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36,871,865 | D008297:Male; D006801:Humans; D005260:Female; D006965:Hyperplasia; D008099:Liver; D056784:Leukoencephalopathies; D014652:Vascular Diseases; D008107:Liver Diseases | [
"D008297",
"D006801",
"D005260",
"D006965",
"D008099",
"D056784",
"D014652",
"D008107"
] | Liver pathology in retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations: vasculopathic disease beyond nodular regenerative hyperplasia. | Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) is a rare autosomal dominant disease resulting from a frame-shift mutation in TREX1, an intracellular 3'-5' exonuclease 1. Hepatic findings include an elevated alkaline phosphatase (ALP) and nodular regenerative hyperplasia (NRH). Affected individuals typically succumb to brain lesions before clinically apparent hepatic manifestations; thus, little else is known about the hepatic pathology. Autopsy reports and a liver section from each (n = 11) of three unrelated kindreds with the most common mutation in TREX1 (V235Gfs∗6) were studied with standard and immunohistochemical stains. Cases were compared with "normal liver" controls from similar autopsy years. Cases consisted of six men and five women who died at a median age of 50 yr (range, 41-60 yr.). Seven had elevated ALP. Two had liver atrophy. Foci of NRH were variably detected in all. Inhomogeneous distribution of other findings included patternless parenchymal fibrous bands, approximation of vascular structures, and commonly, architectural changes of vascular structures. Only bile duct epithelia were unaffected. In addition, small trichrome-positive nodules were found along vein walls or isolated in the parenchyma. Rare foci of non-NRH hepatocytic nodules were noted in 3. Increased CD34 and altered α-SMA IHC expression were variably noted. Periportal ductules and perivenular K7 IHC expression were increased to unpredictable degrees. The extensive but inhomogeneous histopathologic findings in livers of autopsied patients with RVCL-S appear to involve hepatic vascular structures. These findings validate inclusion of vascular liver involvement beyond NRH in this complex hereditary disorder. | null | false | Liver pathology in retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations: vasculopathic disease beyond nodular regenerative hyperplasia. Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) is a rare autosomal dominant disease resulting from a frame-shift mutation in TREX1, an intracellular 3'-5' exonuclease 1. Hepatic findings include an elevated alkaline phosphatase (ALP) and nodular regenerative hyperplasia (NRH). Affected individuals typically succumb to brain lesions before clinically apparent hepatic manifestations; thus, little else is known about the hepatic pathology. Autopsy reports and a liver section from each (n = 11) of three unrelated kindreds with the most common mutation in TREX1 (V235Gfs∗6) were studied with standard and immunohistochemical stains. Cases were compared with "normal liver" controls from similar autopsy years. Cases consisted of six men and five women who died at a median age of 50 yr (range, 41-60 yr.). Seven had elevated ALP. Two had liver atrophy. Foci of NRH were variably detected in all. Inhomogeneous distribution of other findings included patternless parenchymal fibrous bands, approximation of vascular structures, and commonly, architectural changes of vascular structures. Only bile duct epithelia were unaffected. In addition, small trichrome-positive nodules were found along vein walls or isolated in the parenchyma. Rare foci of non-NRH hepatocytic nodules were noted in 3. Increased CD34 and altered α-SMA IHC expression were variably noted. Periportal ductules and perivenular K7 IHC expression were increased to unpredictable degrees. The extensive but inhomogeneous histopathologic findings in livers of autopsied patients with RVCL-S appear to involve hepatic vascular structures. These findings validate inclusion of vascular liver involvement beyond NRH in this complex hereditary disorder. |
36,402,355 | D011247:Pregnancy; D006801:Humans; D005260:Female; D000959:Antihypertensive Agents; D011225:Pre-Eclampsia; D054038:Posterior Leukoencephalopathy Syndrome; D006973:Hypertension; D049590:Postpartum Period | [
"D011247",
"D006801",
"D005260",
"D000959",
"D011225",
"D054038",
"D006973",
"D049590"
] | Tight vs liberal control of mild postpartum hypertension: a randomized controlled trial. | High-quality evidence to inform the management of postpartum hypertension, including the optimal blood pressure threshold to initiate therapy, is lacking. Randomized trials have been conducted in pregnancy, but there are no published trials to guide management in the postpartum period.
This study aimed to test the hypothesis that initiating antihypertensive therapy in the postpartum period at a threshold of 140/90 mm Hg would result in less maternal morbidity than initiating therapy at a threshold of 150/95 mm Hg.
We performed a pragmatic multicenter randomized controlled trial of patients aged 18 to 55 years with postpartum hypertension. Patients with chronic hypertension, gestational hypertension, and preeclampsia without severe features were randomized to 1 of 2 blood pressure thresholds to initiate treatment: persistent blood pressure of ≥150/95 mm Hg (institutional standard or "liberal control" group) or ≥140/90 mm Hg (intervention or "tight control" group). Our primary outcome was composite maternal morbidity defined as: severe hypertension (blood pressure ≥160/110 mm Hg) or preeclampsia with severe features, the need for a second antihypertensive agent, postpartum hospitalization >4 days, and maternal adverse outcome secondary to hypertension as evidenced by pulmonary edema, acute kidney injury (creatinine level ≥1.1 mg/dL), cardiac dysfunction (eg, elevated brain natriuretic peptide level) or cardiomyopathy, posterior reversible encephalopathy syndrome, cerebrovascular accident, or admission to an intensive care unit. Secondary outcomes included hospital readmission for hypertension, persistence of hypertension beyond 14 days, medication side effects, and time to blood pressure control. We calculated that 256 women would provide 90% power to detect a relative 50% reduction in the primary outcome from 36% in the standard blood pressure threshold group to 18%, with a 2-sided alpha set at 0.05 for significance. Data were analyzed using R statistical software.
