we reported a woman with chronic ( long - term ) exposures to dichlorvos , which resulted in liver injury and cirrhosis . she was diagnosed after a second liver biopsy , which was correlated with laboratory findings . at the same time a detailed inquiry of medical history and liver biopsy are necessary for the diagnosis of toxin - induced aih . autoimmune hepatitis ( aih ) is a chronic necroinflammatory liver disease of unknown etiology with yearly increases in incidence . the diagnosis of the disease is based on the clinical and laboratory findings , as well as the exclusion of other causes of chronic liver diseases , such as drug - induced liver injury ( dili ) , viral hepatitis , wilson disease and overlap syndrome ( 1 - 5 ) . recently , a growing number of drug - induced autoimmune liver diseases ( diaild ) were reported . the dili is a potential complication that can occur with the intake of many medications , herbs and/or dietary supplements . multiple drugs and environmental chemicals are capable of evoking a certain degree of liver injury . several drugs have been identified to cause aih that may persist after discontinuation , suggesting that they triggered true autoimmunity . these include oxyphenisatin , nitrofurantoin , minocycline , chlometacin and alpha - methyl dopa ( 6 , 7 ) . recently , drug - induced autoimmune hepatitis ( diaih ) has been reported to be caused by several drugs , while toxin agent induced aih is rare ( 8) . we reported here a woman with chronic ( long - term ) exposures to dichlorvos , which resulted in liver injury and cirrhosis . she was diagnosed with aih after a second liver biopsy , correlated with laboratory features . at the same time a 49-year - old chinese woman was admitted to our hospital for the second time with complaints of loss of appetite , tiredness , feeling weak , intermittent dark colored urine and abnormal liver function for two and a half years . two and half years prior to admission , the patient presented for the same symptoms and also jaundice . initially , she presented the following values for serum parameters : alanine transaminase ( alt ) 1558 u / l ( normal 5  40 u / l ) , aspartate transaminase ( ast ) 1267 u / l ( normal 10  40 u / l ) , total bilirubin ( tbil ) 133.5 umol / l ( normal 3  20 umol / l ) , alkaline phosphatase ( akp ) 182 u / l ( normal 15  130 u / l ) , albumin ( alb ) 45.5 g / l ( normal 35  55 g / l ) , prothrombin time ( pt ) 11.5 seconds ( normal 10  14 seconds ) , international normalized ratio ( inr ) 0.96 ( normal 0.8  1.2 ) . the hbsag , anti - hav , anti - hcv and anti - hev were negative . anti - nuclear antibody ( ana ) , anti - smooth muscle antibody ( sma ) and anti - mitochondrial antibody ( ama ) were negative . she was admitted to the local hospital and treated with glycyrrhizic acid , for one month , with recovery of liver enzymes levels . one year ago , when the patient was admitted to our hospital for the first time , she was alert and oriented to time , place , and person . her body temperature was 36.5c , pulse rate 76/min , respiratory rate 20/min , and blood pressure 120/80 mmhg . her liver function tests showed : alt 335 u / l , ast 657 u / l , tbil 208.5 umol / l , direct bilirubin ( dbil ) 141.3 umol / l , alb 24.3 the laboratory examination findings included : red blood cell count ( rbc ) 3.04  10/l , white blood cell count ( wbc ) 4.3  10/l , platelet count ( plt ) 42  10/l , hemoglobin ( hb ) 10 g / l , pt 18 seconds , inr 1.52 , negative ana , negative ama . abdominal ultrasonography revealed cirrhosis , which led to a diagnosis of decompensated cirrhosis for this patient . on 5th day of admission , a couple of hours later , she reported impaired vision and within several hours , she was totally blind . she could not see movement of hand at the distance of 0.2 m. there was no light perception , although the papillary direct and consensual reflexes to light were normal in both eyes . she was treated with branched chain amino acid supplements , lactulose , and ornithine aspartate . after 18 hours , serum ammonia level dropped to 21 umol / l , she was alert and oriented , and her vision returned . because of her elevated liver enzymes and tbil , the patient was treated with glutathione , silibinin , glycyrrhizic acid , and