Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of the kallikrein-kinin system, as indicated by increased plasma kallikrein and depleted plasma kininogen, prekallikrein, and kallikrein inhibitor, was observed in five patients with Rocky Mountain spotted fever. Four of the patients had petechial rashes characteristic of vasculitis. Three patients had alterations in coagulation consistent with disseminated intravascular coagulation, although no hemorrhagic syndrome was found. Our data, along with the known physiologic actions of kinins, suggest a possible role for the kallikrein-kinin system in the pathophysiology of vasculitis, disseminated intravascular coagulation, circulatory shock, and other complications of infection with Rickettsia rickettsii.
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PMID:Activation of the kallikrein-kinin system in Rocky Mountain spotted fever. 30 54

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

A patient with laboratory-acquired Rocky Mountain spotted fever (RMSF) and concomitant influenza virus infection was studied from the third day of clinical illness. The course of his illness was marked by petechial rash, thrombocytopenia, and elevation of fibrin split products. No evidence of complement activation was observed. Plasma proteins were elevated in a pattern characteristic of the "acute phase reaction." The patient recovered completely, and vascular collapse or clinically important disseminated intravascular coagulation had developed. In febrile patients who had influenza or a clinically similar noninfluenzal respiratory syndrome, no changes in coagulation, complement, or plasma proteins developed. We conclude that aberrations in the patient's laboratory values reflected RMSF, and that complement played no critical role in his illness.
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PMID:Coagulation and complement studies in Rocky Mountain spotted fever. 64 36

We observed and recorded clinical and laboratory data from 54 children with fever and a maculo-papular rash admitted to Soroka Medical Center, Beersheva, Israel suffering from serologically confirmed rickettsial spotted fever. The rash generally began on the palms and soles and extended centripetally to the torso. Other clinical findings included myalgia, headache, hepatomegaly, and splenomegaly. None had a "tache noire". A left shift in the white cells, leucopenia, thrombocytopenia, hyponatraemia and impaired liver function tests were common laboratory abnormalities. All recovered following oral doxycycline therapy. Serious sequelae such as myocarditis, encephalitis, and disseminated intravascular coagulation, as reported in Rocky Mountain spotted fever, did not occur.
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PMID:Israeli rickettsial spotted fever in children. A review of 54 cases. 288 43

Skin lesions, an important clue to the cause of septicemia, result from five main processes: (1) disseminated intravascular coagulation and coagulopathy; (2) direct vascular invasion and occlusion by bacteria or fungi; (3) immune vasculitis and immune complex formation; (4) emboli from endocarditis; and (5) vascular effects of toxins. Disseminated intravascular coagulation probably plays only a minor role in pathogenesis. Vascular invasion by bacteria may result in a severe inflammatory reaction, as in meningococcemia, or in a minimal reaction, as in ecthyma gangrenosum. Gram-stained smears of scrapings from the base of skin lesions--a frequently neglected procedure--is an important diagnostic adjunct. Skin biopsies are particularly important in the diagnosis of Rocky Mountain spotted fever and infections caused by Candida.
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PMID:Skin clues in the diagnosis of life-threatening infections. 351 82

A method is described for the measurement of soluble thrombin-altered fibrinogen (circulating fibrin) in human plasma. This method is dependent upon the enzymatic incorporation of glycine ethyl ester-(14)C (GEE-(14)C) into circulating fibrin by the action of the fibrin-stabilizing enzyme, factor XIII. The mean incorporation of GEE-(14)C into the fibrinogen of normal human plasma controls was 167 +/-47 dpm/mg fibrinogen. The addition of 0.03 NIH U/ml of thrombin to normal human plasma resulted in a two to threefold increase in the incorporation of GEE-(14)C into the fibrinogen. The addition of plasmin split products of fibrinogen to normal plasma did not increase the incorporation of GEE-(14)C unless these products were also exposed to thrombin. The addition of plasmin split products of a fibrin clot resulted in only minimal increase in the incorporation of GEE-(14)C (57 dpm/mg fibrinogen) at 37.5% concentration. The method was therefore sensitive to thrombin alterations of fibrinogen but insensitive to plasmin alterations of fibrinogen and fibrin.Clinically, the method was found to provide useful information for the diagnosis and treatment of disseminated intravascular coagulation in two patients with meningococcemia, two patients with Rocky Mountain spotted fever, and three patients in whom therapeutic abortions were induced by the injection of hypertonic saline.
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PMID:Detection of intravascular coagulation. 509 9

