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)

Human ehrlichiosis is a zoonotic disease, caused by a rickettsia that infects leukocytes. It was described for the first time in the United States of America in 1986. More than 300 cases have been reported in that country. One case has been reported in Portugal, two in France and one more in a tourist coming from Mali (Africa). In Venezuela, a tropical country, where ehrlichiosis is endemic in dogs and horses, the first case of human ehrlichiosis is reported in a seventeen month old girl. She initially had symptoms compatible with a viral illness. Then she developed a rash, acute respiratory failure, hepato-splenomegaly, neurologic abnormalities, renal failure and hematologic alterations including pancytopenia and disseminated intravascular coagulation (DIC). Different diagnoses were given before it was concluded that it was a case of ehrlichiosis. She was treated with tetracycline and very soon recovered. The initial diagnosis was made using buffy coat blood smears stained with Diff Quick Stain. Indirect Immunofluorescence (IFA) test was used to detect antibodies against Ehrlichia chaffeensis (1:126) but not to other rickettsias. Also the presence of platelets with ehrlichia bodies similar to E. platys from dogs, it was demonstrated, in peripheral blood from the child. The presence of these bodies in human platelets has not been previously reported. In this case, it could not be proved that the disease was transmitted by a tick bite. The presence of ehrlichia bodies in platelets from the girl's peripheral blood is also described.
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PMID:[Human ehrlichiosis: report of the 1st case in Venezuela]. 892 30

Human parvovirus B19 (HPV-B19) has been known as the etiologic agents of erythema infectiosum in normal childhood, and chronic anemia and thrombocytopenia in immuno-compromised patients. Recently, this virus has been reported as the association with rheumatic manifestation such as rheumatoid arthritis and systemic lupus erythematosus (SLE). We described here a patient whose HPV-B19 infection was mimiking atypical symptoms of SLE at diagnosis, and was persistent because of immuno-suppressive therapy for SLE. A 34-year-old female was admitted to our hospital on 22 June 1995, presenting fever episode and cervical lymph node swelling. Before eighteen months, she was received methyl-predonisolone pulse therapy and plasma exchange by fresh frozen plasma for the treatment of Stevens-Johnson syndrome, and after several weeks these therapy she was suffered from viral infection with lymphadenopathies with a transient appearance of atypical lymphocytes in her peripheral blood smear. On laboratory examination at the present admission, her peripheral blood showed anemia, thrombocytopenia with atypical lymphocytes. Throughout her hospitalization, anti-nuclear antibody (ANA) suspected SLE including anti-DNA and anti-Sm antibody were all negative except of transient week positive ANA screening test. Her physical condition presented poor clinical course with fever elevation, increased ascites and renal dysfunction showing the elevation of CRP and circulating immune-complex (Clq binding method). Her serum was positive for IgM and IgG antibody against VP-1 and VP-2 antigen of HPV-B19 by ELISA in April 1996. And then, HPV-B19 DNA by polymerase chain reaction (PCR) was positive in bone marrow sample in March 1996, and also positive in spleen necropsy at death. We confirmed persistent chronic HPV-B19 infection by measurement of HPV-B19 IgM and IgG antibody by ELISA and HPV-B19 DNA by PCR. The plasmapheresis and administration of intravenous immunoglobulin showed the possible efficacy for her symptom throughout this clinical course. Moreover, bone marrow smear showed the finding of virus-associated hemophagocytic syndrome, and finally, she was died of cervical hemorrhage accompanied with disseminated intravascular coagulation syndrome on July 1996. HPV-B19 infection can present an atypical clinical picture that is highly suggestive of SLE. We suggest that the therapy of steroids and immuno-suppressive agents should be cautious, because these may potentially cause persistent chronic HPV-B19 infection and induced life-threatening clinical course.
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PMID:[Human parvovirus B19 infection mimicking systemic lupus erythematosus: case report]. 931 Dec 85

Use of hyperthermia in the treatment of cancer and viral infection has received renewed interest. However, the in vivo relationship between hyperthermia and direct versus indirect effects upon hemostasis are incompletely defined, although we do know that disseminated intravascular coagulation (DIC) is a common sequel to heat stroke. The purpose of the present study was to more precisely define the relationship between hyperthermia and derangements of hemostasis, thereby providing a guideline for the development of safe hyperthermia treatment regimens. The present investigation examined the in vivo effects of high-grade whole-body hyperthermia (WBH) (42.5 degrees C, 90 min) on hemostasis in a canine model. Induction of hyperthermia via extracorporeal circulation of heated blood (ECC-WBH) caused thrombocytopenia, increased plasma fibrin degradation products (FDPs), prolonged clotting times, increased serum liver enzymes, and evidence of spontaneous bleeding. However, when WBH was induced by peritoneal lavage (PL-WBH), transient thrombocytopenia was the only significant alteration. Temporal correlation between hemostatic alterations and elevations in serum alanine aminotransferase (ALT) levels in the ECC-WBH treatment group suggested that liver injury is responsible, at least in part, for the coagulopathy associated with high-grade hyperthermia and that in the absence of liver injury, identical degrees of hyperthermia cause only incidental decreases in platelet numbers.
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PMID:Alterations in hemostasis associated with hyperthermia in a canine model. 1091 78

