Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some clinical manifestations of severe malaria resemble those of sepsis and there may be mediators of the host response that are common to both sepsis and malaria. Phospholipase A2 (PLA2), a proinflammatory enzyme whose expression is induced by tumor necrosis factor (TNF), has been implicated in the pathogenesis of complications of the sepsis syndrome. We examined levels of circulating PLA2 in Plasmodium falciparum malaria and studied the association of PLA2 with disease severity. Plasma PLA2 and TNF were measured in 75 Malawian children with P. falciparum malaria. The mean (SD) plasma PLA2 activity in children with acute malaria was 53,804 (37,256) units/ml as compared with 424 (349) units/ml in 34 healthy controls (P < 0.00001). The mean PLA2 activity in 45 convalescent patients was 2,546 (7,372) units/ml (P < 0.00001). In 48 patients with pretreatment PLA2 activity less than 60,000 units/ml, mortality was 8.3%, while in 27 patients with pretreatment PLA2 levels greater than 60,000 units/ml, mortality was 33.3% (P = 0.008). There were significant correlations between PLA2 and TNF (r = 0.471, P < 0.01), density of parasitemia (r = 0.443, P < 0.0001) and a decrease in hematocrit (r = 0.352, P < 0.005). These data show that P. falciparum malaria is associated with a markedly increased circulating PLA2, especially in patients with severe disease, as manifested by high parasite burden, anemia, coma, and death.
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PMID:Increased serum phospholipase A2 activity in Malawian children with falciparum malaria. 821 74

Tumor necrosis factor-alpha (TNF-alpha) has been implicated in several late consequences of trauma such as sepsis, multiple organ failure, and ischemia-reperfusion injury. However, no data are available to indicate whether TNF-alpha is involved in the initial pathophysiologic response to trauma. To address this issue, serum TNF-alpha was determined (by ELISA) longitudinally (first blood sample on admission) in 100 randomly selected trauma patients admitted to the emergency department and trauma division at Jefferson Medical Center, Philadelphia. The TNF-alpha levels were detectable at one or more time points in 35 patients. Mean values tended to be elevated (50.3 +/- 11.5 pg/mL) during the first 5 days, but this trend did not differ statistically from that in healthy controls (n = 12) and did not correlate with the severity of injury (Injury Severity Score and Glasgow Coma Scale score). The TNF-alpha response was not dependent on the mechanism and site of injury, the presence of shock (systolic blood pressure < 90 mm Hg), and the need for emergent surgery. Also, serum TNF-alpha levels were not significantly elevated in patients who subsequently developed multiple organ failure (n = 4), septic shock (n = 5), or both (n = 3). Taken together, these data do not support a role for circulating TNF-alpha in the initial acute inflammatory response to trauma.
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PMID:Serum tumor necrosis factor-alpha profile in trauma patients. 823 Mar 32

Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. Metocurine and morphine were given hourly during induction and maintenance of hypothermia. Rewarming was at a rate of 1 degree C per 4 h beginning 48 h after intravascular temperature had reached 33 degrees C. Muscle relaxants and sedation were continued until core temperature reached 35 degrees C. There were no cardiac or coagulopathy-related complications. Seizure incidence was lower in the hypothermia group (Fisher's exact text, p = 0.019). Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.
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PMID:A phase II study of moderate hypothermia in severe brain injury. 825 39

Infection is one of the major complications of severe head trauma in children. To assess whether intravenous immunoglobulin (IVIg) decreases the incidence of secondary infection after head injury in children, a randomized, double-blind trial was performed. Thirty-three children (mean age, 6.67 years; mean injury severity score, 32.8; mean Glasgow coma score, 6.1) with severe head injuries were enrolled; 1 child was excluded, 18 received IVIg, and 14 received the placebo preparation. Four hundred milligrams per kilogram of IVIg or albumin placebo was administered within 48 hours of admission. IgG levels were obtained before the infusion and then 1 week later. Patients were monitored for evidence of infection for the next 21 days. There was a 66% increase in mean IgG levels in the treatment group compared with 45% in the control group (P = .057). One death occurred in the IVIg group and two in the placebo group. No significant differences in the incidence of pneumonia, sepsis, presumed sepsis, or any other type of infection was noted. There was no difference in the number of days on mechanical ventilation or in number of hospital days. There were no side effects. It is concluded that prophylactic administration of commercial IVIg at a dose of 400 mg/kg, although safe, had no effect on the incidence of secondary infections in children with severe head injuries.
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PMID:Safety and efficacy of intravenous immunoglobulin prophylaxis in pediatric head trauma patients: a double-blind controlled trial. 830 58

