Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 45 patients with acute obstructive cholangitis (AOC) endoscopic sphincterotomy (ES) was performed within 24 hours after admission. Criteria for the diagnosis of AOC were as follows: clinical symptoms consisting of fever and chills, right upper abdominal pain, and jaundice (Charcot's triad) with coexisting laboratory data as elevated WBC, ERS, bilirubin level and evidence of obstructive biliary disease confirmed by endoscopic retrograde cholangiopancreatography. The causes of AOC were: in 38 patients (84.5%)--common bile duct stones, in 2 patients (4.5%)--carcinoma of the papilla of Vater, and in 5 patients (11%)--benign stenosis of the papilla of Vater. A rapid clinical improvement was observed in 40 patients after ES. Within 24 hours after ES patients had relief of pain, fever subsided and white blood cell count returned from 11.7 +/- 6.9 G/l to 7.0 +/- 3.0 G/l. Bilirubin level decreased from 101 +/- 86 mumol/l to 77 +/- 68 mumol/l. Endoscopic drainage failed only in 4 patients (9%) who required surgery. One patient (2%)--died. In the treatment of acute obstructive cholangitis urgent endoscopic sphincterotomy should be a method of choice. Surgery should be reserved only for patients in whom ES failed.
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PMID:[Emergency endoscopic sphincterotomy in acute obstructive cholangitis]. 186 19

We describe the clinical features, liver histology, and ultrastructure in reversible diclofenac-induced hepatitis and review previous reports of this entity. Although rarely reported, diclofenac hepatitis may be severe, and even fatal. Symptoms, which develop from 1 week to 11 months after starting the drug, include jaundice, pruritus, fever, abdominal pain, nausea, vomiting, and rash. Bilirubin and alkaline phosphatase are mildly elevated, transaminases often markedly so. The nature of the idiosyncratic injury appears variable, some cases having features of a hypersensitivity reaction, most being more suggestive of a toxic metabolic effect. Light microscopy shows a nonspecific hepatitis with portal and lobular activity, and focal hepatocellular injury that may progress to zonal or massive necrosis. The ultrastructural features in our case are typical of drug or toxin injury. This may be of value in distinguishing this entity from other forms of hepatitis, which is important in view of the frequent reversibility of this potentially lethal form of injury.
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PMID:Reversible hepatitis associated with diclofenac. 203 30

A retrospective was designed to analyse the mode of presentation, clinical signs and haematological and biochemical abnormalities in 225 consecutive Black (Zulu) patients who were admitted to a general medical ward between the years 1970 and 1981 and in whom cirrhosis was later diagnosed. The most common presenting complaint was swelling of the body (60% of the patients), followed by abdominal pain (32%) and episodes of bleeding, mainly from the gastrointestinal tract (19%). On examination, hepatomegaly was encountered in 66% of the patients, with moderate to massive enlargement in 40%. Ascites was detected in 56%, with tense abdominal distension in 34%. Jaundice was present in 38% and emaciation, mental disturbance and splenomegaly in over 25%. Spider naevi (found in 2 patients) and Dupuytren's contracture (found in 1) were very rare. Thrombocytopenia and a high ESR were common. Over 90% of patients had low albumin and high globulin concentrations (albumin less than 20 g/dl and globulin greater than 60 g/dl in 25%). Bilirubin and alkaline phosphatase levels and the prothrombin index were found to be within normal limits in 32%, 24% and 52% of cases respectively. Histologically the lesion was most commonly micronodular (73%) with variable deposits of fat and iron. Peritoneoscopy was the most useful special investigation in the diagnosis of cirrhosis, leading to a correct diagnosis in 77% of cases. In conclusion, the clinical signs, biochemical abnormalities and histological features suggest that the factors causing cirrhosis in the community studied are mixed; it may result from the combined effects of alcohol abuse, malnutrition and chronic viral (e.g. hepatitis B) infections.
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PMID:Clinical presentation and biochemical abnormalities in black (Zulu) patients with cirrhosis in Durban. 707 88

Hydatid hepatic cyst rupture into bile duct is a complication of hydatid disease. The rupture is more frequent in right or left epatic duct and occasionally in common bile duct (7-9%). A 50-year old man came to emergency room owing to jaundice, fever and abdominal pain. TC show an hydatid cyst with daughter's cyst of left liver and dilatation of biliary tree. Laboratory data of significance included an increased of liver function tests (Bilirubin, Alkaline ph., SGOT, SGPT), VES and leukocytosis. The patients was surgically treated, by total pericystectomy, colecystectomy and coledocotomy with lavage o common bile duct; finally we placed one Kehr drainage and two abdominal drainage. After 15 days of postoperative hospitalization patient was discharged. The best treatment of hydatid cyst is total pericystectomy (when possible). An alternative surgical treatment is possible for the presence of communication with biliary tree. ERCP is very important for a correct diagnosis and for a complete surgical treatment.
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PMID:[Obstructive jaundice caused by hydatid cyst rupture in main bile duct]. 1069 98

Sickle cell disease (SCD) is an autosomal recessive abnormality of the beta-globin chain of hemoglobin (Hb), resulting in poorly deformable sickled cells that cause microvascular occlusion and hemolytic anemia. The spleen is almost always affected by SCD, with microinfarcts within the first 36 months of life resulting in splenic atrophy. Acute liver disorders causing right-sided abdominal pain include acute vaso-occlusive crisis, liver infarction, and acute hepatic crisis. Chronic liver disease might be due to hemosiderosis and hepatitis and possibly to SCD itself if small, clinically silent microvascular occlusions occur chronically. Black pigment gallstones caused by elevated bilirubin excretion are common. Their small size permits them to travel into the common bile duct but cause only low-grade obstruction, so hyperbilirubinemia rather than bile duct dilatation is typical. Whether cholecystectomy should be done in asymptomatic individuals is controversial. The most common laboratory abnormality is an elevation of unconjugated bilirubin level. Bilirubin and lactate dehydrogenase levels correlate with one another, suggesting that chronic hemolysis and ineffective erythropoiesis, rather than liver disease, are the sources of hyperbilirubinemia. Abdominal pain is very common in SCD and is usually due to sickling, which resolves with supportive care. Computed tomography scans might be ordered for severe or unremitting pain. The liver typically shows sickled erythrocytes and Kupffer cell enlargement acutely and hemosiderosis chronically. The safety of liver biopsies has been questioned, particularly during acute sickling crisis. Treatments include blood transfusions, exchange transfusions, iron-chelating agents, hydroxyurea, and allogeneic stem-cell transplantation.
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PMID:Gastrointestinal and hepatic complications of sickle cell disease. 2021 64

Congenital agenesis of the gallbladder is a rare anomaly which is usually asymptomatic and found incidentally. In some cases, however, patients are symptomatic. Common symptoms include right upper quadrant abdominal pain, nausea, and vomiting. Jaundice is present in some symptomatic cases and is due to associated choledocholithiasis (Fiaschetti et al. 2009). In this case, a 63-year-old female presents with jaundice and episodic right upper quadrant abdominal pain with nausea and vomiting. Bilirubin and alkaline phosphatase were found to be markedly elevated. Upper endoscopic ultrasound (EUS) revealed choledocholithiasis, and the patient required multiple endoscopic retrograde cholangiopancreatography (ERCP) sessions before successful extraction of all stones. Subsequent surgical exploration revealed congenital agenesis of the gallbladder. Although this is a rare finding, patients with agenesis of the gallbladder are at increased risk of developing de novo choledocholithiasis which may be challenging to extract.
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PMID:Gallbladder Agenesis with Refractory Choledocholithiasis. 2618 91