African swine fever (ASF) is an asymptomatic infection of warthogs and bushpigs, which has become an emergent disease of domestic pigs, characterized by hemorrhage, lymphopenia, and disseminated intravascular coagulation. It is caused by a large icosohedral double-stranded DNA virus, African swine fever virus (ASFV), with infection of macrophages well characterized in vitro and in vivo. This study shows that virulent isolates of ASFV also infect primary cultures of porcine aortic endothelial cells and bushpig endothelial cells (BPECs) in vitro. Kinetics of early and late gene expression, viral factory formation, replication, and secretion were similar in endothelial cells and macrophages. However, ASFV-infected endothelial cells died by apoptosis, detected morphologically by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and nuclear condensation and biochemically by poly(ADP-ribose) polymerase (PARP) cleavage at 4 h postinfection (hpi). Immediate-early proinflammatory responses were inhibited, characterized by a lack of E-selectin surface expression and interleukin 6 (IL-6) and IL-8 mRNA synthesis. Moreover, ASFV actively downregulated interferon-induced major histocompatibility complex class I surface expression, a strategy by which viruses evade the immune system. Significantly, Western blot analysis showed that the 65-kDa subunit of the transcription factor NF-kappaB, a central regulator of the early response to viral infection, decreased by 8 hpi and disappeared by 18 hpi. Both disappearance of NF-kappaB p65 and cleavage of PARP were reversed by the caspase inhibitor z-VAD-fmk. Interestingly, surface expression and mRNA transcription of tissue factor, an important initiator of the coagulation cascade, increased 4 h after ASFV infection. These data suggest a central role for vascular endothelial cells in the hemorrhagic pathogenesis of the disease. Since BPECs infected with ASFV also undergo apoptosis, resistance of the natural host must involve complex pathological factors other than viral tropism.
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PMID:African swine fever virus infection of porcine aortic endothelial cells leads to inhibition of inflammatory responses, activation of the thrombotic state, and apoptosis. 1158 5

The case of a healthy and immunocompetent five-year-old boy, who developed a disseminated intravascular coagulation during chickenpox is described. Disseminated intravascular coagulation manifestations were extremely severe and included macroscopic hematuria, necrotic purpura and cerebrovascular thrombosis. The outcome in this patient was a complete recovery. Nevertheless, the possibility of a seriously complicated course of chickenpox even in low-risk children subgroups suggests that the Varicella-Zoster virus infection should not be underestimated. More accurate information about the impact of chickenpox and its complications on the population is needed, in order to provide a contribution for the debate about the costs associated with this disease and the potential benefits of both the early antiviral therapy and the vaccinal prophylaxis.
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PMID:[Disseminated intravascular coagulation in chickenpox. Report of a case in a child]. 1174 Apr 41

Dengue virus infection can cause a wide spectrum of illness. Thrombocytopenia with concurrent haemoconcentration differentiates dengue haemorrhagic fever from classical dengue fever. Only cases with shock or unstable vitals signs need admission in the pediatric intensive care. The management is essentially supportive and symptomatic. The key to success is frequent monitoring and changing strategies. A rise in hematocrit of 20% along with a continuing drop in platelet count is an important indicator for the onset of shock. Patients in grade I and II should be closely monitored for signs of shock. The management of dengue shock syndrome (grade III and IV) is a medical emergency needing prompt and adequate fluid replacement for the rapid and massive plasma losses through increased capillary permeability. Early and effective replacement of plasma losses with plasma expanders or fluid and electrolyte solutions results in a favourable outcome in most cases. The ideal fluid management should include both cystalloids and colloids (including albumin). Cystalloids are given as boluses as rapidly as possible, and as many as 2 to 3 boluses may be needed in profound shock. Colloidal fluids are indicated in patients with massive plasma leakage and in whom a large volume of cystalloids has been given. Frequent recording of vital signs and determinations of haematocrit are important in evaluating the results of treatment. Apart from correction of electrolyte and metabolic disturbances, oxygen is mandatory in all patients of shock. Some patients develop DIC and need supportive therapy with blood products (blood, FFP and platelet transfusions). Polyserositis, in the form of pleural effusion and ascitis, are common in cases of dengue shock syndrome, and if possible, drainage should be avoided as it can lead to severe hemorrhages and sudden circulatory collapse. The prognosis depends mainly on the early recognition and treatment of shock.
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PMID:Management of dengue fever in ICU. 1177 Feb 41

