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)

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

There are occasional reports in medical literature of peripheral gangrene and subsequent extremity amputation following systemic infection. Although the authors of these case reports speculated that the gangrene was due to septic embolization, pathologic study of the amputated tissue failed to reveal evidence of septic emboli. In reviewing reports of amputation following scarlet fever, varicella, pneumococcemia, and appendicitis, we found cases with clinical, hematologic, and pathologic evidence of disseminated intravascular coagulation (DIC). We describe 2 patients who required extremity amputation following an acute, systemic infection: transmetatarsal and Lisfranc amputation following meningococcal meningitis and bilateral below-knee amputation following pneumococcal meningitis. Both of these patients had clinical, hematologic, and pathologic evidence of DIC. Following amputation, both of these patients had significant problems with skin healing and prosthetic fitting. The presence of an acute systemic bacterial or viral infection, coagulation abnormalities and pathologic tissue indicative of DIC, and skin lesions of the extremities progressing to dry gangrene and ultimately requiring bilateral amputation are the key clinical features of this syndrome. We conclude that DIC is a major pathophysiologic mechanism responsible for peripheral gangrene following systemic infection.
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PMID:Extremity amputation: disseminated intravascular coagulation syndrome. 736 47