1/238. sarcoidosis with selective involvement of a second liver allograft: report of a case and review of the literature.A case of sarcoidosis recurrent in a patient's second liver allograft is described. There was no granulomatous disease seen in the patient's first liver allograft. After the second orthotopic liver transplantation (OLT), the patient was successfully treated for acute rejection, aspergillus infection, and cytomegalovirus viremia. Approximately 2 months after the second OLT, the patient was treated with long-term interferon-alpha for recurrent hepatitis c. Five years after the operation, he experienced liver failure secondary to recurrent hepatitis and underwent a third OLT. This is only the second reported case of sarcoidosis recurrent in the liver parenchyma of a transplanted organ and the first in which interferon-alpha might have played a role.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/238. Clinical usefulness of conjugated bilirubin levels in patients with acute liver diseases.We used a specific method to measure conjugated bilirubin levels in patients with acute liver diseases to examine its clinical usefulness. Conjugated and total bilirubin levels were measured in 102 samples obtained from six patients with acute liver diseases (three with fulminant hepatic failure, one with acute severe hepatitis and two with acute hepatitis; see text for criteria). Total and conjugated bilirubin levels were measured with Iatro T (total)-Bil and D (direct)-Bil kits (Iatron laboratories tokyo, japan) and with conventional Nescauto T(total)-Bil and D(direct)-Bil VE kits (Nippor Shoji, Osaka, japan). The Iatro D-Bil kit measures conjugated bilirubin correctly, while the Nescauto D-Bil VE kit measures some nonconjugated bilirubin and delta bilirubin as well as conjugated bilirubin. Total bilirubin levels determined by the two methods showed good correlation. The conjugated bilirubin level measured with the Iatro D-Bil kit was strongly correlated with the direct bilirubin level measured with the Nescauto D-Bil VE kit, but there was no correlation between the conjugated-to-total bilirubin ratio and the direct-to-total bilirubin ratio. When we examined the changes in bilirubin levels in our patients with respect to outcome, we found that the two patients in whom the ratio of conjugated-to-total bilirubin exceeded 0.3 died, while all four patients in whom the ratio remained below 0.3 survived. The ratio of direct-to-total bilirubin was unrelated to outcome. The conjugated bilirubin level measured with the Iatro kits was therefore considered useful for the diagnosis and follow-up of acute liver diseases.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
3/238. An inborn error of bile acid synthesis (3beta-hydroxy-delta5-C27-steroid dehydrogenase deficiency) presenting as malabsorption leading to rickets.Deficiency of 3beta-hydroxy-delta5-C27-steroid dehydrogenase (3beta-HSDH), the enzyme that catalyses the second reaction in the principal pathway for the synthesis of bile acids, has been reported to present with prolonged neonatal jaundice with the biopsy features of neonatal hepatitis. It has also been shown to present between the ages of 4 and 46 months with jaundice, hepatosplenomegaly, and steatorrhoea (a clinical picture resembling progressive familial intrahepatic cholestasis). This paper reports two children with 3beta-HSDH deficiency who developed rickets during infancy and did not develop clinically evident liver disease until the age of 3 years. bile acid replacement resulted in considerable clinical and biochemical improvement. The importance of thorough investigation of fat soluble vitamin deficiencies in infancy is emphasised.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
4/238. nitrofurantoin-induced immune-mediated lung and liver disease.A 60-year-old woman with multiple sclerosis and recurrent urinary tract infections (UTI) was evaluated for the recent onset of a dry cough, dyspnea on exertion, and jaundice. Investigation demonstrated interstitial lung disease with bilateral infiltrates and unilateral effusion, as well as a severe chronic active hepatitis with marked fibrosis. Other notable features were positive antinuclear antibodies and anti-smooth-muscle antibodies and the absence of any possible cause except for nitrofurantoin treatment (Macrodantin, 100 mg/day), which the patient had been taking for the previous 3 years as a prophylactic measure against UTI. The patient died of pneumococcal septicemia less than 30 days after presentation. Pulmonary or hepatic injury caused by nitrofurantoin treatment is rare; their combined occurrence is hardly ever described. Combined drug-induced pulmonary and hepatic toxicity is reviewed and should be considered early in the differential diagnosis to allow reversibility and avoid serious outcomes.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
