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)

The aim of this retrospective study was to determine whether total parenteral nutrition-related liver disease was improved by intravenous antibiotics given for systemic sepsis. Liver function tests were performed 1 month before, during and 1 month after one episode of sepsis treated for 4 weeks (mean, range: 2-12), with systemic antibiotics, in 12 patients receiving parenteral nutrition for 13 months (mean, range: 1-71) for short bowel syndrome in 10 of them. Cholestatic liver disease appeared in all during nutrition (mean serum alkaline phosphatase activity > 4 N). Liver test abnormalities observed at the beginning of antibiotics treatment were not significantly different from those observed 1 month before sepsis. Antibiotic administration was followed by a significant decrease (P < or = 0.03) in serum activities of alkaline phosphatases, ALT and AST and bilirubinemia of 38, 41, 23 and 47%, respectively. These results support the concept that parenteral nutrition-associated cholestatic liver disease may be related to intestinal bacterial overgrowth and suggest that it may be improved by intravenous antibiotherapy.
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PMID:[Total parenteral nutrition-related cholestatic hepatopathy, is it an infectious disease?]. 818 92

The Nippon-Zeon (NZ) ventricular assist device is a sac type, air driven, heterotopic, external pump. Its performance has been evaluated in Japan as a bridge to myocardial recovery. Few data are available on the device as a bridge to heart transplantation. Since 1991, 10 patients (9 men) were bridged to heart transplantation with NZ, all in biventricular support. The mean age was 39 +/- 13 years (range, 21-60 years), mean body weight was 75 +/- 13 kg (range, 51-95 kg). Five patients had a dilated cardiopathy, and five were ischemic (three acute myocardial infarctions). Despite maximal inotropic support, including enoximone in seven, epinephrine in three, and intraaortic balloon pumping in one, eight patients were anuric, three were in acute hepatic failure, and three were intubated. Preoperative hemodynamic and biologic values were: cardiac index, 1.57 +/- 0.4 l/min/m2; pulmonary capillary wedge pressure, 34 +/- 5 mmHg; creatinine, 200 +/- 80 mumol/l; blood urea nitrogen, 17.5 +/- 8 mmol/l; total bilirubin 36 +/- 6 mumol/l; aspartate aminotransferase, 1,000 +/- 2,000 IU/l. In all patients, a biventricular assist device was implanted without the use of cardiopulmonary bypass. Improvement occurred immediately in all but one. Mean left ventricular flow was 4.5 +/- 0.8 l/min. Anticoagulation was maintained with intravenous heparin. Recently for bleeding was required in one case (10%), and two patients had positive blood cultures that were successfully treated. There was no mechanical failure. Hemolysis was not significant (lactate dehydrogenase, 378 +/- 50 IU/l; plasma-free hemoglobin below 10 mg/dl). Each device was free of thrombi and deposits at time of explantation. One patient died while on assist. Nine patients (90%) were transplanted after 11 +/- 8 days (range, 1-32 days). Three died early after transplantation, one of graft failure, two of sepsis. Six patients (66%) could be discharged. The follow-up ranges from 7 to 28 months. NZ is a simple, reliable, pneumatic device driven by a light, silent console; it can be rapidly implanted without cardiopulmonary bypass in patients in desperate condition who are awaiting cardiac transplantation. The difficulty of patient rehabilitation while using this device should limit the duration of support to weeks to allow the patient to be in optimal condition for heart transplantation.
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PMID:Use of the Nippon-Zeon pneumatic ventricular assist device as a bridge to cardiac transplantation. 855 33

