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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RhGM-CSF is a hematopoietic growth factor which stimulates the proliferation, differentiation and functional activity of neutrophils, monocytes and macrophages. It also stimulates proliferation of endothelial cells and induces the production of other cytokines, such as interleukin (IL-1), tumor necrosis factor (TNF), interferon, prostaglandin E2, and plasminogen activating factor which affects both hematopoietic and non-hematopoietic cell activities. Initial clinical studies in 1987 generally excluded experimental therapy with rhGM-CSF in pediatric patients (age < or = 17 years) unless life threatening illness related to neutropenia and infection developed (i.e., patients with graft failure). Serious complications of patients undergoing autologous bone marrow transplantation (BMT) related to pancytopenia include infection and hemorrhage. Other regimen related complications include venooclusive disease, pneumonitis and mucositis. As a result of these complications, patients require intensive medical support including antibiotics and hyperalimentation. Initial hospital duration following marrow reinfusion is generally 4 to 5 weeks. Hematopoietic growth factors have been administered to patients undergoing autologous BMT as an attempt to reduce regimen related toxicity.
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PMID:RhGM-CSF in bone marrow transplantation: experience in pediatric patients. 130 85

Disturbances of blood coagulation were studied in 32 consecutive patients with typhoid fever on their admission to hospital. Estimations of prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation products (FDPs), factors VII, VIII and XII, alpha I antitrypsin, plasminogen, CI esterase inhibitor, and platelet counts were performed as well as liver function tests and blood counts. Five patients had laboratory evidence of disseminated intravascular coagulation (DIC) and two had a generalised bleeding disorder which in the other three was inapparent. The platelet count in the group as a whole was low (P less than 0.05) and the FDPs in most cases were mildly elevated. The pre-kallikrein values were depressed in three of the five with DIC, whereas factor XII was not reduced. These results indicate that bleeding disorders in typhoid fever are uncommon. The depression of pre-kallikrein indicates that the DIC is probably triggered by activation of the intrinsic coagulation pathway. Most patients had lymphopenia and monocytopenia but only two had neutropenia.
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PMID:Disturbances of blood coagulation associated with Salmonella typhi infections. 335 16

A heterologous rabbit anti-rat neutrophil serum (ANS) based on peptone-stimulated peritoneal exudate neutrophils (PMNLs) from Sprague Dawley rats was prepared. Leucoagglutination and indirect immunofluorescence assays revealed high titres of antibodies to rat PMNLs (1/2560), lower titre of antibodies to rat lymphocytes (1/160) and a very low titre against rat platelets (1/20). ANS given intravenously (i.v.) to rats in doses of up to 42 mg of protein/kg b.w. caused transient neutropenia, lasting about 10 min after administration, and thrombocytopenia, lasting about 5 min. Two minutes after an i.v. injection of 21 mg of ANS/kg b.w. there was profound uptake of 51Cr-labelled PMNLs in the lung, increased release of 51Cr to plasma, an increased amount of 51Cr in the spleen and consumption of greater than 98% of total complement (CH50). Two hours later there was high activity of 51Cr in the plasma, spleen and liver, while lung radioactivity had decreased to below baseline and CH50 had recovered to 55% of baseline. An intraperitoneal (i.p.) injection of ANS was followed by prolonged neutropenia with a maximum after 12 h. Simultaneously peripheral mononuclear cells slightly decreased. There was no change in the number of peripheral platelets in the blood or in the plasma concentration of fibrinogen, alpha 2-antiplasmin, plasminogen or plasminogen activators. Intraperitoneal administration of ANS did not affect CH50. It was concluded that the raised ANS had good specificity against rat PMNLs and was able to induce prolonged neutropenia after i.p. injection without affecting the complement of fibrinolytic system.
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PMID:Antiserum-induced neutropenia in the rat: characterization of a rabbit anti-rat neutrophil serum. 381 3

Haematological changes in the septic patient are, primarily, neutropenia or neutrophilia, thrombocytopenia and disseminated intravascular coagulation (DIC). Thrombocytopenia frequently arises from DIC although inhibition of thrombopoiesis or immunological platelet damage also occur. DIC contributes to bleeding and microvascular thrombosis, leading to multiple organ failure. Tissue factor release, primarily mediated by tumour necrosis factor, activates the clotting system; fibrinolysis is initially activated, but later becomes inhibited by the release of plasminogen-activator inhibitor (PAI-1), further fostering multiple organ failure. Most septic patients have compensated, chronic DIC, detectable by assays of molecular markers; the earliest signs are already found during the systemic inflammatory response syndrome. Compensated DIC later becomes decompensated with rapid consumption of factors including inhibitors such as antithrombin III (AT III) and proteins C and S. AT III concentrations of < 60-70% of the normal values predict outcome. Management of DIC must address the underlying disease, interrupt the activated haemostasis system and replace consumed coagulation constituents. Interruption of haemostasis with heparin may be attempted, but bleeding may worsen. Administration of a natural anticoagulant, such as AT III, may arrest clotting without concomitant risk of bleeding. In several animal models of DIC, AT III concentrates shortened the duration of DIC and reduced multiple organ failure and mortality. Similar benefits have been reported in early studies of patients with DIC, especially in the absence of sepsis. Studies are under way to determine whether outcome will improve if patients with sepsis are treated before the development of shock and plasma AT III concentrations are maintained at 100-150% of normal.
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PMID:The haematological manifestations of sepsis. 951 Oct 82