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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute, nonobstetric abdominal pain is a common complaint during pregnancy. Both anatomic and physiologic variations in pregnancy cloud the clinical picture when attempts at clinical decision-making and triage are made. Abdominal disorders such as appendicitis, gallbladder disease, pancreatitis, bowel obstruction, liver disease, pyelonephritis, and inflammatory bowel disease are explored from an obstetric triage perspective. Key triage points are noted to augment clinical assessment by the practitioner.
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PMID:Obstetric triage: management of acute nonobstetric abdominal pain in pregnancy. 1063 14

Polycystic liver disease can result in massive enlargement of the liver with resultant debilitating symptoms of abdominal pain, chronic fatigue, and severely compromised functional status. Fenestration of hepatic cysts has been advocated as a treatment for polycystic disease. However, in patients with predominant small cyst replacement, fenestration alone often results in limited hepatic volume reduction without improvement in patient functional status. Liver transplantation has also been previously advocated for polycystic liver disease with predominant small cyst replacement, but, with the severe shortage of donor organs, alternative treatment should be considered. In this report we present a case of massive enlargement of the liver with severe clinical debilitation due to polycystic liver disease. Transverse hepatectomy provided a safe and effective alternative to fenestration or liver transplantation.
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PMID:Transverse hepatectomy for symptomatic polycystic liver disease. 1066 87

Nonalcoholic steatohepatitis (NASH) is a histological diagnosis applied to a constellation of liver biopsy findings that develop in the absence of alcohol abuse. Steatosis, a mixed cellular inflammatory infiltrate across the lobule, evidence of hepatocyte injury and fibrosis are the findings that can be seen. This entity is often identified during evaluation of elevated aminotransferases after exclusion of viral, metabolic and other causes of liver disease. Obesity is a major risk factor for NASH. The role of diabetes is less certain, although evidence is accumulating that hyperinsulinism may play an important pathophysiological role. Patients sometimes suffer from right upper quadrant abdominal pain and fatigue; examination may reveal centripetal obesity and hepatomegaly. Although patients are often discovered because of persistent aminotransferase elevations, these enzymes can be normal in NASH. When they are elevated, the alanine aminotransferase level is typically significantly greater than the aspartate aminotransferase level. This can be particularly helpful for excluding occult alcohol abuse. Imaging studies identify hepatic steatosis when the amount of fat in the liver is significant; however, imaging does not distinguish benign steatosis from NASH. Ultimately a liver biopsy is needed to diagnose NASH. The biopsy may be useful for establishing prognosis based on the presence or absence of fibrosis and for excluding other unexpected causes of liver enzyme elevations. Weight loss is the mainstay of treatment for obese patients. About 15% to 40% of NASH patients develop fibrosis; how many of these cases progress to cirrhosis is unknown, but about 1% of liver transplants are performed with a pretransplant diagnosis of NASH.
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PMID:Nonalcoholic steatohepatitis: an evolving diagnosis. 1079 85

Symptoms related to fungal esophagitis were studied in patients with alcoholic liver disease who underwent upper gastrointestinal endoscopy. Data of 517 patients were studied retrospectively (group I) and 100 alcoholic liver disease patients, that were successively admitted to hospital, were enrolled in the prospective part (group II). Out of the 41 cases with fungal esophagitis found in group I, data of 38 could be evaluated. In group II 13 of the 93 evaluable patients had fungal esophagitis; according to Kodsi's grading 10 patients had grade 1., one patient grade 2. and two patients grade 2-3. oesophagitis. There was no case with grade 4. esophagitis. The rate of symptoms among the 51 patients with fungal esophagitis was: anorexia 23 (45.0%), abdominal pain 22 (43.1%), vomiting 17 (33.3%), nausea 15 (29.4%), occult gastrointestinal bleeding 12 (23.5%), weight loss 9 (17.6%), melena 7 (13.7%), bloating 6 (11.7%), acidic regurgitation 3 (5.8%), haematemesis 2 (3.9%), thoracic pain 2 (3.9%), singultus 1 (1.9%), odynophagia 0 and dysphagia 0. In 7 patients (13.7%) none of the studied symptoms could be identified. Despite the relatively high frequency of symptom free fungal esophagitis reported in the literature, the total lack of odynophagia and dysphagia in our patient group was remarkable. In the lack of deglutition disorders the other symptoms do not raise the suspicion of esophagitis. The diagnosis in such cases can be established only by endoscopy.
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PMID:[Symptoms of fungal esophagitis in alcoholic liver disease]. 1094 8

