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)

A 33-year-old woman presented 42 days after allogeneic bone marrow transplantation for acute monocytic leukemia (AML, FAB M5) with persistent thrombocytopenia, acute renal failure and Coombs negative hemolytic anemia. In the absence of the disseminated intravascular coagulation the diagnosis of hemolytic uremic syndrome due to immunosuppression with cyclosporin A was supposed. Because cessation of cyclosporin A and therapeutic infusions of fresh frozen plasma had failed, plasmaseparation therapy was started on day 79 after bone marrow transplantation. While hemolytic anemia improved during ongoing plasmaseparations the patient developed cholestatic liver failure due to hepatic manifestation of HUS. The histological lesions of liver involvement in thrombotic microangiopathies are discussed and a review of the literature is presented.
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PMID:Hepatic manifestation of hemolytic uremic syndrome in an allogeneic bone marrow transplant recipient. 852 59

The hemolytic uremic syndrome in adults is an uncommon clinical entity consisting of microangiopathic hemolytic anemia, thrombocytopenia, and renal dysfunction. A previously healthy 42-year-old man, after a 2-day prodromal phase, developed severe pain and coldness in both legs, with purpura in the face and extremities. On admission, hepatorenal dysfunction and disseminated intravascular coagulation were evident. These complicated signs and symptoms led to nonspecific supportive therapy because of delayed diagnosis. The patient's condition gradually improved except for ischemia of the legs, which progressed into symmetrical necrosis; eventually, bilateral below-knee amputation was required. This is the first reported case of the hemolytic uremic syndrome complicated by bilateral leg ischemia. A presumed cause of the ischemia was disseminated intravascular coagulation, a rare complication of the hemolytic uremic syndrome.
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PMID:The hemolytic uremic syndrome presenting as bilateral leg ischemia. 921 26

We report 81 of 107 cases of hemolytic uremic syndrome (HUS), admitted between July 1994 and February 1996, following an outbreak of Shigella dysenteriae type 1 dysentery in Kwazulu/Natal. All patients, excluding 1, were black with a mean age of 38 months (range 1-121); 50 (61.7%) were males. The mean duration of dysentery was 11.3 days (range 1-41) and HUS 15 days (range 1-91). Most patients had acute oliguric renal failure (90.1%), 42 (51.6%) required peritoneal dialysis. Complications included encephalopathy 30 (37.0%), convulsions 12 (14.8%) and hemiplegia 2 (2.3%), gastrointestinal perforation 8 (9.9%), protein losing enteropathy 26 (32.1%), toxic megacolon 4 (4.9%), rectal prolapse 5 (6.2%), hepatitis 11 (13.6%), myocarditis 5 (6.2%), congestive cardiac failure 3 (3.7%), cardiomyopathy 3 (3.7%), infective endocarditis 1 (1.2%), septicemia 15 (18.5%), disseminated intravascular coagulation 17 (21%). Leukemoid reactions were found in 74 (91.3%) patients, hyponatremia in 56 (69.1%), and hypoalbuminemia in 67 (82.7%). Stool culture for Shigella dysenteriae type I was positive in only 7 (8.6%) patients; Shiga toxin assays were not performed. Outcome was as follows: recovery 32 (39.5%), impaired renal function 8 (9.9%), chronic renal failure 26 (32.1%), end-stage renal disease 1 (1.2%), and death 14 (17.3%) patients.
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PMID:Post-dysenteric hemolytic uremic syndrome in children during an epidemic of Shigella dysentery in Kwazulu/Natal. 932 80

