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)

Refractory thrombocytopenia (RTC) is a counter-concept to refractory anemia, which is characterized by isolated thrombocytopenia associated with clonal chromosomal abnormality. The diagnosis of RTC is difficult to establish based on morphologic features alone. And steroid therapy for RTC is often ineffective. We examined 3 patients with RTC to identify its characteristics and measured serum thrombopoietin levels. The mean platelet count was 5.1 x 10(4)/microl and the mean age was 64 years. None of our patients had clinical nor laboratory evidence of liver dysfunction, renal disease or disseminated intravascular coagulation. All patients were negative for antiplatelet antibody, PA-IgG and anticardiolipin-beta2GPI antibody. Leukocyte alkaline phosphatase level was low in two patients. Clonal chromosomal abnormalities of different types were detected in all patients. Bone marrow smears showed micromegakaryocytes. But there were no apparent morphological abnormalities of erythroid and granuloid series. Thrombopoietin levels, as determined by enzyme-linked immunosorbent assay, varied from <0.2 to 1.40 fmol/ml. We could not find the screening tool of RTC. In conclusion, there is a need to identify RTC from isolated thrombocytopenia because the patients with RTC don't have good prognosis as patients with isolated thrombocytopenia. Cytogenetic analysis is necessary to establish the diagnosis of RTC. We recommend that a patient above 50 years of age presenting with isolated thrombocytopenia and a low leukocyte alkaline phosphatase score should be suspected of having RTC.
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PMID:Clinical analysis and TPO levels in three patients with refractory thrombocytopenia. 1050 5

40 patients with infective endocarditis (IE) abusing intravenous drugs (heroin, opium surrogates) and 9 IE patients predisposed to heart diseases were examined by Duke diagnostic criteria. IE in drug abusers is characterized by acute course of the disease with affection of the intact valves of the right heart (97.5%) and septicemia provoked by high-virulent microflora (Staph. aureus in 65%). Drug abusers showed the following principal clinical syndromes of IE: thromboembolic (65%); septic with formation of acute DIC syndrome (75%), development of pyodestructive foci in the organs and polyorganic insufficiency (23.3%); acute circulatory insufficiency (37.5%); secondary nephropathy (100%). In IE abusers with predisposition to heart diseases IE ran subacutely in the presence of bacteriemia caused by low-virulent microflora (Strept. viridans in 11%) or in the absence of microbial growth in blood seeding (78%). High IE lethality in drug abusers (40%) is explained both by severe complications and concomitant diseases (viral hepatitis B and C, HIV infection, etc.).
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PMID:[The course of infectious endocarditis in IV drug abusers and in subjects predisposed to heart diseases]. 1158 79

Fatal calciphylaxis (CPX) occurred in two 71-year-old females both requiring haemodialysis for end-stage renal disease. Case 2 also had an associated follicular lymphoplasmocytoid lymphoma. Although laboratory tests disclosed normal coagulation parameters, this woman had a striking cutaneous histological picture of vessel thrombosis and finally died of disseminated intravascular coagulation. CPX is a rare but potentially life-threatening complication of renal failure. The clinical picture is primarily characterized by livedoid purpura with subsequent cutaneous ischaemia and painful ulcerations. Cutaneous ischaemic phenomena are sustained by a progressive process of vascular calcification and thrombosis involving small to medium size arteries of the dermis and subcutis. Although not yet clearly explained, the pathogenetic role of a predisposing hypercoagulability state is currently the most frequently considered hypothesis.
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PMID:Calciphylaxis in two patients with end-stage renal disease. 1176 76

An increased concentration of fibrin(ogen) degradation products (FDPs) commonly is used in conjunction with other hemostatic test abnormalities to identify patients with disseminated intravascular coagulation (DIC). Positive FDP results, however, have been observed in dogs without clinical evidence of DIC. The purpose of this study was to evaluate FDP concentrations in a group of clinically ill dogs with a variety of disorders. Dogs included in the study had the following hemostatic parameters evaluated: prothrombin time, activated partial thromboplastin time, fibrinogen concentration, platelet count, and FDP concentration. Two rapid latex agglutination methods were compared for detecting FDP in serum samples (Thrombo-Wellcotest, International Murex Technologies Corp) and plasma samples (FDP Plasma, American Bioproducts Inc). Results of the serum FDP method were positive in 8% (4/50) of the dogs tested: 3 with DIC and 1 with immune-mediated hemolytic anemia and liver disease. Results of the plasma FDP test were positive in 60% (30/50) of the animals tested: 6 with DIC, 3 with confirmed thrombosis, and 21 with a variety of conditions, including neoplasia, immune-mediated hemolytic anemia, pancreatitis, gastric dilatation-volvulus, heat stroke, severe trauma, sepsis, protein-losing nephropathy, liver disease, hyperadrenocorticism, and chronic heart failure. Because the plasma FDP test was positive more frequently than the serum FDP test in ill dogs, it may be more sensitive for the detection of canine FDP.
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PMID:Serum and plasma latex agglutination tests for detection of fibrin(ogen) degradation products in clinically ill dogs. 1202 12

