Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extrahepatic biliary obstruction due to mechanical obstruction of the common bile duct is a relatively rare complication of pancreatic pseudocyst. When jaundice does occur, clinical or laboratory evidence of associated primary hepatobiliary disease or acute pancreatitis has invariably been present. The patient described had a 3-month history of painless juandice, 40-lb weight loss, pruritus, and hepatomegaly, but no clinical or biochemical evidence of acute or chronic pancreatitis. After initial evaluation, including an abdominal echogram and a transhepatic cholangiogram, carcinoma of the head of the pancreas was diagnosed preoperatively. At laparotomy, a small pancreatic pseudocyst obstructed the terminal portion of the common bile duct. This case illustrates that a pancreatic pseudocyst should be considered in the differential diagnosis of obstructive jaundice, even in the absence of clinical evidence of pancreatitis or pseudocyst formation.
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PMID:Silent pancreatic pseudocyst. An unusual cause of extrahepatic biliary obstruction. 113 Mar 80

When larvae of C. sinensis reach the biliary system and mature, the flukes provoke pathological changes, both as a result of local trauma and of toxic irritation. The appearances vary with duration and severity of the infestation, but they are sufficiently distinctive and characteristic to allow a classification into four phases as follows; 1st phase, desquamation of epithelial cells, 2nd phase, hyperplasia and desquamation of epithelial cells, 3rd phase, hyperplasia and desquamation of epithelial cells, and adenomatous tissue formation, and 4th phase, marked proliferation of the periductal connective tissue with scattered abortive acini of epithelial cells and fibrosis of the wall of the bile duct. The onset of symptoms and signs is at times gradual, at times sudden. Chill and fever up to 40 degrees C occur during the acute stage, i.e. the period less than a month after parasite invasion. And a few weeks later, the chronic stage follows with the classical clinical features. In general, symptoms and signs can be classified as follows: mild, essentially symptomless, progressive, with irregular appetite, gastrointestinal disturbances, oedema, hepatomegaly, etc., and severe, with a syndrome associated with portal cirrhosis and hypertension. Pathogenic changes and complications are generally restricted to foci, but may eventually affect the whole liver. Calculi, acute suppurative cholangitis, recurrent pyogenic cholangitis, cholecystitis, hepatitis, and acute pancreatitis are important complications. Carcinoma of the liver is often found in association with clonorchiasis, too.
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PMID:Clonorchis sinensis: pathogenesis and clinical features of infection. 639 2

Type IA glycogenosis, or von Gierke disease, is the most common among the glycogenoses with enlarged liver. Acute pancreatitis is a rare manifestation of type IA glycogenosis and has been attributed to elevated serum fat levels. We report a case of type IA glycogenosis with acute pancreatitis. The radiologists should be familiar with the computed tomography findings in this rare complications of type IA glycogenosis.
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PMID:[Type IA glycogenosis with acute pancreatitis]. 786 70

The purpose of this study was to characterize the incidence, clinical features, and prognosis of acute pancreatitis in cats with hepatic lipidosis. Of 13 cats histologically diagnosed with hepatic lipidosis between July 1988, and November 1989, 5(38%) were also histologically diagnosed with acute pancreatitis. In cats with hepatic lipidosis alone, the signalment, history, physical examination, and clinicopathologic findings were generally indistinguishable from those of cats with concurrent acute pancreatitis except that cats with acute pancreatitis were more likely to be cachectic and to have coagulation abnormalities. Hepatomegaly was seen on abdominal radiographs in both groups. Of the 5 cats with concurrent acute pancreatitis, abdominal ultrasonography detected 1 cat with a hypoechoic pancreas and 5 with peritoneal effusion; those abnormalities were not seen in cats without concurrent acute pancreatitis. Cats with concurrent acute pancreatitis had only a 20% recovery rate, compared with a 50% recovery rate in cats with hepatic lipidosis alone. We conclude that cats with hepatic lipidosis should be rigorously evaluated for concurrent acute pancreatitis because of 1) the rate of disease coincidence, 2) the inability of signalment, history, physical examination, and clinicopathologic findings to adequately distinguish between hepatic lipidosis and acute pancreatitis, 3) the worse prognosis associated with concurrent acute pancreatitis, and 4) the opposing nutritional strategies for hepatic lipidosis and acute pancreatitis.
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PMID:Acute pancreatitis in cats with hepatic lipidosis. 1146 88

