text:
Psychiatric diagnosis according to ICD 10
\r\n\tThe objective of this book is to provide knowledge appropriate for students, scientists, both experienced and inexperienced horticulturists and, in general, for anyone wishing to obtain knowledge and experience on the topic of olive culture (and increasing productivity and improving product quality).
\r\n\tIt will cover all aspects of production from site selection, recommended varieties, pest and disease control, through to primary and secondary processing.
What is motivation? From a psychological point of view it is a force, of psychic nature, which makes the individual show certain behaviour. Freud said that each behaviour, also the most strange, always responds to a motivation and the motivation's meaning is often unknown not only by people in contact with the subject but also by the subject himself. If we wanted to contextualise motivation within the alliance relationship, we could consider the last one as an interaction between two poles: one is the therapist the other is the patient, each with his own intrapersonal and interpersonal features, in a specific space defined by the setting, motivation is one of the intrapersonal patient's characteristics. Therapeutic alliance is a strong predictor of outcome in individual psychotherapy across diverse treatment orientations and modalities both with adult patients [14], [26] and adolescents [10], [13]. Patient's motivation, within the working alliance, during therapeutic intervention has been much studied [21], [7], [15], [30], [24], [25], [29], whereas the motivation associated with the diagnostic moment has been given less importance in scientific literature [22], [17]. Close to the theory there is clinical experience related to the centre we work in. Longitudinal studies about adolescents' therapeutic compliance and clinical evolution done within our Services [9], [10], [11] showed most of adolescents did not follow therapeutic suggestion about undergoing psychotherapy after the diagnostic process. Compliant and not compliant adolescents were different because of motivation expressed during the diagnostic process: the most of motivated adolescents started therapy, whereas the most of unmotivated adolescents did not. The clinical evolution resulted in association with adolescents' motivation as well: after six months a clinical improvement was statistically more frequent among motivated than among unmotivated adolescents.
These results and other ones from literature, evidencing that an early alliance has been found to be a better predictor of outcome than alliance averaged across sessions or measured in the middle or late phase of treatment [26], [12], stimulated us to think of and to evaluate, during clinical practice, some strategies to favour adolescent's motivation to follow therapeutic suggestion given at the end of the diagnostic process. For this reason we think of a diagnostic protocol which considers, with psychiatric diagnosis (ICD 10) and clinical evaluation (psychopathological investigation), to pay particular attention to motivational aspects. To do that we referred to the experience of interviewing used at the Brent Centre of Young People of London.
Looking at the literature we can deduce that the word "interviewing" has been introduced quite recently. Few authors discussed this process (interviewing) itself. The idea of "Interviewing" with adolescents at the Brent Centre comes from the belief held by M. Laufer that most adolescents were not able to engage in and make use of long term psychoanalytic psychotherapy without some preparatory work, as theorized by Freud (the development of the "observing Ego"). The word "assessment" wasn't used because it reminded to a psychiatric meaning. When the Centre was founded adolescents could come and "walk-in" for any reason. According to the presenting problem, the clinician provided the connection with the general practitioner (GP), the lawyer or the social worker. The aim was to focus on vulnerable adolescents to work on the accessibility, the potentiality for making therapeutic connections. It was considered to work on a long term base and to involve only trained analysts because it takes time and experience to modify the defenses. The results of the first researches showed that the Centre was working with severe neurotic patients and it was considered extremely important to engage the adolescents in order to offer a preventive help. P. Wilson [32] linked intervention in adolescence to the developmental model conceptualized by Laufer and stressed the importance of making an assessment before starting any kind of intervention: " Whatever the extent of intervention, it should be based on an assessment of his feelings about himself, his body and relation to his parents, and designed to contribute towards facilitating progressive movement and so serve to prevent breakdown and the possibility of mental ill-health in adulthood". From his words, it's possible to consider the interviewing as the preliminary work with the adolescent in which there is an assessment about his way of coping with the adolescence tasks. In 'Adolescence and developmental breakdown' [17] it is again stressed that the application of the developmental model to the assessment of psychopathology in adolescence is fundamental to make further decisions about management and treatment of the adolescent. The word "interviewing" appears in the paper written by C. Bronstein and S. Flanders in 1998 [4]. In it, the emphasis is put to another meaning of this process, linked to psychotherapy. The process that develops in this first contact with the adolescents we call interviewing, though it could also be described as psychotherapeutic consultation. It is stressed that a mere assessment followed by therapy can't give the adolescent the possibility to understand what therapy means, leading to a further drop out. It means that the aims of interviewing are both to assess the extent and the nature of the patient's disease and to give the adolescent the possibility to express his feelings and fears, to come into touch with anxiety, to make the "unknown" less frightening. Another aim of the interviewing process could be to set up the framework for further treatment, if this is considered necessary. It means dealing with "plans, arrangements, preparation, undertakings" because it can allow the adolescent and his parents to understand better the meaning of further treatment. It is stressed the importance of making the adolescent an active part of the process and of involving him in it. For example the interviewer can use the explanation to make easier the understanding and to involve more the adolescent; the adolescent is made aware of the interviewer's concerns and of severity and implications of his problems in his present and future life. On the other hand the interviewer has to guide the intervention. Any reaction is "within the strict limits set by our specific role" [19] and it is important to avoid collusion, carefully not trying to take sides and allocate blame [18]. It's also part of the process setting up the framework of further treatment, if it's necessary. It means helping the adolescent and the family in understanding the meaning of the therapy but also talking together about practical problems [17].
The study involved patients attending the Daily Service for Adolescents at the Neuropsychiatric Unit for Children and Adolescents in Padua. The main purposes of this service are the care and rehabilitation of adolescents with severe psychopathological disorders (mood disorders, psychotic disorders, antisocial behavior and personality disorders), particularly optimizing their welfare and providing intervention for these young patients through an integrated clinical and pedagogical approach. Various professional figures cooperate on the therapeutic project and this multi-professional team includes a child and adolescent neuropsychiatrist, a psychologist, two educators and a social worker. Adolescents attending the center undergo an initial diagnostic process, leading to a psychiatric diagnosis formulated according to the ICD 10 [33] and the therapeutic project involves attending a day center.
The centre receives adolescents (males and females from 12 to 18 years of age) with various types of psychiatric and behavioral disorder of moderate to severe degree: it has a capacity to treat approximately 25 patients in all and can simultaneously accommodate up to six adolescents, with the ratio of one operator to every two patients.
The adolescents attend from Monday to Friday from 09.00 to 17.00. Access to the structure is based on individual projects prepared by the team, which establishes the number of weekly visits and their duration. The educators can also implement tailored and/or home-based interventions in situations where an adolescent suffers from significant social isolation, and in acute cases requiring temporary hospital stays, acting as companions and providing support while the patient is in hospital. Patients can also be received in emergency situations (moments of acute crisis, or when a "buffer intervention" is needed while a patient is waiting to join a residential community). These latter interventions do not follow the normal enrolment protocol.
The general goals of the service are:
to optimize the patient care and education measures for adolescents in situations of particular mental illness and at particularly crucial times;
to support the families in their educational role;
to construct an integrated clinical and pedagogical project with the various services on different levels and with different institutional roles;
to improve the social involvement of adolescent in their living environment.
The multidisciplinary team consists of: a developmental neuropsychiatrist responsible for the service, a psychologist-psychotherapist, two educators, a social worker, a coordinator, and an administrative assistant.
There are also trainee psychologists, trainees on the degree course for professional educators at the Faculties of Education Sciences and Psychology, and physicians training in developmental neuropsychiatry.
The team holds the following meetings:
a weekly meeting to coordinate their clinical-pedagogical work and program the educational activities;
a weekly team meeting to discuss the cases;
periodical meetings with social-sanitary operators and clinicians to report on the cases being treated in the semi-residential setting to discuss the clinical issues, assess the adolescent's progress, and recommend new patients for the treatment;
a monthly supervisory team meeting with an outside psychiatrist-psychotherapist.
The phase for assessing and enrolling an adolescent at the semi-residential center for adolescent psychopathologies is completed according to the following protocol.
The case is presented to the team operating at the semi-residential service for adolescent psychopathologies by the psychologist or neuropsychiatrist proposing their enrolment at the Neuropsychiatric Unit for Children and Adolescents and a file is prepared for the patient being recommended.
The case is discussed and, where applicable, a preliminary period of observation and assessment of the adolescent is decided.
A meeting is held with the patient and family to formalize the proposal to start with a preliminary period for the adolescent to get to know the semi-residential service. In addition to patients and their parents, this meeting is also attended by the clinician referring them and an educator.
The observation period starts, normally involving four meetings according to the following schedule:
the first meeting is for introductions, observations and free activity (playing, computer, exploring spaces);
the second meeting is when an observation file is completed (a semistructured interview) by a "third party" educator, i.e. an educator who has had the least to do with the adolescent so far, in order to guarantee the utmost neutrality in the administering the assessment tool. Then activities are proposed in small groups to see how the adolescent functions in group situations;
at the third meeting activities are proposed on the basis of the adolescent's interests emerging from the previous interview;
the fourth and last meeting is where, in addition to the activities already begun at the third meeting, there is also space for a conversation and exchange of ideas with the adolescent, to provide feedback relating to the previous meetings, the adolescent's mode of participation and greater or lesser willingness to enroll at the semi-residential center.
The reference educator completes an initial observation file on the trend of the four meetings.
The team assesses the observation period within two weeks after its completion and decides whether to recommend that the adolescent continue with the semi-residential experience or terminate it.
The patient and family are informed about the child's progress so far and there is an exchange of ideas relating to the adolescent's and the family's experiences and motivations. If all concerned agree to the semi-residential program, this decision is shared and signed jointly by the family and by the physician referring the case to the team, and these parties agree on a first integrated, tailored therapeutic and educational project, and an initial schedule for the adolescent's attendance at the center.
This phase is completed by the working team and the object is to prepare a first project in the light of the findings during the preliminary observation period. A record is made of patients' and their families' demographic details, the motives for enrolment on the program, the internal and external activities conducted, the established goals, the general and specific objectives of the course of therapy, a description of the integrated intervention designed for each adolescent of and the timing for assessing their progress and the project.
