Medical History Of Hepatitis Research Articles

An uncommon complication during management of gastric varices

A 69-year-old woman presented to the emergency department with melena for 3 days. She has a medical history of hepatitis B virus-related cirrhosis. The esophagogastroduodenoscopy showed a gastric varix, GOV-2, with an ulcer on its surface. Histoacryl injection was attempted, but massive bleeding ensued just as the needle touched it. Five milliliters of a 1:1 mixture of N-butyl-2-cyanoacrylate and lipiodol were injected into the varix (1 mm per injection, at the same site). The patient was then transferred to the intensive care unit. Shortness of breath with frequent dry cough developed 1 day later. The patient was slightly tachycardic at 97 beats per minute, tachypneic at 27 times per minute, and normotensive at 132/54 mmHg, with SpO2 of 98%. Physical examination showed bilateral clear breath sounds. Laboratory investigations showed a hemoglobin level of 7.1 g/dL, platelet count of 15 × 103/μL, and D-dimer of 1285.4 ng/ml. Arterial blood gas analysis showed pH 7.436, pCO2 34.9 mmHg, pO2 120.6 mmHg (under O2 nasal cannula 3 L/min), and bicarbonate 23.8 mEq/L. The chest X-ray showed branching opacities over left hilum (Figure 1). What is the diagnosis? Non-contrast chest computerized tomography showed hyperdense material in the left pulmonary branches (Figure 2), and the diagnosis of acute pulmonary embolism after histoacryl injection was made. The patient was under mechanical ventilation support for total 18 days, with only supportive treatment during this period. She was discharged smoothly without any oxygen support. Histoacryl injection therapy is effective for the gastric varices. The overall complication rate ranged from 0.5% to 5%,1 and pulmonary embolism is an unusual but potentially life-threatening one,2 especially in patients with large varices requiring large volumes of sclerosant.3 Other contributory factors include the rate of injection and ratio of the constituent components of the sclerosant.3 Although a leak through an arteriovenous pulmonary shunt or an open foramen ovale had been proposed,4 there was no such abnormality in our case. Hyperdense segments of the pulmonary arteries with respect to the surrounding vessels are the image features on chest X-ray (the so-called “vascular cast sign”), and a confirmatory non-contrast computerized tomography will be more suitable than a contrasted one in detecting the radio-opaque lipiodol.5 All endoscopists should keep this rare complication in mind, and timely recognition—if it occurs, unfortunately—relies on the physician's timely awareness. The authors declare no conflict of interest. According to the institutional review board (IRB), there is no need of IRB approval for an image article in our hospital. A written informed consent was obtained before starting, and the authors followed the principles outlined in the WMA Declaration of Helsinki throughout the writing process.

ODP499 Myxedema Coma: A Challenging Presentation of an Uncommon Disease

Abstract Myxedema coma is a rare diagnosis but if not early recognized, this medical emergency possesses a high mortality rate. Over the years, it has been described predominantly in elderly women with history of hypothyroidism and as a precipitant factor that converges to evolve in a full presentation. We report a case of myxedema coma in a young male without risks for this disease. A 38 y/o Latin-American male with medical history ofhepatitis C virus and intravenous drug abuser that was brought to the emergency department after being found in the streets. The patient was agitated, oriented only to person, had slurred speech and reports last dose of heroin was two days ago. Denied other condition or medications. Vital signs BP 103/90mmHg, pulse: 41 bpm, T: 35.8°C RR: 19 rpm, SPO2: 99% at room air and BMI: 23.9. kg/m 2 . Physical examination pertinent for a disheveled male with anasarca, diffused dry skin with piloerection without surgery scars, non-palpable nor tender thyroid gland, bilateral exophthalmos, decreased bowel sound, positive fluid wave and abdomen diffusely tender to palpation with bilateral lower extremities infected ulcers. Blood workup showed impaired renal function, severe azotemia, hyponatremia, hypoglycemia and normocytic anemia. TSH 147uIU/mL. Imaging studies remarkable for bilateral pleural effusions, intestinal ileus, and negative brain CT scan. Patient was admitted with diagnosis of uremic encephalopathy, drug withdrawal and soft skin tissue infection. Patient was treated with emergent hemodialysis, drug withdrawal measures and IV antibiotics. Despite treatment, patient's clinical condition began to decline. He was found obtunded requiring endotracheal intubation. TSH was persistently elevated in 55.7uIU/mL with suppressed free T4 <0.42ng/dL. Patient noted with persistent sinus bradycardia, hypothermia, ileus, ascites, bilateral pleural effusions, and hypotension. Patient was consulted to endocrinology department who evaluated the overall clinical presentation and myxedema coma was diagnosed. He was treated with levothyroxine 100mg IV for two days, but eventually developed multiorgan failure and unfortunately died. Myxedema coma is a complication of severe hypothyroidism that slows down the functions of multiple organs and directly affects their function. It is an endocrinologic emergency that leads to decline of the clinical presentation of patients. The epidemiology favors this presentation in patients with history of hypothyroidism, more specifically elderly women. Multiple conditions may present with similar signs and symptoms. Physicians must be aware that myxedema coma must be suspected in a patient with altered mental status, hypothermia, hypoglycemia, hypotension, anasarca among others even in the presence of more common conditions and in rare populations like our patient. Opioid Induced Endocrinopathies still remain a complication that is underdiagnosed. The aim of this case is to createmedical awareness on the importanceto consider myxedema coma in patients with Opioid abuse and withdrawal. Presentation: No date and time listed

