Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we present a case of late-puerperal onset of thrombohemorrhagic complications in a 33-yr-old woman with known antiphospholipid syndrome (APS) and heterozygosity for factor V Leiden gene mutation. Antithrombotic prophylaxis with low-molecular-weight (LMW) heparin was given since the 12th gestational week. Pregnancy and cesarean delivery were uncomplicated. Five weeks postpartum, the patient developed a severe hemorrhagic diathesis with marked thrombocytopenia accompanied by vaginal, nasal and cutaneous bleeding. A variety of autoimmune phenomena were also detected, partly at clinical presentation and partly later on, despite ongoing steroid treatment. Platelet counts recovered to normal values within a few weeks secondary to high-dose steroids and intravenous immunoglobulin administration. An ultrasound of both legs, performed because of persistent complaint of moderate calf pain, revealed bilateral deep venous thromboses (DVT). The clinical and biochemical findings were not consistent with thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT) or the 'hemolysis, elevated liver enzymes and low platelet syndrome' (HELLP). The diagnostic criteria for systemic lupus erythematosus (SLE) were not fulfilled either. The complex of thrombohemorrhagic complications and autoimmune phenomena seen in this case is unusual and not previously described in the late puerperal stage of APS-related pregnancies.
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PMID:Late puerperal thrombohemorrhagic complications in a patient with antiphospholipid syndrome. 1552 67

Three-hundred fifty-one women were referred for thrombosis and hemostasis evaluation after suffering recurrent miscarriages. All patients were referred by a high-risk obstetrician or reproductive medicine specialist after anatomic, hormonal or chromosomal defects had been ruled out. These patients were assessed over a three year period. The mean patient age at referral was 34 years and the mean number of miscarriages was 2.9 (2-9). All patients underwent a thorough evaluation for thrombophilia and, when indicated, a hemorrhagic disorder. Of the 351 patients, 29 (8%) had no defect. Of the remaining 322 patients, 7 (2%) had a bleeding disorder: 3 with platelet dysfunction, 1 with Factor XIII deficiency, 3 with von Willebrand's and 3 with Osler-Weber-Rendu. The remainder of the patients had a thrombophilia as follows: 195 (60%) had antiphospholipid syndrome, 64 (20%) had Sticky Platelet Syndrome, 38 (12%) had MTHFR mutation, 23 (7.1%) had PAI-1 polymorphism, 12 (3.7%) had Protein S deficiency, 12 (3.7%) had Factor V Leiden, 3 (1%), had AT deficiency, 3 (1%) had Heparin-Cofactor II deficiency, 3 (1%) had TPA deficiency, and 6 (2%) had Protein C deficiency. There were a total of 364 defects found in the 312 patients harboring thrombophilia; thus, several harbored two and a few harbored three separate defects. All patients with thrombophilia were treated with preconception ASA at 81 mg/day with the immediate post-conception addition of heparin or LMW heparin (Dalteparin). Both ASA and heparin/LMW heparin were used to term. The first 120 patients were treated with unfractionated heparin at 5,000 U every 24 hours, subcutaneously and the last 192 have been treated with Dalteparin at 5,000 U/day subcutaneously. The patients with MTHFR were also treated with folate at 5 mg/day + pyridoxine at 50 mg/day. All patients were carefully monitored with CBC and platelet counts, anti-Xa levels, frequent ultrasounds and physical exams. Only 2 of the thrombophilia patients suffered another miscarriage; all others had a normal term delivery. There were no pregnancy-related thromboses, no delivery complications and no episodes of post-partum thrombosis. The only bleeding consisted of 1-4 cm bruises at injection sites. No episodes of thrombocytopenia (HIT) were noted. In our experience, thrombophilia is a common cause of recurrent miscarriage and all patients with no anatomical, hormonal or chromosomal defect should be evaluated for thrombophilia or a bleeding disorder. The success rate of normal term delivery in these 312 patients was 94% using ASA + heparin or Dalteparin. In addition, side effects of therapy were minimal.
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PMID:Recurrent miscarriage syndrome and infertility due to blood coagulation protein/platelet defects: a review and update. 1567 68

Thrombocytopenia can be a severe complication of nonsteroidal anti-inflammatory drug treatment. We report a case of a 58 year old patient who developed severe thrombocytopenia during treatment with ketoprofen. Within several days the platelet count decreased to undetectable values in routine blood count. In parallel, symptoms of severe hemorrhagic diathesis occurred. Immunoenzymatic tests and result of bone marrow trepanobiopsy ruled out underlying cancer and idiopathic thrombocytopenic purpura (antiplatelet antibodies were not detected). After discontinuation of ketoprofen and treatment with corticosteroids, the patient's platelet count returned to normal and remained stable at 6 months of follow-up.
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PMID:[Thrombocytopenia as a complication of nonsteroidal anti-inflammatory drug treatment]. 1678 95

