Cases reported "Jaundice"

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1/12. liver failure with steatonecrosis after jejunoileal bypass: recovery with parenteral nutriton and reanastomosis.

    Two women, aged 41 and 51 years, developed jaundice, encephalopathy, and hypoprothrombinemia during rapid weight loss four and 12 months after jejunoileal bypass for refractory obesity. Both were treated for liver failure and received a prolonged course of nutrition parenterally and orally. Serial liver biopsy specimens demonstrated extensive alcoholic-like hepatitis and cirrhosis that improved with nutritional repletion and reanastomosis. Postoperative biopsy specimens later demonstrated minimal portal fibrosis in one patient and inactive mild cirrhosis in the other. Although previous reports indicate that patients usually die when they develop liver failure of this severity after jejunoileal bypass, prolonged intensive nutritional repletion was associated with sufficient clinical and histologic improvement in these two patients so that intestinal reanastomosis could be performed safely.
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2/12. Adverse reaction to a dietary supplement in an elderly patient.

    OBJECTIVE: To describe the case of an elderly patient who experienced hepatic enzyme elevations and symptoms of hepatitis associated with the administration of a dietary supplement. CASE SUMMARY: A 92-year-old white woman with no history of hepatic disease developed jaundice and increased confusion associated with increased hepatic enzymes. The hepatitis panel, abdominal ultrasound, and antinuclear antibody screen indicated no abnormalities. A drug regimen review revealed that the patient was receiving a dietary supplement, Nutrilite Double X Multivitamin-Multimineral. Following discontinuation of the supplement, the patient's symptoms resolved and the hepatic enzymes decreased or returned to the reference range at evaluations occurring 1 week and 1 month after intervention. An objective causality assessment revealed this to be a probable adverse drug event. DISCUSSION: While the association of certain herbal preparations with hepatotoxicity has been demonstrated, the potential for this adverse effect is easily overlooked. In this patient, infectious or autoimmune causes of acute hepatitis were ruled out, and drug-induced causes were considered. The resolution of symptoms and laboratory values following discontinuation of the supplement support a relationship between the dietary supplement and this episode of hepatitis. CONCLUSIONS: Our case indicates that there was a probable relationship between the dietary supplement Nutrilite Double X Multivitamin-Multimineral and the development of acute hepatitis. Due to the multi-ingredient formulation of the product, as well as lack of data describing manufacturing procedures, it is difficult to determine which component may be associated with this effect. Over-the-counter supplements should be considered as a part of the differential diagnosis in patients presenting with increased liver enzymes and related symptoms.
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3/12. levofloxacin-induced autoimmune hemolytic anemia.

    OBJECTIVE: To report a case of autoimmune hemolytic anemia (AIHA) secondary to levofloxacin. CASE SUMMARY: An 82-year-old white man was treated with levofloxacin 500 mg/d for cellulitis. Three days following completion of levofloxacin therapy, the patient presented to the emergency department with severe jaundice, dizziness, and loss of vision. He received packed red blood cells (PRBCs) and was discharged home. Two days later at the follow-up visit, he was diagnosed with AIHA secondary to levofloxacin. The patient was hospitalized and treated with a tapering dose of prednisone and additional PRBC infusion. He was discharged from the hospital in stable condition after 3 days. Repeated hematologic laboratory studies following discharge demonstrated that the hemolytic anemia had resolved. DISCUSSION: Hemolytic anemia due to levofloxacin is an extremely rare, but potentially fatal, adverse drug event. An objective causality assessment revealed that the adverse reaction was probable. To our knowledge, this is the first published case of levofloxacin-induced AIHA. However, there are published case reports of hemolytic anemia with other fluoroquinolones including ciprofloxacin (n = 12) and temafloxacin (n = 95). Temafloxacin was withdrawn from the market in 1992 due to this adverse effect. The mechanism by which levofloxacin triggers hemolytic anemia is unknown. We believe that an immune-mediated reaction is most likely. CONCLUSIONS: levofloxacin-induced AIHA is a rare but serious complication of therapy. Immediate discontinuation of the offending medication and treatment of the hemolytic anemia are essential. Until more information is available, levofloxacin should not be prescribed for patients with previous reactions to any fluoroquinolone.
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4/12. Cavernous transformation of the portal vein causing jaundice, presenting in the form of Wilson's disease.

    The following is a case review of portal vein cavernous malformation presenting with intermittent cholestasis and jaundice in a 4 year old child. Correct assessment was supported by radiology, later laparoscopy, yet hindered by histopathology representative Wilson's disease and elevated urinary copper excretion. During surgical procedure the stenosis of the common bile duct secondary to extremely dilated portal vein reticulation was solved by Roux-en-Y choledochojejunostomy. After a one-year follow up the child remains asymptomatic.
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5/12. halothane induced hepatitis: case report.