Rocky Mountain spotted fever and Mediterranean spotted fever are rickettsial infections primarily of endothelial cells that normally have a potent anticoagulant function. As a result of endothelial cell infection and injury, the hemostatic system is perturbed and shows changes that vary widely from a minor reduction in the platelet count (frequently) to severe coagulopathies, such as deep venous thrombosis and disseminated intravascular coagulation (rarely). Changes favoring a hypercoagulable state include endothelial injury and release of procoagulant components, activation of the coagulation cascade with thrombin generation, platelet activation, increased antifibrinolytic factors, consumption of natural anticoagulants, and possibly high levels of coagulation-promoting cytokines. Yet, most studies have been performed on endothelial cell cultures that provide nonphysiologic, reductionistic, experimental conditions. The lack of flow, platelets, and WBCs makes these experiments far from simulating the response of endothelial cells in the human body. Coagulopathies and thrombotic events should be considered as potential complications of severe Rocky Mountain spotted fever and Mediterranean spotted fever.
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PMID:Hemostatic changes in Rocky Mountain spotted fever and Mediterranean spotted fever. 1043 95

Rocky Mountain spotted fever (RMSF) was diagnosed in 30 dogs examined at North Carolina State University, Veterinary Teaching Hospital between 1984 and 1997. Historical, physical examination, and laboratory abnormalities were reviewed. Diagnostic criteria included a four-fold rise in antibody titer to Rickettsia rickettsii (R. rickettsii) (n=15) or a single R. rickettsii antibody titer of 1:1,024 or greater (n=15; when this initial titer was determined one week or more after the onset of clinical signs). Fifteen (50%) dogs were greater than seven years of age, and 13 (43%) dogs were between two and seven years of age. There was no sex predilection. Only five (17%) dogs had a history of known tick exposure. Presumably due to delayed diagnosis, dogs with antibody titers of 1:1,024 or greater at the time of presentation had a higher incidence of more severe neurological dysfunction (e.g., ataxia, hyperesthesia, vestibular disease, and seizures) and cutaneous lesions (e.g., hyperemia, edema, petechiae, ecchymoses, and necrosis). Laboratory findings included anemia, leukocytosis accompanied by toxic granulation of neutrophils, hypoalbuminemia, and coagulation abnormalities; signs were generally more severe in the 15 dogs with R. rickettsii antibody titers of 1:1,024 or greater at the time of presentation. Twelve (40%) dogs in this study were severely thrombocytopenic (less than 75 x10(3) platelets/microl; reference range, 200 to 450 x 10(3)/microl), without clinical evidence of fulminant disseminated intravascular coagulation. In this study, the survival rate following R. rickettsii infection was 100%.
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PMID:Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases. 1120 76

Rocky Mountain spotted fever (RMSF) is a disease caused by the Gram-negative coccobacillus Rickettsia ricketsii which has been on the rise since the last decade in the USA. The symptoms are common to the many viral diseases, and the classic triad of fever, rash and headache is not always present when RMSF is diagnosed. It may progress to severe cases such as renal failure, disseminated intravascular coagulation and septicaemia. This report aims to present a fulminant case of RMSF associated with sepsis. It describes a female patient's case that quickly progressed to sepsis and death. The patient showed non-specific symptoms for 5 days before being admitted to a hospital. The fact that she lived in an area highly infested with Amblyomma aureolatum ticks was unknown to the medical staff until the moment she died.
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PMID:Association between sepsis and Rocky Mountain spotted fever. 2322 Aug 32