A 42-year-old woman was diagnosed as systemic lupus erythematosus (SLE), because of the findings of polyarthritis, leukopenia, positive antinuclear antibody, and positive anti DNA antibody. She was treated with predonisolone (PSL) at 10 mg per day. She was admitted to our hospital on October 2000 because of spiking high fever, skin eruption, and lymph node swelling. Since her illness of SLE was considered to be worsening, high dose of corticosteroids were given. However, high fever persisted and liver dysfunction was developed with increased serum ferritin. Her bone marrow smear showed hemophagocytosis. We made a diagnosis of hemophagocytic syndrome (HPS) complicated by disseminated intravascular coagulation (DIC). HPS was thought to be induced by viral infection, even though causative viral infection was not detected. Her general condition worsened with persistent high fever and liver dysfunction. Plasma exchange was carried for two consecutive days, followed by cyclosporine A and lipo-dexamethasone, which improved her fever rapidly. Her general condition gradually improved. Serum levels of ferritin, soluble interleukin 2 receptor (sIL 2-R), interferon-gamma and interleukin 6 decreased associated with improvements of her clinical condition. We thought plasma exchange could be effective to decrease serum levels of cytokine, which was suggested to be the pathogenic to HPS. However serum levels of IFN-gamma and IL 6 after plasma exchange did not change in this case. Further studies are required to confirm the effects of plasma exchange for HPS.
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PMID:[Case report of systemic lupus erythematosus patient with hemophagocytic syndrome, treated with plasma exchange, with specific reference to clinical profile and serum cytokine levels]. 1183 Oct 15

Xenotransplantation of porcine organs carries the risk of reactivation of latent virus in donor and recipient tissues as well as transmission of viruses between species. We have investigated the activation of baboon cytomegalovirus (BCMV) and porcine CMV (PCMV) in a pig-to-primate model of xenotransplantation. Tissues originating from a series of six swine-to-baboon composite thymokidney xenotransplants were investigated. Four immunosuppressed baboons died (survival range, 7 to 27 days) with the graft in situ. Increases in BCMV DNA copy numbers occurred in three (75%) of these baboons and was thought to be responsible for pneumonitis and the death of one animal. In two baboons, disseminated intravascular coagulation was successfully treated by graftectomy and discontinuation of immunosuppression. PCMV was upregulated in five of six xenografts (83%). PCMV infection was associated with ureteric necrosis in one xenograft. Although significantly increased in native tissues, low levels of BCMV and PCMV were also detected in tissues other than that of the native viral host species. The cross-species presence of CMV did not appear to cause clinical or histological signs of invasive disease. Thus, viral infections with clinical disease were restricted to tissues of the native species of each virus. Intensive immune suppression currently required for xenotransplantation results in a significant risk of reactivation of latent infections by BCMV and PCMV. It is not yet known whether viral DNA detected across species lines represents cellular microchimerism, ongoing viral infection, or uptake of free virus. The observation of graft injury by PCMV demonstrates that CMV will be an important pathogen in immunosuppressed xenograft recipients. Strategies must be developed to exclude CMV from porcine organ donors.
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PMID:Activation of cytomegalovirus in pig-to-primate organ xenotransplantation. 1196 90

Purpura fulminans is a rare but dramatic disease which occurs most commonly during or after an infection. It is characterized by extensive involvement of the skin and extremities and involvement of visceral organs. Purpura fulminans, when occurring after a viral infection such as varicella, is usually characterized by purpuric lesions involving the trunk, usually with sparing of the visceral organs. In this report we describe a child with purpura fulminans due to a transient protein C deficiency as a complication of chickenpox infection. A seven-year-old girl developed bruise-like lesions on her extremities on the fifth day after eruption of varicella exanthem. She had no previous history of bleeding tendency or thrombosis. Family history was also negative. On the seventh day of her illness she was admitted to Marmara University Hospital with widespread echymotic an partially crusted chickenpox lesions. CBC, urinalysis and blood chemistries were within normal limits. She had a prolonged aPT and apt with low serum fibrinogen and high D-dimers suggestive disseminated intravascular coagulation (DIC). Protein C activity was low. Punch skin biopsy was consistent with purpura fulminans. She was treated with heparin and fresh frozen plasma which helped her to recover clinically as well as hematologically. She was discharged with still low protein C activity that returned to normal by the next follow-up visit.
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PMID:A case of purpura fulminans secondary to transient protein C deficiency as a complication of chickenpox infection. 1271 82

Renal involvement in influenza A virus infection has been rarely reported. To define the clinical characteristics and the factors contributing to the development of renal involvement in influenza A virus infection, we reviewed the clinical characteristics, laboratory data, pediatric risk of mortality (PRISM) score, and the number of systemic inflammatory response syndrome (SIRS) criteria and dysfunctional organs in 45 hospitalized children with influenza A virus infection. Eleven (24.4%) patients had renal involvement. All patients with renal involvement suffered from sepsis and multiple organ dysfunction syndrome (MODS) and 5 developed acute renal failure (ARF). The incidences of dehydration, hypotension, disseminated intravascular coagulation (DIC), and rhabdomyolysis were significantly higher in patients with renal involvement. PRISM scores, the numbers of SIRS criteria and dysfunctional organs, and mortality rate were also higher in patients with renal involvement. Influenza A RNA was absent in the renal tissues of 3 patients with ARF. These results suggested that renal involvement in influenza A virus infection occurred in patients with sepsis and MODS; dehydration, hypotension, DIC, and rhabdomyolysis were factors contributing to its development; direct viral injury to the kidney did not seem to occur in influenza A virus infection.
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PMID:Renal involvement in children with influenza A virus infection. 1269 31


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