Multiple organ dysfunction (MOD) is the leading cause of mortality in septic patients with circulatory shock. Recent evidence suggests that the overproduction of the cytokine, tumor necrosis factor-alpha(TNF), and oxygen free radical molecules may mediate the progression of sepsis to MOD and death. In this study, we have examined the ability of MDL 101,002, a free radical scavenger, to reduce organ dysfunction and cytokine secretion induced by lipopolysaccharide (LPS) administration in rats. Treatment with MDL 101,002(10-60 ng/kg, i.p.) 30 min prior to an LPS challenge resulted in a dose-dependent reduction in several markers indicative of organ dysfunction and mortality. MDL 101,002 markedly decreased LPS-induced liver and kidney damage as indicated by serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) or urea and creatinine, respectively. MDL 101,002 also prevented LPS-induced pulmonary edema, but did not prevent leukopenia and only partially reduced thrombocytopenia. Associated with these improvements in organ dysfunction and survival was a modest decrease in LPS-stimulated interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) secretion and a marked ( > 90%) inhibition of TNF secretion by MDL 101,002. The data are consistent with a role for oxygen free radicals in the development of endotoxin-induced organ dysfunction and shock and suggest that free radical scavengers could reduce the mortality consequent to sepsis by decreasing organ dysfunction, at least in part, through a reduction in free radical stimulated cytokine secretion.
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PMID:Reduction in endotoxin-induced organ dysfunction and cytokine secretion by a cyclic nitrone antioxidant. 858 85

Tissue injury is a common occurrence in multiple organ failure, a possible clinical complication of Gram-negative bacterial sepsis. Gram-negative bacteria, in part through lipopolysaccharide (LPS), tumor necrosis factor, and other cytokines, activate neutrophils to increase oxygen consumption and produce reactive oxygen species (ROS). ROS have been suggested to play a critical role in the pathogenesis of multiple organ failure. Accordingly, we hypothesized that the susceptibility of tissues to ROS can be reduced by augmenting the antioxidant status of the affected tissues. Rats were challenged intravenously with LPS (Escherichia coli: 0111:B4) at a dose of 1 mg/kg body weight, and 0, 2, 4, or 6 h later were treated intravenously with plain liposomes or alpha-tocopherol liposomes (20 mg alpha-tocopherol/kg body weight); treated rats were then killed 24 h after LPS challenge. Animals challenged with LPS were extensively damaged in the liver, as evidenced by an increase in plasma alanine aminotransferase and aspartate aminotransferase activities, and also in the lung, as indicated by a decrease in pulmonary angiotensin-converting enzyme and alkaline phosphatase activities. The injection of LPS also resulted in increased myeloperoxidase activities in the two organs, suggestive of activation of the inflammatory response. Within the pulmonary and hepatic organs of LPS-challenged animals, the involvement of oxidative stress mechanisms was evident, because a significant decrease in reduced glutathione and an increase in lipid peroxidation were observed. In contrast, the administration of alpha-tocopherol liposomes in the post-LPS-challenge period resulted in a significant alleviation of both lung and liver injuries, evidenced by a general reversal of the altered biochemical indices toward normal among treated animals. The therapeutic effect was found to be greater when liposomal alpha-tocopherol treatment was given earlier during the development of injury. Plain liposomes administered immediately after LPS injection also protected hepatic and pulmonary tissues from injuries. However, unlike alpha-tocopherol liposomes, plain liposomes did not confer any beneficial effect when administered at later timepoints post-LPS injection. These data suggest that alpha-tocopherol, administered in a liposomal form, may serve as a potentially effective pharmacological agent in the treatment of LPS-induced tissue injuries.
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PMID:Treatment of LPS-induced tissue injury: role of liposomal antioxidants. 882 99

