Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the fact that the clinical experience with TPN has been gathered from patients of all age groups suffering from a variety of underlying diseases running very different clinical courses and often complicated by a number of septic metabolic and therapeutic problems, certain points can be made with regard to predisposing factors. 1) Prematures and neonates are particularly at risk. 2) Cholestasis occurs earlier and has a greater chance of leading to chronic liver disease in surgical patients. 3) Hepatobiliary abnormalities are more likely to develop after a prolonged period of TPN and are less frequent in patients who are also receiving oral feedings. Definition of the mechanism of hepatobiliary complications remains a problem. Although calcium bilirubinate appears to be responsible for sludge and stones, there is as yet no explanation for the presence of large amounts of indirect-reacting bilirubin in gallbladder and hepatic bile in patients on TPN. The pathogenesis of cholestatic liver disease remains an enigma; the lack of normal gastrointestinal stimuli for bile formation, abnormalities of bile acid metabolism, and sepsis might play roles, but attention has recently been attracted to amino acid toxicity and this possibility deserves further study.
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PMID:Hepatobiliary complications associated with TPN: an enigma. 393 7

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.
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PMID:Cholestyramine induced hyperchloremic metabolic acidosis. 659 13

To assess the prevalence and long-term impact of HCV on kidney transplant recipients, we assayed 716 pre-transplant sera using a first-generation ELISA. The anti-HCV positive sera were confirmed by a 6-antigen radioimmunoassay (RIA). Patients were followed up for 5 years. Graft survival, function, evidence of chemical hepatitis (AST > 2x normal), patient mortality and cause of death were evaluated. The prevalence of anti-HCV antibody was 10.3%. In the 638 patients who were followed up for 5 years, there were no differences in graft function, graft survival, overall mortality, or death from sepsis or liver disease. Peak AST levels were significantly higher in anti-HCV positive patients compared to anti-HCV negative patients. At 5 years, the AST levels remained significantly higher in the anti-HCV positive group, however, this was only 6 U/1 > normal. Liver biopsies performed 3 to 7 years post-transplant in 80% of anti-HCV positive patients with chemical hepatitis showed 12% CAH, 50% mild hepatitis and 38% normal histology. Six (9.7%) patients seroconverted from anti-HCV positive to anti-HCV negative 2 to 5 years post-transplant. The presence of anti-HCV does not appear to alter long-term patient or graft survival, and histologic evidence of severe chronic liver disease was rare in anti-HCV positive patients with chemical hepatitis. From these results, the presence of anti-HCV antibody should not preclude kidney transplantation.
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PMID:Long-term outcome in kidney transplant patients with hepatitis C (HCV) infection. 759

There is a high incidence of chronic liver disease in end-stage renal failure patients on dialysis. Hepatitis C virus appears responsible for 80% of posttransfusion hepatitis, and up to 80% of sporadic hepatitis and cryptogenic cirrhosis. Anti-HCV antibodies correlate highly with the presence of active infection. The clinical implications of HCV infection in patients undergoing renal transplantation is unknown. Part I: We undertook a descriptive cross-sectional study of all renal failure patients admitted for kidney transplant between 1/84 and 12/88. Pretransplant sera were assayed for anti-HCV using an ELISA. Patients were divided into anti-HCV-positive (study group) and anti-HCV-negative (controls). Part II: A cohort study was performed with both groups followed from the time of transplantation to the present. Comparisons were made by t tests, chi-square analysis with Yates correction, Mann Whitney test for nonparametric results and multiple regression analysis. Part I: Anti-HCV was present in 76 of 716 sera assayed. There were no differences in sex, age, number of previous transplants, and underlying renal disease. Four variables predicted the presence of anti-HCV: number of blood transfusions; duration on dialysis; i.v. drug abuse, and nonwhite race. Part II: A group of 596 patients was further analyzed. The mean duration of follow-up was not different between the two groups. There were no differences in graft survival, overall mortality, or mortality secondary to liver disease or sepsis. Based on these results, the presence of anti-HCV should not be a contraindication for kidney transplantation.
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PMID:Hepatitis C--its prevalence in end-stage renal failure patients and clinical course after kidney transplantation. 767 27

Vibrio vulnificus infection, which is a rare and fatal disease, can be categorized clinically as either primary septicemia or wound infection. The clinical presentation of patients with primary septicemia can vary from fever alone to a more severe illness including high-grade bullous lesions, hypotension, and shock. Wound infection typically results from either injury to the skin in a marine environment or contact of a preexisting wound with sea water. We reported eight cases with Vibrio vulnificus infection in Chang gung Memorial Hospital and reviewed ten other cases previously reported with details in Taiwan. Fourteen patients presented with primary septicemia, and four with wound infection. Thirteen patients had alcoholism or chronic liver disease, two had peptic ulcer disease, one was steroids abuser, and one patient had thalassemia and chronic liver disease. Overall mortality was 55.6% (ten patients). Patients with hypotension within 48 hours of admission had higher mortality than normotensive patients (77% vs. 0%, P = 0.007). Patients with chronic liver disease or liver cirrhosis also had tendency to a higher mortality than not (64% vs. 25%, P = 0.274). Chronic liver diseases and liver cirrhosis are common disease in Taiwan. They take a high risk for Vibrio vulnificus infection. Clinician should keep in mind of this potentially fatal infection in these patients reporting a history of recent raw oyster consumption and presented with sepsis and characterized skin lesions. Prompt empirical antibiotics treatment and aggressive surgical treatment may be lifesaving for this acute and fatal disease.
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PMID:Vibrio vulnificus infection--report of 8 cases and review of cases in Taiwan. 785 Jun 49