BACKGROUND: Leptospirosis (LS) and Hantavirus (HV) infection have many common clinical manifestations, including acute renal failure. In as much as clinical experience with these diseases is quite limited in urban centers, we identified cases of Leptospira and HV-induced acute renal failure and compared the clinical course and evolution of these diseases. METHODS: Patients hospitalized with acute renal failure, suspected to be caused by infection, were retrospectively studied over a 13-year period (1985-1998). Based on pertinent clinical data and positive serology, a total of 26 patients were included in the study, 17 patients with LS and 9 patients with HV infection. RESULTS: Both diseases presented as flu-like syndromes with high fever. In LS, 2 patients presented with acute meningitis and died soon after admission. Symptoms and signs from other organs began after the fifth day of illness. Jaundice occurred in 71% of LS patients but not in HV. Hemorrhagic phenomena occurred in both diseases but affected predominantly patients with icteric LS. Anuria or oliguria occurred in 76% of patients with LS and 78% with HV infection. Laboratory studies demonstrated minor transaminase elevations in all patients with LS and in 44% with HV. Hypoprothrombinemia or thrombocytopenia was uncommon, although disseminated intravascular coagulation (DIC) developed in 2 patients that had icteric Ls and major bleeding. Nephropathy was associated with haematuria in 71% with LS and all patients with HV. Proteinuria was evident in 35% of patients with LS compared to 78% with HV. Abnormal chest radiographs were seen in 24% with LS and in 33% with HV. In both diseases, aggressive supportive treatment was given, including hemodialysis or peritoneal dialysis in 4/26 patients. Of the 26 patients, 22 survived and four died. The latter all had LS, and the causes of death were meningitis and DIC with multiple organ failure. Follow-up, after 6 months, showed that renal function had returned to normal in the 22 survivors. CONCLUSION: It is important to include LS and HV infection in the differential diagnosis of acute renal failure. Both diseases present with flu-like symptoms and may be complicated by thrombotic microangiopathy with hemorrhagic phenomena and hepatic and pulmonary involvement. Jaundice should alert the physician to icteric LS, a severe disease associated with significant mortality that requires antimicrobial treatment.
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PMID:Acute renal failure caused by leptospirosis and Hantavirus infection in an urban hospital. 1206 23

A survey was carried out among the European Group for Blood and Marrow Transplantation (EBMT) centres to determine the incidence, risk factors, treatment and outcome of thrombotic thrombocytopenic purpura (TTP) following allogeneic haematopoietic stem cell transplantation. TTP was defined as the simultaneous occurrence of red cell fragmentation, laboratory findings of haemolysis, red cell transfusion requirement and de novo or persistent thrombocytopenia caused by consumption, in the absence of disseminated intravascular coagulation. Forty-five centres reported all patients (n = 406) transplanted between July and December 1996. Twenty-three patients developed TTP; the risk of developing TTP was 6.7% at 2 years (95% CI: 4.1% to 9.3%). The median time of onset was 44 d (range 13-319) post transplantation. Significant risk factors for the development of TTP were female gender (P = 0.005) and an unrelated donor (P = 0.046). To treat TTP, cyclosporin administration was discontinued in 10 cases, plasma exchanges were performed in five cases and 12 patients received plasma infusions without plasma exchange. TTP resolved in 13 of the 23 patients (57%). The only factor predictive of resolution of TTP was the absence of nephropathy. Seven patients (30%) were alive at follow-up of 38-45 months from the onset of TTP. Sixteen patients died; the causes were multiple, only three patients had TTP as a central factor. The median time to death was 41 d (range 1-762 d) from the onset of TTP. TTP is a relatively frequent complication of allogeneic stem cell transplantation and it is associated with high mortality, though death is usually caused by multiple factors.
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PMID:Thrombotic thrombocytopenic purpura after allogeneic stem cell transplantation: a survey of the European Group for Blood and Marrow Transplantation (EBMT). 1219 93

