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)

We present the case of a young male with 2-month history of intermittent upper abdominal pain who developed diarrhea, anorexia, tea-color urine, and decreased urine output. He was found to be in severe acute renal failure requiring hemodialysis, four sessions in 10-day period. By the end of the second week of hospitalization renal function gradually improved with total recovery of function to a baseline creatinine of 1.1 mg/dl 25 days after the diagnosis of acute renal failure. His workup included Ham's test, water sugar test, and RBC fragility test which confirmed the diagnosis of paroxysmal nocturnal hemoglobinuria.
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PMID:Acute reversible renal failure in a patient with paroxysmal nocturnal hemoglobinuria. 979 72

A 54-year-old man, who had been diagnosed as having MPO-ANCA-related glomerulonephritis in 1993, developed severe anemia and was admitted to our hospital on October, 1997. Endoscopic examination of the upper gastrointestinal tract revealed melena due to duodenal ulcer (Dieulafoy type). The level of ANCA titer was elevated considerably (640 EU), but otherwise there was no evidence of systemic vasculitis activation such as fever, arthralgia, skin eruption, renal insufficiency, and rise in C reactive protein. A renal biopsy showed neither crescentic formation nor necrosis of glomerulus. Subsequently he developed hematochezia and renal dysfunction rapidly progressed thereafter. Angiographical examination of superior mesenteric artery revealed that the bleeding was responsible for the lesion of the small intestine, probably the ileum. In spite of TAE (transarterial embolization) he had recurrence of severe hematochezia three days later. Partial ileotomy was performed and progression of the anemia was stopped. Multiple ulcer was found in the resected ileum. The small arteries in the submucosa at the ulceration showed fibrinoid necrosis of the vessel walls. These findings suggested that ANCA-related vasculitis had relapsed. The patient received methylprednisolone pulse therapy, followed by oral administration of prednisolone after the operation. Both serum levels of creatinine and MPO-ANCA gradually decreased after the initiation of treatment. However, 24 days later, he suddenly manifested severe abdominal pain, and was diagnosed as having perforation of the stomach or duodenum. Due to supportive therapy and reduction of the steroid dose, peritonitis subsided, but symptoms caused by systemic vasculitis developed. Later raised the dose of steroid suppressed the activity of systemic vasculitis. In this case, elevation of the ANCA titer demonstrated recurrence of MPO-ANCA-related vasculitis as gastrointestinal bleeding.
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PMID:[A case of MPO-ANCA-related vasculitis that recurred as gastrointestinal bleeding and presented difficulty in treatment]. 980 23

Cirrhosis of the liver results from a variety of mechanisms that cause progressive hepatic injury. It is the sixth leading cause of death in all patients between the ages of 35 and 55. This study attempts to correlate the morbidity and mortality of spontaneous bacterial peritonitis in liver failure patients to numerous etiologic and clinical variables. A retrospective review of 26 patients with spontaneous bacterial peritonitis associated with chronic liver disease was performed in a university hospital. Demographics (age and gender), clinical variables (etiology of liver failure, Child's classification, prior history of ascites, fever, abdominal pain, encephalopathy, and upper gastrointestinal hemorrhage), and laboratory variables (ascitic polymorphonuclearcyte count and cultures, serum albumin, bilirubin, creatinine, and prothrombin time) were studied. All of the patients had Child's C liver disease. Mortality rate was 46 per cent. Alcohol (46%) and hepatitis (30%) were the most common etiologies. Escherichia coli and Klebsiella pneumoniae were the most common culture isolates. All of the infections were monomicrobial. The only significant predictor of mortality (P < 0.05) in this study was the peritoneal fluid polymorphonuclear (PMN) cell count. PMN count >1000 PMN/mm3 was associated with a mortality of 88 per cent. Few patients with spontaneous bacterial peritonitis are ultimately transplanted.
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PMID:Spontaneous bacterial peritonitis in liver failure. 984 34