A 30-year-old HBsAg-positive woman was admitted to the hospital because of 6 days of progressive shortness of breath. She was in severe respiratory distress with circulatory collapse. She had an enlarged liver but no stigmata of chronic liver disease or signs of cirrhosis. She had rapidly developed respiratory arrest and was transferred to intensive care unit. Heart ultrasonography and Doppler scan showed right heart straining and high pulmonary artery pressure. Despite cardiovascular and respiratory support she died a few hours after admission. Autopsy revealed combined hepatocellular-cholangiocarcinoma infiltrating the entire liver, metastatic invasion of lung blood vessels and absence of right ventricular hypertrophy. The incidence of hepatocellular-cholangiocarcinoma, a variant of hepatocellular carcinoma, is roughly 2-3% and the presenting symptoms are abdominal pain, weight loss, jaundice, fever or decompensation of liver disease. Associated HBsAg positivity and cirrhosis are reported in 20-30% and 60% of patients, respectively. Metastases to lungs are relatively frequent but this is the first report of hepatocellular-cholangiocarcinoma presented with acute respiratory distress due to massive pulmonary embolism.
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PMID:Combined hepatocellular-cholangiocarcinoma presented with massive pulmonary embolism. 1102 Aug 95

Lactic acidosis and hepatic steatosis caused by mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI) is a rare cause of liver disease with a high mortality rate. This report describes a male, HIV-positive patient with a 4-week history of nausea, vomiting and abdominal pain. His medication consisted of prednisone 5 mg od (because of auto-immune thrombocytopenia), didanosine (for 2 years) and stavudine (for 3 months). Laboratory studies showed cholestasis and elevation of aminotransferases. Lactic level was not measured. Liver biopsy revealed steatosis and cholestatic hepatitis. In the absence of other causes of liver disease a probable diagnosis of stavudine-induced hepatic toxicity was made. After discontinuation of NRTI, he recovered completely. Because lactic acidosis had not been confirmed, stavudine was restarted and within 1 week the lactate level increased significantly. Therefore stavudine was discontinued again. One year later the patient is doing well on a double protease inhibitor regimen. In conclusion, clinicians treating patients with NRTI should be aware of the risk of lactic acidosis and hepatic steatosis. When this is suspected, all NRTI must be stopped. The diagnosis can be made when elevated lactate levels and hepatic steatosis are present in the absence of other causes of liver disease.
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PMID:Hepatic steatosis and lactic acidosis caused by stavudine in an HIV-infected patient. 1106 65

Our article concentrates on two acute states, which develop less dramatically but their after-effects may be very serious: Spontaneous bacterial peritonitis and Ogilvie's syndrome. Spontaneous bacterial peritonitis is a bacterial infection of the ascitic fluid without any intraperitoneal source of infection. Ascites is a condition of the disease but need not be clinically manifested. Spontaneous bacterial peritonitis comes usually during heavy hepatic impairment. Diagnosis can be set according: 1. Positive cultivation of ascitic fluid, 2. PMN levels higher than 250/mm3, 3. No infection, which may require a surgical intervention is apparent. Liver disease, which brings about the spontaneous bacterial peritonitis can be: 1. Chronic (e.g. alcoholic cirrhosis), 2. Subacute (e.g. alcoholic hepatitis), 3. Acute (e.g. fulminant hepatic failure). Mortality of this form of peritonitis can reach up to 46%. The most frequent etiological factor is alcohol and viral hepatitis, the most frequent agents are E. coli and Klebsiella pneumoniae. The disease is most effectively cured by cefalosporins of the third generation. With inadequate treatment, prognosis may be poor. Intestinal pseudoobstruction syndrome has clinical symptomatology of a serious impairment with ileus without signs of any mechanical intestinal obstruction. Syndrome can be classified according to its development: 1. Acute form--acute intestinal pseudoobstruction syndrome--Ogilvie's syndrome, 2. Chronic form--chronic intestinal pseudoobstruction syndrome. Pathogenic mechanism of the syndrome is not known. The disease is related to immobility, administration of some drugs, electrolyte imbalance and concomitant diseases (most frequently malignant tumors). Clinical symptomatology dominates nausea, vomiting, diffuse abdominal pain, constipation or diarrhoea. For diagnostics the first step should be termination of all medication, which could have causing affects, then taking native abdominal X-ray picture where gaseous intestinal distension can be prominent (coecum distended up to 9-12 cm). Identification of fluid surfaces is not usual. Endoscopic examination can exclude obstruction in the distal part of gut minimally. The most frequent complication is perforation of coecum. Pharmacological treatment relays on prokinetics. The basic intervention remains decompression by a rectal catheter or an effective coloscopic decompression with subsequent introduction of a cannula. Mortality of the disease fluctuates between 43 and 46%.
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PMID:[Acute states in gastroenterology: spontaneous bacterial peritonitis and the acute intestinal pseudoobstruction syndrome]. 1150 91

