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)

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

Cholescintigraphy has proven useful in diagnosis of acute and chronic cholecystitis and evaluation of common bile duct obstruction. Common bile duct obstruction may be due to mechanical obstruction such as impact stone in the common duct or functional obstruction due to sepsis with intra-hepatic cholestasis or acute viral hepatitis. We present a cholescintigram of a patient with acute pancreatitis showing complete common bile duct obstruction.
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PMID:Cholescintigraphic demonstration of transient and functional common bile duct obstruction in a patient with acute pancreatitis. 160 Mar 63

Three hundred ninety-seven insulin-dependent diabetic dialysis patients were screened by nursing staff for analgesic-seeking behavior. Thirty-eight patients were identified and classified as prescription abusers (n = 26) or illicit drug users (n = 12). The nine cocaine users, when compared with 14 insulin-dependent diabetics on dialysis matched by protocol, were found to be similar in terms of diabetic retinopathy and metabolic neuropathy. Although statistically not significant, cerebrovascular and cardiovascular complications were more common in the study group. Gastroenteropathy with malnutrition was more common the study group (P less than 0.025). Infection rate and severity were markedly worse in the cocaine group: bacterial cellulitis, sepsis, and abscess each increased greater than fourfold. All the visceral infections were in the cocaine-using group. Hepatitis viral antigen and antibody was increased 10-fold in the cocaine users. Recommendations for management of dialysis patients with analgesic-seeking behavior are formulated in light of these findings.
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PMID:Increased infection rate in diabetic dialysis patients exposed to cocaine. 188 27

While CsA has improved renal-allograft survival rates in the first 2 years compared with Aza, Terasaki's multicenter study (1) failed to show any difference in long-term graft survival in CsA-Pred versus Aza-Pred-treated recipients. The present study examines the long-term graft-survival rates at a single center using CsA immunosuppression and seeks to discern the causes of 58 graft losses among 343 patients with functioning grafts beyond 2 years posttransplantation. The 6-year primary and cadaveric actuarial graft survival at this institution is 59% with a graft half-life of 10 years, which is better than the 40% and 7.7 years, respectively, reported by Terasaki (1) for primary cadaveric recipients on Aza-Pred. It is also better than the 41%, 6-year survival and 5.5-year half-life for primary cadaveric recipients treated with CsA-Pred as reported in the multicenter study. (1) Less experience with the use of CsA may explain the latter comparison. Primary LRD grafts at this institution (2/3 haploidentical) have a 6-year actuarial survival of 77% and a half-life very closely approximating that of HLA-identical LRD grafts under Aza (23.4 years). These results demonstrate that CsA mitigates the effects of HLA incompatibility to reduce graft survival. The most common cause of graft loss beyond 2 years was chronic rejection (36.2%) followed by noncompliance (27.6%). Patient deaths resulted in 13 of the 58 graft losses; most of the deaths were related to cardiovascular diseases. Only 3 patients died from causes that could be attributed to CsA immunosuppression; 2 from sepsis and 1 from viral hepatitis. Acute rejection caused 8.6% of the graft losses on continuous CsA therapy. When immunologic risk factors were analyzed, the entire graft-loss group had a significantly higher proportion of retransplant patients than the graft-survival group (P less than 0.005), suggesting that prior transplantation imposes a higher risk for graft loss not only acutely but long term as well. However, retransplanted patients were significantly less likely to lose their grafts because of noncompliance (P less than 0.005). Male patients were found to be significantly more noncompliant.
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PMID:Causes of graft loss beyond two years in the cyclosporine era. 230 64

Alterations of the gallbladder wall is a well known sonographic sign of acute cholecystitis. But thickening of the gallbladder wall is also found in patients without intrinsic gallbladder disease. We present our experience on this regard in patients with cirrhosis, acute viral hepatitis, infectious mononucleosis, halothane hepatitis, fulminant hepatic failure, malaria due to plasmodium falciparum, heart failure, severe malnutrition due to gastric obstruction, septicemia, pyogenic hepatic abscess, amoebic hepatic abscess and in a 14 years old patient with fracture of the skull-acute anemia-shock. Most of these diseases affected the liver directly or indirectly. Knowledge of these alterations of the gallbladder wall in these circumstances are important in order to avoid a the erroneous diagnosis of acute cholecystitis.
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PMID:[Ultrasonographic changes in the gallbladder wall in non-gallbladder diseases]. 253 57