5/238. Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome.OBJECTIVE: To describe the laboratory and physical manifestations of lamotrigine toxicity presenting as anticonvulsant hypersensitivity syndrome. CASE SUMMARY: A 49-year-old white man presented to our institution with a two-day history of low-grade fever, erythema, and edema involving the periorbital area. Five days earlier, he had been placed on lamotrigine treatment for bipolar disorder. He inadvertently received four daily doses of lamotrigine 2700 mg each. physical examination was significant for periorbital edema and discrete and confluent blanching red macules and papules involving the face, trunk, and extremities. Laboratory tests revealed leukocytosis, hepatitis, and acute renal failure. With normalization of the laboratory results, the eruptions and edema gradually resolved. DISCUSSION: Lamotrigine toxicity can lead to periorbital edema, rash, and multiorgan system abnormalities. This presentation has clinical and laboratory similarities with anticonvulsant hypersensitivity syndrome, which suggests that at some threshold concentration the amount of lamotrigine may overwhelm the body's ability to metabolize the drug, leading to a similar hypersensitivity reaction. Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent. CONCLUSIONS: Healthcare providers should be aware that lamotrigine overdose may present with multiorgan involvement, similar to anticonvulsant hypersensitivity syndrome.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
6/238. Successful use of clopidogrel for cerebrovascular accident in a patient with suspected ticlopidine-induced hepatotoxicity.OBJECTIVE: To report a case of successful clopidogrel use in a patient who developed suspected ticlopidine-induced hepatotoxicity during therapy for a cerebrovascular accident. CASE REPORT: A 79-year-old white woman with a history of hypertension, type 2 diabetes, alzheimer disease, and coronary artery disease started receiving ticlopidine 250 mg twice daily three days after hospital admission for a cerebrovascular accident. Medications prior to admission included quinapril, furosemide, insulin, atorvastatin, conjugated estrogen, medroxyprogesterone, donepezil, and vitamin e. The estrogen, medroxyprogesterone, and donepezil were discontinued on admission. Laboratory tests on admission revealed that total bilirubin, alkaline phosphatase, and aspartate aminotransferase (AST) were within normal limits. On day 39 of hospitalization, laboratory tests showed marked increases in alkaline phosphatase, AST, alanine aminotransferase, gamma-glutamyl-transferase, and 5' nucleotidase. physical examination revealed no signs of jaundice or hepatomegaly, and laboratory tests for viral hepatitis were negative. A presumptive diagnosis of ticlopidine-induced hepatotoxicity was made and ticlopidine was discontinued. The following day, clopidogrel 75 mg/d was initiated. liver function tests returned to baseline over the following four months with ongoing clopidogrel therapy. DISCUSSION: ticlopidine-induced hepatotoxicity is well documented in the literature. In the present case, clopidogrel, a structurally similar thienopyridine, was substituted for ticlopidine following the development of presumptive ticlopidine-induced hepatotoxicity. serum liver enzyme concentrations returned to baseline with continued clopidogrel therapy, suggesting that clopidogrel is a suitable alternative in patients who develop ticlopidine-induced hepatotoxicity. CONCLUSIONS: Clopidogrel may be a suitable alternative for patients who develop ticlopidine-induced hepatotoxicity.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
7/238. Oxaprozin-induced symptomatic hepatotoxicity.OBJECTIVE: To describe a case of symptomatic hepatotoxicity attributed to oxaprozin use. CASE SUMMARY: A 41-year-old white woman was admitted to the hospital with malaise, anorexia, and right upper quadrant pain. The patient was found to have severe jaundice with liver enzyme elevation. Laboratory test results for potential etiologies were negative, except for the use of oxaprozin for the preceding six weeks. diagnosis of drug-induced hepatotoxicity was made by liver biopsy. The patient's symptoms resolved and liver enzymes normalized after oxaprozin was discontinued. DISCUSSION: Symptomatic hepatic effects attributable to most nonsteroidal antiinflammatory drugs (NSAIDs) are rare and usually mild. Oxaprozin has been shown to cause mild elevation of liver enzymes in clinical studies. This is the second reported case of presumed oxaprozin-induced icteric hepatitis. The mechanism of oxaprozin-induced hepatotoxicity is unclear, but is thought to be due to metabolic idiosyncrasy. Most NSAID reactions are hepatocellular and occur because of individual susceptibility (idiosyncrasy). In general, people aged >40 years and women are more predisposed to NSAID-induced liver injury. CONCLUSIONS: Although this toxicity is rare, clinicians should be aware of the potential for oxaprozin to cause hepatotoxicity and use caution when prescribing this medication. This case also stresses the importance of careful inquiry regarding drug or toxin exposure in cases of unexplained hepatitis.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