We measured the platelet distribution width, the mean platelet volume, the volume percentage of platelets, and the platelet-to-large-cell ratio in 15 elderly patients with disseminated intravascular coagulation (DIC). Peripheral venous blood mixed with ehtylenediaminetetraacetic acid was analyzed with a Sysmex E-4000 analyzer. The underlying diseases were sepsis, pneumonia, pyelonephritis, and other inflammatory diseases. The mean duration of survival from the onset of DIC was 16.9 +/- 23.9 days. The distribution of red cell sizes before the onset of DIC did not differ significantly from that in patients without DIC, but fragmentation of erythrocytes on blood films was more common in the early stage of DIC (p < 0.01). Before the onset of DIC, the two groups did not differ significantly in the frequency of giant platelets on blood smears. At the onset of DIC, the platelet distribution width, the mean platelet volume, and the platelet-to-large-cell ratio were significantly higher than in patients without DIC. The concentration of glutamic-oxaloacetic transaminase and those of other serum enzymes did not change significantly, but the serum creatinine concentration and the blood urea nitrogen level increased as the platelet-to-large-cell ratio increased. No significant relation was evident between the levels of serum C-reactive protein and creatinine, between the platelet-to-large-cell ratio and the mean volume of red blood cells, or between the platelet-to-large-cell ratio and the distribution of red cell sizes. These data suggest that studies of platelets are more useful in the diagnosis of DIC at early stages of impaired organ function than are other indicators of inflammation such as the level of C-reactive protein.
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PMID:[Changes in erythrocyte structure and in platelets in elderly patients with disseminated intravascular coagulation]. 899 5

Nine pediatric patients (mean age, 10 years) with biliary atresia, who had hypoxemia related to intrapulmonary shunting, underwent living related liver transplantation. The effects of hypoxemia during the early postoperative period after liver transplantation on cardiopulmonary and renal function, as well as on transplanted liver, were analyzed. Based on the degree of shunt ratio calculated by technetium-99m macroaggregated albumin scintigraphy, the nine patients were included in the moderate group (shunt ratio under 40%, n=4) or the severe group (shunt ratio over 40%, n=5). Partial pressure of arterial oxygen was maintained at normal range in the moderate group, while that in the severe group persistently had very low values (<50 mmHg), in spite of a high degree of oxygen supply. However, all patients in the severe group maintained stable cardiopulmonary vital signs, including systemic blood pressure, heart rate, respiratory rate, and cardiac index. They also demonstrated stable renal function. None of the patients died of cardiopulmonary or renal insufficiency after transplantation, but three patients died of portal vein thrombosis, sepsis, and intracranial hemorrhage (one each). The minimal adverse effect of hypoxemia on the transplanted liver was confirmed by a rapid increase of arterial ketone body ratio, low peak values (under 200 IU/L) of aspartate aminotransferase, and a steady decrease of serum total bilirubin. Four patients encountered surgical complications, including two bile leaks from the cut liver surface, two leaks from bilioenteric anastomosis, and one intestinal perforation. Six patients suffered from bacterial infections, including four wound infections, three right subphrenic abscesses, one cholangitis, and two systemic sepses. All patients in the moderate group recovered from hypoxemia, but four of five patients in the severe group have not recovered during the follow-up period between 4 and 9 months. It was concluded that the adverse effects of hypoxemia on cardiopulmonary and renal function and transplanted liver were minimal, so that patients with severe hypoxemia could tolerate the stress of liver transplantation without special management. However, the high incidence of surgical complication and infection suggested the adverse effects of hypoxemia on wound healing and resistance to bacteria infection.
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PMID:Effects of hypoxemia on early postoperative course of liver transplantation in pediatric patients with intrapulmonary shunting. 903 32

Progressive liver failure in parenteral nutrition (PN)-dependent children with short bowel syndrome carries significant morbidity and mortality. The authors retrospectively reviewed 47 consecutive patients with short bowel syndrome diagnosed from October 1985 through October 1995. All patients were treated according to a protocol designed to promote intestinal motility and discourage bacterial translocation. Elements of the protocol included the use of taurine, vigilant prevention and aggressive treatment of sepsis, meticulous catheter care, early PN cycling, appropriate enteral feeding, and measures designed to inhibit gastrointestinal bacterial translocation, especially gram-negative rods. Complete blood counts and serum liver function studies were compiled from both clinic visits and hospital admissions for each patient every 3 to 6 months while they were on PN. Three patients were lost to follow-up after they had moved out of state. The length of time on PN ranged from 3 months to 9.4 years with an average of 2.2 years. Elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and glutamyltransferase (GGT) were present in 82%, 66%, and 84% of patients, respectively. Alkaline phosphatase was elevated in 58% of patients. Eight patients (18%) are still on PN, and 31 (70%) have been weaned off PN. Five patients have died (11%). Three patients (7%) developed cholecystitis requiring cholecystectomy. No patients developed progressive liver failure. These results suggest that PN-related liver failure may be prevented in most patients with short bowel syndrome. Specific measures to prevent PN-related cholestatic jaundice need further investigation.
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PMID:Prevention of liver failure in parenteral nutrition-dependent children with short bowel syndrome. 909 21

