Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HRS occurs frequently in patients with advanced cirrhosis of the liver and fulminant hepatitis. The pathogenesis of HRS is not clearly understood; reduced effective plasma volume and intense renal cortical vasoconstriction seem to have important roles. The HRS is a diagnosis by exclusion, and it [table: see text] is often difficult to differentiate this entity from prerenal azotemia and ATN. The HRS is characterized by its relentless progression and usually fatal outcome. The essential steps in the management of HRS are to identify and correct the precipitating factors leading to HRS and avoidance of potential hepatotoxic and nephrotoxic drugs. Patients with potentially reversible liver diseases should be treated aggressively. Volume expansion is important and should be tried first, even though hypovolemia may be not clinically evident. Dialysis may benefit patients with fluid overload and electrolyte imbalance or those awaiting liver transplantation. In selective cases, peritoneovenous shunt may be of value. Liver transplantation is the only curative therapy available at present.
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PMID:The hepatorenal syndrome. 219 63

Liver transplantation in neonates represents a major medical and technical challenge particularly in babies weighing less than 5 kg. The authors report the experience of 10 liver transplants in 9 babies (6 boys and 3 girls), mean age, 6 weeks (range, 2 to 11); median weight, 3.7 kg (range, 2.4 to 5). All had fulminant hepatic failure caused by neonatal haemochromatosis (n = 3), non-A non-B hepatitis (n = 3), total parenteral nutrition induced (n = 1), hepatitis B (n = 1), and hepatic haemangio-endothelioma (n = 1). One child underwent retransplantation for hepatic artery thrombosis. Immunosuppression was by Cyclosporine A-based triple therapy in all cases. All received a reduced size graft consisting of left lobe (n = 1), left lateral segment (n = 6) and monosegment III (n = 3). In nine cases the donor hepatic artery was anastomosed to an iliac artery conduit from the infrarenal aorta, and a Roux loop was used for bile duct reconstruction. Primary abdominal wound closure was possible in six patients, skin closure alone in one, and a silastic patch was used in three. Complications included infection (n = 5), bowel perforation (n = 2), diaphragmatic perforation (n = 2), bile leak (n = 1), hepatic artery thrombosis (n = 1), and portal vein thrombosis (n = 1). None of the babies experienced acute rejection. Currently five of the nine recipients are alive with good graft function at a mean follow-up of 22 months (range, 5 to 58). Of the four deaths, two were related to infection (one in combination with portal vein thrombosis), one to multiorgan failure and fluid overload, and one to early graft dysfunction and sepsis after undergoing retransplantation for hepatic artery thrombosis. From our experience liver transplantation offers a promising option for the treatment of severe liver disease in children less than 3 months old.
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PMID:Hepatic transplantation in children under 3 months of age: a single centre's experience. 909 24

A 16-year-old, previously healthy Thai girl presented with DHF grade III. Fifteen hours after the first episode of shock, she had received an excessive amount of crystalloid isotonic solution and 20 ml per kilograms of Dextran-40 however she still had persistently rapid pulse rate and high hematocrit but also had polyuria with more than 4 ml/kg/hr of urine output. She was re-evaluated. Clinical signs showed severe dehydration with some ascites without signs of pleural effusion. Blood gas revealed increased anion gap metabolic acidosis. The cause of polyuria and metabolic acidosis was identified with hyperglycemia, ketouria and glucosuria. Afterwards she was diagnosed and treated as DHF grade III and DKA. Besides insulin administration, fluid resuscitation was very crucial. Intravenous fluid rehydration was needed while the unnecessary extra-volume could cause massive plasma leakage and later on fluid overload. Volume replacement was adjusted to degree of dehydration when signs of volume overload were monitored closely. She was out of DKA at 14 hours after the start of insulin and the intravenous fluid was stopped at 27 hours (36 hours after the first episode of shock). The final diagnosis was DHF grade III, diabetes mellitus with DKA and hepatitis.
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PMID:Dengue hemorrhagic fever grade III with diabetic ketoacidosis: a case report. 2204 83