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 order to identify the predictive factors of hospital mortality in cirrhotics with spontaneous bacterial peritonitis (SBP), we studied 64 patients who fulfilled the accepted diagnostic criteria. All cases were treated with cefotaxime up to 2 days after the infection was considered cured (7.7 +/- 2.9 days). Eleven patients (17%) died while in hospital, six of them before SBP was cured. After uni- and multivariate analyses, only seven routine clinical, biological, and bacteriological variables studied were independently associated with hospital mortality. These were: the presence of upper gastrointestinal bleeding at admission (beta = 2.01), the absence of abdominal pain as presenting symptom (beta = -1.29), the polymorphonuclear count (%) in the ascites (beta = 0.48), prothrombin rate (beta = -0.22), and serum Na (beta = -0.64), creatinine (beta = 0.50), and cholesterol (beta = -0.68). When the equation obtained was computed in a randomly selected sample of the patients studied, it correctly predicted the outcome in 92.3% of the cases. We conclude that short-term outcome of SBP patients depends on the existence of recent gastrointestinal bleeding, the severity of SBP, and the degree of liver and renal failure. The prognostic value of this model needs prospective validation in a new series of patients.
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PMID:Short-term prognosis of cirrhotics with spontaneous bacterial peritonitis: multivariate study. 843 46

We made a retrospective study of 233 episodes of spontaneous bacterial peritonitis that were treated at our Service between January 1980 and September 1996 in order to analyze the clinical presentation, microbiological data, possible pathogenic factors, treatment, and evolution of this clinical entity. Ascites, abdominal pain, and fever were the most frequent symptoms. Only 3.43% of the episodes developed asymptomatically. Thirty-six episodes resulted in the patient's death (15.45%) and, of all the factors analyzed, only a prothrombin time of < 35%, bilirubin > 8 mg/dl, and serum creatinine > 2.1 mg/dl were statistically correlated with a higher death rate. The culture of the ascitic fluid gave a positive result in 47.6% of the cases, whereas no clinical differences were noticed between these patients and those with negative results. The most frequently isolated microorganisms turned out to be Gram negative (49.54%). A proportion of 71.24% of the episodes were treated with cephotaxime (i.v.), whereas 28.76% were treated with other drugs or pharmacological combinations. The death rate was much lower with cephotaxime (4.81% vs. 41.79%, p < 0.01%).
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PMID:Spontaneous bacterial peritonitis. Clinical and microbiological study of 233 episodes. 895 29

One hundred and forty-four episodes of spontaneous bacterial peritonitis (SBP) treated in our service between July 1988 and September 1995 were studied retrospectively to assess the clinical presentation, microbiological findings, possible pathogens, treatment and course. Ascites, abdominal pain and fever were the most common symptoms. Only 3.5% of cases were asymptomatic. The outcome was fatal in 12 (8.33%). Among the factors analyzed, only a prothrombin time of less than 35% correlated significantly with a higher mortality rate (60% and 8.33%, respectively; p < 0.01). Ascitic fluid culture was positive in 43.05% of cases; significant differences existed between these patients and those with negative ascitic fluid culture with respect to clinical findings or course. Gram-negative microorganisms were those most frequently isolated (48.38%). Treatment was initiated within 12 hours in 77.7% of the patients, between 12 and 72 hours in 11.8% and later in 10.41%. Intravenous cefotaxime was administered in 86.1% of cases and other drugs or drug combinations in only 13.9%; the mortality rate was much lower with cefotaxime (2.4% vs 45%; p < 0.01).
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PMID:Spontaneous bacterial peritonitis: clinical study, microbiological findings and clinical course. 914 99

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.
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PMID:[Ischemic hepatitis in congestive heart failure after an episode of hypotension]. 915 12