Access is always formulated on the basis of a tailored individual project and the adolescent's weekly attendance is constantly monitored. Punctuality and adherence to the agreed frequency of attendance is an important tool for assessing the adolescents' and their families' compliance with the agreed educational project, as well as being a necessary premise for implementing the semi-residential program. For each patient, a schedule is agreed with the family, the specialist and the adolescent concerned, starting from a minimum of two attendances a week (lasting four hours each).
For each patient, there are periodical clinical meetings with their own doctors to monitor their psycho-developmental trends and personal response to the therapy. The parental couple is also followed up with regular meetings with a clinician (neuropsychiatrist or psychologist), possibly with the support of an educator.
This action on the families needs to be supported and empowered to help parents establish a different image of their child from the one they knew before, and make sense of the changes taking place in the child during the period in semi-residential care, as well as providing input on how the parents themselves need to respond to the child on a daily basis. A course of psychotherapy proper for both the adolescents and their parents is often recommended and implemented.
After the first six months of attendance at the semi-residential centre, the educational project is reviewed, and the goals and/or operating methods are expanded and/or diversified, based on a first structured assessment of the adolescent's progress that involves completing and checklist of specific indicators relating to the various areas of intervention (relational, social, autonomy).
The ongoing assessment of the adolescent's progress is based on various methods:
periodic team discussions,
periodic meetings with reference clinicians,
periodic meetings with family,
periodic meetings with teachers,
periodic assessment of files completed by the reference educator,
observation/assessment charts recorded before and after laboratory activities,
the periodic administration of standardized tests (YSR 11-18) [1] at the baseline, when the patient is taken into care and subsequently every six months,
the periodic completion by the team of the Global Assessment of Functioning test [31] (at the time of compiling the therapeutic and educational project and subsequently every six months).
This assessment and constant monitoring procedure enables the ongoing adjustment of the objectives of the integrated individual projects, which is normally done every 3-6 months. The tests can also be used as a tool for pre-and post-assessment of the effects of the intervention at the start and end of a specific laboratory activity to evaluate it efficacy.
The end of the course of therapeutic intervention can be decided by various factors. In the most favorable of outcomes, the project may be concluded because the preset goals have been achieved and the adolescents have regained their social contacts and schooling experience, and the course of therapy undertaken can be consolidated.
Attendance at the centre may also be interrupted due to poor compliance on the part of the adolescent and/or the family (with repeated and unjustified failures to attend appointments at the semi-residential centre or meetings with clinicians, or inadequate cooperation). The program may also be stopped by the need to include the patient in a residential community. In each case, the conclusion of the project is confirmed during the course of a final meeting attended by all the parties involved (the adolescent, the family, the reference educator, the psychologist and the neuropsychiatrist).
The object of the pedagogical activities is to support the adolescents in the course of their development by means of a relationship with the figure of the educator, who serves as an "auxiliary ego" and consequently as a supportive companion. This is achieved by providing a space, which takes practical shape in the rooms at the semi-residential centre, and by designing a project that involves customized objectives and timings.
In experiences of research applied to different educational settings, various functions have been identified on which the educator's action is concentrated. The educator thus has several functions [23], [28]:
as a mediator between the adolescent and the adult world,
to provide protection in relation to the adolescent's interior conflicts,
to accompany the patient on a path towards a normalizing educational context,
as containment, providing stability and helping the adolescent to manage the dynamics of his/her daily life.
The general educational goals of the educational process providing the starting point of an individual educational project tailored to each patient include:
helping the adolescents to gain awareness of their own sentiments, impulses and behavior;
helping them to test their abilities in a protected setting and to raise their self-esteem;
helping them to realistically assess their living environment.
The activities in which the psycho-educational process takes shape are designed to achieve the individual objectives of each adolescent's project and rely on fundamental tools, such as providing a setting as a framework in which to enable to the experience of meeting, using the operator's capacity for empathy to create a relationship that can help the adolescent to let their emotional experiences resound inside themselves and thereby increasingly gain control over them, promoting organized behavior patterns, abilities and motivations that can pave the way to satisfactory social relations and an adequate performance in the completion of tasks and the achievement of goals. During their attendance at the center, the adolescents conduct activities designed to develop their personal interests, acquire skills and reinforce their self-esteem. Outings, the preparation of a newspaper, painting, watching films, playing, writing, and dramatizations are activities conducted at the center, individually and in small groups, in the constant presence of the educators. There are also structured laboratories involving pet therapy, horse therapy, art therapy and naturalistic experiences at teaching farms organized in cooperation with other associations, as well as participation in therapeutic winter and summer holiday camps. For many young people, these activities are the only opportunities they have to put themselves to the test away from their usual living environments, to measure themselves against an adventure outside the home, and thereby testing their capacity to manage on their own, to experiment with detachment from the family, to live in groups and share the group's behavioral rules.
Finally, courses are also organized to support the adolescents' formal education in cooperation with their schools. This involves formulating tailored teaching programs and the presence of teachers at the semi-residential centre.
Sample is formed by adolescents who, during a semester, consecutively came to the Neuropsychiatric Unit for Children and Adolescents in Padua, Italy, requesting a psycho diagnostic evaluation and then were suggested to undergo multimodal intervention at the Daily Service for Adolescents. The main purposes of this service are the care and rehabilitation of adolescents with severe psychopathological disorders (mood disorders, psychotic disorders, antisocial behavior and personality disorders), particularly optimizing their welfare and providing intervention for these young patients through an integrated clinical and pedagogical approach. Various professional figures cooperate on the therapeutic project and this multi-professional team includes a child and adolescent neuropsychiatrist, a psychologist, two educators and a social worker. They are 50 individuals, 33 males (66%) and 17 females (34%), aged 13 to 18 years (mean 15,6 y.). The only exclusion criteria were age below 13, chronic rather than acute psychotic state, QI < 70 and presence of known organic pathology associated with mental disease.
Neuropsychiatric consultation was articulated into 5 diagnostic interviews with adolescent and his parents, separately. The last session was deputed to communication of psychiatric diagnosis and therapeutic suggestion. We added to this protocol, which was the usual one, another semistructured meeting finalised to the discussion about therapeutic indication. This difference with respect to usual diagnostic protocol (where the diagnostic communication and therapeutic suggestion formed the last meeting with the adolescent) was set up with the aim of giving information about semiresidential treatment (what it is, how it works, what it is useful for) (1) and raising adolescent's questions, doubts, fantasies and anxieties about therapy and to talk about them with the specialist (2); the hypothesis was that giving voice to these issues and receiving information could be useful to create motivation towards multimodal intervention.
Adolescent's motivation was evaluated at the beginning and at the end of the diagnostic process, considering these three elements according to Marcelli and Bracconier [23]:
Awareness of the disease,
Worry about his/her own psychological state,
Self observing and describing capacities.
Recognising and admitting an uneasy state is the first step to deal with it. Being preoccupied with it means to be in touch with anxiety caused by one's own condition and to hinge on this to desire to change. Having the capacity to self observe and describe means to be in touch with one's own inner world and to quite tolerate anxiety coming from conflicts.
An anamnesis schedule collecting data about adolescent's identification, his/her family, psychosocial situation and clinical elements was filled in for each subject.
The psychiatric diagnosis was formulated using ICD 10 [33]. Additionally, we grouped subjects into three categories according to the severity of the psychopathology and pathologic personality organisation as described by Kernberg [16]. Neurotic personality organization is characterized by psychostructural conditions that include: 1) intact reality testing, 2) a consistent sense of self and of other people, and 3) generally rely on mature defense mechanisms when stressed. At the opposite end of the personality organization dimension are severely disorganized personalities, the Psychotic one which is characterized by: 1) severely compromised reality testing, 2) an inconsistent sense of self and others, and 3) utilize immature defenses. Along the middle of this dimension are personalities organized at the borderline level: 1) the syndrome of identity diffusion, 2) the predominance of primitive defensive mechanisms centering around splitting, and 3) maintenance of reality testing.
Data about patient's therapeutic compliance and clinical evolution were collected during a visit of control after nine months by the last diagnostic session. They are based on both what was referred by the patient about subjective perception of health state and on what the specialist verified about psychosocial functioning changes in a nine months period. Clinical evolution was evaluated throughout the Global Assessment Functioning Scale (GAF) [31], which was filled in before and nine months after the beginning of the semiresidential intervention. The GAF is a scale used by the operators to rate a patient's psychosocial functioning and activities, regardless of the nature of their psychiatric disease. It corresponds to Axis V of the DSM IV [2]. The GAF scale comprises 10 levels (further divided into 10 points) and each patient is assigned to a given level on the strength of a scoring system: the higher the score the better the patient's psycho- social functioning. The patients were retested nine months later: an improvement was considered when the GAF score changed to an upper level, an unvaried situation when the score remained in the same level and an aggravation when the score decreased to an under level with regard to the initial scoring.
Statistical analysis: data analysis considers the variable motivation in relation with gender (male/female); age (13-15 years old, 16-18 years old); educational level of family - valued on parent's education degree (low, middle, high); arrival status (voluntary, by referral); support by parents - evaluated by empathetic capacities towards adolescent, availability to come to the interviews, collaborative capacities about therapeutic project (supportive family, not supportive family); diagnosis (ICD 10); compliance with therapeutic project (in therapy, drop out, therapy never started); nine months follow up (better, unvaried, worse).
The data are expressed as frequencies and percentages. Variables are expressed using nominal and ordinal scales. Cross-tabulations were analyzed using the chi-square test, considering P<0.05 as significant. The analyses were performed using SPSS rel. 14.