X-linked adrenoleukodystrophy (X-ALD) is an inherited disorder of peroxisomal beta-oxidation, which results in accumulation of very long-chain fatty acids, causing damage to the nervous system, adrenal cortex and testis. The two most frequent phenotypes are childhood cerebral adrenoleukodystrophy (CCALD) and adrenomyeloneuropathy (AMN). Some affected males demonstrate no clinical signs (asymptomatic ALD), whereas female carriers can also be affected. Patients with X-ALD have been treated with Lorenzo's oil, a 4:1 combination of oleic acid and erucic acid, with thrombocytopenia as the main side effect and sometimes leading to a hemorrhagic diathesis. We studied platelet count, size and membrane surface exposure of platelet activation antigens in 17 adult X-ALD patients. Eight patients used the prescribed amount of erucic acid (as glyceroltrierucate) or more (very compliant), five used less(compliant), and four did not use the diet. All eight very compliant patients had highly enlarged platelets and seven manifested thrombocytopenia. An enhanced in vivo platelet activation status was established by increased platelet surface expression of P-selectin (CD62P, PADGEM, GMP-140) in five of the seven thrombocytopenic patients, and of increased fibrinogen receptor exposure (measured with the antibody PAC-1) in three of these five patients. The other nine compliant or untreated patients had normal platelet counts and, generally, normal P-selection and fibrinogen receptor expression. A diet-induced 7- to 27-fold enrichment of erucic acid was observed in the platelets of the four patients studied. We conclude that the thrombocytopenia in AMN patients using Lorenzo'soil is associated with circulating platelets that have an increased erucic acid content, size and activation status. We hypothesize that the erucic acid in some way induces the increased size and thus, directly or indirectly, increased platelet activation or instability in vivo. This then causes the thrombocytopenia, with circulating platelets representing a population that has not yet been sufficiently changed to be removed, but has clear signs of activation.
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PMID:Lorenzo's oil and platelet activation in adrenomyeloneuropathy and asymptomatic X-linked adrenoleukodystrophy. 1679 44

The purpose of this study was to describe the clinical characteristics of cats with disseminated intravascular coagulation (DIC), including associated diseases and hemostatic abnormalities, and to identify risk factors for death and treatments that potentially altered outcome. Medical records for cats with DIC from 1990-2004 were evaluated retrospectively. Inclusion criteria were the presence of an underlying disorder associated with DIC and either postmortem examination findings of intravascular fibrin deposition or thrombosis, or both of 2 or more organs or coagulation profiles that meet 3 of 5 criteria: prolonged prothrombin time (PT), activated partial thromboplastin time (aPTT), presence of fibrin degradation products (FDP), low plasma fibrinogen (FIB) concentration, and thrombocytopenia (<160,000 platelets/microL). Signalment, historical data, clinical findings, clinicopathologic data, underlying disorders, management, and outcome were recorded. Forty-six cats fulfilled the criteria for DIC. Cats ranged in age from 7 weeks to 17 years (median, 9 years). Hemorrhage was noted in 7 of 46 cats (15%). Three of 46 cats (7%) survived, whereas 43 of 46 (93%) died or were euthanized. The most common underlying disorders were lymphoma, other forms of neoplasia, pancreatitis, and sepsis. There was no association detected between outcome and signalment; underlying disease; hemorrhage; abnormalities in aPTT, FIB, FDPs, platelet count; transfusion of blood products; and heparin therapy. However, the median PT of nonsurvivors was more prolonged than in survivors (P < .005). DIC in cats can result from a variety of neoplastic, infectious, and inflammatory disorders, and is associated with a high case fatality rate.
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PMID:Disseminated intravascular coagulation in cats. 1718 39

Crimean-Congo hemorrhagic fever is a tick-borne viral disease reported from more than 30 countries in Africa, Asia, South-East Europe, and the Middle East. The majority of human cases are workers in livestock industry, agriculture, slaughterhouses, and veterinary practice. Nosocomial transmission is also well described. Clinical manifestations are nonspecific and symptoms typically include high fever, headache, malaise, arthralgia, myalgia, nausea, abdominal pain, and nonbloody diarrhea. Patients may show signs of progressive hemorrhagic diathesis. Laboratory abnormalities may include anemia, leukopenia, thrombocytopenia, increased AST/ALT levels, and prolonged prothrombin, bleeding, and activated partial thromboplastin times. Diagnostic methods include antibody detection by enzyme-linked immunosorbent assay, virus isolation, antigen detection, and polymerase chain reaction. The mainstay of treatment of Crimean-Congo hemorrhagic fever is supportive, with careful maintenance of fluid and electrolyte balance, circulatory volume, and blood pressure. The Crimean-Congo hemorrhagic fever virus is susceptible to ribavirin in vitro. There is no controlled study evaluating oral versus intravenous ribavirin in treating Crimean-Congo hemorrhagic fever patients, but few studies have evaluated oral ribavirin. This article reviews the epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, prevention, and prognosis of Crimean-Congo hemorrhagic fever with a special focus on oral ribavirin as a choice of medical treatment.
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PMID:Crimean-Congo hemorrhagic fever. 1736 25