A total of 256 patients were randomized, including 128 to the "tight control" group (140/90 mm Hg) and 128 to the "liberal control" group (150/95 mm Hg). Patients in the "tight control" group had a higher body mass index at delivery (37.1±9.4 vs 34.9±8.1; P=.04); other demographic and obstetrical characteristics were similar between groups. The rate of the primary outcome was similar between groups (8.6% vs 11.7%; P=.41; relative risk, 0.73; 95% confidence interval, 0.35-1.53). The rates of all secondary outcomes and the individual components of the primary and secondary outcome measures were also similar between groups.
In the postpartum period, initiation of antihypertensive therapy at a lower blood pressure threshold of 140/90 mm Hg did not decrease maternal morbidity or improve outcomes compared with a threshold of 150/95 mm Hg. | null | false | Tight vs liberal control of mild postpartum hypertension: a randomized controlled trial. High-quality evidence to inform the management of postpartum hypertension, including the optimal blood pressure threshold to initiate therapy, is lacking. Randomized trials have been conducted in pregnancy, but there are no published trials to guide management in the postpartum period.
This study aimed to test the hypothesis that initiating antihypertensive therapy in the postpartum period at a threshold of 140/90 mm Hg would result in less maternal morbidity than initiating therapy at a threshold of 150/95 mm Hg.
We performed a pragmatic multicenter randomized controlled trial of patients aged 18 to 55 years with postpartum hypertension. Patients with chronic hypertension, gestational hypertension, and preeclampsia without severe features were randomized to 1 of 2 blood pressure thresholds to initiate treatment: persistent blood pressure of ≥150/95 mm Hg (institutional standard or "liberal control" group) or ≥140/90 mm Hg (intervention or "tight control" group). Our primary outcome was composite maternal morbidity defined as: severe hypertension (blood pressure ≥160/110 mm Hg) or preeclampsia with severe features, the need for a second antihypertensive agent, postpartum hospitalization >4 days, and maternal adverse outcome secondary to hypertension as evidenced by pulmonary edema, acute kidney injury (creatinine level ≥1.1 mg/dL), cardiac dysfunction (eg, elevated brain natriuretic peptide level) or cardiomyopathy, posterior reversible encephalopathy syndrome, cerebrovascular accident, or admission to an intensive care unit. Secondary outcomes included hospital readmission for hypertension, persistence of hypertension beyond 14 days, medication side effects, and time to blood pressure control. We calculated that 256 women would provide 90% power to detect a relative 50% reduction in the primary outcome from 36% in the standard blood pressure threshold group to 18%, with a 2-sided alpha set at 0.05 for significance. Data were analyzed using R statistical software.
A total of 256 patients were randomized, including 128 to the "tight control" group (140/90 mm Hg) and 128 to the "liberal control" group (150/95 mm Hg). Patients in the "tight control" group had a higher body mass index at delivery (37.1±9.4 vs 34.9±8.1; P=.04); other demographic and obstetrical characteristics were similar between groups. The rate of the primary outcome was similar between groups (8.6% vs 11.7%; P=.41; relative risk, 0.73; 95% confidence interval, 0.35-1.53). The rates of all secondary outcomes and the individual components of the primary and secondary outcome measures were also similar between groups.
In the postpartum period, initiation of antihypertensive therapy at a lower blood pressure threshold of 140/90 mm Hg did not decrease maternal morbidity or improve outcomes compared with a threshold of 150/95 mm Hg. |
16,271,710 | D000199:Actins; D000368:Aged; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017544:Aortic Aneurysm, Abdominal; D050197:Atherosclerosis; D002478:Cells, Cultured; D042783:Endothelial Cells; D019332:Endothelin-1; D005455:Fluorescent Antibody Technique; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular; D032389:Myocytes, Smooth Muscle; D017395:Plasminogen Activator Inhibitor 1; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D052243:Resistin; D020133:Reverse Transcriptase Polymerase Chain Reaction | [
"D000199",
"D000368",
"D015703",
"D015214",
"D017544",
"D050197",
"D002478",
"D042783",
"D019332",
"D005455",
"D006801",
"D007150",
"D008264",
"D008297",
"D008875",
"D009131",
"D032389",
"D017395",
"D019408",
"D012333",
"D052243",
"D020133"
] | Resistin is secreted from macrophages in atheromas and promotes atherosclerosis. | OBJECTIVE
Resistin belongs to a family of cysteine-rich secreted polypeptides that are mainly produced by monocytes/macrophages in humans. Recently, high concentrations of resistin were shown to induce vascular endothelial dysfunction and vascular smooth muscle cell proliferation. We examined if resistin was secreted from macrophages locally in atheromas and if it affected vascular cell function in human.
RESULTS
Immunohistochemical staining of human vessels showed that aortic aneurysms exhibited resistin-positive staining areas along macrophage infiltration, while normal arteries and veins did not. Co-localization of resistin and CD68 (a marker for macrophages) was observed in immunofluorescent double staining of aneurysms. Resistin mRNA was expressed much higher in cultured monocytes/macrophages than in human vascular smooth muscle cells (VSMCs) and human umbilical venous endothelial cells (HUVECs). This suggested that the resistin in aneurysms originates from macrophages within the vessels. To determine the effects of resistin on atherosclerosis, HUVECs and human VSMCs were incubated with resistin (10-100 ng/mL for 4 approximately 24 h). In HUVECs, plasminogen activator inhibitor (PAI)-1 release was assayed by ELISA, while the PAI-1 and endothelin (ET)-1 mRNA levels were analyzed by Northern blotting. Both were increased significantly with resistin treatment by factors of 1.3-2.5 (p<0.05). Migratory activity of VSMCs measured by scratched wound assay also increased significantly (1.6 times, p<0.05). In summary, macrophages infiltrating atherosclerotic aneurysms secrete resistin, and resistin affects endothelial function and VSMC migration.