DISSEMINATED HISTOPLASMOSIS IN A NON-HIV PATIENT: A CASE REPORT

Histoplasmosis is a systemic infectious disease caused by the fungus Histoplasma capsulatum, which is present in contaminated soils. Infection occurs by inhaling microconidia from the filamentous phase of the fungus, and 1 of the variations of the clinical spectrum of this disease is to affect immunocompromised patients. A female patient, 41 years old, complained of dysphagia and weight loss. Her habits were positive for alcoholism, and she was a nonsmoker, with a medical history of hepatitis B, ganglionar and pulmonary tuberculosis, and intestinal histoplasmosis 4 years ago, negative for HIV infection. Intra-oral examination showed a granulomatous ulcer in soft and hard palate transition on the right and presence of lymphadenopathy at the submandibular region bilaterally. The incisional biopsy was performed, and material was sent for polymerase chain reaction analysis of leishmaniasis, with negative result. Histopathologic examination confirmed histoplasmosis. Treatment with amphotericin B was started, and after 2 months the oral lesion regressed but gut infection persisted. Histoplasmosis is a systemic infectious disease caused by the fungus Histoplasma capsulatum, which is present in contaminated soils. Infection occurs by inhaling microconidia from the filamentous phase of the fungus, and 1 of the variations of the clinical spectrum of this disease is to affect immunocompromised patients. A female patient, 41 years old, complained of dysphagia and weight loss. Her habits were positive for alcoholism, and she was a nonsmoker, with a medical history of hepatitis B, ganglionar and pulmonary tuberculosis, and intestinal histoplasmosis 4 years ago, negative for HIV infection. Intra-oral examination showed a granulomatous ulcer in soft and hard palate transition on the right and presence of lymphadenopathy at the submandibular region bilaterally. The incisional biopsy was performed, and material was sent for polymerase chain reaction analysis of leishmaniasis, with negative result. Histopathologic examination confirmed histoplasmosis. Treatment with amphotericin B was started, and after 2 months the oral lesion regressed but gut infection persisted.