8/238. Inflammatory pseudotumor of the liver in a patient with chronic hepatitis c: difficulty in differentiating it from hepatocellular carcinoma.A case of an inflammatory pseudotumor of the liver in a 75-year-old female with chronic hepatitis c whose radiologic features simulated that of hepatocellular carcinoma (HCC) is presented. On imaging studies, hypervascularity by CO2 ultrasound (US) angiography, enhancement at an early phase and isodensity at a late phase by incremental dynamic computed tomography (CT), perfusion defect by CT during arteriography (CTAP), and clinical background of hepatitis c virus (HCV) infection strongly suggested HCC. A US-guided needle biopsy revealed a mainly diffuse and polyclonal proliferation of lymphocytes positive for leukocyte common antigen (pan-lymphocyte cells), L-26 (B cell lymphocytes), and UCHL-1 (T cell lymphocytes), negative for both kappa and lambda light chains and sparsely distributed neutrophils and histiocytes. No lymphoid follicles were observed. The liver tissue around this tumor showed chronic hepatitis with mild activity and mild fibrosis. These histopathologic findings suggested that the diagnosis of inflammatory pseudotumor of the liver was tenable. As it is difficult to differentiate between inflammatory pseudotumor of the liver and HCC by imaging studies alone, supplemental biopsy, where possible, should be obtained when diagnostic imaging of tumors suggesting HCC is carried out. We emphasize that histopathology is a true gold standard in the diagnosis of this disease.- - - - - - - - - - ranking = 3.5keywords = hepatitis (Clic here for more details about this article) |
9/238. Autoimmune liver disease in patients with neoplastic diseases.BACKGROUND: Development of de novo autoimmune liver disease has not been well documented in patients with malignant diseases. methods/RESULTS: In this paper we report on a series of six patients with neoplastic disorders who acquired liver disease with autoimmune features. Five patients had suffered from haematological neoplasms and one from colonic cancer. In two patients, liver disease was detected at the time of presentation with malignancy. In the remaining four, all of whom were successfully treated for malignancies, features of liver disease presented at intervals 24-72 months after the cancer diagnosis. Twelve liver specimens (11 biopsies and one hepatectomy specimen) were obtained at time intervals of 1-76 months after initial presentation of neoplastic disease. Biopsies from three patients showed features of hepatitis (one acute, one sub-acute, one chronic). Two patients had histological features suggestive of an overlap syndrome (one autoimmune hepatitis/primary biliary cirrhosis, one autoimmune hepatitis/primary sclerosing cholangitis). The sixth patient had features of autoimmune cholangiopathy. All but one responded well to steroid therapy with complete clinical and biochemical remission obtained 4 weeks to 8 months after steroid introduction. We discuss briefly possible aetiologies of autoimmune liver disease in these patients. CONCLUSIONS: Autoimmune liver disease may be precipitated by therapy for neoplastic disease or malignant disease itself. The unusually heterogeneous clinicopathological findings in this group as well as the response to treatment support the concept of a wide spectrum of manifestations of autoimmune liver disease. The results may also suggest that autoimmune liver disease may be possibly added to the list of paraneoplastic syndromes. Further prospective studies are required to confirm a causal association and to determine whether the mechanisms involved are disease- or treatment-related.- - - - - - - - - - ranking = 1.5keywords = hepatitis (Clic here for more details about this article) |
10/238. Progressive liver calcifications in neonatal coxsackievirus infection.Coxsackievirus group B can cause a severe systemic disease in the perinatal period. Severe manifestations like meningitis, encephalitis, hepatitis, and myocarditis have been previously reported. A case of a twin neonate infected by coxsackievirus group B is described, who developed progressive extensive hepatic calcifications demonstrated by ultrasound and computed tomography with follow-up. Hepatic calcifications in coxsackievirus infection have not been previously reported.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
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