The sample is formed by 50 individuals, 33 males (66%) and 17 females (34%), aged 13 to 18 years. They were divided in 2 age groups: 13-15 years old (24 subjects, 48%) and 16-18 years old (26 subjects, 52%). 6% attended primary school, 36% secondary school, 56% college and 2% had abandoned school. Gender/age cross tabulation shows that males are younger (61% in age range13-15, 39% in age range16-18) than females (23.5% in age range 13-15, 76.5% in age range 16-18). The family's educational level the adolescents come from, results low in 18%, middle in 62% and high in 20% of cases. Arrival status is by spontaneous request for psychodiagnostic consultation in 40% of cases and by referral in 60% of cases. Diagnosis are summarised in table 1, where comorbility is referred to depressive mood disorder and personality disorder.
|\n\t\t\t\tDiagnosis (ICD 10)\n\t\t\t\n\t\t\t
|\n\t\t\t\tPercent (%)\n\t\t\t\n\t\t
|anxiety disorders\n\t\t\t
|mood disorders\n\t\t\t
|psychotic disorders\n\t\t\t
|personality disorders\n\t\t\t
|behaviour disorders\n\t\t\t
|eating disorders\n\t\t\t
|mental retardation\n\t\t\t
|comorbility (depression and personality disorder)\n\t\t\t
Adolescent's motivation has been evaluated on the basis of three elements: knowledge of a disease, preoccupation about personal psychological state and self observing and describing capacities. Three categories have been individuated on the basis of this evaluation: motivated adolescents –38%-(who recognise the disease, are worried about it and desire to change it), indifferent adolescents –34%-(who admit and describe the disease, but do not seem worried and tend to minimise their psychological condition) and contrary adolescents 28%-(who arrive to the service obliged by parents, do not recognise a disease and say that it is others' fault if they are there) (graphic 1). The difference between indifferent and contrary categories, considering the psycho-relational way of functioning, is the dimension respectively passive and active which characterizes their resistance to meet the clinician.
The motivation, evaluated at the first interview, shows that less than half of the cases (38%) agrees on diagnostic process. This result suggests that adolescent's motivation to be helped is an aim of an intervention rather than an assumption. This is confirmed by literature [23] and agrees with the result about arrival status which shows that more than 50% of subjects came because they were referred by others rather than coming by themselves and also in this last case, the visit was requested by parents and not by the adolescent. We wanted to determine whether the variable initial motivation was significantly different among groups defined by gender, age, educational level of family and diagnosis. Statistical analysis evidences that diagnosis, gender and educational level influence in some way adolescent's initial motivation. Actually, distribution of initial motivation in adolescents grouped for sex, educational level and diagnosis is not casual, while age doesn't seem affect initial motivation like the other factors (tables 2, 3, 4 ).
|\n\t\t\t\tInitial motivation categories\n\t\t\t\n\t\t\t
|% within gender\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within gender\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within gender\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|Chi-Square Tests\n\t\t\t
|Asymp. Sig. (2-sided)\n\t\t\t
|Pearson Chi-Square\n\t\t\t
|\n\t\t\t\tInitial motivation categories\n\t\t\t\n\t\t\t
|\n\t\t\t\tfamily\'s formal education\n\t\t\t\n\t\t\t
|% within education\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within education\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within education\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within education\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|Chi-Square Tests\n\t\t\t
|Asymp. Sig. (2-sided)\n\t\t\t
|Pearson Chi-Square\n\t\t\t
|\n\t\t\t\tInitial motivation categories\n\t\t\t\n\t\t\t
|\n\t\t\t\tpsychopathological categories\n\t\t\t\n\t\t\t
|% within diagnosis\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within diagnosis\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within diagnosis\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|% within diagnosis\n\t\t\t
|% within motivation\n\t\t\t
|% of Total\n\t\t\t
|Chi-Square Tests\n\t\t\t
|Asymp. Sig. (2-sided)\n\t\t\t
|Pearson Chi-Square\n\t\t\t
With respect to gender (table 2 a), motivated are prevalently females, while indifferent and contrary are prevalently males; these differences are statistically significant (p=0.033). This could be explained by the general tendency of females to be more reflexive and capable of insight than males teenagers, added to the fact that in our sample females are older than males and then more mature.
With regard to the educational level of family (table 2b), the most of motivated adolescents come from family with a middle educational level, the most of indifferent come from family with a low educational level, and contrary prevalently come from family with high educational level (p=0.033). Considering initial motivation in relation with nosographic categories, anxiety disorders and eating disorders are the most frequent diagnosis among motivated; acute psychosis, mood disorders and borderline mental retardation (70<QI<85) are more frequent among indifferent; conduct disorders and personality disorders are prevalent among contrary adolescents (p=0.007).
We considered motivation categories in relation to Kernberg's personality organisation categories too. It is interesting to note that the association between motivation categories and personality organisation categories (motivated -nevrosis, indifferent- psychosis and contrary- borderline), as showed in table 2c, reminds about the kind of bond that usually characterises the clinical relationship with the patient according to different psychofunctional level: the neurotic one (patients motivated to get better given their good reality test and a differentiated sense of social tact and sensitivity), borderline one (patients ambivalent and often oppositive towards therapist, given their lack of capacity for a mature empathy with others, and a lack of mature evaluation of other people, who are seen either as idealized, persecutory or devalued persons), psychotic one (patients often not conscious of their diseases, with a rigid relational modalities and then mainly indifferent towards therapy).
The aim of the diagnostic process, and overall aim of the last interview, was to create a relationship with the patient whose objective was to become aware of the disease and to want to change. So we tried to change the situation where the specialist evaluates the patient and at the end delivers a verdict - instead we tried to build a collaborative relation with adolescent where the main objective is to give a sense to the symptoms, to verify where the adolescent had stopped and to make the therapy to be perceived as something useful.
Motivation at the beginning of the psychodiagnostic process
Adolescent's motivation was evaluated again at the end of the diagnosis process (basing on the same elements). The result was an increase of motivated and a decrease of indifferent and contrary adolescents (scheme 2), without relevant difference regarding gender within the three categories (p=0.19). The relation between motivation and diagnosis looses statistical significance too (p=0.09), whereas educational level remains significant in regard to adolescent's motivation (X2=11.38 (DF4), p=0.023). This result suggests that sociocultural aspects (like educational background) influences thinking capacity more than other more constitutional factors (like gender or psychiatric disorder); moreover, it could make operators inclined to differentiate the way of approaching psychopathology in case of particular cultural conditions, like the realization of more supportive rather than expressive intervention with people coming from a low socio-cultural background. It is interesting to note that the change to a motivated category is bigger among contrary than among indifferent adolescents: actually first halved during the diagnostic process, showing major capacities of mobilization (compare scheme 1 and 2). This could be linked to what was said before about the psychopathological features of these subjects: indifferent who are mainly psychotic organised are characterised by a defending setting and a psychorelational functioning which are less flexible and changeable than the one of contraries who enter mainly the borderline and neurotic psycho structural organisations.
Motivation at the end of the psychodiagnostic process
Evaluation of adolescents and their family showed, among contrary subjects, high frequency of difficult relationships and conflict with parents. This aspect seems preponderant in influencing the adolescent's feeling towards the specialist and psychological space. It is as if the difficulty with the parents is expressed by the difficulty and refusal in regards to psychiatric consultation, to which the adolescent has been lead by parents rather than coming by him self. In these cases, focusing on problematic relations and working on the relationship with the parental couple in terms of separation/ individuation, seems to favour the use of psychodiagnostic space as one's own rather than as something to be used to attack parents. This was shown by contrary adolescents as major capacity to thinking for them selves, to recognise personal difficulties and to accept help to sort them out. Contrary adolescents, even if more oppositional evidently, are more "malleable" than indifferent adolescents whose defences are rigid and whose emotive distance makes it difficult to establish an emphatic relationship.
A nine months follow up have permitted verification of therapeutic compliance and clinical evolution. 84% of the adolescents are compliant, 8% have dropped out and 8% have never started psychotherapy. 62% of the adolescents have improved, 34% have not varied and 4% have got worse. There are significant statistical differences both in regard to therapeutic compliance and clinical evolution: motivated and indifferent adolescents mainly follow the therapeutic suggestion at the end of the diagnostic procedure, whereas contrary do not even start therapy (p=0.006) (scheme 3). In parallel after nine months motivated get better, indifferent do not vary and contrary adolescents do not vary or get worse (p=0.000) (scheme 4). The evidence of a missed clinical improvement nine months later even if indifferent are compliant for 90%, suggests - and confirms what said before about that - the presence of stronger rigidity of personality structure and defence mechanisms and/or necessity of a longer period to get better in these subjects.
Motivation in relation with therapeutic compliance after nine months by the beginning of the semiresidential treatment.
Motivation in relation with outcome nine month by the beginning of the semiresidential treatment.
This result is relevant because it indicates that adolescent's motivation is linked not only to therapeutic compliance but also to therapeutic efficacy. In fact the elements we considered to define motivation are significant ingredients to build an alliance relationship; this one is an important factor in regard to efficacy of therapeutic process [20], [14], [5], [8],[3].
Significant, statistically only in the latter case, the result about parents' collaboration in regard to therapeutic compliance and clinical evolution: 10% of adolescents do not start multimodal treatment or drop out among supportive families, whereas the percentage becomes 30% among not supportive families. With respect to clinical evolution: nine months later there was a clinical improvement in 73% of cases with supportive families, while the improvement regarding 31% of subjects with not supportive families (p=0.005).
This data seems to indicate that parental support for adolescents is more important to the efficacy of intervention than to compliance, as if adolescent's motivation was fundamental to start treatment, but then the family's support becomes significant as well to get clinically better.
Yesterday R's mother (Mrs A) phoned to confirm the appointment and asked if it would be possible to speak to me before his son would. Today Mrs A arrived at the Institute on time and the secretary found her screaming asking for someone, from the balcony upstairs on the first floor. Mrs A said she couldn't find anyone immediately upon entering the building and she didn't know where to go. Mrs A asked the secretary if she could speak to me before I saw R (R was waiting into the car). The secretary said she could spend the first 10 minutes with me whilst R was present – then she went to get R.
After I had introduced myself, we entered the room together and R's mother started to speak to me about R. "R has been suffering panic attacks for 4 months, he has got very nervous, he can't sleep, he has a lot of difficulties with his exams, he needs help in facing going to university, panic attacks, girls…" Furthermore she asked for medication to help him to sleep. She was very agitated and I felt R's anxiety rising while she was speaking. After a while I asked her to leave and wait for R. Then I asked R what he thought and he replied that what his mother had said was true, and he started to tell me about his panic attacks. They started since February when he had to do his first exam. He was at home, having a shower; his heart started to beat faster, he couldn't understand what was going on and he went to his mum (who was in the kitchen) to ask for help. I wondered within myself what he was doing or thinking while having a shower. His mum suggested he drink a glass of water but it didn't work. His legs and arms started to tremble and he was not able to control them. So his mum took him to the hospital where he had a lot of tests; everything was all right medically.