In a retrospective survey of patients hospitalized in the Department of Medicine of the University Hospital, Basel, Switzerland, from 1980 to 1986, we found 269 patients with history of past or current drug abuse. The charts of these patients were analyzed for infectious complications according to defined criteria. Heroin was the principal drug consumed by 95%. In 127 patients (47%) at least one infectious complication was diagnosed. In 125 (31%) of 404 admissions, the infectious problem was the main reason for hospitalization. Among the 269 patients, 217 infective episodes occurred. Pulmonary infections were the most frequently occurring (52 episodes). There were 44 cases of viral hepatitis, 30 of human immunodeficiency virus infection, and 25 of minor genital infections. Bone and joint infections and sepsis/endocarditis were diagnosed in seven cases each. The overall mortality was 4.1%; however, only three of the 11 deaths were attributed to infections. Intravenous drug addiction is complicated by a high morbidity because of infections that were seldom lethal during the observed period.
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PMID:Infectious complications in drug addicts: seven-year review of 269 hospitalized narcotics abusers in Switzerland. 274 5

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41

The patient who has clinical jaundice, abnormal results on liver function tests, or both presents a difficult diagnostic challenge. Many infectious diseases affect the liver, and the extent of involvement determines the degree of clinically apparent jaundice. Some diseases that affect the liver minimally cause no jaundice at all. An important clue to the cause of the disorder is the pattern of abnormal results on liver function tests. Increased alkaline phosphatase predominates with Q fever, secondary or tertiary syphilis, clonorchiasis, and hepatic candidiasis, while elevated levels of serum transaminases characterize viral hepatitis, leptospirosis, mononucleosis syndromes, legionnaires' disease, typhoid fever, toxic shock syndrome, and yellow fever. Increases in serum bilirubin are typical with jaundice caused by clostridial myelonecrosis, severe bacterial sepsis, and relapsing fever (borreliosis). These findings together with the patient's history, physical findings, and basic laboratory tests provide a presumptive diagnosis in most cases.
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PMID:Systemic infections affecting the liver. Some cause jaundice, some do not. 305 Sep 27

We describe our experience in the treatment of acute liver failure in 620 patients who developed grade 3 or 4 encephalopathy between 1973 and June 1985. The principal aetiologies were paracetamol-induced hepatic necrosis, viral hepatitis, halothane hepatitis and idiosyncratic drug reactions. Cerebral oedema is a major cause of death in these patients and is most effectively treated with mannitol (20%). Renal failure occurs in between 30% and 75% of cases, depending on aetiology, and is most effectively managed by haemodialysis. Electrolyte and acid-base abnormalities are common. Haemodynamic abnormalities encountered include a high cardiac output, low peripheral vascular resistance, hypotension and venodilatation. Assisted mechanical ventilation is frequently required to treat hypoxia caused by pneumonia, atelectasis, haemorrhage and oedema. A coagulopathy is always present but coagulation factors and platelets are given only when the patient is clinically bleeding. These patients are prone to sepsis and this is a significant cause of death. Hypoglycaemia is common and must be actively and frequently sought. The use of charcoal haemoperfusion has been associated with improved survival, especially when it is started during the grade 3 phase of encephalopathy. Recently survival figures of between 47% and 60% have been achieved for patients with paracetamol-induced liver failure and hepatitis A and B. However the figure for non A non B hepatitis and halothane- and drug-induced liver failure are disappointing at around 15% and liver transplantation is being explored as a treatment option in these patients.
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PMID:Management of acute liver failure. 308 71

The diagnosis of acute viral hepatitis is based on a thorough history (with a detailed review of possible modes of transmission), consistent physical findings (in which stigmata of chronic liver disease are absent), and laboratory tests confirming the presence of acute hepatocyte damage. Specific etiologic entities can be identified by serologic testing. In some cases, infection by more than one hepatitis virus may be revealed. The occurrence of HBV/HDV coinfection may lead to typical, uncomplicated acute hepatitis. In some patients, however, the development of a prolonged prothrombin time and encephalopathy indicates the presence of fulminant disease. The management of patients with such disease usually requires admission to an intensive care unit in order to increase the likelihood that complications will be recognized at an early stage, when intervention might make a difference. Standard interventions include vigorous treatment of hypoglycemia, attention to electrolyte and acid-base disturbances, and antibiotic therapy for bacterial sepsis. Despite aggressive management by experienced teams, fatality rates remain exceedingly high: As many as 75% to 100% of patients with severe encephalopathy die. Liver transplantation has been attempted in a number of cases. Its role remains ambiguous. Survival rates of 50% to 60% have been reported, but selection bias may turn out to have contributed to this apparently favorable outcome. In the patient under discussion, results of a follow-up physical two months after discharge were entirely normal. Liver chemistries were within normal limits, but a test for HBsAg was still positive. During the course of the examination, the patient admitted to having accidentally pricked his skin nearly two months before the onset of his illness while holding a needle that a friend had used for the intravenous injection of heroin. One year later, HBsAg was no longer detectable, but tests for anti-HBc and anti-HBs were both positive. The anti-HBc positivity was attributable to IgG rather than IgG anti-HBc. A test for anti-HDV was negative.
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PMID:Fulminant hepatitis due to HBV/HDV coinfection. 311 12


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