CONCLUSIONS
Resistin secreted from macrophages may contribute to atherogenesis by virtue of its effects on vascular endothelial cells and smooth muscle cells in humans. | null | false | Resistin is secreted from macrophages in atheromas and promotes atherosclerosis. OBJECTIVE
Resistin belongs to a family of cysteine-rich secreted polypeptides that are mainly produced by monocytes/macrophages in humans. Recently, high concentrations of resistin were shown to induce vascular endothelial dysfunction and vascular smooth muscle cell proliferation. We examined if resistin was secreted from macrophages locally in atheromas and if it affected vascular cell function in human.
RESULTS
Immunohistochemical staining of human vessels showed that aortic aneurysms exhibited resistin-positive staining areas along macrophage infiltration, while normal arteries and veins did not. Co-localization of resistin and CD68 (a marker for macrophages) was observed in immunofluorescent double staining of aneurysms. Resistin mRNA was expressed much higher in cultured monocytes/macrophages than in human vascular smooth muscle cells (VSMCs) and human umbilical venous endothelial cells (HUVECs). This suggested that the resistin in aneurysms originates from macrophages within the vessels. To determine the effects of resistin on atherosclerosis, HUVECs and human VSMCs were incubated with resistin (10-100 ng/mL for 4 approximately 24 h). In HUVECs, plasminogen activator inhibitor (PAI)-1 release was assayed by ELISA, while the PAI-1 and endothelin (ET)-1 mRNA levels were analyzed by Northern blotting. Both were increased significantly with resistin treatment by factors of 1.3-2.5 (p<0.05). Migratory activity of VSMCs measured by scratched wound assay also increased significantly (1.6 times, p<0.05). In summary, macrophages infiltrating atherosclerotic aneurysms secrete resistin, and resistin affects endothelial function and VSMC migration.
CONCLUSIONS
Resistin secreted from macrophages may contribute to atherogenesis by virtue of its effects on vascular endothelial cells and smooth muscle cells in humans. |
7,585,281 | D001281:Atrial Fibrillation; D002121:Calcium Channel Blockers; D002986:Clinical Trials as Topic; D004110:Diltiazem; D005260:Female; D006333:Heart Failure; D006439:Hemodynamics; D006801:Humans; D008297:Male; D015337:Multicenter Studies as Topic; D016032:Randomized Controlled Trials as Topic; D013599:Systole; D018487:Ventricular Dysfunction, Left; D014700:Verapamil | [
"D001281",
"D002121",
"D002986",
"D004110",
"D005260",
"D006333",
"D006439",
"D006801",
"D008297",
"D015337",
"D016032",
"D013599",
"D018487",
"D014700"
] | Calcium channel blockers for heart rate control in atrial fibrillation complicated by congestive heart failure. | OBJECTIVE
To review the safety and efficacy of verapamil and diltiazem with respect to ventricular response in atrial fibrillation (AF) in the setting of left ventricular (LV) systolic dysfunction.
METHODS
Pertinent articles were identified through a MEDLINE search of the English language literature from 1984 to 1993, followed by a manual search of the bibliographies of pertinent articles.
METHODS
Studies selected were case reports, controlled trials, review articles and editorials.
METHODS
Effects of verapamil and diltiazem on hemodynamics, ventricular response in AF, clinical parameters and mortality were reviewed.
RESULTS
There are limited data about the effects of verapamil and diltiazem on ventricular function in patients with congestive heart failure. In vitro diltiazem has fewer negative inotropic effects than verapamil. Clinically there are some reports of hemodynamic and clinical deterioration in patients with significant LV dysfunction given verapamil although most patients improve with verapamil. There are more data concerning diltiazem in the setting of AF complicated by congestive heart failure. The drug does not appear to exacerbate heart failure, although hypotension can result. In chronic AF complicated by heart failure, there is concern that diltiazem may increase mortality. Options for therapy are digoxin, beta-blockers and atrioventricular node ablation.
CONCLUSIONS
Calcium channel blockers may have a role in the acute reduction of ventricular response in patients with AF complicated by congestive heart failure; however, their safety in chronic heart rate control remains to be proven. | null | false | Calcium channel blockers for heart rate control in atrial fibrillation complicated by congestive heart failure. OBJECTIVE
To review the safety and efficacy of verapamil and diltiazem with respect to ventricular response in atrial fibrillation (AF) in the setting of left ventricular (LV) systolic dysfunction.
METHODS
Pertinent articles were identified through a MEDLINE search of the English language literature from 1984 to 1993, followed by a manual search of the bibliographies of pertinent articles.
METHODS
Studies selected were case reports, controlled trials, review articles and editorials.
METHODS
Effects of verapamil and diltiazem on hemodynamics, ventricular response in AF, clinical parameters and mortality were reviewed.
RESULTS
There are limited data about the effects of verapamil and diltiazem on ventricular function in patients with congestive heart failure. In vitro diltiazem has fewer negative inotropic effects than verapamil. Clinically there are some reports of hemodynamic and clinical deterioration in patients with significant LV dysfunction given verapamil although most patients improve with verapamil. There are more data concerning diltiazem in the setting of AF complicated by congestive heart failure. The drug does not appear to exacerbate heart failure, although hypotension can result. In chronic AF complicated by heart failure, there is concern that diltiazem may increase mortality. Options for therapy are digoxin, beta-blockers and atrioventricular node ablation.
