Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course of necrotizing fasciitis in 8 patients is compared with observations on 22 other patients with erysipelas. In necrotizing fasciitis the early erythematous areas turn into a dusky blue colour with later vesiculation and formation of bullae. An important finding is a non-pitting oedema extending outside the erythematous patches. The disease often progresses and involves further skin areas proximal to the initial ones. Gangrene tends to follow in multiple sites after the 1st week of illness. Group A streptococci in conjunction with widespread thrombosis and vascular necrosis of the involved skin are two major factors in the pathogenesis of the gangrene. Early debridement and excision of necrotic tissue in combination with large doses of penicillin and cloxacillin are confirmed as mandatory to remove toxaemia and inhibit further necrosis of the skin. In 3 of the 8 patients with necrotizing fasciitis the syndrome of disseminated intravascular coagulation complicated the course of the disease. A promising therapeutic result was seen in 2 further patients exhibiting alarming signs and symptoms of early necrotizing fasciitis; the combination of heparin, given intravenously in therapeutic doses guided by activated partial thromboplastin time studies, and of systemic antibiotics alleviated the symptoms, which vanished within 10 days of the start of treatment.
Br J Dermatol 1977 Apr
PMID:Erysipelas and necrotizing fasciitis. 32 13

The lupus anticoagulant is an antiphospholipid antibody found in association with systemic lupus erythematosus and in a variety of other diseases, as well as in healthy individuals. In the laboratory, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis, mainly of the larger veins and arteries. The case of a young woman who developed superficial migratory thrombophlebitis in association with a high titer lupus anticoagulant is presented. Her diagnosis was initially missed because the partial thromboplastin time was not elevated. This appears to have resulted from the use of a specific thromboplastin relatively insensitive to the presence of the antibody. Retesting with a more sensitive reagent showed a markedly prolonged partial thromboplastin time.
Int J Dermatol 1990 Apr
PMID:Superficial migratory thrombophlebitis and the lupus anticoagulant. 211 May 53

The term antiphospholipid syndrome is used to characterize a complex of clinical and pathologic findings mediated by a group of antibodies formed against a family of antiphospholipids. These antiphospholipid antibodies were originally found in patients with lupus erythematosus in whom the partial thromboplastin time was prolonged and in patients with other autoimmune diseases; subsequently, they have been observed in association with a variety of other conditions, including infections, reactions to drugs, malignant neoplasms, human immunodeficiency virus disease, and as an isolated finding. In recent years, there has been some clarification of the significance of the various tests for antiphospholipid antibodies, including the lupus anticoagulant test and the anticardiolipin antibody tests, in predicting the antiphospholipid syndrome. The mechanism of disease, however, has not been well defined. The most common cutaneous lesion seen in seven patients with lupus anticoagulant and anticardiolipin antibody who have the antiphospholipid syndrome was ulceration due to thrombosis of dermal veins and arteries. Often there is a reactive vascular proliferation around the thrombosed vessels. The presence of primary thrombosis of both veins and arteries in thrombotic disorders is unusual and may provide insight into the mechanism of thrombosis in antiphospholipid syndrome.
Arch Dermatol 1990 Sep
PMID:Cutaneous histopathologic findings in 'antiphospholipid syndrome'. Correlation with disease, including human immunodeficiency virus disease. 211 49

A lupuslike disease with cutaneous manifestations secondary to the use of chlorpromazine (Thorazine) is presented. Skin biopsy specimens demonstrated classic findings consistent with lupus erythematosus and abundant mucin deposition in the cutaneous lesions--a finding not previously reported to occur in drug-induced lupuslike disease. Laboratory and serologic examinations included a positive antinuclear antibody titer, presence of single-stranded deoxyribonucleic acid (DNA), absence of double-stranded DNA, presence of antihistone antibodies, normal complement level, increased IgM level, and prolongation of partial thromboplastin time. These data confirmed our clinical and histologic diagnosis. Cessation of the medication (chlorpromazine) led to resolution of the skin abnormalities. Electron microscopy revealed electron-dense drug metabolites in vascular endothelial cells, as well as tubuloreticular inclusion bodies. This is only the second reported case of chlorpromazine-induced lupuslike disease with cutaneous manifestations.
J Am Acad Dermatol 1985 Jul
PMID:Chlorpromazine-induced lupuslike disease. Case report and review of the literature. 299 78