2278 Rapidly Progressive Hepatitis C After Liver Transplantation Treated With Glecaprevir/Pibrentasvir

INTRODUCTION: Hepatitis C recurrence following liver transplantation occurs in all patients with chronic HCV infection who have detectable serum HCV RNA levels prior to transplant. Less than 10% of these patients develop an acute and severe phenotype called fibrosing cholestatic hepatitis, which often involves fibrosis, rapid graft loss and decreased survival. The introduction of direct-acting antiviral agents (DAAs) have changed the paradigm of treatment of these patients. CASE DESCRIPTION/METHODS: A 62-year-old woman with a medical history of hepatitis C infection, hepatocellular carcinoma status post orthotropic liver transplantation, diabetes mellitus and hypertension who was hospitalized for fatigue and elevated liver chemistries following her liver transplantation. Laboratory tests showed a white cell count 6.67 × 103/μL, creatinine 1.1 mg/dL, aspartate aminotransferase 592 U/L, alanine aminotransferase 504U/L, alkaline phosphatase 312 U/L, bilirubin 3.5 mg/dL, albumin 2.9 g/dL. Acute hepatitis work up showed a positive hepatitis C virus antibodies with genotype 1B, with a viral load of 80 million IU/mL HCV RNA. HBsAg, HBc IgG, HBc IgM, and hepatitis A virus IgM were negative. Evaluation for Epstein-Barr virus, cytomegalovirus and herpes simplex virus were negative. Ultrasound of the abdomen revealed that the liver is normal in size, echotexture and contours. No focal hepatic lesions. Normal hepatic blood flow. The patient underwent liver biopsy that showed lymphocytic portal inflammation with frequent lobular apoptosis consistent with active chronic hepatitis C (MHAI: 5-6/18). Mild portal fibrosis (ISHAK FIBROSIS STAGE: 1/6) and minimal evidence of acute t cell-mediated rejection (rejection activity index: 1/9). During the patient hospitalization her liver chemistries significantly worsened and peaked to aspartate aminotransferase 740 U/L, alanine aminotransferase 511U/L, alkaline phosphatase 312 U/L, bilirubin 3.5 mg/dL. We decided to start the patient on Glecaprevir/Pibrentasvir for acute and severe hepatitis. Fourteen days after starting Glecaprevir/Pibrentasvir, the patient viral load decreased to 782 IU/mL HCV RNA and normalized liver chemistries with AST19 and ALT 27. The patient denied any adverse events due to the treatment. DISCUSSION: To our knowledge, this is the first case report of treating early and aggressive form of HCV recurrence with Glecaprevir/Pibrentasvir. The dramatic improvement of the patient suggest that DAA might be safe and effective in this situation.

The Mysterious Hand

CASE REPORTA 50-year-old man with medical history of hepatitis C (with a low viral load treated a decade prior) initially presented to an outside provider with a progressive rash, digit swelling, and joint pain and was evaluated for oligoarticular synovitis. Joints affected included the right knee,

Multiple Idiopathic Cervical Root Resorptions in Patients with Hepatitis B Virus Infection

Multiple idiopathic cervical root resorptions are a rare finding. The diagnosis is perplexing, and treatment is a challenge. It is a debilitating condition that often leads to extraction of all the involved teeth. Various theories have been given for explanation of the disease entity; however, the etiology remains elusive. This report describes a case of an 18-year-old man with idiopathic cervical resorption that progressed aggressively and involved 20 teeth. The medical history of hepatitis B virus infection made this case unique in the literature. The mechanism of increased osteoclastic activity in patients with hepatitis B virus infection is discussed as a predisposing factor for the development of root resorption.

Rapid Progression of Chronic Hepatitis C Virus Infection Following Treatment Failure With Harvoni: A Case Report

Patient is a 71-year-old African American male with medical history of hepatitis C virus infection S/P failed Harvoni therapy, hypertension, diabetes mellitus type II, chronic kidney disease stage IV, nicotine dependence and marijuana use. Was diagnosed of HCV infection about 16 years prior treatment was initiated. Treatment for Hepatitis C with Harvoni was started on (2/20/16) and completed 12 week course treatment with about 96% compliance. Following treatment patient HCV viral load became undetectable. 6-month post treatment HCV was detected with associated NS5A drug resistance. Patient remained asymptomatic except for fatigue that started during Harvoni treatment. Patient presented to the emergency department with pain was described has dull, located in the epigastric area, non-radiating, no known aggravating factor, relieved with pain medications, associated with loss of appetite, weight loss and constipation. On examination patient was cachetic, jaundiced, no asterixis, normal cardiovascular and decrease breath sounds in the lower lung zones worse on the right, tender hepatomegaly. Laboratory test result include Hepatitis C genotype 1a, fibrosis score 0.41, F, fibrosis stage F1-F2, necroinflammation A1-A2, Alpha 2-Macroglobulins 370mg/dL(high). Resistance test showed no RAV (Resistance associated variant) for NS5B but possible RAV to NS5A1. Hepatitis Be core Ab Positive, Hepatitis B surface Ab non-reactive, Hep A ab Neg, AFB Serum, Tumor Marker (3.3ng/Ml). CT abdomen pelvis showed heterogeneous liver mass with portal vein tumor thrombus, favoring hepatocellular carcinoma. Patient underwent Liver and lung biopsy which confirmed Hepatocellular carcinoma and squamous cell carcinoma of the lungs. Patient was started on palliative radiotherapy but died; primary cause of death respiratory failure and sepsis. Various factors have been associated with chronicity and probably progression to liver cirrhosis and hepatocellular cancer. Progression is variable with no linear relationship. Risk factors include old age, male gender, coinfection with hepatitis B, metabolic factor (obesity, insulin resistance, steatosis), use of alcohol, use of Marijuana, use of coffee and HCV genotype 3A. Other risk factors include duration of disease and being of African American descent. Studies have shown higher SVR, as high has 99% to 100% in patients treated for 24 weeks. Patients with multiple risk factors are likely to benefit from longer course of treatment.Figure

