fibrin and Purpura

Topics: Administration, Topical; Adolescent; Adult; Aged; Anabolic Agents; Animals; Child; Child, Preschool; Chronic Disease; Endothelium; Ethylestrenol; Female; Fibrin; Fibrinolysin; Fibrinolysis; Follow-Up Studies; Histocytochemistry; Humans; Inflammation; Leg Ulcer; Male; Middle Aged; Phenformin; Purpura; Rats; Skin Diseases; Thrombophlebitis; Vascular Diseases; Wound Healing

Topics: Acute Disease; Adolescent; Adult; Child; Child, Preschool; Chronic Disease; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Immune Complex Diseases; Immunoglobulin A; Immunoglobulin G; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Middle Aged; Nephritis; Nephrosis; Nephrotic Syndrome; Purpura; Streptococcal Infections

The experimental and clinical observations analyzed in this review suggest that the deposition of fibrin within glomeruli is an important pathogenic mechanism in the series of events leading to progressive destruction of glomerular capillaries. Neither the causal factors nor the consequences of this type of reaction are peculiar to the glomerulus. Fibrin deposits can occur in any injured blood vessel and, if not rapidly dealt with by fibrinolysis, will lead to endothelial changes and the development of organizing thrombi. It seems that glomerular capillaries are especially vulnerable; there are several reasons for this. First, some immunologic reactions are triggered within the glomeruli and thus produce a local inflammatory response, leading to fibrin deposition. Secondly, the glomerular filtration function allows a progressive local accumulation of potentially damaging particles, such as circulating fibrinogen derivatives (formed during generalized intravascular clotting), or phlogistic immune complexes (as a result of systemic antigen-antibody interaction); these too cause local injury and fibrin deposition. Finally, the glomerular obliteration resulting from the organization of such fibrin deposits leads to irreversible damage and so has more serious implications for the patient than if the lesions occurred elsewhere, where the formation of functionally useful new capillaries is often possible. It seems reasonable to propose, therefore, that the use of anticoagulant may be natural therapy in cases with the risk of rapid, massive, and continuous fibrin accumulation in glomeruli, where glomerular sclerosis and irreversible renal failure are likely.

Topics: Anticoagulants; Antigen-Antibody Complex; Antigen-Antibody Reactions; Basement Membrane; Blood Coagulation; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Endocarditis, Bacterial; Fibrin; Glomerulonephritis; Humans; Hyalin; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Phagocytosis; Purpura

In two young patients with an elevated temperature, a girl aged 6 months and a boy aged 10 months, purpura and oedema were noticed on the face, ears, arms and legs. On one occasion the boy lost blood anally. A histopathological examination revealed leucocytoclastic vasculitis with fibrin deposits. The diagnosis was 'acute haemorrhagic oedema of infancy' (AHOI), a relatively unknown variant of palpable purpura due to leucocytoclastic vasculitis affecting infants and young children (up to two years of age). AHOI is characterised clinically by marked oedema and fever as well as large palpable purpuric and ecchymotic skin lesions in a target-like pattern mainly on the face, ears and extremities. The skin lesions heal spontaneously within one to three weeks and internal organs are rarely affected. This is in contrast to Henoch-Schönlein purpura, which was observed in a 5-year old boy suffering from similar skin lesions on the legs as well as painful joints, in whom IgA deposits were found in the vasculitis. Henoch-Schönlein purpura is clinically characterised by palpable purpura on the extensor surfaces of the legs and on the buttocks, whereas in AHOI larger purpura and ecchymoses are found on the face, ankles and wrists, with far more extensive oedema. There are also histological differences: in AHOI there is more extensive vasculitis with fibrin deposits and IgA deposits are seen in a minority of cases. Awareness of this relatively unknown form of leucocytoclastic vasculitis will assist in making an early diagnosis possible, thereby avoiding unnecessary treatment and concern.