CONCLUSIONS
Calcium channel blockers may have a role in the acute reduction of ventricular response in patients with AF complicated by congestive heart failure; however, their safety in chronic heart rate control remains to be proven. |
26,491,537 | D000493:Allopurinol; D000818:Animals; D015536:Down-Regulation; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde; D020011:Protective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha; D015854:Up-Regulation; D001743:Urinary Bladder; D014969:Xanthine Oxidase; D051028:bcl-2-Associated X Protein; D048051:p38 Mitogen-Activated Protein Kinases | [
"D000493",
"D000818",
"D015536",
"D048049",
"D048031",
"D015227",
"D008297",
"D008315",
"D020011",
"D019253",
"D051381",
"D017207",
"D017382",
"D015427",
"D015398",
"D014409",
"D015854",
"D001743",
"D014969",
"D051028",
"D048051"
] | Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders. | Bladder ischemia-reperfusion (I/R) injury results in the generation of reactive oxygen species (ROS) and markedly elevates the risk of lower urinary tract symptoms (LUTS). Allopurinol is an inhibitor of xanthine oxidase (XO) and thus can serve as an antioxidant that reduces oxidative stress. Here, a rat model was used to assess the ability of allopurinol treatment to ameliorate the deleterious effects of urinary bladder I/R injury. I/R injury reduced the in vitro contractile responses of longitudinal bladder strips, elevated XO activity in the plasma and bladder tissue, increased the bladder levels of tumor necrosis factor-α (TNF-α), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase, reduced the bladder levels of extracellular regulated kinase (ERK), and decreased and increased the bladder levels of Bcl-2 and Bax, respectively. I/R injury also elevated lipid peroxidation in the bladder. Allopurinol treatment in the I/R injury was generated significantly ameliorating all I/R-induced changes. Moreover, an in situ fluorohistological approach also showed that allopurinol reduces the generation of intracellular superoxides enlarged by I/R injury. Together, the beneficial effects of allopurinol reducing ROS production may be mediated by normalizing the activity of the ERK, JNK, and Bax/Bcl-2 pathways and by controlling TNF-α expression. | 7,298,571 | true | Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders. Bladder ischemia-reperfusion (I/R) injury results in the generation of reactive oxygen species (ROS) and markedly elevates the risk of lower urinary tract symptoms (LUTS). Allopurinol is an inhibitor of xanthine oxidase (XO) and thus can serve as an antioxidant that reduces oxidative stress. Here, a rat model was used to assess the ability of allopurinol treatment to ameliorate the deleterious effects of urinary bladder I/R injury. I/R injury reduced the in vitro contractile responses of longitudinal bladder strips, elevated XO activity in the plasma and bladder tissue, increased the bladder levels of tumor necrosis factor-α (TNF-α), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase, reduced the bladder levels of extracellular regulated kinase (ERK), and decreased and increased the bladder levels of Bcl-2 and Bax, respectively. I/R injury also elevated lipid peroxidation in the bladder. Allopurinol treatment in the I/R injury was generated significantly ameliorating all I/R-induced changes. Moreover, an in situ fluorohistological approach also showed that allopurinol reduces the generation of intracellular superoxides enlarged by I/R injury. Together, the beneficial effects of allopurinol reducing ROS production may be mediated by normalizing the activity of the ERK, JNK, and Bax/Bcl-2 pathways and by controlling TNF-α expression. |
34,599,610 | D001237:Asphyxia; D001238:Asphyxia Neonatorum; D002648:Child; D015331:Cohort Studies; D005260:Female; D006801:Humans; D020925:Hypoxia-Ischemia, Brain; D007223:Infant; D007231:Infant, Newborn; D011247:Pregnancy; D011446:Prospective Studies | [
"D001237",
"D001238",
"D002648",
"D015331",
"D005260",
"D006801",
"D020925",
"D007223",
"D007231",
"D011247",
"D011446"
] | Profile of minor neurological findings after perinatal asphyxia. | OBJECTIVE
To characterise the spectrum of findings in sequential neurological examinations, general movements (GM) assessment and magnetic resonance imaging (MRI) of infants with perinatal asphyxia.
METHODS
The prospective cohort study of term infants with perinatal asphyxia treated at Helsinki University Hospital's neonatal units in 2016-2020 used Hammersmith Neonatal Neurological Examination (HNNE) and brain MRI at 2 weeks and Hammersmith Infant Neurological Examination (HINE) and GM assessment at 3 months of age.
RESULTS
Analysis included 50 infants: 33 displaying perinatal asphyxia without hypoxic-ischaemic encephalopathy (HIE), seven with HIE1 and 10 with HIE2. Of the infants with atypical HNNE findings, 24/25 perinatal asphyxia without HIE cases, 5/6 HIE1 cases and all 10 HIE2 cases showed atypical findings in the HINE. The HINE identified atypical spontaneous movements significantly more often in infants with white matter T2 hyperintensity.
CONCLUSIONS
In this cohort, most infants with perinatal asphyxia, with or without HIE, presented atypical neurological findings in sequential examinations. The profile of neurological findings for children with perinatal asphyxia without HIE resembled that of children with HIE. White matter T2 hyperintensity was associated with atypical spontaneous movements in the HINE and was a frequent MRI finding also in perinatal asphyxia without HIE. | null | false | Profile of minor neurological findings after perinatal asphyxia. OBJECTIVE
To characterise the spectrum of findings in sequential neurological examinations, general movements (GM) assessment and magnetic resonance imaging (MRI) of infants with perinatal asphyxia.