A disturbance in endothelial cell (EC) function may be pathogenetic in the thrombotic tendency of patients with the lupus anticoagulant (LA). The ability of serum from normal subjects and patients with systemic lupus erythematosus (SLE), with and without the LA, to modulate the release of prostacyclin (PGI2) and the expression of procoagulant activity by cultured human EC was investigated. Only the 10% and 20% serum concentrations from patients with SLE-LA produced a significantly greater inhibition of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) release (the stable metabolite of PGI2) than control serum. However, when patients with SLE-LA having Raynaud's phenomenon were excluded from this group, there was then no significant difference between the effect of the patient and control serum. Serum from patients with SLE +/- LA caused a significant increase in EC procoagulant activity compared to healthy controls. The two-stage partial thromboplastin time expressed in seconds decreased from 66 (normal) to 34 (SLE - LA) and 31 (SLE + LA), but there was no significant difference between the patients with and without the LA. The significantly increased EC procoagulant activity induced by serum from patients with SLE +/- LA may account for the observed increased incidence of thrombotic events in patients with SLE. Our data suggest that factors other than decreased prostacyclin release are responsible for the altered hemostasis observed in patients with SLE + LA.
J Invest Dermatol 1988 May
PMID:Effects of the lupus anticoagulant in patients with systemic lupus erythematosus on endothelial cell prostacyclin release and procoagulant activity. 312 19

An 18-year-old white woman admitted for an incomplete septic abortion was found to have thrombocytopenia, anemia, and increased activated partial thromboplastin time (PTT). Additionally, results of nontreponemal serologic tests for syphilis were positive, and the fluorescent antinuclear antibody was weakly positive. A mixture of the patient's plasma with normal control plasma showed that the elevation in activated PTT was the result of a circulating anticoagulant, not an inherent clotting defect. Sclerodermoid features were present and consisted of bound-down, hairless skin and scattered subcutaneous indurated plaques. A faint pattern consistent with livedo reticularis was recognized on all extremities. Biopsy specimens of sclerodermoid lesions showed increased and thickened dermal collagen consistent with morphea. We believe that this patient's condition represents an unusual connective tissue disease syndrome consisting of abortion, livedo reticularis, thrombocytopenia, circulating "anticoagulant," negative or slightly positive antinuclear antibodies, and false positive results on nontreponemal serologic tests for syphilis. Sclerodermoid lesions were also a unique feature in our patient.
J Am Acad Dermatol 1988 Nov
PMID:Connective tissue disease associated with sclerodermoid features, early abortion, and circulating anticoagulant. 314 41

Bismuth subgallate is an effective agent in preventing hemorrhage after adenotonsillectomy. The experiments described demonstrate that this may occur through the activation of Hageman factor by this agent. Bismuth subgallate shortened the clotting time of whole blood, an action localized to an effect on the early steps of the intrinsic pathway; bismuth subgallate did not accelerate the thrombin time or prothrombin time of normal plasma, but could be substituted for kaolin as an activator of coagulation in assays of the partial thromboplastin time. The action of bismuth subgallate was localized to an effect on Hageman factor. It did not induce coagulation of plasma samples deficient in any of the recognized factors participating in the intrinsic pathway of thrombin formation, but it shortened the clotting time of plasma deficient in factor VII, a component of the extrinsic pathway. Evidence was obtained that Hageman factor exposed to bismuth subgallate corrected the defect of Hageman factor-deficient plasma and acquired amidolytic properties in the absence of other clotting factors. These studies provide a rationale for the hemostatic properties of bismuth subgallate.
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PMID:Activation of Hageman factor (factor XII) by bismuth subgallate, a hemostatic agent. 317 56