Complications of oral contraceptives (OCs) affecting the gastrointestinal tract, liver and pancreas are rare but potentially serious. Hepatobiliary complications are by far the most frequent and varied. Hepatic lesions will probably decline in frequency as low-dose OCs replace higher dosed pills. Intrahepatic cholestasis induced by OCs resembles that of pregnancy. There may be a genetic predisposition to both conditions involving a dose-dependent estrogen effect of decreasing bile secretion. Intrahepatic cholestasis appears within 6 cycles of OC use. Symptoms include pruritus with anorexia, asthenia, vomiting, and weight loss without fever, rash or abdominal pain. Termination of OCs clears the condition without sequelae within 1-3 months, sometimes after a temporary aggravation. A moderate and asymptomatic cytolysis may appear when OC treatment is begun. Sinusoidal dilatation has been conclusively linked to OCs although few cases have been published. Clinical manifestations other than hepatomegaly are variable. Abdominal pain and fever are the most common. The condition is not related to duration of use and disappears 5-15 days after OC use is terminated. The relative risk of Budd-Chiari syndrome in OC users is estimated at 2.37. OCs increase the prevalence of hepatic adenomas as a function of duration of treatment. They are usually discovered fortuitously but may be revealed by vague abdominal pains. Hemorrhagic complications are more likely in OC users. It may be difficult to distinguish between adenomas, hepatocellular carcinoma, and focal nodular hyperplasia. A puncture biopsy guided by sonography may aid diagnosis. The natural history of adenomas is poorly understood and treatment remains controversial. OCs do not appear to increase the risk of focal nodular hyperplasia but they increase the size of the tumor and the risk of hemorrhage. OCs should be terminated because of risk of hemorrhage. Surgical resection is not indicated unless there are complication or diagnostic doubts. While hepatocellular carcinoma is very rare, its risk is increased by a factor of 7-20 in women using OCs for 8 years or more. Use of combined OCs appears to speed development of lithiasis in predisposed women. Risk of lithiasis is linked to estrogen content in women under 30. Several cases of acute pancreatitis in the 1st 3 months of treatment have been reported in women with preexisting lipid metabolic anomalies. Cases of ischemic lesions of the small intestine or colon have been reported in OC users with A positive blood type. Such lesions can be fatal without early diagnosis and termination of OCs. Gastric esophageal reflux is increased by progestins. Preexisting constipation may be aggravated and the incidence of Crohn's disease increased by OCs. It is advisable to rule out preexisting hepatic pathology before prescribing OCs. OCs should be stopped in case of viral hepatitis.
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PMID:[Contraception and hepatogastroenterology]. 1231 76

A 22-year-old woman had suffered from several episodes of acute pancreatitis since the age of 11. Other than exercise intolerance since early childhood, her psychomotor development was normal. At age 21, she experienced two episodes of generalized muscle weakness including acute respiratory failure and hepatomegaly. Liver biopsy indicated fatty metamorphosis, and muscle biopsy revealed vacuolar myopathy with lipid accumulation. Biochemical investigations demonstrated elevated serum creatine kinase and elevated 2-hydroxylglutaric, pyruvic, ethylmalonic, hippuric, adipic, and seburic acids in urinary organic acid analysis. These findings confirmed the diagnosis of glutaric aciduria type II. Although acute pancreatitis in glutaric aciduria type II has been reported previously, this is the first reported case of recurrent pancreatitis occurring in glutaric aciduria type II. We treated the patient with l-carnitine and riboflavin. As of the latest follow-up 2.5 years later, the patient has had no further episodes of muscle weakness or pancreatitis. We suggested analyzing urine organic acid when lipid storage myopathy is suspected.
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PMID:Riboflavin-responsive glutaric aciduria type II with recurrent pancreatitis. 1535 Oct 24

In this case report, a young woman with gallbladder sludge and acute pancreatitis due to acute hepatitis A (HAV) is presented. She was admitted to our hospital with abnormal hepatic enzymes. Five days prior to her admission, an initial abdominal ultrasound was performed at another hospital and revealed no abnormality, while her serum aspartate aminotransferase (AST) level was at the upper limit of normal (ULN) x 8. A second ultrasound was performed at our hospital and revealed a gallbladder wall thickness (9.3 mm), gallbladder sludge in the gallbladder lumen, pancreatic edema, ascites, and hepatomegaly while AST was at the ULN x 50. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed imaging features of an acute stage of pancreatitis and gallbladder wall thickness with coexisting sludge in the gallbladder lumen. HAV infection was diagnosed by the detection of immunoglobulin M against HAV in the serum. The patient underwent two repeated abdominal ultrasound examinations on the 5th (AST was at the ULN x 3) and the 20th days (AST was at the normal) after her discharge, and both revealed normal findings. In our case, we observed reversible changes in the hepatobiliary and pancreatic system which was related to the severity of hepatic necro-inflammation. HAV-associated pancreatitis may be due to the formation of biliary sludge during the acute phase of the viral illness, but this association needs further investigation.
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PMID:Gallbladder sludge and acute pancreatitis induced by acute hepatitis A. 1790 17