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

The HELLP syndrome is a dangerously severe form of preeclampsia associated with multiorgan system damage and occurs in 0.2-0.6% of all pregnancies. It usually presents with abdominal pain, often in the setting of preeclampsia. In most cases, HELLP is initiated by inadequate placental vessel development with subsequent placental ischemia, leading to the release of circulating vasoconstrictors. These powerful vasoconstrictors include thromboxane A2, angiotensin, prostaglandin F2, and endothelin-1. The ischemic placenta also produces fewer vasodilators, such as prostacyclin, prostaglandin, E2, and nitric oxide. The ensuing imbalance in vasoactive substances causes intense systemic vasospasm and multiorgan endothelial damage. Multiple genetic, coagulation, and immunologic disorders also appear to contribute to the endothelial damage. Fibrin and platelets are then deposited on the endothelial surfaces leading to the hemolytic anemia, elevated liver enzymes, and low platelets of the HELLP syndrome. The most reliable laboratory tests for the diagnosis of HELLP are a complete blood count with peripheral smear, lactate dehydrogenase, serum transaminases, and urinalysis. Supportive tests include serum haptoglobin, D-dimer fragment levels, lactate dehydrogenase isoenzymes, total bilirubin, prothrombin times, and activated partial thromboplastin times. Lactate dehydrogenase and the platelet count are the two best tests to monitor the course of the disease. Prompt delivery is the treatment of choice. The intensity of the HELLP syndrome peaks 24 hours after delivery. Extended atypical HELLP has been successfully treated with plasma exchange. The clinical laboratory professional plays an important role in the diagnosis, follow-up, and treatment of patients with the HELLP syndrome.
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PMID:HELLP! A cry for laboratory assistance: a comprehensive review of the HELLP syndrome highlighting the role of the laboratory. 984 23

The occurrence of hepatocellular carcinoma (HCC) in renal transplant recipients has typically been associated with hepatitis B or C infection. We encountered two cases of HCC in renal transplant recipients with negative hepatitis B and C markers and no underlying liver pathology, in whom immunosuppression therapy consisted of prednisone and azathioprine (AZA). Patient no. 1 is a 66-year-old man with diabetes who underwent cadaveric renal transplantation 13 years before presentation. An ultrasound obtained for evaluation of a prolonged prothrombin time and decreased serum albumin level showed a suspicious nodular lesion in the left lobe of the liver. A computed tomographic (CT) scan confirmed a 4- x 5- x 5-cm mass that, on biopsy, was determined to be well-differentiated HCC. There was no evidence of metastasis, and the results of random biopsies of the surrounding parenchyma were normal. The patient underwent a left lateral segmentectomy, did well, and an initial alpha-fetoprotein (AFP) level of 85995 ng/mL decreased to 9 ng/mL. Approximately 20 months postoperatively, however, a surveillance CT scan showed three hypervascular lesions in the right lobe of the liver and the AFP level increased to 28,370 ng/mL. Subsequent percutaneous alcohol injections yielded good results, and the patient is alive and well 13 months later. Patient no. 2 is a 57-year-old man who underwent cadaveric renal transplantation 24 years earlier. A CT scan of the abdomen obtained for evaluation of lower abdominal pain showed a 4- x 4- x 6.5-cm mass in the right lobe of the liver that, on biopsy, was found to be poorly differentiated HCC. Multiple biopsies of adjacent liver parenchyma showed no evidence of cirrhosis, AFP level was normal, and imaging studies showed no evidence of tumor spread. The patient underwent a right hepatic lobectomy and is doing well without evidence of recurrence 27 months postoperatively. Our two patients had no evidence of viral hepatitis, cirrhosis, or metabolic liver disease, yet both developed HCC. The use of AZA may have had a role in the development of HCC. In renal transplant recipients on long-term immunosuppression therapy, particularly AZA, it is prudent to maintain a high index of suspicion for HCC when liver enzyme level or function abnormalities are encountered.
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PMID:Hepatocellular carcinoma after renal transplantation in the absence of cirrhosis or viral hepatitis: a case series. 987 92