    halothane as a cause of hepatitis is rare and may be overlooked when evaluating a patient with sudden onset jaundice. A 34-year-old lady, a nurse, presented to the liver clinic with sudden onset non-pruritic jaundice. Viral and collagen serological tests were all normal, malaria and sickling tests were negative, but transaminases were elevated. She reported inadvertent exposure to halothane in surgical theatre where she works. She improved on conservative management, then had a re-exposure to halothane after three weeks and developed a similar clinical picture, which improved on conservative management. In an area endemic of malaria, hepatitis and haemolysing conditions like sickle cell anaemia, the diagnosis of halothane hepatitis requires high index of suspicion. The mechanism of halothane-induced hepatic damage in this patient is very likely idiosyncratic. This is because of the modest dose at first exposure and more severe clinical picture at re-exposure.
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6/12. hyperemesis gravidarum presenting as jaundice and transient hyperthyroidism complicated with acute pancreatitis.

    hyperemesis gravidarum is an extreme form of nausea and vomiting during pregnancy. Its presenting symptoms include vomiting, disturbed nutrition, electrolyte imbalance, ketosis, extreme weight loss, renal and/or liver damage. It is rare for a hyperemesis gravidarum patient to present with jaundice, hyperthyroidism and idiopathic acute pancreatitis during the same hospitalization period. Here, we report such a case. A 25-year-old pregnant woman without underlying liver or thyroid disease was admitted due to jaundice noted for 2 days at 8 weeks of gestational age. hyperthyroidism symptoms of tachycardia and finger tremor also bothered her. After treatment with parenteral fluid and antithyroid agents, her clinical condition improved. However, an episode of idiopathic pancreatitis occurred after nausea and vomiting subsided. Bowel rest with parenteral fluid and nutrition supplement was given and the increased pancreatic enzyme level gradually subsided. Follow-up liver and thyroid function were normal after gestational age of 26 weeks. She delivered a healthy female baby without low birth body weight at gestational age of 39 weeks. Rapid diagnosis and supportive care are important for the hyperemesis gravidarum patient with the complication of acute pancreatitis.
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keywords = nutrition
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7/12. A patient with early syphilis complicated by fatty liver who showed an alleviation of hepatopathy accompanied by jaundice after receiving anti-syphilitic therapy.

    A 42-year-old male with visceral obesity and a fatty liver presented with hepatopathy accompanied by jaundice and was diagnosed to have early syphilis based on the results of standard serologic tests and clinical findings. Both the subjective and objective findings including hepatopathy were rapidly alleviated by anti-syphilitic therapy. Severe hepatopathy accompanied by jaundice used to be considered a rare complication. However, due to contemporary unhealthy lifestyle patterns characterized by hypernutrition and a lack of exercise the occurrence of fatty liver is now dramatically increasing. Our findings suggest that the occurrence of fatty liver can exacerbate the damage to the hepatic parenchyma due to a treponema pallidum infection.
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8/12. cytodiagnosis of hepatic amyloidosis by fine needle aspiration cytology: a case report.

    BACKGROUND: Amyloid in fine needle aspirates tends to be overlooked due to its rarity. It may appear at virtually any site and can be identified by special stains. CASE: In a case of amyloidosis of the liver, where fine needle aspiration cytology was instrumental in making the primary diagnosis. Smears revealed normal hepatocytes and chronic inflammatory cells. Amorphous material (amyloid) was extensively present between compressed hepatocytic clusters. It stained pale green in Papanicolaou-stained preparations and reddish purple with Giemsa stain. This material was initially thought to be hyalinized granulomas. However, it was later confirmed to be amyloid by using congo red stain. CONCLUSION: Whenever amorphous material is present in smears, a high index of suspicion for amyloid needs to be maintained.
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9/12. manganese levels in a jaundiced long-term total parenteral nutrition patient: potentiation of haloperidol toxicity? Case report and literature review.

    manganese is vital in human nutrition. When oral intake is precluded, the recommended parenteral supplementation is 0.15 to 0.8 mg/day. manganese is excreted primarily in the bile; during cholestasis, serum manganese levels may rise, and manganese toxicity ensue. Neuropsychiatric symptoms are prominent. Phenothiazine-derivative drugs may potentiate manganese toxicity. serum or whole blood manganese levels should guide manganese therapy in jaundiced patients.
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10/12. Measurement of hepatocellular function with deconvolutional analysis: application in the differential diagnosis of acute jaundice.

    A direct, noninvasive technique was developed to quantitate hepatocyte function with computer assessment of scintiscans obtained after administration of technetium-99m disofenin in 53 patients with acute jaundice: 32 patients with normal livers, 10 patients with acute biliary obstruction, and 11 patients with acute hepatocellular dysfunction. In all patients a final clinical diagnosis was obtained with follow-up for a minimum of 4 months and, in most patients with obstruction or dysfunction, with surgery, intraoperative cholangiography, ultrasound, and/or computed tomography. heart (blood pool) and liver time-activity curves were generated for 32 minutes after intravenous injection of 5-15 mCi (185-555 MBq) of Tc-99m disofenin and were subjected to deconvolutional analysis to determine the first-pass hepatocyte extraction fraction (HEF) of the tracer. The difference in HEF between patients with obstruction and those with dysfunction was highly significant (P = 3.3 X 10(-19)). Deconvolutional analysis eliminates the effects of tracer recirculation, thus permitting direct measurement of hepatic disofenin extraction, and appears to provide functional information useful in evaluation of the patient with acute jaundice.
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