Topics: Acute Disease; Child, Preschool; Diagnosis, Differential; Ecchymosis; Edema; Female; Fever; Fibrin; Humans; IgA Vasculitis; Immunoglobulin A; Infant; Male; Purpura; Skin; Syndrome; Vasculitis, Leukocytoclastic, Cutaneous

Livedoid vasculitis is characterized clinically by smooth or depressed ivory-white scars surrounded by hyperpigmentation and telangiectasia with or without preceding purpuric infiltrated papules and plaques and histologically by intravascular deposition of fibrin. Its etiology remains obscure and therapy very difficult.. Our purpose was to test the efficacy of low-dose danazol in the treatment of livedoid vasculitis.. Seven patients with active lesions of livedoid vasculitis were treated with low-dose danazol (200 mg, orally, daily). Laboratory coagulation and fibrinolysis parameters, including antithrombin III, protein C, protein S, tissue plasminogen activator, plasminogen, alpha 2-antiplasmin and fibrinogen, were evaluated before and during the therapy.. Six of the 7 patients completed the treatment. After the therapy, all 6 patients had rapid cessation of new lesion formation, prompt reduction in their pain and healing of ulcers. A significant elevation of plasminogen and a decrease in fibrinogen levels were noted 1 month after initiation of the therapy (p = 0.028). The level of fibrinogen seemed to parallel the disease activity in individual patients. In addition, in most of these patients, the levels of antithrombin III, protein C, protein S and alpha 2-antiplasmin tended to increase after the treatment. However, the differences were not statistically significant. Abnormalities of tissue plasminogen activator levels were less consistent. Low-dose danazol was well tolerated without major side effects.. We concluded that low-dose danazol was effective in the treatment of livedoid vasculitis, without unacceptable side effects.

Topics: Administration, Oral; Adult; alpha-2-Antiplasmin; Antithrombin III; Blood Coagulation; Blood Vessels; Cicatrix; Danazol; Estrogen Antagonists; Female; Fibrin; Fibrinogen; Fibrinolysis; Humans; Hyperpigmentation; Male; Plasminogen; Protein C; Protein S; Purpura; Remission Induction; Safety; Skin Diseases, Vascular; Skin Ulcer; Telangiectasis; Tissue Plasminogen Activator; Vasculitis; Wound Healing

A plasmin generation method to determine tissue plasminogen activator (t-PA) activity in plasma is described. A protein solution of homogenized fibrin was used as a stimulator in the presence of plasminogen and the plasmin generated was measured by the release of para-Nitroanilide (p-NA) from the chromogenic substrate S-2251. Plasmin generation by 5 iu/mL t-PA in the presence of 1 CU/mL of plasminogen and 850 micrograms/mL of fibrin solution reaches a peak at about 5 h incubation whilst in plasma, plasmin generation peaks after about 16 h incubation. The highest t-PA activity in plasma was determined using an assay involving 18 h incubation. In the 21 subjects studied by this method the t-PA activity at rest ranged from 0.34 to 0.92 iu/mL with a mean of 0.57 +/- 0.15 iu/mL of plasma whilst in the post-occlusion state the activity ranged from 1.12 to 18.0 iu/mL, with a mean of 5.25 +/- 4.49 iu/mL of plasma. We also found that subjects who developed petechiae during occlusion had significantly higher t-PA activity both at pre- and post-occlusion when compared with those who did not develop petechiae. The t-PA activity of acid-treated plasma stored at -70 degrees C showed no significant changes in activity after 12 weeks of storage when compared with the t-PA activity of the same plasma tested prior to storage.

