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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with calcitriol-resistant rickets caused by a defect in the ligand-binding domain of the vitamin D receptor are described. Eight patients, 1.7 to 13.8 years of age, received high doses of elemental calcium (range, 0.4 to 1.4 gm/m2) through indwelling intracaval catheters for periods of 1.8 to 3.8 years. Two other patients, aged 1.1 and 2.2 years, were given oral calcium therapy as the sole mode of treatment. In five of the intravenously treated patients, oral calcium therapy was initiated after radiologic evidence of healing of the rickets. To maintain normal serum calcium concentration, the patients required daily doses of elemental calcium of 3.5 to 9 gm/m2 body surface area. Clinical improvement was observed within a week of the start of intravenous therapy, with disappearance of bone pain; several of the younger patients started to walk for the first time. Growth velocity increased within 2 to 3 months, from a pretreatment rate of -0.8 to -6.3 standard deviation score (SDS), to a posttreatment rate of +0.1 to +5.1 (SDS). Serum calcium, parathyroid hormone, phosphorus, and alkaline phosphatase values returned to normal within a year. Radiologic signs of healing occurred more rapidly in the intravenous treatment groups and in younger patients. Episodes of septicemia occurred frequently in those receiving parenteral therapy and required replacement of the catheter. We recommend that in the treatment of calcitriol-resistant rickets, oral calcium therapy be started at the youngest possible age, in doses to the limit of intestinal tolerance. When rickets is present, calcium should be infused through a large vessel in doses high enough to produce normocalcemia, normophosphatemia, and suppression of parathyroid hormone. Only after radiologic healing has been observed can oral calcium therapy be introduced.
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PMID:Calcium therapy for calcitriol-resistant rickets. 133 89

This paper presents further preliminary results of a trial of the prophylaxis of sepsis in 165 patients undergoing vascular surgery. The efficacy and safety of a single dose of teicoplanin was examined and compared with three doses of cephradine plus metronidazole. No significant differences were detected in the prophylactic efficacy in either group. The first interim report indicated abnormalities in liver function, maximum at 7 days, in both groups. These findings are confirmed in this second interim report. Raised levels of GGT and alkaline phosphatase are more prominent in patients receiving teicoplanin. Liver function improved by 28 days, however, suggesting that any abnormality is transient.
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PMID:Teicoplanin vs cephradine and metronidazole in the prophylaxis of sepsis following vascular surgery: an interim analysis of an ongoing trial. 138 43

The purpose of this study is to evaluate the modifications in biochemical parameters before and after the initiation of nutritional therapy, and to observe whether there is a relationship between the patient's development (exitus or improvement) and the presence of sepsis. The study was performed on 578 adults treated in our hospital from January 1988 to October 1989. The parameters analyzed were the following: glucose, triglycerides, total proteins, albumin, cholesterol, alkaline phosphatase, GOT, GPT, bilirubin, GGT, urea, urates, creatinine and electrolytes. The average initial values of each parameter were compared against those obtained after interrupting the PN by means of the Student t test. The results showed that within the parameters indicating the hepatic function, GGT and alkaline phosphatase were those that showed the most significant differences after ceasing the PN. Furthermore, the parameters indicating hepatic function and the electrolytes showed greater variations, regardless of the clinical evolution of the patient (improvement or exitus). The remainder of the parameters showed significant variations based on the clinical evolution.
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PMID:[Changes in the biochemical parameters during parenteral nutrition. The experience in Hospital de Bellvitge]. 142 Apr 86

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylsulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AlT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 +/- 0.36 to 5.65 +/- 0.20 mumoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 +/- 0.69 mumoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 +/- 0.49 mumoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 +/- 37.3 mumoles/g wet tissue) and rose by 55% to 261.7 +/- 55.8 mumoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tourniquet release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxygen-derived free radicals mediate liver damage in rats subjected to tourniquet shock. 148 82