METHODS
The prospective cohort study of term infants with perinatal asphyxia treated at Helsinki University Hospital's neonatal units in 2016-2020 used Hammersmith Neonatal Neurological Examination (HNNE) and brain MRI at 2 weeks and Hammersmith Infant Neurological Examination (HINE) and GM assessment at 3 months of age.
RESULTS
Analysis included 50 infants: 33 displaying perinatal asphyxia without hypoxic-ischaemic encephalopathy (HIE), seven with HIE1 and 10 with HIE2. Of the infants with atypical HNNE findings, 24/25 perinatal asphyxia without HIE cases, 5/6 HIE1 cases and all 10 HIE2 cases showed atypical findings in the HINE. The HINE identified atypical spontaneous movements significantly more often in infants with white matter T2 hyperintensity.
CONCLUSIONS
In this cohort, most infants with perinatal asphyxia, with or without HIE, presented atypical neurological findings in sequential examinations. The profile of neurological findings for children with perinatal asphyxia without HIE resembled that of children with HIE. White matter T2 hyperintensity was associated with atypical spontaneous movements in the HINE and was a frequent MRI finding also in perinatal asphyxia without HIE. |
34,124,862 | D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000971:Antineoplastic Combined Chemotherapy Protocols; D000069286:Bortezomib; D019008:Drug Resistance, Neoplasm; D005260:Female; D006801:Humans; D007564:Japan; D000077269:Lenalidomide; D008297:Male; D008875:Middle Aged; D009101:Multiple Myeloma; D009842:Oligopeptides; D010865:Pilot Projects; D011379:Prognosis; D011446:Prospective Studies | [
"D000328",
"D000368",
"D000369",
"D000971",
"D000069286",
"D019008",
"D005260",
"D006801",
"D007564",
"D000077269",
"D008297",
"D008875",
"D009101",
"D009842",
"D010865",
"D011379",
"D011446"
] | Prognostic impact of resistance to bortezomib and/or lenalidomide in carfilzomib-based therapies for relapsed/refractory multiple myeloma: The Kyoto Clinical Hematology Study Group, multicenter, pilot, prospective, observational study in Asian patients. | Combinatory strategies with carfilzomib (CFZ), a second-generation proteasome inhibitor, plus dexamethasone (DEX) with or without lenalidomide (LEN) have shown promising efficacy for patients with relapsed/refractory multiple myeloma (RRMM) in pivotal clinical trials. However, their effects on patients who were resistance to bortezomib (BTZ) and/or LEN have not been fully evaluated in a daily practice setting.
To evaluate the real-world efficacy and safety of CFZ-based treatments; that is, CFZ with LEN plus DEX (KRD therapy) and CFZ with DEX (KD therapy), in Asian patients, we conducted a multicenter pilot prospective observational study in the Kyoto Clinical Hematology Study Group.
All 50 patients with RRMM enrolled in this study were treated with CFZ-based treatments between 2017 and 2019. KRD and KD were administered to 31 and 19 patients, respectively. The overall response rates (ORRs) were 80.6% with KRD and 73.7% with KD. Two-year progression-free survival (PFS) and overall survival (OS) were 58.5% and 79.7% with KRD, and 23.1% and 52.6% with KD. By multivariate analysis, refractoriness to BTZ and to LEN were identified as independent unfavorable factors for both PFS and OS. The common non-hematologic AEs included hypertension (42.0%), fever (24.0%), fatigue (24.0%), and infection (16.0%). No serious heart failure was observed. This study is registered as UMIN000025108.
This study suggests the need of the development of novel CFZ-containing strategy which can overcome the refractoriness to BTZ and/or LEN, while both KRD and KD were shown to be mostly feasible in Asian patients in a daily practice setting. | null | false | Prognostic impact of resistance to bortezomib and/or lenalidomide in carfilzomib-based therapies for relapsed/refractory multiple myeloma: The Kyoto Clinical Hematology Study Group, multicenter, pilot, prospective, observational study in Asian patients. Combinatory strategies with carfilzomib (CFZ), a second-generation proteasome inhibitor, plus dexamethasone (DEX) with or without lenalidomide (LEN) have shown promising efficacy for patients with relapsed/refractory multiple myeloma (RRMM) in pivotal clinical trials. However, their effects on patients who were resistance to bortezomib (BTZ) and/or LEN have not been fully evaluated in a daily practice setting.
To evaluate the real-world efficacy and safety of CFZ-based treatments; that is, CFZ with LEN plus DEX (KRD therapy) and CFZ with DEX (KD therapy), in Asian patients, we conducted a multicenter pilot prospective observational study in the Kyoto Clinical Hematology Study Group.
All 50 patients with RRMM enrolled in this study were treated with CFZ-based treatments between 2017 and 2019. KRD and KD were administered to 31 and 19 patients, respectively. The overall response rates (ORRs) were 80.6% with KRD and 73.7% with KD. Two-year progression-free survival (PFS) and overall survival (OS) were 58.5% and 79.7% with KRD, and 23.1% and 52.6% with KD. By multivariate analysis, refractoriness to BTZ and to LEN were identified as independent unfavorable factors for both PFS and OS. The common non-hematologic AEs included hypertension (42.0%), fever (24.0%), fatigue (24.0%), and infection (16.0%). No serious heart failure was observed. This study is registered as UMIN000025108.