Topics: Adult; Dose-Response Relationship, Drug; Female; Fibrin; Fibrinolysin; Humans; Male; Purpura; Tissue Plasminogen Activator

Topics: Aged; Complement System Proteins; Cryoglobulins; Female; Fibrin; Humans; Immunoglobulin M; Middle Aged; Purpura; Waldenstrom Macroglobulinemia

The urinary concentration of fibrin-fibrinogen degradation products (F.D.P.) was measured in 90 patients with proteinuria above 2 g/1 and correlated with proteinuria, differential protein clearances, serum urea and creatinine, and renal biopsy findings. There was a linear correlation (r equals 0-7; P less than 0-001) between the urinary F.D.P. excretion and the selectivity of the proteinuria such that patients with highly selective proteinuria excreted only small amounts of F.D.P. whereas those with non-selective proteinuria excreted much higher levels. There was a significant correlation between the urinary F.D.P. excretion and the urine:serum (U:S) ratio of IgG excretion but not with the U:S ratio or urinary excretion of albumin or transferrin. Sephadex G200 column chromatography of the concentrated urine in 26 cases showed that patients with highly selective proteinuria excreted predominantly F.D.P. of low molecular weight in the urine whereas those with non-selective proteinuria excreted mainly fibrinogen and products of high molecular weight. Hence the type and quantity of F.D.P. in the urine are determined primarily by the differential filtration of fibrinogen and the various degradation products from the plasma through the glomerular basement membrane, which in turn is determined by the "pore size" of the basement membrane. In clinical nephrology measurement of the urinary F.D.P. level provides a rapid and convenient means of estimating the differential protein clearance.

Topics: Albuminuria; Amyloidosis; Chromatography; Fibrin; Fibrinogen; Filtration; Glomerular Filtration Rate; Glomerulonephritis; Humans; Hypersensitivity; Hypertension, Malignant; Immunodiffusion; Immunoglobulin G; Lupus Erythematosus, Systemic; Molecular Weight; Nephrotic Syndrome; Proteinuria; Purpura; Thrombosis; Transferrin

Topics: Amyloid; Arthritis, Rheumatoid; Basement Membrane; Biopsy; Blood Proteins; Complement System Proteins; Diagnosis, Differential; Fibrin; Glomerulonephritis; Glycoproteins; Granulomatosis with Polyangiitis; Histocytochemistry; Humans; Hypersensitivity; Immunoglobulins; Kidney Glomerulus; Methenamine; Methods; Proteins; Purpura; Silver; Staining and Labeling

Topics: Child; Child, Preschool; Female; Fibrin; Fibrinogen; Hematuria; Humans; Infant; Kidney Diseases; Male; Nephritis; Nephrosis; Nephrotic Syndrome; Proteinuria; Purpura; Urinary Tract Infections

Biopsy of renal tissue from four patients with idiopathic focal nephritis and three patients with Henoch-Schönlein syndrome showed that C3 and properdin were deposited with IgA in the glomerular mesangium, C1q could not be detected. These observations suggest that glomerular injury in disorders characterized by mesangial deposits of IgA and C3 is mediated via the properdin system.

Topics: Biopsy; Complement System Proteins; Fibrin; Fluorescent Antibody Technique; Glycine; Glycoproteins; Humans; Immunoglobulin A; Immunoglobulin G; Kidney Glomerulus; Nephritis; Properdin; Purpura

Topics: Fibrin; Glomerulonephritis; Hemolytic-Uremic Syndrome; Kidney Diseases; Nephrosis; Purpura; Urinary Tract Infections

Topics: Adolescent; Child; Child, Preschool; Female; Fibrin; Glomerulonephritis; Hematuria; Humans; Hypersensitivity; Immunoglobulin A; Immunoglobulin G; Immunosuppression Therapy; Male; Proteinuria; Purpura; Respiratory Tract Infections; Serum Globulins

Topics: Adrenal Glands; Aneurysm; Aorta; Autopsy; Biopsy; Disseminated Intravascular Coagulation; Fibrin; Humans; Kidney; Kidney Glomerulus; Male; Meningococcal Infections; Myocarditis; Pulmonary Veins; Purpura; Renal Artery Obstruction; Testis; Thrombosis; Urinary Bladder; Vasa Vasorum; Vena Cava, Superior