We report a 3-year analysis (1986 to 1989) of the management of 63 home parenteral nutrition patients, 40 with short-bowel syndrome and 23 with chronic intestinal obstruction with or without intestinal resection. Intravenous fluid requirements varied from 0.9 to 6 L/day, and the content of glucose varied between 46 and 531 g/day, protein varied from .0 to 85 g/day, fat from .0 to 100 g/day, sodium from 37 to 695 mEq/day, potassium from 30 to 220 mEq/day, chloride from 60 to 760 mEq/day, and acetate from 0 to 200 mEq/day. Body weight was normalized and well maintained in the majority of patients, but using the strict definition of deficiency as the presence of one abnormal value during 3 years, more than half had abnormal plasma chloride, glucose, alkaline phosphatase, serum glutamic oxaloacetic transaminase, total protein, albumin, selenium, and iron concentrations, and more than a third had low calcium, magnesium, vitamin D, and vitamin C levels. Normochromic anemia was seen in 73% and high blood creatinine associated with low urine volumes in 42%. Most (78%) returned to relatively normal lifestyles, but employability was occasionally impaired by loss of third-party insurance coverage resulting from a therapy that may cost $100,000 per year. Overall mortality was low (5% per year), but 73% needed readmission to hospital, mainly for suspected catheter sepsis. The results indicate that home parenteral nutrition has allowed many patients to survive gut failure and return to work but problems with chronic fluid, electrolyte and micronutrient deficiencies, catheter sepsis, and insurance coverage often restrict optimal rehabilitation.
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PMID:Home parenteral nutrition--a 3-year analysis of clinical and laboratory monitoring. 850 44

Hepatic dysfunction is a frequent finding in sepsis and peritonitis. In the present study, hepatic function in experimental peritonitis in the rat was determined by measuring serum levels of bilirubin, alkaline phosphatase (ALP), glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT), together with antipyrine (AP) clearance as a determinant of microsomal function. Peritonitis was induced by intraperitoneal injection of 3 x 10(8) colony-forming units of E. coli together with either 1.0 ml bile or saline. E. coli + bile peritonitis rats had significantly elevated levels of bilirubin, ALP, GOT and GPT as compared with both controls and rats with peritonitis induced by E. coli alone. The derangements gradually increased with time over the 10-hour period studied. In contrast, no reduction of AP clearance was observed in the peritonitis models. On the contrary, AP clearance was enhanced at 10 hours after induction of peritonitis by E. coli alone. In conclusion, hepatic dysfunction as revealed by routine laboratory tests is seen early in experimental peritonitis in the rat, but this is not accompanied by a reduced AP clearance rate.
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PMID:Effect of bile on liver function tests in experimental E. coli peritonitis in the rat. 176 53

A 5-year prospective study was performed to monitor liver function tests (LFTs) in patients receiving total parenteral nutrition (TPN). A gradual and progressive rise was seen in the plasma concentration of bilirubin, aspartate transaminase, and alkaline phosphatase. The rate of rise was not increased in patients with LFT abnormalities before the start of TPN. Half of the patients had an episode of sepsis during TPN, but overall abnormal LFTs did not appear more common in these patients than in those without obvious sepsis. Patients with malignant disease, those requiring long-term TPN, and those requiring a nonstandard TPN regimen were more likely to develop raised LFTs.
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PMID:Liver function tests in patients receiving parenteral nutrition. 190 Nov 8

The progression of changes in biochemical liver test results during moderate and severe sepsis (SS) was studied prospectively in 43 patients admitted to a surgical intensive care unit. Using predetermined criteria, severity of sepsis was assessed by physicians blinded to the liver test results. Linear regression analysis showed that bilirubin levels increased at a rate approximating 0.95 mg/dl/day in patients with SS, whereas alkaline phosphatase levels did not rise initially in these patients. Following peak hyperbilirubinemia, however, alkaline phosphatase levels increased at approximately 4 IU/L/day. In patients with moderate sepsis (MS), bilirubin levels increased slowly (approximately 0.4 mg/dl/day) but alkaline phosphatase levels increased rapidly (approximately 29 IU/L/day). Following peak hyperbilirubinemia, alkaline phosphatase levels did not change. These data define patterns of liver test abnormalities of clinical importance. Rapidly rising bilirubin levels with little change in alkaline phosphatase levels are associated with SS, whereas markedly elevated alkaline phosphatase levels may indicate MS or resolution of SS. In critically ill surgical patients subjected to many potential hepatic insults, recognition of liver dysfunction with these patterns should alert the clinician to the possibility of underlying sepsis.
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PMID:Patterns of liver test abnormalities in patients with surgical sepsis. 192 83

