Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten episodes of Torulopsis glabrata fungemia occurring in nine patients with terminal illnesses are described. Eight patients had underlying malignancies and one patient had a plastic anemia. Two episodes of fungemia were considered transient since they were clearly related to the administration of intravenous hyperalimentation (IVH). Most patients were adult women and had solid tumors of the genitourinary tract. Contributory factors were: antibiotic therapy (100%), immunosuppressive drugs (75%), abdominal surgery (63%), IVH (50%), neutropenia (38%), and diabetes mellitus (13%). The clinical course was indistinguishable from a severe bacterial infection. However, endotoxic shock was not observed. The infection was rapidly fatal in four patients. In the remaining five patients, the infection was altered favorably by the discontinuation of infected intravenous hyperalimentation catheters. However, tissue invasion by T. glabrata was found in two of these patients who died shortly thereafter from tumor progression. At autopsy, T. glabrata was identified in tissue sections of the lungs, kidneys, and mucosas of the gastrointestinal and genitourinary tracts. In all cases there was tissue necrosis with a minor inflammatory response consisting of mononuclear cells. To our knowledge, this is the single largest series of T. glabrata fungemia ever reported.
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PMID:Fungemia due to Torulopsis glabrata in the compromised host. 82 17

This study examined 1) the effects of infusion of LTB4 and 2) the potential role of LTB4 in the sequelae to endotoxic shock in the rat. Control rats were anesthetized with Ketamine/xylazine and given LTB4 (2 micrograms/kg) bolus i.v. followed by a 1 microgram/kg/min infusion for 10 min. LTB4 induced systemic hypotension and a three-fold increase in circulating band neutrophils which contributed to a 70% increase (P less than 0.05) in the total peripheral neutrophil count. LTB4 did not cause changes in circulating mature (segmented) neutrophils, lymphocytes, platelets, or hematocrits. Pretreatment (1 min) with LY233978, an LTB4 antagonist (10 mg/kg bolus i.v.), inhibited LTB4-induced systemic hypotension (-16.1 +/- 6.1 mmHg [n = 3] vs. -38.8 +/- 5.9 mmHg [n = 4], P less than 0.05). Salmonella enteritidis endotoxin (10 mg/kg bolus i.v.) induced systemic hypotension, hemoconcentration, leukopenia, and thrombocytopenia, which was greatest at 5 and 15 min postendotoxin. The leukopenia was characterized by lymphopenia, band neutropenia, and segmented neutropenia. LY233978 (10 mg/kg bolus i.v. immediately before endotoxin administration and followed by an infusion at 0.67 mg/kg/min for 90 min) attenuated endotoxin-induced hemoconcentration at 60 and 90 min postendotoxin (P less than 0.05), and systemic hypotension at 15 min postendotoxin (P less than 0.05). The LTB4-receptor antagonist LY255283 (10 mg/kg bolus i.v., 10 min before endotoxin followed by a 5 mg/kg bolus i.v. 30 min postendotoxin) completely inhibited endotoxin-induced systemic hypotension and partially attenuated endotoxin-induced hemoconcentration from 15 min to 90 min postendotoxin (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of LTB4 receptor antagonists in endotoxic shock in the rat. 166 29

The role of lipoxygenase metabolites as inflammatory mediators in endotoxic shock remains uncertain. In the present study, the effects of a selective leukotriene (LT) D4/LTE4 antagonist, LY171883, 1-[2-hydroxy-3-propyl-4-[4-(1H-tetrazol-5-YL)-butoxy]-phenyl ethanone], on endotoxin-induced sequelae in the rat were assessed. LY171883 was given as a bolus (30 mg/kg i.v.) 10 min before Salmonella enteritidis endotoxin (40 mg/kg) in ketamine-anesthetized (200 mg/kg i.m.) rats, followed by an infusion (10 mg/kg/hr) starting at 30 min postendotoxin. Carotid artery blood pressures were determined at 10 min before and at intervals up to 240 minutes postendotoxin administration. Compared to shocked vehicle controls LY171883 attenuated (analysis of variance, P less than .02) the initial (0-30 min), but not the later, endotoxin-induced hypotension. LY171883 prevented completely (analysis of variance, P less than .001) the neutropenia (0-180 min), but not the thrombocytopenia induced by endotoxin. Hemoconcentration resulting from endotoxemia was reduced by LY171883 compared to the vehicle control group (P less than .02). These data demonstrate that this LTD4/LTE4 antagonist has significant salutary actions in endotoxemia and suggest that LTs may contribute to some endotoxin-induced sequelae.
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PMID:Protective effect of a selective leukotriene antagonist in endotoxemia in the rat. 299 35