short course steroid therapy . after 15 days , liver enzymes and bilirubin decreased significantly , and a liver biopsy was performed . liver histology revealed severe cirrhosis ( figure 1 a ) , and the possible reason was toxin or drug induced liver injury . her medication history and toxic material contacting history were inquired repeatedly . after 2 days , the patient told us that she had a habit of using dichlorvos painting bed mat to kill bed flea , and she had done this for several years the hepatoprotective drugs and low - dose of steroids were used after discharging from hospital . eleven months later , the patient admitted to our hospital for the second time for abnormal liver function . this time , the laboratory results included alt 304 u / l , ast 292 u / l , tbil 18 umol / l , dbil 7.4 umol / l , akp 123 u / l , ggt 239 u / l , alb 41.9 g / l , glb 31.7 g / l , pt 10.1 seconds , prothrombin activity ( pta ) 132.6% ( 80  150 ) , inr 0.94 , activated partial thromboplastin time ( aptt ) 33.2 seconds ( 21  38 seconds ) , fibrinogen 2.04 g / l ) , thrombin time 19.8 seconds ( 14  20 seconds ) . the hemoleucogram parameters were wbc 4.3  10/l , rbc 4.68  10/l , hb 114.4 g / l , plt 92.4  10/l , ana h : n 1:1000 , igg 19.3 liver biopsy was performed again because of unfavorable therapeutic result and discontinuation of low - dose inhaled corticosteroids , and this time the liver histology showed the portal inflammation , interface hepatitis , cirrhosis and relieved bridging necrosis ( figure 1 b ) . presence of plasma cells in portal and intra - acinar structures , and rosette formation were features that favored aih . six scores were obtained from the simplified criteria for the diagnosis of aih , the second time in our hospital , therefore supporting a possible diagnosis of aih . we reviewed the first presentation of the patient , with clinical history and liver biopsy with the same criteria , and the score was 3 , and the diagnosis of aih was excluded . . with long term treatment and low dose clycocorticosteroid therapy , the clinical symptoms and liver biochemical indicators of the patient improved . dichlorvos is an organophosphoric insecticide , widely used for controlling internal and external parasites in livestock and domestic animal , and also insects in houses and in fields . dichlorvos is highly toxic by inhalation , dermal absorption and ingestion ( 9 - 11 ) . acute ( short - term ) and chronic ( long - term ) exposures of humans to dichlorvos result in the inhibition of an enzyme , acetylcholinesterase , with neurotoxic effects , including perspiration , vomiting , diarrhea , drowsiness , fatigue , headache , and , at high concentrations , convulsions and coma . yang j s study aimed to assess the metabolomic profile and related histopathological outcomes of rat plasma after chronic low - dose exposure to dichlorvos , and significant changes in several of the metabolites were found in all the treated groups , compared with the control group ( 10 , 12 ) . lysopc ( 15:0/0:0 ) , lysopc ( 16:0/0:0 ) , lysopc ( 17:0/0:0 ) , lysopc ( 0:0/18:0 ) , sphingosine , sphinganine , c16 sphinganine , c17 sphinganine , and arachidonic acid were decreased in the treated groups . our patient has a history of long - time low - dose dermal exposure to dichlorvos . dichlorvos could be absorbed easily through the skin , and a small amount of long - term absorption can lead to toxic - induced liver injury . this patient had abnormal liver function for one and half years , and was admitted four times to hospital without identifying the true reason of liver injury . this rare medical record of long - time and low - dose dermal exposure to dichlorvos provides important clues and basis for the diagnosis of toxic liver injury . therefore , a thorough medical history from the patient is very important for the physician in the diagnosis of liver diseases ( 13 ) . at least three clinical types have been proposed , which refers to diaild : aih with dili ( that is patients with known aih with high probability of association , which often leads to fibrosis on histology ) , diaih and immune mediated dili ( im - dili ) with clinical , biochemical , and histological signs similar to aih . characteristic for diaih are patients with unrecognized aih