Patients with the acquired immune deficiency syndrome (AIDS) frequently develop hepatic dysfunction. Although hepatic injury may indirectly result from malnutrition, hypotension, administered medications, sepsis, or other conditions, the hepatic injury is frequently due to opportunistic hepatic infection, directly related to AIDS. Infection with Mycobacterium avium intracellulare typically occurs in patients with advanced immunocompromise and with systemic symptoms due to widely disseminated infection. In contrast, hepatic tuberculosis often occurs with less advanced immunocompromise. Cytomegaloviral infection may produce a hepatitis. Cytomegaloviral and cryptosporidial infections have been implicated as causes of acalculous cholecystitis and of a secondary sclerosing cholangitis. About 10-20% of patients with AIDS have chronic hepatitis B infection. These patients tend to develop minimal hepatic inflammation and necrosis. The clinical findings in patients with hepatic cryptococcal infection are usually due to concomitant extrahepatic infection. Hepatic histoplasmosis usually develops as part of a widely disseminated infection with systemic symptoms. Hepatic involvement by Kaposi's sarcoma is rarely documented ante mortem because an unguided liver biopsy is an insensitive diagnostic procedure. Patients with non-Hodgkin's lymphoma of the liver typically have lymphadenopathy, hepatomegaly, and systemic symptoms. As a pragmatic approach, patients with liver dysfunction and HIV-related disease should have a sonographic or computerized tomographic examination of the liver. Patients with dilated bile ducts should undergo endoscopic retrograde cholangiopancreatography because opportunistic infection may produce biliary obstruction. Patients with a focal hepatic lesion should be considered for a guided liver biopsy. Patients with a significantly elevated serum alkaline phosphatase level should be considered for a percutaneous liver biopsy. When performed for these indications, liver biopsy will demonstrate a significant disease involving the liver in about 50% of patients with AIDS and in about 25% of patients who are HIV seropositive but who are not known to have AIDS. The clinical impact of a diagnostic biopsy is blunted by a lack of efficacious therapy for many opportunistic infections.
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PMID:Hepatobiliary manifestations of the acquired immune deficiency syndrome. 198 33

Five of 23 patients with recurrent nasopharyngeal carcinoma (NPC) were diagnosed to have bone marrow metastasis. They all had advanced local-regional disease, and were treated with neoadjuvant chemotherapy and definitive radiotherapy after the initial diagnosis. Bone marrow metastasis developed 4-24 months later. The clinical features were anemia (5 of 5), leukopenia (3 of 5), thrombocytopenia (4 of 5), sepsis (3 of 5), tenderness of the sternum (3 of 5), and fever (4 of 5). Patients frequently had elevation of serum lactic dehydrogenase (LDH), alkaline phosphatase (ALK-P), and IgG and IgA antibody titers to Epstein-Barr viral capsid antigen when bone marrow involvement was diagnosed. However, clinical manifestations and laboratory tests were not specific. It is important that three patients had normal bone scans. All five patients had a rapid downhill course; four patients died within 23 days, and the fifth 3 months after the diagnosis of bone marrow metastasis. We concluded that bone marrow was a common metastatic site in NPC patients. Bone marrow metastasis adversely affected patients' survival and required a high index of suspicion for diagnosis. We suggested that bone marrow biopsy should be considered as a routine staging procedure in NPC patients and indicated especially when patients presented with abnormal blood counts, sepsis, bone pain, or tenderness of the sternum. It may be positive in the face of a normal bone scan.
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PMID:Nasopharyngeal carcinoma with bone marrow metastasis. 198 43


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