Percutaneous Tricuspid Valve Annuloplasty Under Conscious Sedation (With Only Fluoroscopic and Intracardiac Echocardiography Monitoring)

A 74-year-old woman with severe functional tricuspid regurgitation (FTR) was admitted with New York Heart Association functional class III with signs of right-sided heart failure. She had a medical history of hepatitis B–related liver disease, permanent atrial fibrillation, and previous stenting

A Palpable Painless Axillary Mass as the Clinical Manifestation of Castleman's Disease in a Patient with Hepatitis C Disease.

Introduction. Castleman's disease (CD) is a rare lymphoproliferative disorder. CD is divided into two clinical subtypes: the most common unicentric and the less usual multicentric subtype. The majority of unicentric CD affects the mediastinum, while neck, abdomen, and axilla are less common locations. Case Presentation. Herein, we describe a rare case of unicentric CD in the right axilla in a 36-year-old white male with a medical history of hepatitis C virus infection admitted to our hospital due to palpation of a painless mass in the right axilla. Complete excision of the lesion was performed and, one year after the diagnosis, patient was free of the disease. Conclusions. Although infrequent, it is important to include CD in the differential diagnosis when evaluating axillary lymphadenopathy particularly in young patients with a low-grade inflammation process and chronic disease even in the absence of an abnormal blood picture or organomegaly.

Drug eluting beads on cytology smears

To the Editor, Transarterial chemoembolization (TACE) is the most widely used primary treatment for unresectable hepatocellular carcinoma (HCC). TACE increases the in-situ dwell time and concentration of drug through vascular occlusion by drug-eluting beads (DEB). DEB consist of injectable polymeric microspheres of calibrated size that can be loaded with various antineoplastic solutions.[1] We describe here the appearance of doxorubicin drug eluding beads on cytology in a 60-year-old African-American male with a past medical history of hepatitis C, hypertension, HCC, hypothyroidism, and arthritis. The patient underwent three TACE procedures within the year for treatment of HCC. Four months after the last chemoembolization, a computed tomography (CT) scan showed a suspicious lesion next to the TACE area. An ultrasound guided fine needle aspiration and core biopsies were done of the suspicious lesion. The cytology showed moderately cellular smears composed of groups of neoplastic cells with endothelial wrapping consistent with HCC. Intermixed with hepatocytes were circumscribed dense eosinophilic globules consistent with the DEB from chemoembolization [Figures ​[Figures11–3], done 4 months ago. The core biopsy showed nests of malignant cells with focal pseudoacinar pattern, in background of cirrhosis. On reticulin stain the tumor showed decreased staining with thickened trabeculae confirming the diagnosis of HCC seen on smears. A total of four fine needle passes and two 18 gauge core biopsies were done. The chemoembolization beads were seen only in one air dried smear. Figure 1 Drug eluting beads on cytology smear (4× diff quik stain) Figure 3 drug eluting beads on cytology smear (4× diff quik stain) Figure 2 Drug eluting beads on cytology smear (4× diff quik stain) Developed in mid-2000, DEB can be loaded with cytotoxic drugs for the chemoembolization of hypervascular tumors.[2] These beads slowly release the cytotoxic drug in a controlled fashion into the tumor, inflicting local ischemia while reducing systemic drug concentrations.[2] In our patient the doxorubicin eluting beads were used. These were seen as homogenous, well circumscribed purple, foreign body globules measuring in size from 100–300 μm on air dried cytology smears stained with Romanowsky stain [Figures ​[Figures11–3]. Previously described microscopic appearance of drug eluting and radioactive beads has been reported in histology tissue sections.[1,3–5] The rationale of using these DEB is based on the assumption that the vector releases its chemotherapeutic agent, which is able to diffuse locally in the embolized area and causes the necrosis of the target tissue.[1] The tissue adjacent to beads shows characteristic coagulative necrosis and an inflammatory–fibrotic reaction few weeks after the procedure. The DEB have been demonstrated in the tissue sections from explanted liver, but to our knowledge they have not yet been described in a cytology preparation. In the current case we did see a foreign body type giant cell [Figure 4] but did not see any necrosis or fibro-inflammatory reaction adjacent to the beads. Figure 4 Foreign body type of giant cell (400× diff quik stain)