This study suggests the need of the development of novel CFZ-containing strategy which can overcome the refractoriness to BTZ and/or LEN, while both KRD and KD were shown to be mostly feasible in Asian patients in a daily practice setting. |
36,077,285 | D006333:Heart Failure; D006353:Heart-Assist Devices; D006801:Humans; D009206:Myocardium; D032383:Myocytes, Cardiac | [
"D006333",
"D006353",
"D006801",
"D009206",
"D032383"
] | Novel Targets for a Combination of Mechanical Unloading with Pharmacotherapy in Advanced Heart Failure. | LVAD therapy is an effective rescue in acute and especially chronic cardiac failure. In several scenarios, it provides a platform for regeneration and sustained myocardial recovery. While unloading seems to be a key element, pharmacotherapy may provide powerful tools to enhance effective cardiac regeneration. The synergy between LVAD support and medical agents may ensure satisfying outcomes on cardiomyocyte recovery followed by improved quality and quantity of patient life. This review summarizes the previous and contemporary strategies for combining LVAD with pharmacotherapy and proposes new therapeutic targets. Regulation of metabolic pathways, enhancing mitochondrial biogenesis and function, immunomodulating treatment, and stem-cell therapies represent therapeutic areas that require further experimental and clinical studies on their effectiveness in combination with mechanical unloading. | 761,476 | true | Novel Targets for a Combination of Mechanical Unloading with Pharmacotherapy in Advanced Heart Failure. LVAD therapy is an effective rescue in acute and especially chronic cardiac failure. In several scenarios, it provides a platform for regeneration and sustained myocardial recovery. While unloading seems to be a key element, pharmacotherapy may provide powerful tools to enhance effective cardiac regeneration. The synergy between LVAD support and medical agents may ensure satisfying outcomes on cardiomyocyte recovery followed by improved quality and quantity of patient life. This review summarizes the previous and contemporary strategies for combining LVAD with pharmacotherapy and proposes new therapeutic targets. Regulation of metabolic pathways, enhancing mitochondrial biogenesis and function, immunomodulating treatment, and stem-cell therapies represent therapeutic areas that require further experimental and clinical studies on their effectiveness in combination with mechanical unloading. |
6,607,135 | D000368:Aged; D000787:Angina Pectoris; D001807:Blood Vessel Prosthesis; D003251:Constriction, Pathologic; D001026:Coronary Artery Bypass; D003327:Coronary Disease; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction; D011183:Postoperative Complications; D012008:Recurrence | [
"D000368",
"D000787",
"D001807",
"D003251",
"D001026",
"D003327",
"D005260",
"D005500",
"D006801",
"D008297",
"D008875",
"D009203",
"D011183",
"D012008"
] | Association between early graft patency and late outcome for patients undergoing artery bypass graft surgery. | For a group of 658 patients who received coronary artery bypass graft surgery, we investigated the correlation between the degree of early (6 months) graft patency and recurrence of anginal symptoms, late myocardial infarction, and postoperative coronary-related death. The patients were grouped according to the number of surgically placed grafts, and each group was further subgrouped on the basis of the number of grafts functioning at the early postsurgical follow-up examination. The patients were observed over a period as long as 13 years. The frequency with which angina returned correlated significantly with the degree of patency within each of the groups (one, two, three, or four grafts); patients with a higher percentage of patent grafts experienced longer periods of freedom from angina. On the average, patients with all of their multiple grafts patent experienced at least 7 more years of symptomatic relief than their counterparts with all grafts occluded. Most surprisingly, the rate of the return of angina for those patients who had all grafts patent and were completely revascularized was independent of the number of diseased vessels or the number of grafts placed. The findings for coronary death and postoperative infarction showed similar trends. | 14,811,315 | true | Association between early graft patency and late outcome for patients undergoing artery bypass graft surgery. For a group of 658 patients who received coronary artery bypass graft surgery, we investigated the correlation between the degree of early (6 months) graft patency and recurrence of anginal symptoms, late myocardial infarction, and postoperative coronary-related death. The patients were grouped according to the number of surgically placed grafts, and each group was further subgrouped on the basis of the number of grafts functioning at the early postsurgical follow-up examination. The patients were observed over a period as long as 13 years. The frequency with which angina returned correlated significantly with the degree of patency within each of the groups (one, two, three, or four grafts); patients with a higher percentage of patent grafts experienced longer periods of freedom from angina. On the average, patients with all of their multiple grafts patent experienced at least 7 more years of symptomatic relief than their counterparts with all grafts occluded. Most surprisingly, the rate of the return of angina for those patients who had all grafts patent and were completely revascularized was independent of the number of diseased vessels or the number of grafts placed. The findings for coronary death and postoperative infarction showed similar trends. |
7,472,829 | D016470:Bacteremia; D002648:Child; D002675:Child, Preschool; D003428:Cross Infection; D018450:Disease Progression; D004452:Echocardiography; D004697:Endocarditis, Bacterial; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D010493:Pericarditis; D011446:Prospective Studies; D013203:Staphylococcal Infections; D013211:Staphylococcus aureus; D016896:Treatment Outcome | [
"D016470",
"D002648",
"D002675",
"D003428",
"D018450",
"D004452",
"D004697",
"D005260",
"D006801",
"D007223",
"D007231",
"D008297",
"D010493",
"D011446",
"D013203",
"D013211",
"D016896"