The second panic attack came a month later, at home too, nobody was in. R called his dad who went home and took R to the hospital again. Then panic attacks became more frequent: until two weeks ago they were every day. During these two last weeks R has been feeling a bit better (the exams have finished). His General Practitioner (GP) did not prescribe any medication, instead he suggested R come to the Service. I asked him what he thought about that and he answered he preferred not to take medication at that moment. I asked him about University and he told me the choice to go on to study was a very important one. Before he had been working at his stepfather's shop for nearly one year. Now he has to study a lot, he has no more time for friends and recreation. His life consists of going to university then coming back home and so on again, every day. He did not look worried or sad saying this. He doesn't want to give university up "even if it causes my panic attacks". His words made me remember that his mum had said that 'there are guys who are able to study and guys who aren't able to bear the burden and R should understand if he's able or not; he could eventually leave university…'
After about 20 minutes someone knocked on the door, twice. I went to open it and it was R's mum who wanted to tell me she'd wait for R outside, in the car. In the meantime she was trying to look behind me to see R, at the same time, looking at me making a lot of signs with her face and her hands as if to say "is it all right with him?" I closed the door with a gentle smile and went back to my seat feeling annoyed; I looked at R with a questioning glance. He did not say anything about his mum, he did not seem ashamed or embarrassed or annoyed. He seemed to me a bit relieved instead. I asked him more about his parents: R's mum is from South Italy while his father is North Italian. They divorced when R was 6 because his father had an affair. His mum, who now is a housewife, has been living with another man for 10 years. He told me about the first time he'd met his mother's partner, saying that he'd liked him from the start.
R said he gets on very well with both his dad and his stepfather. It seemed to me it was very important for R to tell me that everything is all right with his family. This picture (intrusive and anxious mum, close family, worry about school, not many friends) gave me the image of a little boy, even though I was listening to a tall, broad, handsome man of 18 years. I felt a sort of big gap between his physical appearance and the way in which his mum treated him plus the way in which his symptoms seemed to ask for care. R was very keen to go on with interviews (what struck me was that he spoke about finding a way to face panic attacks rather then a way to rid himself of them). We agreed to see each other next week at the same time.
R arrived on time, brought by his stepfather who waited for him outside. R had had his hair cut and he was wearing a cap that he did not take off. He started to tell me about his last panic attack that had happened while he was reading an article about a 12 y.o. girl's death. R told me that horror films made him have panic attacks as well. I asked him what he'd felt about the girl's death and he was able to say only that he'd felt strange "how can things like that happen?" Then he told me yesterday he went to his GP who prescribed R some medication (paroxetine) for his shaking. He went on to speak about his panic attacks, how they happen, how he feels and so on, talking very fast and repeating the same things. R links them to the fear of exams, stubbornly, as if he had to convince himself about that.
R said he gets very anxious thinking about his exams. I asked him what he's scared of. He's scared of failing. What could happen if you failed an exam? R answered he wouldn't know what to do. I asked him if it's something to do with him only and he said that he's worried what others could say about him too. He was getting very anxious so I asked him what he was going to do after his graduation. He seemed relieved to change the topic and said he'd like to get a job and a house. I asked him if he would like to live with anyone; he answered it doesn't matter. I asked him about girlfriends: he has never had one and he doesn't care...now he has no time to think of this. He told me he used to speak with his mother about these things, also because she asks him a lot...even if it is not so easy and a bit embarrassing too, he added. I wondered whether he wouldn't find easier to talk to his father about things like this, "between men"…R looked a bit thoughtful then said that yes, probably it'd be easier.
What about friends? He has a few good friends, but now he has no time anymore to go out with them. I asked R what his mum would think about him going to live on his own. R said that it would be difficult for her to accept, but she knows it'll happen one day. He told me he gets on very well with his mum, she's very supportive and that's been very important for R. I asked R if anyone else in his family was suffering panic attacks. He, looking as if he had been discovered of some secret, answered that his mum had had panic attacks too, when she was the same age as R. According to this she used to tell him not to worry because "panic attacks are going to stop spontaneously". He did not look very sure about this. His voice and way of talking made me ask him whether he's worried about his mum. "Yes" he said "because she's worried about me". I took up it looks like a sort of vicious circle and R agreed but he did not add anything else.
R likes music very much; he can play the piano (he had studied in a music school for some years). His dream is to become a musician…I took up he had chosen quite a different subject (computers) and R said it was because after you qualify you can get a job easier.
Towards the end of the session I asked him how he felt and he said with a smile he's feeling much better, he needs to talk to somebody about himself and what's happening "I should have come before". I thought he had been saying only a little of the whole and the way in which he used to speak about his panic attacks (using the most of our sessions talking about them) seemed to me a sort of defense for avoiding different topics or for not telling me something deeper.
R's mother phoned to the service saying that R wasn't very well so he could not come today. He'd phone when he was better. The secretary who answered the phone, told her we would send a new appointment anyway and R's mum said not to do that because R would phone when he felt ready to ask for another appointment.
It was phoned for another appointment.
R arrived on time, he looked anxious as usual, but smiling. As soon as he sat down he started to say that he feels much better. I asked him what had happened (I was referring to last missed interview) and R told me he had managed to confide in his father about something he had been keeping to himself and that had been really hard to bear. He added it had been easier to speak between men and his father had supported and reassured him, so now he feels really well. Furthermore the day after he had spoken with his dad he managed to speak to his mum as well "so now it's all sorted out". He told me when the first panic attack came he was masturbating under the shower. He felt he had damaged his body, he felt really ashamed and scared at the same time. Until now he has been feeling that something wrong had happened to him, he's been fearing he couldn't masturbate anymore, he's been fearing about what might happen with girls…. Now the truth has come out he feels really better. It's all over. He has no fear anymore; he has not had panic attacks since he managed to talk about it. I asked what his mum had said. She had told R he shouldn't have worried, that's normal, besides the same had happened to his father years ago (!). The mother told him she thought it might be something to do with sex and now he has told her she feels better. R told me he should have spoken before. I commented he'd probably needed a period in order to understand and to face a lot of feelings that had been coming out, not always easy to deal with. He agreed and repeated he had felt really ashamed and guilty. In particular, he had been scared of what his mum could have thought about him. I took up that it was difficult to say such personal things to his mum, especially now that he's growing up, and that growing up could be also be something to feel guilty about. He agreed and said it had been very important to speak to his dad before…because he's a man.
We spoke a bit about girls; R got a bit anxious and it seemed to me he wanted to censor the topic. He repeated he's very well, he wants to go on with University, he's able to go out again and so on. I felt he was censoring interviewing as well so I asked him openly what he had thought about continuing to come here. He seemed relieved by my question and answered that he felt he had received the help he needed and that he was very grateful. I proposed to him to take some time to think about that and to see each other next week again…he seemed more agitated and in trouble, then he repeated his thanks for the help he has received and that he preferred to stop there, because he was really OK and he did not need help anymore.
I took up his anxiety (probably linked to sexuality and body) and his fear in facing it: I told him I thought it would be important for him to have a deeper look inside; I also said that, looking at his anxious state, I could feel that perhaps it was too much for him at that moment and that it was important and right to respect his feelings of being scared by those thoughts and emotions. So I reassured R about the possibility of finding someone to help him here, if and when he decides to ask for further help.
We said goodbye each other.
Six months later, R came and ask for psychotherapy. He was chosen a male therapist for him. The compliance has been good from the beginning.
Results of this study suggest that it is possible to work on adolescent's motivation using relational instruments. Data from follow up indicates the importance of preparing the adolescent and his family, since during the diagnosis process, for treatment with the object of fair compliance and clinical evolution. With regard to that this paper suggests that an improvement of interviews, specifically used to discuss therapeutic referral, could be methodologically useful to improve motivation. In conclusion the motivation influences both compliance and clinical evolution, so it is important to pay attention to motivation since the start of the diagnosis process. This study moreover suggests that it is important to work with adolescent's parents too to obtain effective results from the treatment. If we consider that a missed therapy opportunity for psychological disease during the developmental age could become a psychiatric disease in adult age [6], [27], then what mentioned before gains the meaning of prevention too.