Acute liver failure and haemolytic syndrome appeared quite suddenly as the first manifestations of Wilson disease (WD) in five of our patients previously regarded as healthy persons (although an interview showed that 2-4 weeks prior to the illness the patients complained of several non-specific symptoms, such as abdominal pain, headaches, fever, weakness or behavioural changes). All the patients were young women (17-23 years), none of them had any history of liver disease. They were admitted with icterus, nausea, vomiting and symptoms of increasing haemolysis. The diagnosis of WD was given as disturbed copper metabolism. After a short period of observation ascites and anasarca occurred, haemorrhagic diathesis and other symptoms of liver failure increased. Levels of clotting factors decreased rapidly. Despite treatment with D-penicillamine, plasmapheresis, and symptomatic drugs, three of the women died in irreversible liver coma, due to the unavailability of liver transplantation. The fourth woman was carried to the Transplantation Centre, due to aggravation of the symptoms of liver failure, where liver transplantation was performed. Histopathologically micronodular cirrhosis was shown in all these cases. The fifth patient survived having undergone the above treatment without liver transplantation. The main differences between the patient who survived and those who died or underwent transplantation were relatively higher activity of alkaline phosphatase (26 U/l vs. 10-20 U/l), slightly higher levels of clotting factors and prothrombin time, which never fall below 68% of the control (versus 14-44% in other patients). Only in the surviving patient was the Kayser-Fleischer ring present. In four of our patients we found family members who were carriers of WD.
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PMID:Acute haemolytic syndrome and liver failure as the first manifestations of Wilson's disease. 1221 29

We report a case of severe hepatotoxicity associated with ductopenia in a 61-year-old woman. The patient developed jaundice, vomiting, and abdominal pain a few weeks after the beginning of treatment with candesartan cilexetil, 16 mg/d, for essential hypertension. Liver biopsy showed parenchymal bilirubinostasis with portal cholangitis and ductopenia. The drug was immediately withdrawn, and in the following weeks, aminotransferases and serum bilirubin returned to normal levels. The clinical-histologic data and the exclusion of known causes of liver disease led us to make a diagnosis of drug-induced cholestasis. To our knowledge, this is the first description of severe hepatotoxicity associated with ductopenia caused by an adverse reaction to candesartan cilexetil.
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PMID:Candesartan cilexetil-induced severe hepatotoxicity. 1259 Feb 42

We report on the difficult differential diagnosis of liver involvement in disseminated Langerhans' cell histiocytosis (LCH). Three years after treatment of LCH involving the skull and pelvic bones, an 18-year-old girl presented with abdominal pain and cholestatic liver disease. At this time, liver biopsy showed portal infiltrates which were diagnosed as chronic non-suppurative destructive cholangitis. Two years later, she was icteric under progredient hepatic failure. A second liver biopsy revealed biliary fibrosis and granulomatous inflammation with destruction of the portal bile ducts. The morphological changes in both liver biopsies could be identified as LCH by immunohistochemical detection of CD1a and S-100-positive Langerhans' cells. Morphological changes and clinical findings in LCH of the liver may resemble primary sclerosing cholangitis or chronic non-suppurative destructive cholangitis. Therefore, LCH is an important differential diagnosis of chronic destructive cholangitis with cholestatic liver disease, especially in children and young adults. The diagnosis can be verified by S-100 and CD1a immunohistochemistry.
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PMID:[Langerhans' cell histiocytosis of the liver. Differential diagnosis of a rare chronic destructive sclerosing cholangitis]. 1267 1


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