Unexpected Hemoglobin A1c Results

A 52-year-old woman with a medical history of hepatitis B, hyperlipidemia, hypertension, anemia, and depression presented to the internal medicine clinic for a routine visit. Laboratory tests 3 months previously had revealed an impaired fasting glucose concentration of 5.9 mmol/L (106 mg/dL) [reference interval, 3.9–5.6 mmol/L (70–100 mg/dL)]. Therefore, a hemoglobin (Hb)2 A1c analysis was performed. The initial Hb A1c evaluation by cation-exchange HPLC (CE-HPLC) (Hb A1c Program on the VARIANT II TURBO Link System; Bio-Rad Laboratories) showed an Hb A1c value of 115.8% (reference interval, 4.0%–6.0%) (Fig. 1). Fig. 1. CE-HPLC chromatogram for Hb A1c analysis. Hb S and an aberrant Hb A1c value of 115.8% represented the predominant Hb peaks in the chromatogram. In an effort to determine if the unusual Hb A1c result was due to potential hemoglobinopathies, we performed an Hb variant analysis with the Bio-Rad VARIANT CE-HPLC β-Thalassemia Short Program. The analysis revealed the absence of Hb A and the presence of sickle cell Hb (Hb S) (37.4%), along with normal Hb A2 (3.2%) and Hb F (<1.0%) (Fig. 2). Also evident was another large peak (53.0%) that eluted earlier than Hb A, which we called P2. This study suggested the presence of an Hb variant with a chromatographic retention time virtually identical to that of Hb A1c, in addition to Hb S (Figs. 1 and 2). A subsequent Hb electrophoretic analysis at pH 6.0 (QuickGel Acid; Helena Laboratories) identified Hb S and another abnormal band with a mobility similar to Hb F (not shown). Fig. 2. Chromatogram of Hb variants analysis with the CE-HPLC β-Thalassemia Short Program. Hb S (37.4%), wild-type Hb A2 (3.2%), and Hb F (<1.0%) were identified, but Hb A was not detected. A large peak, which we designated P2, was detected at 53.0%. ### PATIENT FOLLOW-UP To identify the Hb variants, we investigated DNA sequences corresponding to the patient's β-globin genes. This …

Nicardipine-Induced Acute Hepatitis in an Intensive Care Unit Patient

Drug-related hepatotoxicity is now the leading cause of acute liver failure in the United States, especially among patients who have no prior liver disease. Nicardipine is the only IV calcium channel blocker available for the short-term treatment of hypertension with a considerably good safety profile. We report a case of nicardipine-induced hepatitis. A patient with history of hypertension was admitted because of right middle cerebral artery infarction. Computed tomography of the brain showed evolving stroke. The patient went for cerebral angiography and stent placement, and during the procedure he had cerebral hemorrhage. He was transferred to neurosurgery. After surgery, he was started on hypertonic saline, mannitol for cerebral edema, and nicardipine drip for blood pressure control. On the fourth day after operation, he started to have fever with progressive elevation of liver enzymes [Aspartate amino transferase (AST) 450, Alanine amino transferase (ALT) 356, and alkaline phosphatase 299]. Serum bilirubin was 0.6. He did not receive blood transfusion. No medical history of hepatitis or liver disease was reported. Other medications included metoprolol and heparin. White blood cell count was 13,000. Chest x-ray did not show evidence of consolidation. Urine analysis was unremarkable. Cultures were negative. Acute hepatitis panel was negative. Cerebrospinal fluid examination was normal. Liver enzymes were trending up gradually with normal protein and bilirubin. Computed tomography of the abdomen was unremarkable. The patient's medications were reviewed. It was noticed that the patient started to have fever and elevated liver enzymes after administration of nicardipine drip. It was postulated that nicardipine may be the culprit of acute hepatitis. Nicardipine drip was stopped, and the patient was started on labetalol. Fever started to resolve, and liver enzymes started trending down toward normal. The patient remained afebrile after that.