First reported by Thomas Addison (1849) as an atrophic gastritis with autoimmune etiology and co-existing distinctive type of anemia, the autoimmune gastritis (AIG) represents a chronic gastric inflammation with progression to mucosal atrophy, occurring in up to 8% of the general population. Since parietal cells antibodies (PCA) and anti-intrinsic factor antibodies (AIFA) have been first reported by Schwartz (1960) and Irvine (1962), the autoimmune conception of this type of gastritis is recognized. The autoimmune reaction with CD4+ T cells leads to destruction of parietal cells, which are unique cells in the corpus and fundus glands. Therefore, AIG is located in stomach corpus and fundus, which distinguish AIG from other diseases, leading to gastric atrophy (H. pylori infection, drugs etc.). Based on Sydney System, pyloric or intestinal glands replace the oxyntic glands. The consequences of the loss of parietal cells are hypochlorhydria, gastric pH increasement and decreased production of intrinsic factor with concomitant megaloblastic pernicious anemia in the end-stage due to vitamin B12 malabsorption. Patients might suffer from iron deficiency anemia due to hypochlorhydria and inadequate iron uptake. Gastrointestinal symptoms are rarely reported. AIG is often presented with other autoimmune co-morbidities (thyroid autoimmune disease, type 1 diabetes, etc.). Although gastrointestinal symptoms are rarely reported, a malignant transformations, namely intestinal-type gastric cancer and type I gastric carcinoid are observed in respectively 5.3% and ca. 9% of AIG patients [1, 2, 3].\n
Nowadays the prevalence of AIG is difficult to obtain, as the disease occurs asymptomatic in early stages, remains undiagnosed for a long period as symptoms arise with atrophy and mucosal dysplasia progression. Further explanations for the underdiagnosed AIG are the inadequate and not from the right location biopsy sampling and the poor identification of the etiology of anemia, which is one of the AIG manifestations. Estimated incidence is ca. 2% in younger and up to 12% in elderly patients. Studies demonstrate increased prevalence of AIG with advancing age and in patients with H. pylori infection (Zhang et al.). Females are more often affected than males (3:1 ratio), although this has not been consistently observed. Cabreta et al. in their randomized study find no age difference. The reported prevalence of pernicious anemia, which is one of the most typical AIG manifestations, is about 0.1% in the general population and about 2% in elderly (older than 60 years). The prevalence of pernicious anemia does not differ between populations (white, African American and non-white Hispanic). A study of Carmel and Johnson elucidate that African American women develop pernicious anemia at significantly younger age. Association with other autoimmune diseases (autoimmune thyroid diseases - Hashimoto's thyroiditis and Graves' disease, type 1 diabetes, vitiligo, Addison's disease etc.) is documented to additionally increase the prevalence to up to 35%. This consequence determines a multiple autoimmune diseases (MAS) type 3B and 4. Pernicious anemia is present in patients with Graves' disease, Hashimoto's thyroiditis, type 1 diabetes, autoimmune thyroid disease, Addison's disease, primary hypoparathyroidism and vitiligo in 2, 4–12%, up to 4, 2–12, 6, 9 and 3–8%, respectively. Recent data direct the attention to the possible association between H. pylori infection and AIG development in respect to molecular mimicry between H. pylori antigens and the gastric H+/K+ adenosine-triphosphate enzyme (ATPase). Few studies evaluate the incidence of AIG (using histology, PCA positive levels) in patients with iron deficiency anemia (IDA) of unknown etiology. The estimated prevalence varies between 15 and 27%. The profile of patients with IDA and positive PCA are younger females with lower hemoglobin and ferritin levels and who suffer more often from restless legs syndrome. [1, 2, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14].\n
AIG is a chronic inflammation, localized in the gastric corpus and fundus. The inflammatory processes start with lymphocytes and plasma cells infiltration in lamina propria with involvement of deep layers, leading to parietal cells destruction. Because of preservation of relatively normal oxyntic mucosa, a gastric pseudopolyposis appears (also known as "islands in the sea"). The loss of parietal cells results in hypochlorhydria and further in G-cell hyperplasia due to missing negative feedback, leading to higher gastrin secretion in the antrum. A further consequence of the increased gastric pH is the parietal cell pseudohypertrophy. The higher gastrin secretion leads to direct stimulation of enterochromaffin-like (ECL) cells and their proliferation in hyperplastic, dysplastic and neoplastic subtypes that might onset a carcinoid tumor. Pseudopyloric metaplasia ("oxyntic antralization", spasmolytic polypeptide-expressing metaplasia (SPEM)), intestinal metaplasia (IM) and pancreatic metaplasia can be observed. SPEM can be transformed into IM, which represents the replacement of gastric mucosa with intestinal epithelium (small intestinal and colonic). AIG results in microcytic iron deficiency anemia and megalocytic pernicious anemia due to vitamin B12 deficiency [2, 4].\n
AIG and PCA are observed in 20–30% of the family members of patients with pernicious anemia. However, a genetic predisposition has been proposed. Although the association between pernicious anemia and particular HLA haplo/genotypes is weak, studies evaluate HLA DR4, with DR2 and DR5 haplotypes. A genetic heterogeneity is observed in respect to DR3/DR4 genotype, which is found in patients with pernicious anemia and concomitant endocrinopathy. Using murine models, 4 distinct genetic regions of susceptibility genes for AIG were identified (Gasa1, 2, 3 and 4) on chromosomes 4 and 6 and H2 region. Interestingly, three of these genes are nonmajor histocompatibility complex genes and are located on the same locus with those of type 1 diabetes, which could explain the strong concordance between AIG and type 1 diabetes [2, 15, 16, 17, 18].\n
Cell-mediated autoimmunity has a key role for the AIG development. The main trigger of autoimmunity are the 100-kd catalytic α-subunit and the 60- to 90-kd glycoprotein β-subunit of the gastric H+/K + -ATPase, which membrane protein is a proton pump. PCA and AIFA are found in both serum and gastric juice. The higher the PCA titer is, the more severe the corpus atrophy is and the lower the parietal cells concentration is. The loss of parietal cells is a consequence of mainly CD4+ CD25− Th1 resting lymphocyte effectors initiated perforin-mediated cytotoxicity (perforin/granzyme B pathway) or Fas–FasL apoptosis. CD4+ CD25− Th1 resting lymphocyte effectors produce IFN-γ and TNF-α. Submucosa, lamina propria and gastric glands are infiltrated by CD4 + CD25− T-cells, together with macrophages and B lymphocytes, leading to loss of parietal (CD4+ T cells react to H+/K+-ATPase α chain and marginally to the β chain), principal and P/D1 ghrelin-producing cells [2, 5, 15, 19, 20, 21].\n
Two types of antibodies are produced by B cells from activated CD4+ T cells in patients with AIG, namely PCA (antibody to the parietal cells) and AIFA (antibody to the produced by the parietal cells a 60-kDa glycoprotein intrinsic factor). PCA are found in the serum and gastric juice in up to 90% and AIFA in 30–50% of AIG patients. Α catalytic and β subunits of gastric H+/K + -ATPase are bound by PCA. In end-stages of AIG the PCA titer decreases because of parietal cells loss. Researchers have found two types of AIFA from IgG class. Type 1 is present in 70% of patients and acts as a blocking antibody that reacts with the binding site for vitamin B12. Type 2 AIFA is present in 30% of patients and is a precipitating antibody that binds other binding sites from vitamin B12 and impedes binding of intrinsic factor-vitamin B12 to the receptors in the ileal mucosa [5, 22, 23, 24].\n
H. pylori, which is well-established etiological factor for atrophic gastritis development, may induce AIG through mechanisms of molecular mimicry at the T-cell level (autoreactive T cells against gastric proton pump), bystander activation and / or epitope spreading. This hypothesis is supported by recent studies as some patients may have AIG with co-existing H. pylori infection (20–50%). H. pylori leads to development of various antibodies, including PCA and anticanalicular antibodies against the H+/K+ ATPase, which are in fact most frequent. Studies show a high homology between the β subunit of H. pylori urease and the subunit β of gastric proton pump, which is a precondition for cross-reactivity against parietal cells and IFN-γ production, resulting in killing or apoptotic suicide. Some patients with PCA and/or AIFA, who underwent H. pylori eradication, demonstrated loss of antigastric antibodies. However, the correlation between AIG and H. pylori still remains controversial. AIG patients with observed gastric atrophy or IM in the course of H. pylori infection do not decrease their risk for gastric cancer development even after H. pylori eradication [2, 5, 25, 26, 27, 28, 29, 30].\n
AIG is frequently associated with other autoimmune diseases. Emphasized is the link to type 1 diabetes and autoimmune thyroid disease (Hashimoto's thyroiditis and Graves' disease). Reported risk factors for patients with AIG and type 1 diabetes are persistent positive islet cell antibody and positive glutamic acid decarboxylase-65 antibody, which is found in the thyroid gland and stomach except in pancreas and brain. Studies demonstrate that type 1 diabetes itself and not hereditary might be a risk factor for AIG development. Positive thyroid peroxidase autoantibody are reported in up to 50%of AIG patients due to possible cross-reaction. As PCA are verified in up to 40% of patients with autoimmune thyroid diseases, screening the patients of this population for AIG should be recommended. Other reported co-existing autoimmune conditions are polyglandular autoimmune syndromes (mainly type 3B), Addison's disease, vitiligo, perioral cutaneous autoimmune diseases (mainly erosive oral lichen) and myasthenia gravis [2, 4, 7, 31, 32, 33, 34].\n