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

The hemodynamic effects of sepsis have been attributed in part to increased nitric oxide (NO) production and activation of guanylate cyclase, resulting in increased cGMP and relaxation of vascular smooth muscle. Heme oxygenase-1 (HO-1), a heat shock protein, has been shown to increase intracellular cGMP levels by formation of carbon monoxide (CO). We hypothesized that HO may be an important mediator of the hepatic response to infection. Male Swiss Webster mice underwent standard cecal ligation and puncture (CLP, 18 gauge 2X) or sham operation, and received either normal saline (NS) or Zn protoporphyrin IX (ZN PP IX), a competitive HO inhibitor (n = 6-8/group). Hepatic tissue samples were collected at 3, 6, 12, and 24 hr from separate mice. Serum was collected at 3 and 24 hr. A semiquantitative reverse transcriptase polymerase chain reaction method was used to measure HO-1 mRNA levels. Hepatic cGMP levels were measured by ELISA. Groups were repeated (n = 10/group) to assess mortality. Serum was collected at 3 and 24 hr to measure serum aspartate aminotransferase (AST) levels. HO-1 mRNA expression increased significantly by 3 hr after CLP and with HO inhibition alone (P < 0.05 vs sham + NS). HO-1 mRNA remained elevated through 24 hr. CLP animals with HO inhibition showed a significant reduction of hepatic cGMP following CLP compared with CLP + saline at 24 hr (P < 0.05). Mortality was significantly increased in the CLP + ZN PP group at 24 hr (P < 0.05 CLP NS vs CLP ZN PP). CLP caused a marked increase in AST activity, which was increased further with HO inhibition. HO-1 mRNA expression was induced by CLP. AST levels following CLP were markedly increased with HO inhibition. HO-1 function appeared to contribute to elevation of hepatic cGMP during peritonitis and may be an important hepatic adaptive response to infection.
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PMID:Heme oxygenase-dependent carbon monoxide production is a hepatic adaptive response to sepsis. 927 Dec 71

The objective of this paper is to report 5 cases of rhabdomyolysis (RML) in patients with acute leukemia (AL). This occurred consecutively after the administration of chemotherapy, during the ensuing period of myelosuppression. Thirty-six patients with AL received, in a three-month period, 51 cycles of combined chemotherapy which included, in all of them, cytosine arabinoside (ARA-C); among them, along with myelosuppression, five experienced fever, infectious complications, gastrointestinal tract symptoms and severe myalgias. Serum creatine kinase (CK), liver function tests and a light microscopy muscle biopsy were performed on all of them. Ten-17 days after receiving chemotherapy, five patients (4 males and 1 female) with acute lymphoblastic leukemia developed incapacitating myalgias in neck, thighs and arms. CK and/or alanine aminotransferase and aspartate aminotransferase were increased 5-24 times above the normal range in four of these patients, and the muscle biopsy showed focal RML in all five. Myalgias were self-limited and lasted 4-10 days. In addition to the chemotherapy, other factors known to be capable of producing RML, such as sepsis, other medications, and dehydration were found. In conclusion, myalgias were due to focal RML produced probably by a combination of factors, particularly the chemotherapy along with dehydration due to gastrointestinal complications, infection, and the use of diverse antibiotics. The endemic nature of the finding in such a short period of time is outstanding.
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PMID:Rhabdomyolysis in patients with acute lymphoblastic leukemia. 929 34


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