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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complex biologic investigation of thyphoid fever is dictated by the necessity of instituting a pathogenetic therapy, especially in the toxic and complex forms. Performing 178 fuctional-metabolic tests in 50 cases of typhoid fever (of which 10 severe and complicated forms), the authors established the prognostic value energy deficiency (approximately P), lactate, alkaline reserve and GPT. Azotemia is only characteristic in the forms with renal involvement, and the other transaminases may be positive even whe the liver is not enlarged. In one case of repeated digestive hemorrhage no evidence could be found of the mechanism of consumption coagulopathy.
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PMID:[Fuctional-metabolic disorders in typhoid infection]. 13 47

Patients with typhoid fever were studied to determine whether disseminated intravascular coagulation (DIC), circulating bacteria, and endotoxemia were responsible for the signs and symptoms of their illnesses. Coagulation tests in 28 patients detected thrombocytopenia in 17, hypofibrinogenemia in nine, and elevated titers of fibrinogen-related antigens in 20. Repeated testing during convalescence showed a return toward normal values. Intestinal bleeding, however, did not correlate with abnormalities of coagulation tests. Thus, DIC occurred commonly but appeared to be a subclinical event in these patients. In 25 patients with positive blood cultures for Salmonella typhi, quantitative cultures detected from less than 10 to 9 x 10(2) bacteria/ml. Limulus tests for endotoxin in plasma were negative in all 21 patients tested. These results indicated that the concentrations of circulating bacteria and endotoxin in typhoid fever are lower than in other Gram-negative bacterial infections and suggested that circulating bacteria and endotoxin do not play a major role in the pathogenesis of typhoid fever.
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PMID:Typhoid fever. Studies of blood coagulation, bacteremia, and endotoxemia. 62 35

The records of 104 patients with culture-proven enteric fever were reviewed and evaluated as to the clinical signs, laboratory findings, pathologic features and complications of the disease. One patient with fatal disseminated intravascular coagulation and enteric fever is also presented. Fever and bradycardia were the leading clinical signs followed by splenomegaly, hepatomegaly and rose spots. The principal complications of enteric fever included anemia, typhoid hepatitis, relapse and bleeding. Evidence of typhoid hepatitis was present in 30% of the patients tested. The pathology consisted of typhoid nodules of variable frequency and size depending upon the severity of the condition. The relationship of typhoid hepatitis to relapse seems to be more than coincidental as four out of seven patients who had relapse had abnormal liver tests. The occurrence of disseminated intravascular coagulation in enteric fever is rare; however, awareness of such a potential complication may be life-saving to the patient.
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PMID:Enteric fever: a clinicopathologic study of 104 cases. 64 89

A patient with documented typhoid fever had several uncommon manifestations. These included (1) haematemesis as the presenting feature, (2) hepatocellular jaundice with hepatic encephalopathy, (3) acute intravascular haemolysis and (4) probable disseminated intravascular coagulation. Haematemesis as the presenting feature in typhoid fever has not been reported previously.
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PMID:Typhoid fever manifesting with haematemesis, hepatitis and haemolysis. 70 25

Typhoid accounts for 8% of pediatric admissions to the Aga Khan University Hospital in Karachi, Pakistan. Over a 4-year period (1986-1989), 355 children had typhoid documented by culture of blood or bone marrow. Strains of Salmonella, resistant to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole accounted for 20% of these cases. Compared with children infected by drug-susceptible strains of Salmonella, children with multiresistant infection were generally sicker at presentation and were more likely to be assessed as appearing "toxic" (P less than .001), as having disseminated intravascular coagulation (P less than .01), and as exhibiting hepatomegaly (P less than .01). The mortality was 4.2% among children with multiresistant infection and 1.4% among those infected with strains susceptible to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole; the higher mortality in the former group was probably due to a longer duration of illness (P less than .05) and to ineffectual oral antimicrobial therapy before hospitalization.
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PMID:Multidrug-resistant typhoid in children: presentation and clinical features. 196 94

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.
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PMID:Role of kallikrein-kinin system in pathogenesis of bacterial cell wall-induced inflammation. 199 42

Three patients with typhoid fever, initially misdiagnosed, developed intravascular haemolysis, disseminated intravascular coagulation, haemoglobinuria and acute renal failure. 2 of the patients were deficient in erythrocyte glucose-6-phosphate dehydrogenase; Plasmodium falciparum was present in the blood of the third. Among the indigenous population of endemic areas, typhoid fever is the likely diagnosis in any pyrexial illness associated with haemoglobinuric renal failure.
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PMID:Haemoglobinuric renal failure and typhoid fever. 323 92

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

Abnormalities of hemostasis in vivo and in vitro were defined in a prospective study of patients with typhoid fever. In a group of 56 patients with a proven diagnosis of typhoid fever, hemostatic abnormalities were frequently found. In patients with normal clotting tests the fibrinogen level was found to be higher than in normal controls. This finding established a new normal level for patients with typhoid fever. Using this redefined normal level it was found that low fibrinogen was associated with other hemostatic abnormalities. Low fibrinogen levels in patients with typhoid fever are possibly the result of disseminated intravascular coagulation. This process affected 20% of our patients and was often of mild to moderate intensity. Clinically significant bleeding occurred in 18 patients and, in contrast to the results of previously published studies, was found to correlate with clotting abnormalities.
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PMID:Hemostasis in typhoid fever. 720 2

The haematological profile in 20 culture proven patients with typhoid fever of varying age and of both sexes was studied. Significant changes observed were anaemia, leucopenia, eosinopenia, thrombocytopenia and sub-clinical disseminated intravascular coagulation. The bone marrow of typhoid patients showed myeloid maturation arrest, decrease in the number of erythroblasts and megakaryocytes with increased phagocytic activity of histiocytes.
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PMID:Haematological profile in typhoid fever. 750 22


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