The evaluation of AIG-associated autoantibodies (PCA and AIFA), anti-H. pylori antibodies (anti-HP-IgG) and markers for gastric atrophy (gastrin and pepsinogen levels) is used for serological noninvasive diagnosis of AIG ("serological biopsy", the so-called GastroPanel test (ELISA test, Biohit, Helsinki, Finland)). AIG-associated autoantibodies are widely used for screening and diagnosis of AIG. They differ according to their sensitivity and specificity as PCA is higher sensitive (80% compared to 50% sensitivity for AIFA) but less specific for pernicious anemia detection. Studies are controversial whether PCA levels correlate with AIG severity or not. Due to low gastric acid output and G-cells stimulation and elevated gastrin secretion in patients with atrophic autoimmune gastritis, it is crucial to evaluate gastrin levels (usually gastrin 17) as gastrin correlates strong with gastric atrophy based on histopathology. Other useful atrophy markers are the produced by the chief cells of oxyntic mucosa of stomach corpus and fundus pepsinogen I and the secreted by the chief cells and mucous neck cells of the whole stomach mucosa pepsinogen II. In patients with atrophic autoimmune gastritis are demonstrated significant decrease of pepsinogen I (low pepsinogen II levels are not commonly observed) and low Pepsinogen I/Pepsinogen II ratio (<3). In respect to diagnosis of pernicious anemia, a panel of vitamin B12, homocysteine and methylmalonic acid measurement is required. In those patients may be observed thrombocytopenia, increased levels of LDH and bilirubin, and rarely schistocytes in the peripheral smear. Iron deficiency anemia, which is often present in patients with AIG, should be identified by levels of hemoglobin, mean corpuscular volume (MCV), serum iron, ferritin, total iron-binding capacity (TIBS) and serum transferrin receptor (TfR). In patients with suspected carcinoid tumor transformation the measurement of chromogranin A, which is secreted by the ECL cells, can be useful, although it shows low specificity (23%) and false-positive results in patients with inflammatory bowel disease, renal insufficiency and other conditions [4, 23, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45].\n
Of a great importance for AIG diagnosis is the performance of gastroscopy with separately collected biopsies - two from the corpus, two from the antrum and one from the incisura angularis (updated Sydney System recommendations). New endoscopic techniques (magnifying endoscopy, autofluorescence and narrow-band imaging) improve the diagnostic accuracy as they provide information for minimal gastric atrophic changes. A number of endoscopic appearances can be present: polyps (hyperplastic or adenomatous), pseudopolyps, flattened rugal folds, visible submucosal vessels, loss of subepithelial capillary network resembling honeycomb, collecting venules in regular shape and appearance and vascular pattern and swelling of areae gastricae. A combination of them improves the sensitivity and specificity of the procedure. In early AIG stages with minimal or no endoscopical and histological changes, gastric acid production is increased due to hypo- or achlorhydria. Thus, gastric acid measurement (simple intragastric pH measurement or volume of acid secretion) might be useful for early AIG diagnosis [1, 4, 46, 47, 48, 49, 50, 51, 52].\n
Histopathological assessment of biopsies form gastric corpus and fundus remains gold standard for AIG diagnosis even in early stages of the disease. The correct site of biopsy is of great importance for the proper AIG diagnosis, which could be tested by immunohistochemical staining of G cells (gastrin). Histological characteristics change with disease progression. Typical but non-specific for AIG are lymphoplasmacytic infiltration in lamina propria, which is mainly multifocal with accentuation in the deeper; glandular portion in early stage and diffuse lymphoplasmacytic infiltration of the lamina propria in end-stage; focal to profound atrophy of oxyntic mucosa with disease progression. End-stage AIG is further characterized by distinct reduction or total loss of oxyntic glands with pseudohypertrophy of parietal cells due to fragmentary oxyntic glands destruction in end-stage of AIG; SPEM presence; pancreatic or intestinal metaplasia; ECL cells hyperplasia with additional samples immunohistochemical testing with chromogranin A and synaptophysin [1, 4, 11, 53, 54, 55, 56, 57].\n
Symptoms vary during the course of AIG as patients at early stages are most often asymptomatic, which makes the diagnostic approach only on clinical presentation challenging. With disease progression a wide spectrum of gastrointestinal, hematological and neurological signs and symptoms arises [1, 3, 4].\n
Gastrointestinal symptoms are not the leading presentation of patients with AIG. Carabotti et al. report in their recent study frequency of one or more gastrointestinal symptoms in 56.7% of AIG patients. Female gender, younger age (<55 years) and non-smoking are independent risk factors for gastrointestinal symptoms manifestation. More than half of the patients had upper gastrointestinal complains as most frequent one was vague dyspepsia in respect to post-prandial fullness and/or early satiation. Furthermore, as achlorhydria is a major pathogenetic consequence of AIG, patients may suffer from bloating, delayed gastric emptying, small intestinal bacterial overgrowth, and gastrointestinal infections such as Clostridium difficile. Pain and peptic or duodenic ulcers are not reported. Atrophic glossitis due to vitamin B12 deficiency is an early stage AIG manifestation. Interestingly, heartburn (24%) and acid regurgitation (12%) are presented in a study of Miceli et al., which could develop from nonacidic refluxes. Data exist to support the observation that gastroesophageal reflux disease and its complications like Barrett's esophagus may develop even in AIG patients [1, 2, 3, 4, 6, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69].\n
Typical hematological manifestations of AIG are iron deficiency anemia (IDA) in the early stages and pernicious anemia in the end-stage of the disease.\n
IDA is the leading hematological manifestation, occurring in 50% of AIG patients as reported by Hershko et al. Several epidemiological studies demonstrate IDA in younger patients prior to pernicious anemia development. Iron metabolism, which is regulated by an uptake, is impaired in AIG mainly due to the presence of achlorhydria. Different mechanisms of IDA with AIG etiology are observed. For the necessary reduction of the ferric form of inorganic iron (the iron type in food) to ferrous as well as for releasing the ferric/ferrous iron from its protein-complex in order to precede to an iron uptake, gastric acid is needed. Another cause for IDA in AIG is the decreased iron absorption due to lack of ascorbic acid, destroyed in AIG. IDA symptoms vary as the commonly reported are fatigue, brittle nails, hair loss, restless legs syndrome, immune dysfunction, ineffective wound healing, while due to anemia itself tachycardia, shortness of breath, dizziness, lightheadedness and cognitive and physical dysfunction may develop. Pregnant women are at risk of early birth and underweight newborns. Of great importance is that IDA with AIG etiology is refractory to iron therapy [1, 4, 6, 13, 20, 58, 59, 60, 70, 71, 72, 73, 74, 75].\n
Pernicious anemia is usually caused by vitamin B12 deficiency due to loss of intrinsic factor and insufficient releasing of vitamin B12 from the food due to low levels of gastric acid. Vitamin B12 is a key regulator of DNA synthesis. Mostly affected are patients at advanced age due to age-related reduced absorption and minimal turnover with further large stores of vitamin B12. The clinical manifestations vary widely; therefore pernicious anemia is so-called "great pretender". Reported symptoms of pernicious anemia are fatigue, lightheadedness, palpitations, angina pectoris and congestive heart failure and mental disturbances. Patients are at increased risk of endovascular dysfunction and myocardial infarction and pulmonary embolism due to hyperhomocysteinemia and the related thrombosis. Therefore, untreated pernicious anemia may lead to lethal exit [1, 4, 6, 20, 58, 59, 60, 61, 76, 77, 78, 79, 80].\n
Neuronal death due to demyelination and axonal damage leads to the typical neurological manifestation of vitamin B12, which might be present even in patients with no hematological changes. The loss of vibratory and position sensations together with distal paresthesias develop from damages in the lateral and posterior columns of the cervical and upper thoracic segments of the spinal cord. This syndrome is called a subacute combined degeneration and is very specific for pernicious anemia. Other vitamin B12 deficiency presentations are peripheral neuropathy (paresthesia and numbness of the lower extremities), optic neuropathy and neuropsychiatric conditions (dementia, mania, depression, psychosis, obsessive–compulsive disorder, etc.). Proper diagnosis and early vitamin B12 substitution are mandatory to delay progression and for better outcome [1, 4, 81, 82, 83, 84, 85, 86, 87, 88, 89].\n
Patients with AIG are at increased risk of gastric cancer development. The estimated prevalence is about 5.3% as recent studies suggest even higher incidence - 14.2 per 1000 person-years with patients with AIG having risk of gastric cancer development 3 to 6-fold higher than the general population. Recent meta-analysis demonstrates 0.27% per person-year with an overall relative risk of 6.8 (95% CI 2.6–18.1) for gastric cancer development. Elderly people, chronic inflammation due to H. pylori infection, achlorhydria, presence of dysplasia and intestinal metaplasia are significantly risk factors for gastric tumorogenesis [1, 57, 90].\n
Gastric carcinoids are verified in 4–9% of patients with AIG and pernicious anemia. 50–85% of all gastric carcinoids develop in patients with AIG. Three types of gastric carcinoids are established, of which type I is found in patients with AIG, type II is associated with Zollinger-Ellison syndrome and multiple endocrine neoplasia I and type III carcinoid is the most aggressive type. Achlorhydria is a key factor for the development of gastric carcinoids in AIG patients. As described, achlorhydria leads to loss of negative feedback and G-cells stimulation in antrum, followed by hypergastrinemia (typical for type I and II carcinoids). The high gastrin levels demonstrate trophic effects on ECL cells hyperplasia, which further may result in dysplasia and transformation into gastric carcinoid. Gastric carcinoids are quite benign lesions with low metastatic potential (less than 10%). Patients with gastric carcinoids are usually asymptomatic. However, they may complain of dyspepsia, abdominal pain, flushing, diarrhea and symptoms of anemia. Classical carcinoid syndrome is seen very rare. Carcinoids are usually diagnosed incidentally during endoscopy in patients with anemia. Gastroscopy with biopsy sampling with further immunostaining for chromogranin A and/or neuron-specific enolase is the best diagnostic approach. The presence of polyps in the stomach body in patients with AIG is significantly associated with type I carcinoid. As long as polyps might be underdiagnosed during endoscopy, serum chromogranin A levels are more accurate for carcinoids diagnosis. Chromogranin A levels correlate strong with gastrin levels and ECL cell density in the corpus and fundus mucosa, representing high specificity (59%) and sensitivity (100%). According to the algorithm of Gilligan et al. based on size and number, gastric carcinoids in AIG patients, which size is <1 cm and the number is 3–5, should be removed endoscopically, and those >1 cm and/or > 5 should be followed by antrectomy. Surveillance at every 6-month is proposed. Another therapeutic option is the administration of octreotide, which leads to lower gastrin levels, improved ECL status and even spontaneous regression (Ferraro et al.) [1, 2, 4, 45, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110].\n