The serum levels of thrombopoietin (TPO) were measured in 16 patients with thrombotic thrombocytopenic purpura (TTP), 12 with hemolytic uremic syndrome (HUS), 10 with aplastic anemia (AA), 10 with disseminated intravascular coagulation (DIC), and 71 with idiopathic thrombocytopenic purpura (ITP). The serum TPO levels were measured with a sensitive sandwich enzyme-linked immunosorbent assay. The serum TPO level in the ITP group (1.68 +/- 0.85 fmol/ml) were not significantly increased compared with those of the normal subjects. The TPO levels in the TTP (2.77 +/- 1.38 fmol/ml) and HUS groups (5.77 +/- 4.41 fmol/ml) were higher than those of the normal subjects. The patients with AA (12.7 +/- 8.0 fmol/ml) and those with DIC (13.3 +/- 5.7 mol/ml) had significantly higher serum TPO levels than did the normal subjects and ITP patients. The TPO levels were well correlated with the platelet counts in the TTP patients, and were negatively correlated with the platelet counts in the ITP patients. These results suggest that the serum TPO levels in some thrombocytopenic diseases are regulated not only by the platelet count and the megakaryocyte mass, but also by other factors.
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PMID:Increased serum levels of thrombopoietin in patients with thrombotic thrombocytopenic purpura, idiopathic thrombocytopenic purpura, or disseminated intravascular coagulation. 935 24

Cisplatin is a known cause of hemolytic uremic syndrome (HUS). The acute, fulminant form of cisplatin-induced HUS is almost always fatal. We present a 67-year-old Hispanic woman who was treated with cisplatin for squamous cell carcinoma of the tongue. Three days after receiving the treatment, she presented with increasing fatigue, decreased urine output, and confusion. Physical examination was remarkable for tachycardia of 130 beats/min, peripheral edema, and mental obtundation. Laboratory investigations showed a white cell count of 5,500/microL, hemoglobin level of 9.6 g/dL, hematocrit of 29.6%, and platelet count of 13,000/microL. Schistocytes were present on peripheral smear. Screening for disseminated intravascular coagulation was negative. Serum chemistry values included blood urea nitrogen 111 mg/dL, creatinine 3.8 mg/dL, and lactate dehydrogenase (LDH) 927 IU. The patient underwent hemodialysis and therapeutic plasma exchange (TPE), using fresh frozen plasma (FFP). Dialysis was no longer required after the fifth day. TPE was performed daily until the platelet count normalized on the 13th day, after which intertreatment intervals were extended until normalization of LDH levels on the 50th day. We conclude that the normally fatal, fulminant form of cisplatin-induced HUS can be successfully treated with standard TPE, using FFP replacement.
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PMID:Successful treatment of cisplatin-induced hemolytic uremic syndrome with therapeutic plasma exchange. 970 19

The precise etiology of hemolytic uremic syndrome (HUS) is unknown. However, it has been associated with bacterial (Shigella, Salmonella, E. coli, S. pneumoniae), Bartonella, and viral (coxsackie, ECHO, influenza, varicella. Epstein-Barr) infections and with endotoxemia. Recently, we experienced a case of HUS in a 16-year-old boy who was in the acute phase of an Epstein-Barr virus (EBV) infection. He had typical manifestations of HUS and EBV infection. He also transiently presented disseminated intravascular coagulation. His renal dysfunction recovered by supportive care, including hemodialysis, plasmapheresis, antihypertensive medication and aspirin. We present this case with a review of the literature as the second report of HUS associated with EBV infection.
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PMID:A case of hemolytic uremic syndrome associated with Epstein-Barr virus infection. 973 70

Fas, a member of the tumor necrosis receptor superfamily, is 36 kD surface protein containing a single transmembrane region and induces apoptosis by Fas-Fas ligand binding. Soluble Fas (sFas) is produced as the form lacking 21 amino acid residues containing the transmembrane domain by alternative splicing. We found that the plasma sFas levels of 33 patients with thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS), 19 patients with disseminated intravascular coagulation (DIC), and 10 non-DIC patients with multiple organ failure (MOF) were significantly higher than those of 21 non-DIC patients without organ failure and those of 25 healthy volunteers. The plasma sFas ligand levels of the TTP/HUS patients, the DIC patients, and the non-DIC patients with MOF were significantly higher than those of the non-DIC patients without organ failure and those of the healthy volunteers. The plasma sFas levels were significantly correlated with the plasma sFas ligand levels in all subjects. The plasma thrombomodulin (TM) levels were increased significantly in the TTP/HUS patients, the DIC patients, and the non-DIC patients with MOF compared with the levels of the non-DIC patients without organ failure and the healthy volunteers. The plasma sFas antigen levels were correlated significantly with the plasma TM levels in all subjects. These findings suggest that the increases of sFas and sFas ligand that cause apoptosis might be related to the vascular endothelial cell injuries in TTP and DIC with organ failure.
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PMID:Plasma sFas and sFas ligand levels in patients with thrombotic thrombocytopenic purpura and in those with disseminated intravascular coagulation. 1033 7