] | Cardiac complications in children with Staphylococcus aureus bacteremia. | Clinically silent endocarditis was detected in 4 (11%) of 36 hospitalized children with staphylococcal bacteremia who underwent echocardiographic examination. Pericarditis was detected in two further children. Only one child had underlying cardiac disease (patent ductus arteriosus). Echocardiography should be considered in children with staphylococcemia even if an obvious extracardiac focus is apparent. | 14,956,335 | true | Cardiac complications in children with Staphylococcus aureus bacteremia. Clinically silent endocarditis was detected in 4 (11%) of 36 hospitalized children with staphylococcal bacteremia who underwent echocardiographic examination. Pericarditis was detected in two further children. Only one child had underlying cardiac disease (patent ductus arteriosus). Echocardiography should be considered in children with staphylococcemia even if an obvious extracardiac focus is apparent. |
18,094,888 | D000328:Adult; D000367:Age Factors; D000368:Aged; D001938:Brazil; D016022:Case-Control Studies; D002598:Chagas Cardiomyopathy; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D012959:Socioeconomic Factors | [
"D000328",
"D000367",
"D000368",
"D001938",
"D016022",
"D002598",
"D002908",
"D005260",
"D006801",
"D008875",
"D015999",
"D012307",
"D012959"
] | Case-control study of factors associated with chronic Chagas heart disease in patients over 50 years of age. | A case-control study on chronic Chagas heart disease (CCHD) was carried out between 1997 and 2005. Ninety patients over 50 years of age were examined for factors related to (CCHD). Fourty-six patients (51.1%) with Chagas heart disease (anomalous ECG) were assigned to the case group and 44 (48.9%) were included in the control group as carriers of undetermined forms of chronic disease. Social, demographic (age, gender, skin color, area of origin), epidemiological (permanence within an endemic zone, family history of Chagas heart disease or sudden death, physical strain, alcoholism, and smoking), and clinical (systemic hypertension) variables were analyzed. The data set was assessed through single-variable and multivariate analysis. The two factors independently associated with heart disease were age--presence of heart disease being three times higher in patients over 60 years of age (odds ratio, OR: 2.89; confidence interval of 95%: 1.09-7.61)--and family history of Chagas heart disease (OR: 2.833, CI 95%: 1.11-7.23). Systemic hypertension and gender did not prove to hold any association with heart disease, as neither did skin color, but this variable showed low statistical power due to reduced sample size. | 13,633,708 | true | Case-control study of factors associated with chronic Chagas heart disease in patients over 50 years of age. A case-control study on chronic Chagas heart disease (CCHD) was carried out between 1997 and 2005. Ninety patients over 50 years of age were examined for factors related to (CCHD). Fourty-six patients (51.1%) with Chagas heart disease (anomalous ECG) were assigned to the case group and 44 (48.9%) were included in the control group as carriers of undetermined forms of chronic disease. Social, demographic (age, gender, skin color, area of origin), epidemiological (permanence within an endemic zone, family history of Chagas heart disease or sudden death, physical strain, alcoholism, and smoking), and clinical (systemic hypertension) variables were analyzed. The data set was assessed through single-variable and multivariate analysis. The two factors independently associated with heart disease were age--presence of heart disease being three times higher in patients over 60 years of age (odds ratio, OR: 2.89; confidence interval of 95%: 1.09-7.61)--and family history of Chagas heart disease (OR: 2.833, CI 95%: 1.11-7.23). Systemic hypertension and gender did not prove to hold any association with heart disease, as neither did skin color, but this variable showed low statistical power due to reduced sample size. |
22,262,598 | D000328:Adult; D000465:Algorithms; D016208:Databases, Factual; D006801:Humans; D002546:Ischemic Attack, Transient; D017063:Outcome Assessment, Health Care; D011237:Predictive Value of Tests; D020521:Stroke; D054928:Validation Studies as Topic | [
"D000328",
"D000465",
"D016208",
"D006801",
"D002546",
"D017063",
"D011237",
"D020521",
"D054928"
] | A systematic review of validated methods for identifying cerebrovascular accident or transient ischemic attack using administrative data. | OBJECTIVE
To perform a systematic review of the validity of algorithms for identifying cerebrovascular accidents (CVAs) or transient ischemic attacks (TIAs) using administrative and claims data.
METHODS
PubMed and Iowa Drug Information Service searches of the English language literature were performed to identify studies published between 1990 and 2010 that evaluated the validity of algorithms for identifying CVAs (ischemic and hemorrhagic strokes, intracranial hemorrhage, and subarachnoid hemorrhage) and/or TIAs in administrative data. Two study investigators independently reviewed the abstracts and articles to determine relevant studies according to pre-specified criteria.
RESULTS
A total of 35 articles met the criteria for evaluation. Of these, 26 articles provided data to evaluate the validity of stroke, seven reported the validity of TIA, five reported the validity of intracranial bleeds (intracerebral hemorrhage and subarachnoid hemorrhage), and 10 studies reported the validity of algorithms to identify the composite endpoints of stroke/TIA or cerebrovascular disease. Positive predictive values (PPVs) varied depending on the specific outcomes and algorithms evaluated. Specific algorithms to evaluate the presence of stroke and intracranial bleeds were found to have high PPVs (80% or greater). Algorithms to evaluate TIAs in adult populations were generally found to have PPVs of 70% or greater.
CONCLUSIONS
The algorithms and definitions to identify CVAs and TIAs using administrative and claims data differ greatly in the published literature. The choice of the algorithm employed should be determined by the stroke subtype of interest. | null | false | A systematic review of validated methods for identifying cerebrovascular accident or transient ischemic attack using administrative data. OBJECTIVE
To perform a systematic review of the validity of algorithms for identifying cerebrovascular accidents (CVAs) or transient ischemic attacks (TIAs) using administrative and claims data.
