Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

200 patients with pancreatitis were examined for various concomitant and previous diseases, and socioeconomic factors, in a retrospective study. This pancreatitis group (PG) was compared with a control group (CG) of 250 patients. Most frequent amongst the etiological factors, were biliary diseases, especially a state after cholecystectomy. Second in rank, was chronic alcoholism. For women, the incidence was highest in the 7th decade; for men, there was a double peak in the 4th and 6th decade, respectively. The incidence was about equal for both sexes. The following factors were found to play no essential role in the PG: type of profession, cigarette consumption, gastric and/or duodenal ulcers, partial gastric resection, renal and cardiac insufficiency, viral hepatitis, liver cirrhosis of hypertriglyceridemia. There is a significant accumulation of mumps in the history of the PG, which had gone along without any clinically detectable affection of the pancreas in childhood, in practically all cases.
 ...
PMID:[Social profile and accompanying diseases in acute and chronic pancreatitis (author's transl)]. 700 47

Two patients abruptly developed congestive heart failure and elevation in serum transaminase levels when given disopyramide phosphate; enzyme abnormalities and hemodynamic status corrected upon withdrawal of the drug. Both patients had underlying ischemic cardiomyopathy. Myocardial infarction, pulmonary embolism, and viral hepatitis were ruled out in both patients. One patient had a liver biopsy documenting central hepatic necrosis with congestion, consistent with hepatic ischemia and not toxic hepatitis. In the other patient, cardiac decompensation and hepatocellular enzyme elevation were reproduced on rechallenge with the drug. Disopyramide should be used with caution in patients with heart failure.
 ...
PMID:Acute cardiac failure and hepatic ischemia induced by disopyramide phosphate. 722 41

Fulminant hepatic failure is a complication of severe cardiocirculatory failure, with high morbidity and mortality, and is frequently misdiagnosed as fulminant viral hepatitis. We report three cases of patients with chronic severe heart failure who developed cardiogenic shock complicated by elevation of aminotransferase levels above 1,000 soon after the most severe episode of hypotension. All the three patients presented regression of hepatic enzymes 72h after admission. Two patients developed hepatic encephalopathy and renal failure. One underwent the implantation of an artificial left ventricle, followed by orthotopic heart transplantation. One died of systemic multiple organ failure, after he had showed improvement on his hepatic profile, and one was sent to the ward, after 15 days with marked improvement on his clinical status and no signs of hepatic disease.
 ...
PMID:[Acute liver failure secondary to cardiogenic shock in patients with congestive heart failure]. 782 36

Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.
 ...
PMID:[Acute ischemic liver]. 854 28

Intrahepatic cholestasis has rarely been observed in patients with thyrotoxicosis and generally occurs in association with coexistent congestive heart failure. We report the case of a 63-year-old man who was referred to our Institution because of jaundice and hyperthyroidism. During his hospital stay, his plasma bilirubin level reached 27.41 mg/dL. Clinical, biohumoral, and instrumental examinations excluded heart failure and autoimmune or viral hepatitis. After the start of therapy with methimazole, thyroid hormone and plasma bilirubin levels decreased progressively and simultaneously, eventually returning to normal. Plasma bilirubin values as high as the ones we recorded, in the absence of congestive heart failure or autoimmune chronic hepatitis, have not, to our knowledge, been previously reported.
 ...
PMID:[Hyperthyroidism and cholestasis: a case report]. 1034 8

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.
 ...
PMID:Acute liver failure. 1113 56

Many clinical aspects associated with chronic uraemia and long-term dialysis therapy may determine both the qualification for renal transplantation and post-transplant outcome. These include dialysis access, severe hyperparathyroidism, inadequate or excessive erythropoietin production, heart failure, viral hepatitis, defects of urinary tract and malnutrition. Some of them delay the qualification for transplant, the other on contrary make the need for transplantation very urgent. Selected aspects are discussed in this paper.
 ...
PMID:[Patients on dialysis as renal graft recipients]. 1143 86

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.
 ...
PMID:The liver in heart failure. 1251 1

Spontaneous hepatobiliary tumors in non-human primates are uncommon. Here we report a case of hepatic carcinoma and a case of hepatic focal nodular hyperplasia (FNH) and myelolipoma in two captive chimpanzees. A 16-year-old male chimpanzee (4X0392) died after an 8-month history of hepatic amyloidosis and low-grade anemia. Necropsy findings included a hepatic neoplasm with highly pleomorphic hepatocytes arranged into irregular thickened trabeculae. The diagnosis was high-grade hepatocellular carcinoma. A second male chimpanzee (4X0080), 23 years of age, died suddenly of heart failure secondary to cardiomyopathy. An incidental finding at necropsy was a liver mass characterized by multinodularity, prominent fibrous septa, and biliary hyperplasia. These features were consistent with FNH. While 4X0392 had no history of experimental viral exposure, 4X0080 was vaccinated with inactivated hepatitis B virus, an attenuated hepatitis A virus, and was experimentally infected with hepatitis C virus and human immunodeficiency virus. A survey of the literature revealed 68 reported cases of hepatobiliary tumors in non-human primates, including 12 hepatocellular adenomas, eight cholangiocellular adenomas/cystadenomas, 22 hepatocellular carcinomas, seven cholangiocarcinomas, and seven gallbladder adenocarcinomas. The majority of reported cases have been in prosimians and Old World monkeys. Hepatic neoplasia is rare in chimpanzees. Only four hepatic neoplasms have been reported in chimpanzees, three of which were associated with viral hepatitis. FNH has not been previously described in any non-human primate.
 ...
PMID:A case report of hepatocellular carcinoma and focal nodular hyperplasia with a myelolipoma in two chimpanzees and a review of spontaneous hepatobiliary tumors in non-human primates. 1506 32

A 39-year-old white man was referred to our hospital for evaluation of his jaundice and pruritus. The patient was treated with I for diffuse toxic goiter prior to his referral to our hospital. Clinical examination and laboratory investigations excluded viral hepatitis, autoimmune hepatitis, granulomatous disease, primary biliary disease, extrahepatic biliary obstruction, and heart failure. Liver biopsy showed severe intrahepatic and canalicular cholestasis with minimal inflammatory changes. The patient's jaundice promptly resolved with therapy for hyperthyroidism and thyroid storm as bilirubin levels decreased from 35 mg/dL (normal: 0.5-1.2 mg/dL) to 0.4 mg/dL. Thyrotoxicosis can be an uncommon cause of profound cholestasis. Our case differs from all other reports in the literature because of the severity of the cholestasis and its prompt resolution with treatment for thyrotoxicosis.
 ...
PMID:Severe cholestatic jaundice in hyperthyroidism after treatment with 131-iodine. 1559 31


<< Previous 1 2 3 Next >>