The complication of thrombotic thrombocytopenic purpura or hemolytic uremic syndrome (TTP/HUS) can occur in cancer patients. It is characterized by a microangiopathic hemolytic anemia, severe thrombocytopenia, and renal failure. Pulmonary manifestations, especially pulmonary edema, are a common observation. Neurologic changes are also frequently seen. The etiology is unknown at this time. It has been observed in many different types of cancer and is most commonly seen in gastric adenocarcinoma followed by carcinoma of the breast, colon, and small cell lung carcinoma. The hemolysis can be massive and is due to red cell fragmentation, as schistocytes are present in all the cases. Though immune complexes are present in the plasma, the antiglobulin (Coomb's) test is negative. Chemotherapeutic agents, especially mitomycin C, have been implicated as causative factors. There is a correlation of this complication with the cumulative dose. However, chemotherapy cannot account for all the cases as the syndrome can occur in untreated patients. It can be differentiated from disseminated intravascular coagulation by the absence of a coagulopathy. Management should consist of plasma exchange, use of a Staphylococcus aureus column (Prosorba), and control of hypertension. Because of the susceptibility to pulmonary edema, blood volume overloading should be avoided.
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PMID:Thrombotic microangiopathy manifesting as thrombotic thrombocytopenic purpura/hemolytic uremic syndrome in the cancer patient. 1035 89

Maternal death during pregnancy, although uncommon, may result from a broad range of conditions. In this paper, a case of thrombotic thrombocytopenic purpura diagnosed by postmortem examination is presented. Thrombotic thrombocytopenic purpura is one of a subset of diseases that result in the formation of microthrombi within the vasculature, either as a primary or secondary manifestation. Other conditions included in the differential diagnosis during pregnancy are hemolytic uremic syndrome, systemic lupus erythematosus, preeclampsia-eclampsia and the HELLP syndrome, acute fatty liver of pregnancy, antiphospholipid antibody syndrome, and disseminated intravascular coagulation. The histologic manifestations of these diseases can be similar and in most cases do not provide adequate information to accurately differentiate these diseases in the postmortem period. This paper addresses the need for clinical history (i.e., symptomatology, trimester of onset) and antemortem laboratory testing in addition to a thorough autopsy to accurately differentiate among the conditions named previously. In the absence of an adequate clinical history and antemortem laboratory testing, the more general diagnosis of "thrombotic microangiopathy of pregnancy" is acceptable.
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PMID:Death due to thrombotic thrombocytopenic purpura in pregnancy: case report with review of thrombotic microangiopathies of pregnancy. 1041 63

Three patients with hemolytic uremic syndrome (HUS) developed peripheral gangrene. Bilateral carotid artery thromboses occurred in one of these patients after recovery from HUS. One patient had a long history of juvenile rheumatoid arthritis. In the second patient, a flu-like illness preceded the onset of HUS. The third was one of two sisters, with the HUS appearing more than 1 year apart. None had evidence of disseminated intravascular coagulation or infection with Streptococcus pneumoniae. The patient with rheumatoid arthritis had renal cortical necrosis but recovered moderate renal function after treatment with dialysis and plasmapheresis for 6 months. The child with a genetic form of HUS died of renal failure and had massive cortical necrosis and vascular thrombosis at autopsy. This is the first report of peripheral gangrene in children with idiopathic HUS and autosomal recessive HUS.
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PMID:Peripheral gangrene complicating idiopathic and recessive hemolytic uremic syndromes. 1097 12


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