Vibrio vulnificus is an etiologic agent of septicemia and skin lesions. Patients with chronic diseases, and more frequently chronic liver disease, are specially susceptible to this infection. The main risk factor is shellfish ingestion. In this report we present a patient with chronic liver disease who suffered fulminant sepsis and necro-hemorrhagic bullaes secondary to a V. vulnificus infection. The patient had ingested shrimps two days before. A review of the recent literature on the subject is also presented.
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PMID:[Vibrio vulnificus in Mexico: a case report and review of the literature]. 789 42

Functional hyposplenism, seen in some patients with alcoholic liver disease, may contribute to the increased susceptibility to infections. As hyposplenism does not complicate non-alcohol related chronic liver disease, it is probably secondary to a toxic effect of alcohol. Over a two year period the case notes of 82 patients with alcoholic liver disease, whose splenic function had been assessed by the counting of pitted erythrocytes using differential interference microscopy, were reviewed to monitor mortality and the effects of hyposplenism. Thirteen patients (seven with hyposplenism) had serial measurements of pitted erythrocyte count made to assess the effect of abstinence from alcohol on splenic function. Thirty one of the 82 alcoholic patients had pitted erythrocyte counts greater than 2%. Eighteen of 82 (16%) patients died over the two years and 11 of these had been unable to stop drinking. Only one patient died of sepsis. Five patients (6%) had pitted erythrocyte counts comparable with those in splenectomised patients. In 12 of 13 patients who had abstained from alcohol for two months, the pitted erythrocyte count fell from a median of 3 to 1.3% (mean: 8.1 to 2.6%. p = 0.01). The pitted red cell count in two patients increased. One had abstained, the other had continued to drink heavily. Short term mortality in alcoholics is high, particularly if they continue to drink heavily. Only a few of these deaths are secondary to infection. Splenic function, as assessed by these methods, improves in most patients with abstinence, suggesting that the functional hyposplenism may be a result of a direct toxic effect of alcohol on the spleen.
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PMID:Functional hyposplenism in alcoholic liver disease: a toxic effect of alcohol? 820 May 65

We recently saw two unusual manifestations of Haemophilus influenzae infection in adults in the Seattle area: fulminant sepsis in an otherwise-healthy man and three episodes of bacteremia in a woman with chronic liver disease. We retrospectively identified 79 bacteremic and 40 non-bacteremic cases of invasive H. influenzae infection developing in patients > or = 9 years of age between 1 January 1980 and 31 December 1990. The most common clinical presentations among patients with bacteremia included pneumonia (52%), septicemia (27%), meningitis (8%), gynecologic infection (5%), and epiglottitis (5%). Underlying illnesses were common in these patients, and overall mortality was 35.5%. Factors associated with mortality included underlying neurological disease, polymicrobial bacteremia, and advanced age. The clinical presentations of the 40 patients without bacteremia included soft-tissue abscesses (45%), lung abscesses (18%), peritonitis (13%), meningitis (8%), gynecologic infection (8%), epididymitis (5%), mastoiditis (3%), and osteomyelitis (3%). Thus H. influenzae disease has a variety of presentations and is associated with significant mortality in older children and adults. Further study is required to determine whether widespread administration of H. influenzae type b conjugate vaccine to infants will alter the development of subsequent disease in later life.
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PMID:Invasive Haemophilus influenzae infections in older children and adults in Seattle. 821 79

Chronic liver disease is accompanied by a number of circulatory changes including impairment of cardiovascular autonomic reflexes. This occurs irrespective of the aetiology of liver disease, increases in prevalence and severity with worsening hepatic function, and is related at least in part to an autonomic neuropathy. Parasympathetic abnormalities predominate and, although largely subclinical, they may play a role in the altered fluid homeostasis and neurohumoral disturbances associated with cirrhosis. On prospective follow up, the presence of autonomic impairment was associated with a five-fold increased mortality, largely from sepsis and variceal haemorrhage. Defective responses to such stressful events as a result of an afferent defect could possibly explain these findings. Further studies are required to evaluate the natural history of this complication, and determine if it is reversible with improvement in hepatic function or after liver transplantation.
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PMID:Autonomic dysfunction in chronic liver disease. 829 76

Vibrio parahemolyticus is a halophilic marine vibrio commonly associated with outbreaks of acute gastroenteritis which also sometimes causes serious wound infection. It is an uncommon cause of septicemia. A few reports suggest that patients with chronic liver disease and leukemia are more susceptible. A case of liver cirrhosis with septicemia caused by this organism is discussed. The patient's condition rapidly deteriorated, and he died 12 hours after admission.
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PMID:Septicemia caused by Vibrio parahemolyticus: a case report. 829 34


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