or predisposition to aih , in whom aih is induced by dili . these cases have a good response to steroids and may present relapse after withdrawal of immunosuppression , with the need for continued immunosuppressive treatment . the chance for an association of drug intake in a patient with first presentation of aih drug - induced autoimmune or autoimmune like hepatitis is an acute or chronic , and potentially severe , side effect of drugs ( 14 ) . toxin - induced aih is rare ( 8) . in this patient without history of aih , the liver enzyme became abnormal with interruption of low - dose corticosteroids , liver fibrosis progressing to cirrhosis . the titer of ana on the first admittance to our hospital was negative , although on the second admission , the ana titer was positive . also , the igg concentration was higher . the score of simplified criteria for the diagnosis of aih ( 15 ) was 3 on the first admission , and 6 on second admission , and met the established international criteria of aih . the dili is thought to involve a complex interaction between chemical properties of the drug , environmental , genetic and pre - existing host factors ( 16 ) . recognized predisposing factors include ethnicity , cytochrome polymorphisms , concomitant liver disease , age , nutritional status and diet , gender and pregnancy ( 16 ) . the dili is either an overcompensating immune response or a direct cell injury by the drug or its metabolite ( 17 ) . therefore , we think the mechanism of the toxin - induced liver injury was the same as for a drug , which sometimes persists after drug discontinuation , suggesting that they awaken latent autoimmunity . the release of hepatic antigens and consecutive presentation of these autoantigens by immune cells may lead to a continued autoagressive - immune reaction in genetically susceptible individuals . in a long term follow - up , many of them developed cortical blindness is defined as bilateral impairment of vision , with normal ocular structures , normal pupillary light reflex , and absence of nystagmus ( 18 ) . hepatic cortical blindness is an unusual clinical complication of hepatic encephalopathy and must be differentiated with nervous system diseases , such as cerebral vascular disease , ophthalmology disorder , or other cause of lead to binocular vision disorder ( 19 ) . this patient had normal papillary reflexes , and no organic brain lesion on brain ct and tcd , the eeg showed no anomaly , no ophthalmological disorder by ophthalmoscopic exam was evident and slit lamp examination revealed no abnormalities in the ocular fundus ( 20 ) . this patient had decompensated cirrhosis and impaired vision , which were associated with elevated serum ammonia due to eating too much proteins , and the impaired vision disappeared following cessation of high serum ammonia . consequently , we considered that the elevated serum ammonia level was the cause of the hepatic cortical blindness in this patient . the prevalence of hepatic cortical blindness is low , and is easy to miss the diagnosis . therefore , in the clinic , when any patient with abnormal liver enzymes and cortical blindness presents , we should think of this disease . meanwhile , accurate diagnosis is necessary for dili patients with a history of medication , and several of dili tend to develop diaih . a detailed inquiry of medical history is necessary for the diagnosis of toxin - induced aih .
introduction : drug - induced liver injury is a frequent cause of hepatic dysfunction . 
 several drugs have been identified to cause autoimmune hepatitis ( aih ) . 
 environmental chemicals are capable of triggering a certain degree of liver injury . however , toxin induced aih is rare.case presentation : we reported a woman with chronic ( long - term ) exposures to dichlorvos , which resulted in liver injury and cirrhosis . 
 she was diagnosed after a second liver biopsy , which was correlated with laboratory findings . at the same time , she experienced hepatic cortical blindness during her first admission.conclusions:chronic ( long - term ) exposures to dichlorvos can lead to aih . 
 a detailed inquiry of medical history and liver biopsy are necessary for the diagnosis of toxin - induced aih . 
 corticosteroid therapy is associated with favorable evolution .