Alteração de enzimas hepáticas em trabalhadores de refinaria de petróleo

Occupational exposure typical of an oil refinery may alter liver function among the workers. Thus, the objective of the study was to identify risk factors for liver enzyme abnormalities among oil refinery workers. The workers at an oil refinery in Northeastern Brazil underwent routine annual medical examination from 1982 to 1998. This case-control study investigated all the 150 cases of individuals with simultaneous gamma-glutamyltransferase and alanine aminotransferase abnormalities of at least 10% above reference levels. As controls, 150 workers without any liver enzyme or bilirubin abnormalities since starting to work there were selected. Odds ratios and the respective 95% confidence intervals were calculated from logistic regression models. In all the production sectors, the risk of liver enzyme abnormalities was significantly higher than in the administrative sector (OR=5.7; 95% CI: 1.7-18.4), even when the effects of alcohol, obesity and medical history of hepatitis were controlled for. During the period from 1992 to 1994, 88 out of the 89 cases occurred among workers from the various production sectors. Occupational exposure plays an important role in causing liver enzyme abnormalities among oil refinery workers. This is in addition to the specifically biological and/or behavioral risk factors such as obesity and alcohol consumption.

Alterações hepáticas em trabalhadores de uma refinaria de petróleo e em uma população de referência no Estado da Bahia, Brasil

To determine the prevalence of liver changes in workers at an oil refinery located in the state of Bahia, Brazil, as compared to a reference population with no occupational exposure to chemical products, and to describe the factors associated with the observed differences in prevalence. We studied workers at the refinery and at the company's central management office located in the city of Salvador, which is the state capital. Blood samples of 692 refinery workers and 377 workers from the reference population were analyzed. Cases were defined as individuals presenting high serum levels of both gammaglutamyltransferase (GGT) and alanine aminotransferase (ALT) (GGT > 50 U/L for males and > 32 U/L for females; ALT > 50 U/L). Data were collected on age, sex, weight, height, years working for the company, use of alcohol, smoking habits, physical exercise, occupational exposure to chemical products, use of personal safety equipment, and medical history of hepatitis, jaundice, and obesity. The prevalence of liver changes among refinery workers was 15.3% (95% CI: 12.5 to 18.1), vs. 3.8% (95% CI: 1,8 to 5,8) in the reference population. According to multiple logistic regression analysis, the prevalence of liver changes among refinery workers was 3.56 times greater (95% CI: 1,99 to 6,38) than in the reference population, regardless of the presence of other relevant co-variables, such as obesity, exercise, smoking, and alcohol consumption. These results suggest that occupational exposure may play a major role in the development of liver changes among workers at the oil refinery where the study was carried out.

Infective, chronic carriers of hepatitis C virus among blood donors with no history of clinical hepatitis.

We investigated the infectivity of three hepatitis C virus antibody (anti-HCV) positive blood donors with either hepatitis B core antibodies (anti-HBc) (Nos 1 and 2) or raised alanine aminotransferase (ALT) (No. 3). The 57 recipients of blood products from these donors during the period 1971-1990 were identified and the living 23 were tested for anti-HCV. Among these, 11 out of 14 (78%) recipients from Nos 1 and 2, and 1 out of 9 (11%) recipients from No. 3 were anti-HCV positive. The former donors had high titres of anti-C100-3 and high rating scores in the HCV recombinant immunoblot assay (RIBA). They were evidently infective, chronic carriers of HCV but had no clinical signs or medical history of hepatitis. The latter donor had low titres of anti-C100-3 and a low RIBA rating score. She had clinical signs of chronic hepatitis and persistently elevated ALT, but only one of her recipients was anti-HCV positive.

Persistence of transaminase abnormalities in former drug addicts.

A large group of ex-addicts in residence in a rehabilitation program were studied to determine their medical history of hepatitis, the frequency of SH/Au antigen, and the prevalence of liver malfunction. Fifty percent of our population had a history of hepatitis while using drugs. Among the whites, 58.4% had had hepatitis, whereas only 26% of the nonwhites had such a history. The frequency of SH/Au antigen by Ouchterlony technique (1.2/100) was consistent with that of previous studies. There was a significant decline in serum glutamic-pyruvic transaminase (SGPT) values as a function of time free of drug and needle use. There was a 40% frequency of abnormal results (> 50 Karmen units/ml) in tests taken soon after entry into the program; in tests taken after 4 months and up to a year there was a 20% frequency of abnormal results. The persistent abnormal SGPT results and liver biopsy findings in several residents with persistently elevated transaminases showed a high frequency of chronic inflammatory liver disease among the population.