Widespread human exposure to a variety of drugs, chemicals, and biologic products and recent awareness of their toxic manifestations has led to the recognition of toxic nephropathy as an important segment of renal disease in the tropical countries. Tropical nephrotoxins are distinctly different from those seen in the rest of the world and are derived from local fauna and flora or plant and chemical sources. The spectrum of exposure varies from country to country and even from community to community, depending on variations in the distribution of local plants and animal species and prevalent social practices. Acute renal failure (ARF), either alone or in association with liver failure, neurologic abnormalities, metabolic acidosis, disseminated intravascular coagulation, or pulmonary infections is the most common form of presentation. Traditional medicines prescribed by witch doctors (traditional healers) constitute a special class of nephrotoxins among several communities in Africa and Asia. The prevalence of nephropathy caused by traditional medicines is directly related to a combination of ignorance, poverty, lack of medical facilities, lax legislation, and widespread belief in indigenous systems of medicine in rural areas. These medicines are a mix of herbs and unknown chemicals administered orally or as enemas. Clustering of cases after exposure to a particular agent suggests the possibility of a toxic insult. Common animal nephrotoxins are venoms of viper snakes, sea snakes, stinging insects, and raw gallbladder and bile of carp and sheep. Botanical nephrotoxins are encountered both in common edible plants (djenkol beans, mushrooms) and medicinal herbs (impila, cat's claw). Mistaken identification of medicinal herbs by untrained workers and even deliberate trials of toxic substitutes derived from plants frequently lead to renal disease, the most commonly reported being the Chinese herbal nephropathy. Nephrotoxicity caused by chemicals can be secondary to accidental occupational exposure in industrial work places (eg, chromic acid), or after suicidal or homicidal use (eg, copper sulphate, ethylene dibromide, ethylene glycol). Late presentation and multiorgan dysfunction are associated with a high mortality. A high index of suspicion, careful history taking, and an awareness of local practices are essential for proper diagnosis and management of toxic nephropathies in the tropics.
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PMID:Nephropathy associated with animal, plant, and chemical toxins in the tropics. 1256 1

The diagnosis of thrombotic thrombocytopenic purpura (TTP) rests on evidence of microangiopathic hemolytic anemia and thrombocytopenia in the absence of disseminated intravascular coagulation and other known causes of thrombotic microangiopathy. Highly specific diagnostic tools such as serum levels of ADAMTS13 are not routinely available for immediate clinical diagnosis. The presence of schistocytes on a blood smear is the morphologic hallmark of the disease, but no guidelines exist as to the number of schistocytes required to differentiate TTP from other thrombotic microangiopathies. We studied 6 patients with TTP and compared their schistocyte counts with those of 40 normal subjects, 28 patients with chronic renal disease, 5 with preeclampsia, and 5 with normal functioning mechanical heart valves. The mean schistocyte count for the TTP patients was 8.35% versus 0.05% for normal subjects, 0.2% for renal patients, 0.25% for preeclamptic patients, and 0.18% for patients with mechanical valves (P < 0.001). Schistocytes were found on 100% of blood films of TTP patients and ranged from 1.0% to 18.4% of red cells. Schistocytes are found on the smears of 58% of normal individuals and on 80-100% of the other patient groups studied, but always comprise less than 0.5% of the red cell population. An initial schistocyte count of greater than 1% strongly suggests a diagnosis of TTP in the absence of other known causes of thrombotic microangiopathy.
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PMID:Morphologic diagnosis of thrombotic thrombocytopenic purpura. 1469 28

Sepsis continues to have a substantial mortality and morbidity despite advances in the diagnosis and management of this condition. We retrospectively analysed hospital charts of patients diagnosed to have sepsis between January 2002 and June 2003. Demographic characteristics of patients, microbiological findings and predictors of survival were evaluated. Sixty-nine sepsis episodes that occurred in 63 patients were analysed. The most common underlying diseases were hypertension, malignancies and diabetes mellitus. Renal insufficiency, respiratory distress and disseminated intravascular coagulation developed in 52.2, 30.4 and 30.4% of the episodes respectively; 47.7% of the blood cultures yielded an organism. Gram-negative bacteria were the predominant microorganisms (65.9%). Fifty-five patients (87.3%) died. Mechanical ventilation and underlying renal disease were significant determinants of mortality. In conclusion, Gram-negative bacteria remain the major pathogens in sepsis. The mortality remains very high, and a change in the clinical approach to the septic patient should be employed to improve the outcome.
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PMID:Epidemiology and outcome of sepsis in a tertiary-care hospital in a developing country. 1649 Jan 36

Snakebites have the highest incidence in Asia and represent an important health problem. Clinical renal manifestations include proteinuria, hematuria, pigmenturia, and renal failure. Nephropathy usually is caused by bites by snakes with hemotoxic or myotoxic venoms. These snakes are Russell's viper, saw-scaled viper, hump-nosed pit viper, green pit viper, and sea-snake. Renal pathologic changes include tubular necrosis, cortical necrosis, interstitial nephritis, glomerulonephritis, and vasculitis. Hemodynamic alterations caused by vasoactive mediators and cytokines and direct nephrotoxicity account significantly for the development of nephropathy. Hemorrhage, hypotension, disseminated intravascular coagulation, intravascular hemolysis, and rhabdomyolysis enhance renal ischemia leading to renal failure. Enzymatic activities of snake venoms account for direct nephrotoxicity. Immunologic mechanism plays a minor role.
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PMID:Snakebite nephrotoxicity in Asia. 1862 Sep 59


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