Polymorphonuclear neutrophils (PMNs) may contribute to organ injury in both hemorrhagic and endotoxic shock. Both models of shock exhibit a "flight of the leukocytes," but the mechanisms for entrapment of leukocytes in the microcirculation differ. The objective of this study was to investigate lipopolysaccharide (LPS)-induced shock and hemorrhagic shock with similar survival rates, in terms of circulating PMNs, activated circulating PMNs, plasma tumor necrosis factor (TNF) activity, and PMN adhesion. In the LPS protocol, rats received 6.5 mg/kg E. coli LPS i.v., which resulted in 50% survival. In the hemorrhagic shock protocol, rats were maintained for 3 h at 40 mm Hg mean arterial pressure, and survival during a 24-h observation period was 40%. LPS injection and hemorrhage caused rapid neutropenia in survivors and nonsurvivors. Low circulating PMN counts persisted during hypotension in the hemorrhagic protocol and among nonsurvivors in the LPS protocol, but in both protocols a tendency toward significantly higher circulating PMN counts in survivors compared with nonsurvivors was found. In both protocols, survivors had significantly lower fractions of circulating activated PMNs and lower adhesion of circulating PMNs to nylon fibers. In the LPS protocol, higher plasma TNF activity was found in nonsurvivors than in survivors, but no TNF activity in plasma could be found throughout the hemorrhagic protocol. These results indicate that nonsurvivors in both shock models exhibit higher levels of PMN activation. No correlation was detected between PMN activation and plasma TNF activity to suggest that TNF serves as the primary mediator of circulating PMN activation.
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PMID:Neutrophil activation, tumor necrosis factor, and survival after endotoxic and hemorrhagic shock. 869 57

Sixteen cases of acute idiopathic toxaemic colitis developed in a veterinary hospital over a period of three years. Before the onset of colitis, 15 horses had received antibiotics, 11 had undergone general anaesthesia and various surgical procedures, and 10 had been treated with non-steroidal anti-inflammatory drugs. The horses had acute onset, profuse watery diarrhoea, profound depression, mild to moderate abdominal pain, reduced intestinal borborygmi, tachycardia, dehydration and endotoxic shock. Leucopenia, neutropenia and pyrexia were common early indicators of impending colitis. Metronidazole appeared to be an effective treatment; eight horses treated with metronidazole survived whereas five of seven horses that received other treatments, but no metronidazole, died or had to be euthanased. The aetiology of the colitis could not be determined, but the clinicopathological features resembled those of colitis attributed to an intestinal overgrowth of Clostridium perfringens type A. No Salmonella species were isolated from 52 samples of faeces, colonic contents and colonic mucosa which were collected from the horses antemortem and postmortem.
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PMID:Use of metronidazole in equine acute idiopathic toxaemic colitis. 967 Apr 51

A 2-year-old, Quarter Horse filly was referred to Michigan State University, Veterinary Teaching Hospital with a 2-3 day history of depression and partial anorexia progressing to severe, watery diarrhea with severe neurologic abnormalities, including repetitive muscle fasciculations, muscle stiffening, and collapse. Laboratory findings included severe polycythemia, neutropenia, metabolic acidosis, and electrolyte and fluid loss, consistent with watery diarrhea and endotoxic shock. Increased creatine kinase and aspartate transaminase activities were consistent with recent transport and the muscle abnormalities. Severe hyperammonemia (1369.0 micromol/L; control value, 15.3 micromol/L) was found, without other substantial laboratory evidence of hepatic dysfunction. The horse was euthanized because of poor prognosis and rapid clinical deterioration. Necropsy findings were unremarkable with the exception of severe diffuse colitis. Culture of colonic contents recovered >1000 colony-forming units of Clostridium perfringens. Based on these findings, marked hyperammonemia in this filly was attributed to changes in colonic flora leading to increased bacterial production of ammonia that was readily absorbed through the inflamed bowel wall, exceeding the hepatic capacity for deamination. Intestinal bacteria as a source of hyperammonemia in the absence of hepatic disease has been linked rarely to positive culture results for clostridial organisms.
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PMID:Diarrhea and hyperammonemia in a horse with progressive neurologic signs. 1678 24