We studied 13 patients with lipoamide dehydrogenase (LAD) deficiency, originating from seven Ashkenazi Jewish families. Their disease was characterized by recurrent attacks of vomiting, abdominal pain, and encephalopathy accompanied by elevated liver transaminases, prolonged prothrombin time, and occasionally associated with lactic and ketoacidemia or with myoglobinuria. Two patients who presented neonatally suffered from residual neurological damage with attention deficit hyperactive disorder, mild ataxia, motor incoordination, muscle hypotonia, and weakness. Nine patients who presented in early childhood or later suffered from exertional fatigue between decompensation episodes but were otherwise asymptomatic. Two patients died because of intractable metabolic acidosis and multi-organ failure. In all patients LAD activity was reduced to 8 to 21% of the control in muscle or lymphocytes. In four patients LAD protein in muscle was reduced to 20 to 60% of the control. Direct sequencing of the cDNA of the LAD gene showed that 12 of the 14 mutated alleles carried the G229C mutation and two carried an insertion mutation 105insA (Y35X). The patients who presented neonatally and had more severe sequelae were compound heterozygotes for the two mutations; patients who presented in early childhood or later were homozygous for the G229C mutation. Using an allele-specific oligonucleotide hybridization technique, nine heterozygotes for the G229C mutation were identified among 845 anonymous individuals of Ashkenazi Jewish origin disclosing a carrier rate of 1:94. Because of the significant morbidity associated with the disease, screening for the G229C mutation among Ashkenazi Jewish couples should be considered.
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PMID:Molecular basis of lipoamide dehydrogenase deficiency in Ashkenazi Jews. 993 85

A retrospective case note review was undertaken to assess the clinical significance of hepatic dysfunction with jaundice in typhoid fever. Of the 57 patients, 21 (36.8%) had jaundice, while 36 (63.2%) did not have jaundice. Significantly higher proportions of jaundiced patients were females (P = 0.04). Confusion (P = 0.01), upper abdominal pain (P = 0.02), right upper quadrant tenderness (P = 0.0001), and low prothrombin index (P = 0.04) were statistically significant occurrences in jaundiced patients on admission. Admission mean values of serum bilirubin (P = 0.0001), gamma-glutamyltranspeptidase (GGT; P = 0.009), and alanine aminotransferase (ALT; P = 0.0005) were significantly higher in icteric patients while mean values of total serum protein (P = 0.0009) and albumin (P = 0.0001) were significantly higher in anicteric patients. There were no deaths. Glomerulonephritis occurred significantly (P = 0.001) more frequently in icteric patients. It is concluded that hepatic dysfunction with jaundice in typhoid fever indicates more severe hepatic injury, which may precipitate the development of clinically detectable glomerulonephritis.
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PMID:Clinical significance of hepatic dysfunction with jaundice in typhoid fever. 1008 Jan 55

We evaluated the focal therapeutic effect of oily carcinostatic agents administered by transcatheter arterial infusion (TAI) as the initial therapy in patients with hepatocellular carcinoma in a randomized controlled clinical trial. Group A (19 patients) received 4 mg of styrene maleic acid neocarzinostatin in 4 ml of Lipiodol, and group B (18 patients) received 100 mg of epirubicin in 4 ml of Lipiodol via the tumor feeding arteries as peripherally as possible. The grade of Lipiodol accumulation and the tumor regression rate were determined 2 weeks after TAI by computerized tomography. Adverse effects within 2 weeks after TAI were evaluated by subjective signs and symptoms such as fever (maximum body temperature) and the frequency of shaking chills and abdominal pain, and by biochemical parameters such as albumin, prothrombin time, and aspartate and alanine aminotransferases. Lipiodol accumulation in the tumor was significantly greater in group A (12/19; 63.2% showing grade IV Lipiodol accumulation) than in group B (3/18; 16.7% showing grade IV) (P<0.05). The tumor regression rate was also significantly greater in group A (8/17; 47.1% showing more than 25% tumor regression) than in group B (1/13; 7.7% showing more than 25% tumor regression) (P<0.05). Although clinically significant elevations of aminotransferases and reductions of cholinesterase, and shaking chills were observed more often in group A than in group B (P<0.0001), these factors had little influence on the clinical outcome. Our results suggest that styrene maleic acid neocarzinostatin in Lipiodol exerts a more favorable focal therapeutic effect than does epirubicin in Lipiodol in the initial treatment of hepatocellular carcinoma.
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PMID:Focal therapeutic efficacy of transcatheter arterial infusion of styrene maleic acid neocarzinostatin for hepatocellular carcinoma. 1063 37


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