A 43-years-old female was admitted to our hospital because of facial erythema and photosensitivity in 1983 and was diagnosed as systemic lupus erythematosus (SLE). She was treated with betamethazone 2.5 mg/day as an outpatient. Abdominal pain and diarrhea were developed in September, 1995. So she was admitted to our hospital and diagnosed as having paralytic ileus. Ultrasonography showed marked intestinal edema. Forbidden oral intake and given antibiotics, she was satisfactorily improved in a few days, but the symptoms got worse soon. We forbid oral intake again. We performed a pulse therapy with 1 g of methylprednisolone and increased a dose of betamethasone 2.5 to 4.0 mg/day, but the symptoms were not improved. Since October 6th, serum creatinine level (s-CRE) increased to 8.1 mg/dl at October, 20th. We suspected the worsening of SLE nephropathy or drug-induced nephropathy, so we stopped a medication of pravastatin and used 50 mg/day of azathioprine. Moreover, we did a pulse therapy of methylprednisolone and a plasmapheresis. By these treatments, s-CRE level returned to normal range and paralytic ileus was completely improved. The cause of hypercreatininemia was suspected to be rhabdomyolysis due to pravastatin. The main cause of paralytic ileus with intestinal edema was suspected to be vascular disturbance of superior mesenteric arteries. We consider that pulse therapy and plasmapheresis are useful for a patient of SLE with marked intestinal edema and paralytic ileus.
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PMID:[A case of systemic lupus erythematosus complicated with marked intestinal edema and paralytic ileus]. 988 51

Two patients, one 76-year-old-man and one 79-year-old-woman with cardiovascular disease and one 36-year-old-man with Factor-V-Leiden deficiency (activated protein C-resistance) had abdominal pain and elevation of LDH levels. With abdominal CT scan kidney infarction was diagnosed. In two cases a selective kidney arteriography was performed to confirm the diagnosis. Treatment consisted of (re)starting anticoagulant therapy. In unexplained abdominal pain with insufficiently specific results of physical examination combined with a rapid rise of the LDH and sometimes of the serum creatinine, a kidney infarction should be considered in the differential diagnosis.
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PMID:[Three patients with a kidney infarct]. 1002 29

We identified 35 cases of tubulointerstitial nephritis and uveitis (TINU), 31 from a MEDLINE search (1966-1996) of the English literature and 4 from our hospital records (1988-1996). To meet the case definition, the patient had to be less than 18 years old and have TINU of unknown cause. Common presenting symptoms included fatigue, weight loss, fever, and abdominal pain. The uveitis was usually anterior and could occur at any time with respect to the onset of the renal disease. Common laboratory features included anemia, increased erythrocyte sedimentation rate, and decreased creatinine clearance. Most patients (33 of 35) had renal biopsies that commonly revealed an intense inflammatory interstitial infiltrate, glomerular sparing, and negative immunofluorescence studies. Of the 35 patients, 26 received systemic corticosteroid therapy (5 of 26 for eye disease); 22 had follow-up for at least 1 year; 13 of 35 patients had a recurrence of their uveitis. The outcome in all 35 cases was normal renal function with no documented visual loss. In conclusion, TINU is a unique syndrome with characteristic clinical features, laboratory changes, and renal biopsy results. Treatment is controversial, and the outcome in children, even if untreated, is excellent.
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PMID:Tubulointerstitial nephritis and uveitis in children and adolescents. Four new cases and a review of the literature. 1041 64

Recurrent urinary tract infection (UTI) has not been widely recognized as a clinical manifestation of hypercalciuria in children. We studied 59 children with two or more episodes of UTI, a normal urinary tract, and with hypercalciuria. Clinical manifestations were fever, dysuria, straining with micturition, hematuria, polyuria, abdominal pain, and failure to thrive. Urinary calcium/creatinine ratio was 0.36+/-0.15 mg/mg. Renal function studies included serum bicarbonate (21+/-3 mmol/l), urinary/blood PCO2 difference (11+/-11 mmHg), urinary net acid excretion (63+/-3 micromol/min per 1.73 m2), uric acid fractional excretion (13%+/-12%), and maximal urinary osmolality (920+/-236 mosmol/kg). Treatment included promotion of fluid intake, avoiding excessive salt and protein, and keeping dietary calcium between 900 and 1,200 mg/day. Potassium citrate or hydrochlorothiazide were indicated if hypercalciuria persisted. With this treatment, in 95% of the children, no further episodes of UTI occurred once normocalciuria was achieved. It is possible that hypercalciuria may play a predisposing role for recurrent UTI in children by promoting the formation of microcrystals which damage the uroepithelium. We advocate the investigation of urinary calcium excretion in children with recurrent UTI and a normal urinary tract.
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PMID:Hypercalciuria and recurrent urinary tract infection in Venezuelan children. 1041 65