Patients with fulminant hepatic failure have severe circulatory disturbances which may be due to fibrin and cellular plugs in micro-vessels which are a consequence of intravascular coagulation and which can lead to multiorgan failure. Since antithrombin III supplementation has been shown to be beneficial in animal models of septic shock with disseminated intravascular coagulation, a controlled study was performed to investigate the effect of antithrombin III supplementation in fulminant hepatic failure. Twenty-five patients in grade III or IV coma were selected on the basis of evidence of sepsis, intravascular coagulation and a high risk of developing multiorgan failure. Thirteen patients received 3000 units of antithrombin III (Kybernin P; Behringwerke), followed by a further 1000 units every 6 h. Antithrombin III activity increased from 0.26 +/- 0.04 SE U/ml to 0.82 +/- 0.07 U/ml at 3 h post infusion (normal range 0.80-1.20 U/ml) and remained greater than 0.80 U/ml throughout the study without any apparent increase in the frequency of bleeding. However, survival was not improved and markers of intravascular coagulation remained similar between the two groups. Thus, although the antithrombin III deficiency in fulminant hepatic failure can be corrected by supplementation with antithrombin III concentrate, its use in the prevention of intravascular coagulation and to avoid microvessel plugging needs to be studied at an earlier stage in the disease.
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PMID:Controlled trial of antithrombin III supplementation in fulminant hepatic failure. 831 61

Marked deterioration of neurologic function accompanies organ dysfunction in systemic sepsis. Although previous hypotheses have suggested that cerebral hypoperfusion, anoxia or progressive edema of the brain may be causative, the pathogenesis remains unknown. Patients with sepsis with stable or supported hemodynamics and adequate oxygenation may manifest confusion, stupor or coma. Recent evidence has demonstrated that the brain is the source of many classical mediators of inflammation after various forms of injury. These mediators, including the leukotrienes, have pronounced effect on cerebrovascular function. Endotoxin is known to stimulate the release of arachidonate from cell membranes, the rate limiting step in leukotriene synthesis. The current studies were performed to test the hypothesis that neurologic dysfunction associated with endotoxemia is characterized by alterations in cerebrovascular permeability or vasomotor function manifested by intracranial hypertension, or both. We studied the response of miniature swine to experimental endotoxemic shock and compared this response with hemorrhagic hypotension. We observed a dramatic elevation of intracranial pressure in swine subjected to endotoxemic shock, despite arterial hypotension. Moreover, estimation of cerebral blood volume (CBV) by reflectance infrared photoplethysmography demonstrated a dramatic increase in CBV, which corresponded to this elevation in intracranial pressure. However, cerebral cortical oxygen saturation was significantly reduced despite this net increase in CBV, indicative of an increase in the venous volume of the brain, while arterial volume remained the same or decreased from baseline levels. Oxygen extraction across the brain decreased during this same period compared with baseline and control values. These results demonstrate that endotoxemia is associated with the development of intracranial hypertension and an increase in CBV secondary to elevation of cerebrovascular venous volume coupled with reduced oxygen extraction across the brain. This evidence of cerebrovascular dysfunction probably represents blood flow maldistribution, similar to that seen in other organs with sepsis, suggesting a cause for altered neurologic function in systemic sepsis.
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PMID:Alterations in intracranial pressure and cerebral blood volume in endotoxemia. 842 4