Scurvy occurred in an elderly man with fatigue, dyspnea on exertion, and extensive ecchymoses and brawny edema of the legs. Platelet count, prothrombin time, and partial thromboplastin time were normal, but serum ascorbic acid level was very low. Other signs considered to be classic and almost pathognomonic for were absent: bleeding gums, hyperkeratotic follicles, coiled hairs, and perifollicular hemorrhages. Reliance on these well-known features of scurvy may obscure or delay diagnosis of an easily cured disorder Severe scurvy is most commonly suggested by tenderness, extensive ecchymoses, and brawny edema of the lower extremities.
Int J Dermatol 1982 May
PMID:Bachelor scurvy. 709 49

Amyloid precursor protein forms that contain Kunitz protease inhibitor domains are released from activated platelets, T-lymphocytes, and leukocytes and inhibit trypsin, plasmin, and activated factor XI. We investigated the effects of amyloid precursor protein isoforms on activated Hageman factor (factor XII), activated factor X (Stuart factor), and thrombin. Recombinant amyloid precursor proteins with or without the Kunitz domain, 770 and 695 amino acids, respectively, were produced in insect cells by Baculovirus expression (BAC770 and BAC695). Neither BAC695 nor BAC770 inhibited human alpha-thrombin or activated factor X. The partial thromboplastin time was prolonged by both amyloid precursor proteins, only one of which, BAC770, contains the Kunitz protease inhibitor domain. Both forms of amyloid precursor proteins inhibited ellagic acid-induced activation of Hageman factor but did not inhibit activated Hageman factor. Bismuth subgallate, which is an insoluble analog of ellagic acid, lost its ability to activate Hageman factor on being exposed to BAC770. Inhibition of ellagic acid-induced activation of Hageman factor by both forms of amyloid precursor protein was enhanced by heparin. These findings suggested that the heparin-binding domain of amyloid precursor proteins is not in the Kunitz domain. This heparin-binding domain may block the activation of Hageman factor by negatively charged agents. Thus, amyloid precursor proteins may be involved in the control of hemostasis, properties not all dependent on the Kunitz domain.
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PMID:Inhibitory action of amyloid precursor protein against human Hageman factor (factor XII). 784 73

Seventy-four patients with PSS were evaluated with regard to plasma concentration of blood coagulation and fibrinolysis factors: fibrinogen (Fbg), prothrombin time (PT), active partial thromboplastin time (APTT), protein C, thrombin-antithrombin III complex (TAT), antithrombin-III (AT-III), factor XIII (XIII) fibrinopeptide A (FPA), alpha 1-antitrypsin (alpha 1-AT), plasminogen (Pmg), alpha 2-plasmin inhibitor plasmin complex (PIC), alpha 2-plasmin inhibitor (alpha 2-PI), alpha 2-macroglobulin (alpha 2-MG), fibrinopeptide B beta 15-42 (FPB beta-15-42) and soluble fibrin monomer complex (SFMC), FDP (fibrin degradation product) and D-dimer. They were also evaluated with regard to platelet-derived proteins: beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 and 6-keto-prostaglandin F1 alpha (6KF). In the coagulation/fibrinolysis systems high plasma levels of TAT, AT-III, FPA, alpha 2-MG and FPB beta 15-42 could be demonstrated in more than 50% of total PSS patients. There was no statistical correlation between those of TAT and AT-III. Plasma levels of PIC, D-dimer, FDP and SFMC were not always high. There was no statistical correlation between those of TAT and PIC. These data lead us to consider that alpha 2-MG may play an important role for inhibiting PIC, which accelerates the conversion from fibrin into FDP. Subsequently, there were high plasma levels of FPB beta 15-42 converted from fibrin monomer. These data seem to be indicative of an involvement of coagulation and platelet disorder in PSS. These platelet-vessel system disorders might be closely related to the pathophysiology of PSS.
J Dermatol Sci 1996 Mar
PMID:Plasma levels of molecular markers of blood coagulation and fibrinolysis in progressive systemic sclerosis (PSS). 878 74


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