1/187. 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 = 1keywords = jaundice (Clic here for more details about this article) |
2/187. 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 = jaundice (Clic here for more details about this article) |
3/187. Gastrointestinal and hepatic manifestations of human ehrlichiosis: 8 cases and a review of the literature.BACKGROUND: ehrlichiosis has emerged as an increasingly recognized tick-borne rickettsial disease. It can affect multiple organs including the gastrointestinal tract and liver. signs and symptoms include abdominal pain, nausea, vomiting, diarrhea, jaundice, and hepatosplenomegaly. patients commonly have elevated liver transaminases early in the course of illness as well as leukopenia and thrombocytopenia. If not diagnosed and treated in a timely fashion, ehrlichiosis can progress to multiorgan failure. methods: Between 1992 and 1998, 8 patients meeting the CDC criteria for ehrlichiosis were diagnosed and treated at the John L. McClellan Memorial veterans Hospital and University Hospital in Little Rock, Ark. These cases and English-language articles relating to gastrointestinal and hepatic manifestations of ehrlichiosis, identified by searching medline and manually reviewing bibliographies of retrieved articles, are reviewed. RESULTS: Seven of the eight patients had elevated transaminases on presentation which increased rapidly initially and slowly returned to normal. Three of our patients had hyperbilirubinemia. One of the eight patients presented with hepatomegaly. Three had hyperbilirubinemia with a peak bilirubin of 13.8 mg/dl. Two patients (25%) had a rash on presentation. All 8 patients were treated with and responded to doxycycline. One developed multiorgan failure but eventually recovered with intensive medical care and doxycycline. CONCLUSION: To avoid treatment delay and serious complications, in the appropriate clinical setting ehrlichiosis should be considered as a cause of elevated liver transaminases.- - - - - - - - - - ranking = 0.5keywords = jaundice (Clic here for more details about this article) |
4/187. Delayed-onset ticlopidine-induced cholestatic jaundice.An 86-year-old man experienced a rash approximately 2 weeks after starting ticlopidine therapy, necessitating discontinuation of the drug. About 1 month later, despite discontinuation, he developed jaundice and liver test abnormalities. These resolved gradually over the next few months. Based on case reports and the drug's pharmacokinetic profile, a high index of suspicion for ticlopidine-induced jaundice is prudent in patients with recent exposure to the agent who have evidence of liver damage.- - - - - - - - - - ranking = 3keywords = jaundice (Clic here for more details about this article) |
5/187. Obstructive jaundice caused by a huge liver cyst riding on the hilum: report of a case.A 71-year-old man presented to our hospital with obstructive jaundice, found to be caused by a huge liver cyst which was centrally located and riding on the hilum. Percutaneous transhepatic cyst drainage was performed, following which obstruction of the bile duct was relieved and the jaundice subsided. As jaundice recurred after removal of the drainage tube, the patient underwent deroofing, since when he has remained well. Only 13 cases of liver cysts producing obstructive jaundice have been reported in the English literature, most of which were characteristically enormous, located centrally, and riding on the hilum. Liver cysts possessing such features are likely to cause obstructive jaundice by compressing the hepatic hilum. Cyst drainage is helpful for ameliorating the jaundice and making an accurate diagnosis; however, subsequent deroofing or injection therapy is necessary to prevent recurrence.- - - - - - - - - - ranking = 5keywords = jaundice (Clic here for more details about this article) |
6/187. Myeloma and severe cholestasis.amyloidosis is a frequent complication of multiple myeloma. Liver involvement is common in amyloidosis. Hepatic dysfunction and liver chemistry abnormalities are often mild or absent and obstructive jaundice is rare. We report on a 44-year-old patient with multiple myeloma and rapidly deteriorating liver involvement with severe intrahepatic cholestasis. autopsy showed widespread amyloidosis primarily involving the liver. This unusual cholestatic manifestation of hepatic amyloidosis has an uniformly poor prognosis, with death occurring within a few months. We discuss the clinical and pathologic aspects.- - - - - - - - - - ranking = 0.5keywords = jaundice (Clic here for more details about this article) |
7/187. 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 = jaundice (Clic here for more details about this article) |
8/187. 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 = 0.5keywords = jaundice (Clic here for more details about this article) |
9/187. Liver disease in Navajo neuropathy.OBJECTIVE: To describe clinical and histologic features of liver disease in infants and children with Navajo neuropathy (NN). methods: physicians at Navajo Area Indian health Service facilities and neurologists and gastroenterologists at regional referral hospitals were surveyed for identification of patients born between 1980 and 1994 with known or suspected NN. Clinical records and liver histologic findings were reviewed. RESULTS: Liver disease was present in all children with NN. Three clinical phenotypes of NN were observed, based on age at presentation and course: infantile NN presented in 5 infants before 6 months of age with jaundice and failure to thrive and progressed to liver failure before 2 years of age; childhood NN presented in 6 children between 1 and 5 years of age with liver dysfunction, which progressed to liver failure and death within 6 months; and classical NN presented in 9 children with variable onset of liver disease but progressive neurologic deterioration. Liver histologic findings were characterized by multinucleate giant cells, macrovesicular and microvesicular steatosis, pseudo-acini, inflammation, cholestasis, and bridging fibrosis and cirrhosis. Cases of all 3 phenotypes occurred within the same kindred. CONCLUSIONS: Liver disease is an important component of NN and may be the predominant feature in infants and young children. We propose changing the name of this disease to Navajo neurohepatopathy.- - - - - - - - - - ranking = 0.5keywords = jaundice (Clic here for more details about this article) |
10/187. The challenge of diagnosing the cause of jaundice.The patient presenting with jaundice may have a variety of hepatobiliary or hematologic conditions. Understanding the causes of jaundice and the history and physical examination hallmarks provide the basis for choosing the most efficacious laboratory and diagnostic studies. A case report illustrating the reasoning involved in distinguishing between the different causes of jaundice is presented.- - - - - - - - - - ranking = 3.5keywords = jaundice (Clic here for more details about this article) |
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