Topics: Adolescent; Azathioprine; Biopsy; Child; Child, Preschool; Female; Fibrin; Glomerulonephritis; Humans; Immunoglobulin G; Infant; Kidney Glomerulus; Male; Microscopy, Fluorescence; Nephrotic Syndrome; Prednisone; Proteinuria; Purpura; Skin; Syndrome

Topics: Complement System Proteins; Cryoglobulins; Fibrin; Fluorescent Antibody Technique; Humans; Immunoelectrophoresis; Immunoglobulin G; Immunoglobulin M; Immunoglobulins; Inflammation; Purpura; Skin; Urticaria; Vascular Diseases

Topics: Basement Membrane; Blood Vessels; Collagen; Cytoplasmic Granules; Erythema; Fibrin; Humans; Male; Microscopy, Electron; Middle Aged; Mitochondria; Purpura; Skin Diseases

Topics: Adolescent; Anaphylaxis; Biopsy; Child, Preschool; Fibrin; gamma-Globulins; Humans; Kidney; Kidney Glomerulus; Microscopy, Electron; Microscopy, Fluorescence; Purpura

Topics: Adolescent; Adult; Anemia, Hemolytic; Beta-Globulins; Blood Coagulation Disorders; Blood Coagulation Tests; Child; Child, Preschool; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Heparin; Humans; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Nephritis; Nephrotic Syndrome; Purpura; Uremia; Urinary Tract Infections

Topics: Agar; Anaphylaxis; Animals; Epinephrine; Female; Fibrin; Fluorescent Antibody Technique; Kidney; Microscopy; Microscopy, Electron; Microscopy, Fluorescence; Purpura; Rats; Shwartzman Phenomenon

Topics: Animals; Blood Coagulation Disorders; Blood Platelets; Busulfan; Fibrin; Fibrinogen; Hemolysis; Injections, Intravenous; Kidney Glomerulus; Models, Biological; Neoplasms; Platelet Adhesiveness; Purpura; Rabbits; Sepsis; Shock; Shwartzman Phenomenon; Sulfonic Acids; Thrombocytopenia

Topics: Antigen-Antibody Reactions; Arthus Reaction; Basement Membrane; Capillary Permeability; Fibrin; Humans; Hypersensitivity; Microscopy; Microscopy, Electron; Purpura; Skin Manifestations

Topics: Blood Coagulation; Blood Coagulation Disorders; Blood Platelet Disorders; Blood Platelets; Classification; Fibrin; Genetics, Medical; Hemophilia A; Humans; Purpura; Surgery, Oral; Thrombin; Thromboplastin

Topics: Blood Coagulation; Blood Vessels; Fibrin; Fibrinogen; Humans; Hyalin; Pathology; Purpura; Purpura, Thrombotic Thrombocytopenic; Shwartzman Phenomenon; Thrombocytopenia; Thrombosis

Topics: Anemia; Anemia, Hypochromic; Biomedical Research; Blood Chemical Analysis; Collagen Diseases; Enzyme Inhibitors; Fibrin; Hemophilia A; Hepatitis; Hepatitis A; Jaundice; Jaundice, Obstructive; Leukemia; Liver Cirrhosis; Multiple Myeloma; Nephritis; Nephrotic Syndrome; Physiology; Purpura; Thrombin; Uremia

Topics: Coagulants; Fibrin; Fibrinogen; Humans; Purpura; Purpura, Thrombocytopenic; Syndrome; Thrombocytopenia

Topics: Fibrin; Fibrinogen; Humans; Hypnotics and Sedatives; Injections, Intravenous; Purpura; Purpura, Thrombocytopenic; Thrombocytopenia; Urea

Topics: Afibrinogenemia; Blood Coagulation; Fibrin; Humans; Purpura; Purpura Fulminans; Thrombin

Topics: Blood Platelets; Fibrin; Fibrinogen; Humans; Purpura; Purpura, Thrombocytopenic; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia

Topics: Fibrin; Microscopy, Electron; Purpura; Purpura, Thrombocytopenic; Thrombocytopenia