The chronic inflammation, which is an integral part of the pathogenesis of AIG, increases significantly the risk of malignant transformations. Achlorhydria, high dietary salt intake and bacterial overgrowth are proposed risk factors. Furthermore, the concomitant H. pylori infection additionally increases the risk of precancerous lesions. Current studies suggest that cancer stem cells, which might be exposed on mutations, have an important role in cancerogenesis. This concept is assumed as stem cells are well-known for their longevity and inherent capacity for self-renewal. As a consequence of chronic inflammation, stem cells level and proliferation potential increase, which favors their intestinal metaplasia (possible phenotype of stem cells abnormality) and dysplasia. In 1988, Correa and Piazuelo proposed the so-called "Correa hypothesis/cascade" for gastric cancer development in patients with H. pylori infection: unknown genetic and epigenetic factors lead stepwise to 1. chronic inflammation; 2. atrophy gastritis; 3. intestinal metaplasia; 4. low to high grade dysplasia, which finally results in gastric cancer in some patients. H. pylori factors, associated with higher malignancy potential are CagA-positive strains, VacA gene and s1 m1 [1, 4, 5, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120].\n
An attention is paid at the role of tumor-associated autoantigens in immunogenicity and immunodiagnosis, which may detect cancer at early stage. Usually these autoantigens are cellular proteins, which can be ectopically expressed or a result from genetic mutations and rearrangements. Additional mutations in the tumor-associated autoantigens lead to new antigenic epitopes and finally increased immunogenicity. According to a current concept of the immunological response of cancer tissue, tumor-associated antigens lead to autoantibodies production. Autoantibodies with potential clinical usefulness are anti-carcinoembryonic antigen (CEA), anti-p53, anti-survivin, anti-mucin, and anti-livin autoantibodies. The autoantibodies are missing in healthy people and non-cancer diseases. Thus, autoantibodies against tumor antigens can serve as biomarkers and may have the potential to verify an early stage cancer, which may significantly improve patients diagnosis and outcome as the majority of patients with gastric cancer are diagnosed late, when are symptomatic and the management is rather palliative. Studies show significant lower levels of biomarkers after radical tumor resection, which suggest their prominent role in patient monitoring [5, 121, 122, 123, 124, 125].\n
The estimated frequency of detection of anti-carcinoembryonic antigen (CEA) anti-survivin, anti-mucin, and anti-livin autoantibodies is 46–56, 40, 75 and 50%, respectively, as anti-CEA is found in 10% of healthy people. They are present in the early stage of gastric cancer and demonstrate a good prognostic value for survival and postoperative monitoring, especially in patients without anti-p53 antibodies [123, 126, 127, 128, 129, 130, 131].\n
p53 is a key factor in carcinogenesis. In 46% of patients with p53-positive gastric cancer are found increased anti-p53 antibodies levels. Anti-p53 antibodies, which are first reported in patients with breast cancer, correlate significantly with the tumor suppressor gene p53 protein expression, demonstrating about 96% specificity for neoplastic detection. In contrast to anti-carcinoembryonic antigen (CEA) anti-survivin, anti-mucin, and anti-livin autoantibodies, anti-p53 antibodies are not appropriate markers for early diagnosis and prognosis as they are detected in advanced gastric tumors with regional lymph node involvement [123, 126, 132, 133, 134].\n
Extracellular protein kinase A (ECPKA) is a cAMP-dependent intracellular enzyme. Anti- ECPKA antibodies are significantly increased in patients with gastric cancer and other malignancies. They have the potential to be future universal screening method for tumors of different origin as their sensitivity and specificity are very high - 90 and 87%, respectively [135].\n
The presence of substantial number heterogeneous autoantibodies varies widely and demonstrates high specificity but low diagnostic sensitivity. To improve their sensitivity in order to enable their application in clinical practice for screening and diagnosis of gastric cancer; it is reasonable to promote a combination of serological AIG- and tumor biomarkers, microRNAs and/or glycosylation signatures. Using a combination of 5 biomarkers (MAGEA4, CTAG1, TP53, ERBB2_C, and SDCCAG8), Werner et al. demonstrated 32% sensitivity and 87% specificity for diagnosis of early stage gastric adenocarcinoma. In a study of Zhou et al. a combination of 7 markers, namely p53, Koc, p62, c-myc, IMP1, survivin and p16, identified gastric cancer with sensitivity and specificity of 64% and 87%, respectively. Wang et al. verified a panel of 8 biomarkers (IMP1, p62, Koc, p53, c-myc, cyclin B1, survivin and p16), able to detect gastric cancer with 56.1% sensitivity and 86.2% specificity [136, 137, 138, 139, 140, 141, 142, 143, 144].\n
Up-to-date there is no consensus on whom to screen for AIG and how often. The treatment management of AIG with avoiding further complications requires according to the present symptoms, serological results and imaging data proper follow-up. A proper monitoring with testing once a year complete blood count, gastrin, iron and vitamin B12 levels seems to be beneficial. Therapy depends on the stage of AIG, H. pylori infection, current nutrient deficiencies, concomitant autoimmune conditions and (pre)malignant transformation. As described above, H. pylori infection may play a crucial role in AIG pathogenesis. However, screening for H. pylori (serological anti-HP-Ig G and Ig M, fecal HP-antigen, breath tests, histological and cultural methods) in patients with AIG, gastric atrophy, intestinal metaplasia/dysplasia, and hypo- or achlorhydria should be performed. If positive for H. pylori, patients need subsequent treatment and eradication. Studies support H. pylori treatment as H. pylori eradication was associated with decreased levels of PCA and AIFA and AIG early stages healing. Oral supplementation with vitamin B12, iron and folic acid is recommended in early stages of AIG. With neurological symptoms occurring, parenteral vitamin B12 should be applied. As long as various autoimmune diseases are recognized as AIG co-morbidities, attention should be paid at their screening and following treatment. Researchers recommend the routine screening for type 1 diabetes and autoimmune thyroid diseases. On the other hand, in patients, who are diagnosed with type 1 diabetic (positive glutamate decarboxylase-65 antibodies) and autoimmune thyroiditis (positive thyroid peroxidase antibodies), PCA should be investigated at the disease's onset and thereafter yearly for 3 years and later on a longer intervals if there is no AIG clinical signs. Screening for AIG in those patients' populations might avoid the development of IDA and pernicious anemia with their above mentioned serious complications. As long as gastric carcinoid is curative, proper diagnosis and radical treatment are essential. According to size, number and location of gastric cancer /carcinoid, polypectomy, antrectomy (gastrin-producing part), surgical eradication of a gastric tumor, with resection of adjacent lymph nodes or medicamentous treatment with further surveillance is performed. Somatostatin analogs are used as they can reduce gastrin and chromogranin A levels in patients with neuroendocrine tumor (carcinoid). Promising therapeutic option is the gastrin receptor antagonist Netazepide, leading to decreased chromogranin A levels together with cancer size and number. A new technique for carcinoid tumors treatment is the peptide receptor radiotherapy, which would be worth to be tested in AIG patients. Whether to perform surveillance program with regular endoscopic and histological examination in patients with AIG or not remains controversial and guidelines according to AIG surveillance are missing. If mild to moderate dysplasia or ECL cell hyperplasia are observed, an endoscopic surveillance every 5 years is proposed. In contrast to the rare and with far better prognosis carcinoids, gastric cancer development might be fatal. According to the American Society for Gastrointestinal Endoscopy recommendations (2006) for monitoring of patients with H. pylori atrophic gastritis, depending on the primary endoscopic finding the follow-up should be in intervals of 3–5 years (patients with simple, linear/micronodular hyperplasia); every 3 years (patients with extensive atrophy/IM) or every year (patients with adenomas/low-grade dysplasia) [1, 2, 11, 90, 103, 109, 113, 145, 146, 147, 148, 149, 150, 151, 152, 153].\n
Although H. pylori is a leading cause for gastritis, AIG frequency is increasing in elderly people and in those with other autoimmune pathology. As AIG is commonly underdiagnosed, AIG should be considered in the differential diagnosis of patients with anemia, dyspepsia and especially in those with concomitant autoimmune thyroid disease and type 1 diabetes and with relatives with gastric neoplasia. H. pylori presence does not exclude AIG in the pathogenesis of an underlying gastritis. Screening of patients with a panel of serological markers pepsinogen I and II, gastrin, and/or H. pylori antibodies as well as the antibodies PCA and AIFA directs to the need of gastroscopy. However, gastroscopy with separately collected biopsies and histopathological assessment of specimens form gastric corpus and fundus remain the gold standard for AIG diagnosis. Asymptomatic in the early stages of the disease, AIG is not recognized in guidelines as an etiological factor for iron deficiency. However, AIG is often leading to iron deficiency anemia, which requires a different treatment strategy. Untreated pernicious anemia, which is a later manifestation of AIG, could cause both neurological complications and letal cardiovascular events. AIG is a precancerosis for the development of gastric cancer and neuroendocrine tumors. An effort is required to identify a biomarker panel with high sensitivity for early-stage gastric malignancy diagnosis. The treatment of AIG still remains challenging due to asymptomatic early stage and complex pathogenesis of the disease.\n
Proper and early diagnostic approach and prevention, followed by patients' carefully lifelong monitoring at yearly intervals is mandatory to improve the prognosis and outcome of AIG. New therapeutic strategies are needed to delay disease progression and influence the gastric atrophy, making it a reversible entity. Guidelines of AIG surveillance are awaited.\n
The publication of this work was supported by Vladimir Jeglov and Valeri Andreev.\n
There is no conflict.