During routine antimalarial drug efficacy trials, we observed, for the first time, severe thrombocytopenia developing in Aotus monkeys infected with Plasmodium vivax. Data obtained from 26 Aotus infected with the AMRU-1 strain showed that 77% developed severe thrombocytopenia, whereas only 15% had severe anemia, with hemorrhagic diathesis ensuing in 31%. In general, thrombocytopenic monkeys either failed primary treatment with experimental antimalarial drugs or were found to have higher-density parasitemias, longer patency duration, and lower hematocrits. In these monkeys, severe thrombocytopenia inversely correlated to parasitemia (R = -1.0), and animals that received a blood transfusion had significantly higher platelet counts (P < 0.05) by day 38 after inoculation. In conclusion, the AMRU-1 strain of P. vivax, was considered to be highly pathogenic to Aotus monkeys, and thrombocytopenia rather than anemia should be regarded an early indicator of drug treatment failure with this strain.
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PMID:Clinico-pathological observations on the pathogenesis of severe thrombocytopenia and anemia induced by Plasmodium vivax infections during antimalarial drug efficacy trials in Aotus monkeys. 1762 Jun 23

A hemorrhagic diathesis due to neonatal alloimmune thrombocytopenia occurred in a sow herd consisting of F I large white X Landrace females. Colostrum, containing maternal antibodies incompatible with platelet antigens inherited from the sire, was ingested and absorbed by the piglets. Six piglets were affected and displayed signs of lethargy and depression with petechiation, ecchymosis, and severe bruising of the skin. All 6 piglets died or were euthanized by 3 days of age.
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PMID:Neonatal alloimmune thrombocytopenia, purpura, and anemia in 6 neonatal piglets. 1782 32

Idiopathic thrombocytopenic purpura (ITP) of Childhood is a common hemorrhagic diathesis. The purpose of the present work is to summarize the results of 20-year observation over children suffering ITP, to record certain progress in diagnosing and treatment of this disease and to raise the problems still to be solved. The authors have been observing 181 ITP patients (girls 89, boys 92) at the age of 3 months up to 15 years. Childhood ITP mostly occurs at the age of 1 to 6 year i.e. in the so called "critical period" of immune system forming. Several peculiar cases were identified among infants and the children above 10 years old. Clinical manifestation of all the ITP patients was characterized with cutaneous hemorrhagic syndrome. 95% of childhood cases showed deep thrombocytopenia with the thrombocyte level <30X10 9/l. Most of the patients suffered acute form of ITP (87,9%). In the majority of cases illness took its normal predictable course after the glucocorticosteroid therapy. In heavy cases the combination of glucocorticosteroid and intravenous immunoglobulin is recommended. The indications of splenectomy were considered to be heavy, life -threatening, excessive bleeding, mainly in cases of chronic, steadily recurrent forms of ITP. Remissions were achieved in most of cases.
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PMID:[Childhood idiopathic thrombocytopenic purpura (the results of 20-year experience)]. 1980 32

During the 12 months ending May, 1937, 72 rats were observed that manifested typical symptoms of panmyelophthisis. The disease may start as agranulocytosis, thrombocytopenia or pure red cell anemia, leading progressively, often rapidly, to aleukia hemorrhagica with its typical manifestations (epistaxis, melena, hematuria, purpura). Blood examinations revealed correspondingly low white cell, red cell and platelet counts with very pronounced granulocytopenia (0 to 4 per cent). Bone marrow smears and histological findings were consistent with the diagnosis of panmyelophthisis. Suprarenal hemorrhage was a frequent postmortem finding. The pathogenesis of this experimental panmyelophthisis and this hemorrhagic diathesis is confined to special nutritional conditions. These diseases have been observed by us in rats kept on a diet deficient in vitamin B(6), containing cane sugar and supplemented with vitamin B(1) and crystalline natural or synthetic lactoflavin. Lack of vitamin B(6), however, is not a necessary condition, since the disease was encountered in the majority of the animals after the specific deficiency disease which became apparent in rats kept on the B(6) free diet was successfully treated with purified B(6) preparations. Even in the untreated animals kept on the B(6) deficient diet acrodynia was, as a rule, in distinct remission before symptoms of panmyelophthisis and hemorrhagic diathesis became manifest. By means of the addition of Peters' eluate to the basal diet, panmyelophthisis could be prevented and, in animals where it was recognized in an early stage, cured. In view of these facts it is suggested that Peters' eluate contains a specific maturation factor for the primary blood-producing tissue, the reticulo-endothelium, a factor which, being different from lactoflavin, vitamin B(6) and probably also from the so called filtrate factor, constitutes another distinct component of the vitamin B(2) group. Bacteriological studies brought forward no conclusive positive evidence for the infectious etiology of the experimental panmyelophthisis in our rats. The possible relation of this new disease in rats to aleukia hemorrhagica and its partial manifestations in man, as well as to the so called Waterhouse-Friderichsen syndrome, is discussed. Administration of amidopyrine, at least under the conditions chosen, failed to provoke panmyelophthisis in rats kept on the same diet as that given to rats in which the disease spontaneously developed.
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PMID:PANMYELOPHTHISIS WITH HEMORRHAGIC MANIFESTATIONS IN RATS ON A NUTRITIONAL BASIS. 1987 Jun 85


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