During the first 12 months of the Danish Liver Transplantation program, which began in October 1990, 21 transplantations were performed in 11 women, six men and three children. One patient required a retransplant. Fourteen operations were performed electively and six patients were transplanted for acute and subacute fulminant liver failure and coma, two patients had reduced size livers because of large donor liver. There were no peroperative deaths. One of the elective patients died after three weeks from multiorgan failure and sepsis. Two of the emergency patients died after 20 and 22 days. One from graft dysfunction due to stenosis of the celiac trunk and the other of exudative pericarditis. One patient died from chronic rejection and CMV-infection after seven months. Complications were relatively few and acute rejection occurred in 40% of the patients. Fifteen patients are discharged with normal liver function and 11 of these were back at work, school or previous functions in the home. It is concluded that these results are comparable to the best results from other centres but that 21 transplants in 12 months must be a minimum activity.
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PMID:[Liver transplantation in Denmark. First-year experiences]. 845 6

We retrospectively studied 42 patients hospitalized for Stevens-Johnson syndrome at the Veterans General Hospital-Taipei between 1979 and 1991. Twenty-seven patients were males and 15 females; the ages ranged from 7 months to 82 years old with a mean age 50. The most common precipitating factor was drugs among which diphenylhydantion was the leading offender followed by nonsteroidal anti-inflammatory agents and allopurinol. Sixteen cases might be etiologically associated with infection, including 13 with upper respiratory infection, one with acute hepatitis B, one with pulmonary tuberculosis, and one with fever of unknown origin that was suspected to be viral infection. Although mycoplasma infection was thought in the literature to be a common etiologic factor of Stevens-Johnson syndrome, it was scarcely found in our study. Four patients were not treated with systemic steroids but still recovered uneventfully. Systemic steroid as a whole was not proved to be necessary, but early large-dose steroid therapy might abbreviate the course of the disease. The mortality rate was 11.9% which differs unremarkably from the reported rate (5-15%). Two patients died of pneumonia with sepsis, one of hemorrhagic shock (bleeding of adenocarcinoma of stomach), one of aspiration pneumonia, and one of sepsis with disseminated intravascular coagulation, upper gastrointestinal bleeding, and hyperglycemic hyperosmolar nonketotic coma.
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PMID:[Stevens-Johnson syndrome: a review of 42 cases]. 849 Jul 98

The present study on 5330 patients admitted to the internal intensive care unit over the five year period (1990-1994) indicated that consciousness disorders are most frequently associated with poisoning. On admission, the state of consciousness of 665 of these 5330 patients was retrospectively evaluated. Poisoning by drugs was most common among intoxications (93 patients of 154 cases of poisoning). Coma, which is the most severe manifestation of consciousness disorder, occurred very often in these patients. Poisoning caused by other agents was connected with other forms of consciousness disorders. Low Glasgow Coma Score (GCS) was a severe predictor, while the number of deaths among patients with GCS > 10 was low. Sepsis was the next most common cause of consciousness disorder among our patients (88 patients). Death rate in these patients was high, amounting to almost 50%, regardless of GCS on admission, suggesting that the severity of main event determines the outcome. Glycemia disorders, including hypoglycemia, hyperglycemia as well as hyperosmotic state, did not result in lethal outcome, regardless of GCS on admission. The highest death rate was registered in patients with cardiopulmonary arrest and lowest GCS on admission. Patients with cardiogenic shock, despite high GCS on admission, had high death rate.
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PMID:[Causes of disorders of consciousness in internal medicine intensive care units]. 864 56

We report a female patient presenting with sepsis and multi-organ failure following eclampsia and intrauterine childdeath. In the phase of recovery, the patient developed consciousness disorder and coma characterized by fasciculation, generalized myoclonia and respiratory insufficiency. The clinical picture corresponded to that of Lance Adam's syndrome. A quick change in the composition of body fluids in the polyuric phase of renal insufficiency associated with an antidiuretic hormone deficit was a cause of that disorder. Metabolic dysfunction and hyperexcitability of neurons developed as a result. Hyperexcitability of the caudal part of the medulla oblongata was responsible for the development of myoclonia. Following the correction of that disorder, the patient completely improved.
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PMID:[Disorders of consciousness due to disorders of body fluid composition--case report of a female patient]. 864 63


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