METHODS
PubMed and Iowa Drug Information Service searches of the English language literature were performed to identify studies published between 1990 and 2010 that evaluated the validity of algorithms for identifying CVAs (ischemic and hemorrhagic strokes, intracranial hemorrhage, and subarachnoid hemorrhage) and/or TIAs in administrative data. Two study investigators independently reviewed the abstracts and articles to determine relevant studies according to pre-specified criteria.
RESULTS
A total of 35 articles met the criteria for evaluation. Of these, 26 articles provided data to evaluate the validity of stroke, seven reported the validity of TIA, five reported the validity of intracranial bleeds (intracerebral hemorrhage and subarachnoid hemorrhage), and 10 studies reported the validity of algorithms to identify the composite endpoints of stroke/TIA or cerebrovascular disease. Positive predictive values (PPVs) varied depending on the specific outcomes and algorithms evaluated. Specific algorithms to evaluate the presence of stroke and intracranial bleeds were found to have high PPVs (80% or greater). Algorithms to evaluate TIAs in adult populations were generally found to have PPVs of 70% or greater.
CONCLUSIONS
The algorithms and definitions to identify CVAs and TIAs using administrative and claims data differ greatly in the published literature. The choice of the algorithm employed should be determined by the stroke subtype of interest. |
1,338,148 | D000208:Acute Disease; D000368:Aged; D001342:Autonomic Nervous System Diseases; D002545:Brain Ischemia; D002561:Cerebrovascular Disorders; D004562:Electrocardiography; D004569:Electroencephalography; D006801:Humans; D002537:Intracranial Arteriosclerosis; D008875:Middle Aged | [
"D000208",
"D000368",
"D001342",
"D002545",
"D002561",
"D004562",
"D004569",
"D006801",
"D002537",
"D008875"
] | [The characteristics of the autonomic disorders in acute cerebral circulatory disturbances]. | The problem of the role of the autonomic nervous system (ANS) in the mechanism of symptom formation and in the pathogenesis of acute disturbances of cerebral circulation (ADCC) has not been studied well. Bearing this in mind, the authors examined 78 patients who suffered ADCC. The patients were divided into 2 groups. The first group was made up of 50 patients who suffered ischemic brain stroke with a stable neurological defect (SSD), the second one comprised 28 patients who suffered brain stroke with a reversible neurological defect (SRD). It has been established as a result that the initial level of sympatheticotonia and the intensity of the signs of vegetodystonia was higher in patients with SSD. Electrophysiological studies have demonstrated that in SRD, the level of ascending nonspecific brain activation prevailed according to the responsiveness of the reference alpha-rhythm as compared with the first group patients and the control group. The data obtained are discussed from the standpoint of the compensatory role played by the autonomic nervous system in the pathogenesis and course of the clinical forms of ADCC differing in the gravity and prognosis. | null | false | [The characteristics of the autonomic disorders in acute cerebral circulatory disturbances]. The problem of the role of the autonomic nervous system (ANS) in the mechanism of symptom formation and in the pathogenesis of acute disturbances of cerebral circulation (ADCC) has not been studied well. Bearing this in mind, the authors examined 78 patients who suffered ADCC. The patients were divided into 2 groups. The first group was made up of 50 patients who suffered ischemic brain stroke with a stable neurological defect (SSD), the second one comprised 28 patients who suffered brain stroke with a reversible neurological defect (SRD). It has been established as a result that the initial level of sympatheticotonia and the intensity of the signs of vegetodystonia was higher in patients with SSD. Electrophysiological studies have demonstrated that in SRD, the level of ascending nonspecific brain activation prevailed according to the responsiveness of the reference alpha-rhythm as compared with the first group patients and the control group. The data obtained are discussed from the standpoint of the compensatory role played by the autonomic nervous system in the pathogenesis and course of the clinical forms of ADCC differing in the gravity and prognosis. |
1,467,188 | D017541:Aneurysm, False; D000785:Aneurysm, Infected; D017544:Aortic Aneurysm, Abdominal; D002006:Brucellosis; D006801:Humans; D008297:Male; D008875:Middle Aged; D011859:Radiography | [
"D017541",
"D000785",
"D017544",
"D002006",
"D006801",
"D008297",
"D008875",
"D011859"
] | False aneurysm of the abdominal aorta due to Brucella suis. | A 48-year-old man presented with a fissured false aneurysms of the abdominal aorta due to Brucella suis. Clinical findings were lumbosciatic pain, fever, and sudation. Diagnosis was reached through abdominal computed tomographic (CT) scan and arteriograms. An extremely large false aneurysm, thrombosed and perforated posteriorly, was found in the infrarenal aorta. Semiurgent therapy consisted of resection of the aneurysm and prosthetic Dacron graft replacement associated with a transposed omental wrap. Antibiotic therapy was administered for three months. Although bacteriologic specimens were negative, brucellosis was diagnosed because of a positive Wright test and high Brucella antibodies in this patient originating from an endemic area. Six months after surgery he is apparently in good health. | 13,101,780 | true | False aneurysm of the abdominal aorta due to Brucella suis. A 48-year-old man presented with a fissured false aneurysms of the abdominal aorta due to Brucella suis. Clinical findings were lumbosciatic pain, fever, and sudation. Diagnosis was reached through abdominal computed tomographic (CT) scan and arteriograms. An extremely large false aneurysm, thrombosed and perforated posteriorly, was found in the infrarenal aorta. Semiurgent therapy consisted of resection of the aneurysm and prosthetic Dacron graft replacement associated with a transposed omental wrap. Antibiotic therapy was administered for three months. Although bacteriologic specimens were negative, brucellosis was diagnosed because of a positive Wright test and high Brucella antibodies in this patient originating from an endemic area. Six months after surgery he is apparently in good health. |
Subsets and Splits