Authors are listed below with their open access chapters linked via author name:",metaTitle:"IntechOpen authors on the Global Highly Cited Researchers 2018 list",metaDescription:null,metaKeywords:null,canonicalURL:null,contentRaw:'[{"type":"htmlEditorComponent","content":"
New for 2018 (alphabetically by surname).\\n\\n
Philippe Amouyel\\n\\n
Jong-Beom Baek\\n\\n
Giovanni Benelli\\n\\n
Gabriele Berg\\n\\n
Jocelyn Chanussot (chapter to be published soon...)\\n\\n
Yu Chen\\n\\n
C. L. Philip Chen\\n\\n
Jun Chen\\n\\n
Shaowei Chen\\n\\n
Xiaohong Chen\\n\\n
Jonathan N. Coleman\\n\\n
Ilse De Bourdeaudhuij\\n\\n
Mérouane Debbah\\n\\n
Meletios A. Dimopoulos\\n\\n
Andrew Dobson\\n\\n
Shi-Xue Dou\\n\\n
Franz Essl\\n\\n
Ramon Estruch\\n\\n
Muhammad Farooq\\n\\n
Erik Gómez-Baggethun\\n\\n
Josep M. Guerrero\\n\\n
İlhami Gulcin\\n\\n
Michael Hallek\\n\\n
Paul Heremans\\n\\n
Itaru Honma\\n\\n
Rufus Isaacs\\n\\n
Rashid Jalil\\n\\n
Kisuk Kang\\n\\n
David L. Kaplan\\n\\n
Yuekun Lai\\n\\n
Frank L. Lewis\\n\\n
Changjian Lin\\n\\n
Gang Liu\\n\\n
Francois Nosten\\n\\n
Zhijun Ning\\n\\n
Willem A. Nolen\\n\\n
Liberato Manna\\n\\n
Paul W. O'Toole\\n\\n
Huisheng Peng\\n\\n
Burkert Pieske\\n\\n
Russel J. Reiter\\n\\n
Dennis Revicki\\n\\n
Tawfik A. Saleh\\n\\n
Eran Segal\\n\\n
Guy Smagghe\\n\\n
José A. Teixeir\\n\\n
Christine van Broeckhoven\\n\\n
Robert Verpoorte\\n\\n
George M. Weinstock\\n\\n
Somchai Wongwises\\n\\n
Moe Z. Win\\n\\n
Guoyao Wu\\n\\n
Chongwu Zhou\\n\\n
Shu-Feng Zhou\\n\\n
Alimuddin Zumla\\n\\n
Previous years (alphabetically by surname)\\n\\n
Abdul Latif Ahmad 2016-18\\n\\n
Khalil Amine 2017, 2018\\n\\n
Ewan Birney 2015-18\\n\\n
Frede Blaabjerg 2015-18\\n\\n
Gang Chen 2016-18\\n\\n
Junhong Chen 2017, 2018\\n\\n
Zhigang Chen 2016, 2018\\n\\n
Myung-Haing Cho 2016, 2018\\n\\n
Mark Connors 2015-18\\n\\n
Cyrus Cooper 2017, 2018\\n\\n
Liming Dai 2015-18\\n\\n
Weihua Deng 2017, 2018\\n\\n
Vincenzo Fogliano 2017, 2018\\n\\n
Ron de Graaf 2014-18\\n\\n
Harald Haas 2017, 2018\\n\\n
Francisco Herrera 2017, 2018\\n\\n
Jaakko Kangasjärvi 2015-18\\n\\n
Hamid Reza Karimi 2016-18\\n\\n
Junji Kido 2014-18\\n\\n
Jose Luiszamorano 2015-18\\n\\n
Yiqi Luo 2016-18\\n\\n
Joachim Maier 2014-18\\n\\n
Andrea Natale 2017, 2018\\n\\n
Alberto Mantovani 2014-18\\n\\n
Marjan Mernik 2017, 2018\\n\\n
Sandra Orchard 2014, 2016-18\\n\\n
Mohamed Oukka 2016-18\\n\\n
Biswajeet Pradhan 2016-18\\n\\n
Dirk Raes 2017, 2018\\n\\n
Ulrike Ravens-Sieberer 2016-18\\n\\n
Yexiang Tong 2017, 2018\\n\\n
Jim Van Os 2015-18\\n\\n
Long Wang 2017, 2018\\n\\n
Fei Wei 2016-18\\n\\n
Ioannis Xenarios 2017, 2018\\n\\n
Qi Xie 2016-18\\n\\n
Xin-She Yang 2017, 2018\\n\\n
Yulong Yin 2015, 2017, 2018\\n"}]'},components:[{type:"htmlEditorComponent",content:'
New for 2018 (alphabetically by surname).\n\n
Philippe Amouyel\n\n
Jong-Beom Baek\n\n
Giovanni Benelli\n\n
Gabriele Berg\n\n
Jocelyn Chanussot (chapter to be published soon...)\n\n
Yu Chen\n\n
C. L. Philip Chen\n\n
Jun Chen\n\n
Shaowei Chen\n\n
Xiaohong Chen\n\n
Jonathan N. Coleman\n\n
Ilse De Bourdeaudhuij\n\n
Mérouane Debbah\n\n
Meletios A. Dimopoulos\n\n
Andrew Dobson\n\n
Shi-Xue Dou\n\n
Franz Essl\n\n
Ramon Estruch\n\n
Muhammad Farooq\n\n
Erik Gómez-Baggethun\n\n
Josep M. Guerrero\n\n
İlhami Gulcin\n\n
Michael Hallek\n\n
Paul Heremans\n\n
Itaru Honma\n\n
Rufus Isaacs\n\n
Rashid Jalil\n\n
Kisuk Kang\n\n
David L. Kaplan\n\n
Yuekun Lai\n\n
Frank L. Lewis\n\n
Changjian Lin\n\n
Gang Liu\n\n
Francois Nosten\n\n
Zhijun Ning\n\n
Willem A. Nolen\n\n
Liberato Manna\n\n
Paul W. O'Toole\n\n
Huisheng Peng\n\n
Burkert Pieske\n\n
Russel J. Reiter\n\n
Dennis Revicki\n\n
Tawfik A. Saleh\n\n
Eran Segal\n\n
Guy Smagghe\n\n
José A. Teixeir\n\n
Christine van Broeckhoven\n\n
Robert Verpoorte\n\n
George M. Weinstock\n\n
Somchai Wongwises\n\n
Moe Z. Win\n\n
Guoyao Wu\n\n
Chongwu Zhou\n\n
Shu-Feng Zhou\n\n
Alimuddin Zumla\n\n
Previous years (alphabetically by surname)\n\n
Abdul Latif Ahmad 2016-18\n\n
Khalil Amine 2017, 2018\n\n
Ewan Birney 2015-18\n\n
Frede Blaabjerg 2015-18\n\n
Gang Chen 2016-18\n\n
Junhong Chen 2017, 2018\n\n
Zhigang Chen 2016, 2018\n\n
Myung-Haing Cho 2016, 2018\n\n
Mark Connors 2015-18\n\n
Cyrus Cooper 2017, 2018\n\n
Liming Dai 2015-18\n\n
Weihua Deng 2017, 2018\n\n
Vincenzo Fogliano 2017, 2018\n\n
Ron de Graaf 2014-18\n\n
Harald Haas 2017, 2018\n\n
Francisco Herrera 2017, 2018\n\n
Jaakko Kangasjärvi 2015-18\n\n
Hamid Reza Karimi 2016-18\n\n
Junji Kido 2014-18\n\n
Jose Luiszamorano 2015-18\n\n
Yiqi Luo 2016-18\n\n
Joachim Maier 2014-18\n\n
Andrea Natale 2017, 2018\n\n
Alberto Mantovani 2014-18\n\n
Marjan Mernik 2017, 2018\n\n
Sandra Orchard 2014, 2016-18\n\n
Mohamed Oukka 2016-18\n\n
Biswajeet Pradhan 2016-18\n\n
Dirk Raes 2017, 2018\n\n
Ulrike Ravens-Sieberer 2016-18\n\n
Yexiang Tong 2017, 2018\n\n
Jim Van Os 2015-18\n\n
Long Wang 2017, 2018\n\n
Fei Wei 2016-18\n\n
Ioannis Xenarios 2017, 2018\n\n
Qi Xie 2016-18\n\n
Xin-She Yang 2017, 2018\n\n
Yulong Yin 2015, 2017, 2018\n'}]},successStories:{items:[]},authorsAndEditors:{filterParams:{sort:"featured,name"},profiles:[{id:"6700",title:"Dr.",name:"Abbass A.",middleName:null,surname:"Hashim",slug:"abbass-a.-hashim",fullName:"Abbass A. Hashim",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/6700/images/1864_n.jpg",biography:"Currently I am carrying out research in several areas of interest, mainly covering work on chemical and bio-sensors, semiconductor thin film device fabrication and characterisation.\nAt the moment I have very strong interest in radiation environmental pollution and bacteriology treatment. The teams of researchers are working very hard to bring novel results in this field. I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. 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Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). I am a Reviewer for several refereed journals and international conferences, such as IEEE Transactions on Biomedical Engineering, IEEE Transactions on Industrial Electronics, Optic Letters, Measurement Science Review, and also a member of the International Advisory Committee for 2012 IEEE Business Engineering and Industrial Applications and 2012 IEEE Symposium on Business, Engineering and Industrial Applications.",institutionString:null,institution:{name:"Joseph Fourier University",country:{name:"France"}}},{id:"55578",title:"Dr.",name:"Antonio",middleName:null,surname:"Jurado-Navas",slug:"antonio-jurado-navas",fullName:"Antonio Jurado-Navas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/55578/images/4574_n.png",biography:"Antonio Jurado-Navas received the M.S. degree (2002) and the Ph.D. degree (2009) in Telecommunication Engineering, both from the University of Málaga (Spain). He first worked as a consultant at Vodafone-Spain. From 2004 to 2011, he was a Research Assistant with the Communications Engineering Department at the University of Málaga. In 2011, he became an Assistant Professor in the same department. From 2012 to 2015, he was with Ericsson Spain, where he was working on geo-location\ntools for third generation mobile networks. Since 2015, he is a Marie-Curie fellow at the Denmark Technical University. His current research interests include the areas of mobile communication systems and channel modeling in addition to atmospheric optical communications, adaptive optics and statistics",institutionString:null,institution:{name:"University of Malaga",country:{name:"Spain"}}},{id:"6495",title:"Dr.",name:"Daniel",middleName:null,surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/6495/images/1947_n.jpg",biography:"Daniel Eberli MD. Ph.D. is a scientific physician working in the translational field of urologic tissue engineering. He has a medical degree from the Medical School in Zurich, Switzerland, and a Ph.D. in Molecular Medicine from Wake Forest University, Winston Salem, NC. He currently has a faculty position at the Department of Urology at the University Hospital Zurich, where he devotes half of his time to patient care. He is a lecturer at the Medical School of Zurich and the Swiss Federal Institute of Technology. Together with his research team, he is working on novel biomaterials for bladder reconstruction, improving autonomic innervation, cellular treatment of incontinence and tracking of stem cells.",institutionString:null,institution:{name:"University Hospital of Zurich",country:{name:"Switzerland"}}},{id:"6667",title:"Dr.",name:"David",middleName:null,surname:"Pozo",slug:"david-pozo",fullName:"David Pozo",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/6667/images/system/6667.jpg",biography:"Professor of Biochemistry and Molecular Biology, University of Seville Medical School, Seville, Spain.\n\nPrincipal Investigator at the Center for Molecular Biology and Regenerative Medicine (CABIMER), Seville, Spain.\n\nDr. Pozo Perez received his Ph.D (1998) from the University of Seville. He subsequently joined the Division of Immunology at Cambridge University (UK) as an EMBO postdoctoral fellow and Marie Curie Fellow from 2000-2003. He did a second post-doctoral stint at the Department of Immunology of Weizmann Institute of Science (2004) in Israel and short stages as visiting scientist at the Center for Neurologic Diseases, Brigham & Women Hospital, Harvard Medical School (2013, 2015). 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