We report a rare case with multiple renal infarction associated with lupus anticoagulant and SLE. A 20-year old woman presented with remitent fever, butterfly rash and, abdominal pain. Laboratory findings showed leukopenia, positive antinuclear and anti-DNA antibodies, and biological false positive for syphilis. Despite a therapy with prednisolone 25 mg/day, the patient showed hypocomplementemia, high titer of anti-DNA antibody and a development of proteinuria and an elevation of serum creatinine. Renal biopsy revealed no abnormalities. She presented abdominal pain with an elevation of serum LDH. Abdominal dynamic computed tomography demonstrated multiple perfusion defects in both kidneys indicating multiple renal infarction. Brain MRI showed multiple micro infarction in the anterior lobes. She was treated with 80 mg of aspirin and have been in remission for two years. Although there have been reported 18 cases with renal infarction associated with antiphospholipid syndrome, this is the first report in Japan. Renal infarction should be differentiated from renal involvement in patients with SLE who have antiphospholipid antibodies.
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PMID:[Multiple renal infarction associated with lupus anticoagulant in a patient with systemic lupus erythematosus]. 1043 52

Thirty patients with primary hepatocellular carcinoma or liver metastases were entered into a program of chemoembolization with cisplatin, lipiodol, and escalating doses of thiotepa. Doses of cisplatin were 100/m2, and thiotepa doses ranged from 9 mg/m2 to 24 mg/m2. Two of three patients with ocular melanoma had partial responses in the liver metastases for 3+ and 16 months. In patients with either hepatocellular carcinoma (15 patients) or primary cholangiocarcinoma of the liver (three patients), there were two partial responses, for 22 and 33 months. Five patients had minor responses: four with a 40% reduction in tumor and one with a mixed response. There were four early deaths, which involved sepsis in two patients, respiratory failure in one, and acute myocardial infarction in one. Otherwise, toxicity was tolerable and reversible and included abdominal pain and transient elevation of serum creatinine, bilirubin, and transaminases. Less common toxicities included ototoxicity and peripheral neuropathy. Chemoembolization of the liver with cisplatin, thiotepa, and lipiodol can produce responses, but toxicity can be significant. The recommended starting phase II dose for future studies is thiotepa 24 mg/m2 and cisplatin 100 mg/m2.
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PMID:A phase I study of chemoembolization with cisplatin, thiotepa, and lipiodol for primary and metastatic liver cancer. 1044 Jan 93

We report three children with tubulointerstitial renal failure following leptospirosis. All had acute nonoliguric renal failure with mild hypocalemia and mild metabolic acidosis. Maximum blood urea nitrogen (BUN) and creatinine were 217 and 7.1 mg/dl, respectively, on the 6th day of disease, and no patient required dialysis. They presented with acute febrile illness and dehydration, and required intravenous fluid supplements. Myalgia, vomiting, and bleeding were found in two children. Abdominal pain, arthralgia, diarrhea, and conjunctival suffusion were found in one child. Only one child, who had an underlying disease of beta-thalassemia/Hb E, had jaundice, hepatosplenomegaly, anemia, and thrombocytopenia. Penicillin treatment was given in one case. All recovered, with normal renal function. The leptospirosis complement fixation test was used to confirm diagnosis. L. batavia was considered the etiologic agent in two of the children.
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PMID:Tubulointerstitial renal failure in childhood leptospirosis. 1053 63


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