Hemophagocytic syndrome (HS) is a life-threatening condition of hyperinflammation. Main symptoms are: prolonged fever, cytopenia, hepatosplenomegaly, hemophagocytosis, hyperferritinemia, hypertriglyceridemia and hypofibrinogenemia. Primary genetic form and secondary HS associated with infections, malignancies or autoimmune disorders can be distinguished. Untreated HS in most cases leads to death. We analyzed retrospectively 7 cases of HS in children (3 girls, 4 boys; aged 10 days -14 years) treated in 3 different pediatric centers from 2004 to 2009. In 3 cases HS was associated with infections (EBV, CMV, Bacillus Calmette Guerin - BCG), in 1 child with non-Hodgkin anaplastic large cell lymphoma (ALCL), in 1 patients probably with side effect of antiepileptic drug. In 2 cases cause of HS remained unknown. Fever, hepatomegaly, pan- or bicytopenia and hyperferritinemia were present in all children. In addition, splenomegaly was noted in 6 cases, hemophagocytosis in 6 children, impaired function or decreased number of NK cells in 4 cases, hypofibrino-genemia in 5 and hypotriglyceridemia in 4 patients. Among other symptoms and signs we observed: lymphadenopathy, hepatic failure, oedema, rash, neurological symptoms, increased level of LDH and inflammatory markers. In one child acute pancreatitis occurred. Among others, antibiotics, antiviral and immunosuppressive drugs were used in therapy. HLH-2004 protocol was applied in 4 cases. Patient with ALCL was treated with chemotherapy and allogeneic stem cell transplantation. Four patients are alive, 2 died because of HS, child with ALCL died because of generalized infection in peritrans-plantation period. In case of prolonged fever, splenomegaly and cytopenia diagnosis of HS should be considered. Following tests are recommended: complete blood count, ferritin, triglycerides, fibrinogen, bone marrow aspiration and NK cell assessment. Patients should be also screened for infections and malignancies. Early diagnosis of HS and underlying condition is crucial to start lifesaving therapy.
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PMID:[Hemophagocytic syndrome in children with different underlying conditions]. 2134 76

We report the case of a 14 year-old male from Lima. He is a student with a history of bronchial asthma since age 4 receives conditional salbutamol, corticosteroids used for asthma attacks (a crisis in 2010, 1 month ago) Refuses surgery or transfusions. He presented with a two weeks for abdominal pain, nausea, fever, and jaundice. Epigastric pain is colicky and radiated back to righ upper quadrant, refers in addition to nausea and fever, for ten days notice jaundice of skin and sclera. On examen he was lucid, with jaundice of skin and mucous membranes. There was no palpable lymph nodes, abdomen with bowel sounds, soft, depressible, liver span of 15cm, positive Murphy, no peritonitis. The laboratory findings showed hemoglobin 13gr, MCV 90, platelets 461.000/mm3, WBC 4320/mm, lymphocytes 1700 (39%). total bilirubin: 8.8, B Direct: 7.6, ALT (alanine aminotransferase): 3016, AST (aspartate aminotransferase): 984, alkaline phosphatase: 250, albumin: 3.34gr%, globulin: 2.8, amylase: 589 (high serum amylase), TP: 17, INR: 1.6, VHA IgM positive. 89 mg glucose, urea 19 mg%, creatinine 0.5 mg Hemoglobin 13gr, MCV 90 Platelet 461000/mm3, WBC 4320/mm, Lymphocytes 1700 (39%). The nuclear magnetic resonance showed hepatomegaly associated with thickening of gallbladder wall without stones up to 11mm inside. No bile duct dilatation, bile duct 4mm, pancreas increased prevalence of body size. Mild splenomegaly and free fluid in the space of Morrison and right flank. Abdominal ultrasound revealed a gallbladder wall thickness (11mm), without stones in his light. Pancreas to increase volume with peripancreatic fluid free perivesicular with a volume of 430 cc. Findings consistent with acute acalculous cholecystitis and acute pancreatitis. CT-scan showed enlarged pancreas with predominance of body and tail with peripancreatic edema; the gallbladder was thickening. We report this case because the extrahepatic manifestations of viral hepatitis A infection are uncommon, specially the associated with acute acalculous cholecystitis and acute pancreatitis simultaneous.
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PMID:[Acute pancreatitis and acalculous cholecystitis associated with viral hepatitis A]. 2183 59

A 49-year-old female was admitted to our hospital for acute pancreatitis. The abdomen CT scan incidentally showed midline liver with hepatomegaly, centrally located gallbladder, pancreas truncation, right sided small bowel, left sided large bowel, interruption of the inferior vena cava with azygos continuation, preduodenal portal vein, and multiple spleens in the left upper quadrant. In MRCP, the head of pancreas was enlarged and short main pancreatic duct without accessory duct was showed. EUS revealed enlarged ventral pancreas with a main pancreatic duct of normal caliber, absence of the accessory pancreatic duct and the dorsal pancreas. She was diagnosed as polysplenia syndrome with agenesis of dorsal pancreas. It is a rare congenital anomaly frequently associated with various visceral anomalies including multiple spleens, impaired visceral lateralization, congenital heart diseases, gastrointestinal abnormalities and azygos continuation of the inferior vena cava. We report a case of polysplenia syndrome with agenesis of dorsal pancreas presenting acute pancreatitis.
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PMID:Polysplenia syndrome with congenital agenesis of dorsal pancreas presenting as acute pancreatitis and the role of endoscopic ultrasonography in its diagnosis. 2283


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