Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 10 years ago, the first reports about the successful treatment of autoimmune thrombocytopenia with high-dose intravenously administered immunoglobulins (ivIg) were published. Since this time ivIg have been tried for treating almost any autoimmune disease. However, reports about this treatment modality are only anecdotal. So far, ivIg are a widely used and accepted treatment only for autoimmune thrombocytopenia and Kawasaki disease. During the last years many groups tried to gain a better understanding of the mechanisms by which ivIg exert their effects in autoimmune diseases. In systemic lupus erythematosus (SLE) only case reports are available which describe encouraging positive effects of ivIg especially in patients with cytopenia and vasculitis. However in some cases a serious impairment of renal function after ivIg therapy has been reported. This was seen mainly in SLE patients who already had renal involvement before ivIg therapy was started. Therefore, extreme caution should be exercised in these patients until we know more about the pathophysiology of this side effect. We have treated 6 SLE patients with high-dose ivIg (400 mg/kg, 5 days). One patient had a remission for 6 months, another patient for 36 months; in 2 patients with preexisting reduced renal function we observed two acute renal failures and in 1 patient a decrease of the renal function 1 month after ivIg treatment. These preliminary data demonstrate the necessity of controlled clinical trials to prove the effectiveness, to define indications, to find the optimal dosage, and to study the possible mechanisms of action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intravenous administration of immunoglobulins in systemic lupus erythematosus: review of the literature and initial clinical experiences]. 849 42

Human parvovirus B19 causes erythema infectiosum (fifth disease) and aplastic crisis. In pregnancy, B19 may be transmitted on to the fetus resulting in hydrops fetalis. B19 is sometimes associated with thrombocytopenia and vasculitis. In immunocompromised patients, B19 may persist causing chronic infection. Several methods for detecting B19 virus or specific antibodies are now available. B19 infection does not usually require therapy. Efficacy of immunoglobulins in chronic B19 infection has been demonstrated.
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PMID:[[Human parvovirus B19 and its clinical significance]. 856 65

Therapy with blood and blood products related to hemostatic disorders in small animal practice is reviewed. Administration of platelet rich plasma and platelet concentrates in thrombocytopenia or thrombopathia is discussed. Vascular purpuras, vasculitis, and vascular inherited defects are also considered. Inherited coagulation disorders are summarized and the therapeutic choices in treating these disorders are also proposed. In addition, acquired coagulation disorders are briefly reviewed.
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PMID:Use of blood and blood components in canine and feline patients with hemostatic disorders. 861 72

To investigate the prevalence and possible role of anti-endothelial cell antibodies (AECA) in the pathogenesis of systemic lupus erythematosus (SLE), cell membrane antigen was prepared from cultured human umbilical vein endothelial cells and immunoblotting performed to detect AECA in SLE sera. IgG-AECA could be detected in 41 (86%) of 47 SLE patients. They were highly specific and failed to react with membrane antigens of human peripheral blood mononuclear cells or granulocytes. IgG-AECA reacted with endothelial membrane antigens which ranged from 15 to 200 kDa in molecular size. Further analysis of the antigens reacting with IgG-AECA revealed some interesting correlations between specific species of antibodies with certain clinical manifestations. Thus, patients having lupus nephritis, vasculitis, and hypocomplementemia had IgG-AECA against a 66-kDa membrane antigen; those with thrombocytopenia had IgG-AECA against a 55-kDa antigen; those with pleuritis had IgG-AECA against an 18-kDa antigen. These results indicate that IgG-AECA in the sera of SLE patients consist of heterogenous species.
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PMID:Characterization of anti-endothelial cell antibodies in the patients with systemic lupus erythematosus: a potential marker for disease activity. 863 77

We retrospectively analyzed the outcome of bone marrow transplantation (BMT) performed in 26 patients with Wiskott-Aldrich syndrome (WAS) in one center. Twenty-eight transplantation procedures were performed. Ten unselected patients received unmanipulated marrow from a donor with genetically identical human leukocyte antigen (HLA). Eight patients were cured and survive 1.5 to 16.5 years after BMT. One patient successfully received a T-cell-depleted marrow from a matched unrelated donor. Sixteen patients were selected to receive a related HLA partially incompatible BMT because of the occurrence of life-threatening complications from the WAS (i.e., refractory thrombocytopenia, autoimmunity including vasculitis and sepsis). All but one received T-cell-depleted marrow after a conditioning regimen of busulfan and cyclophosphamide. One patient had two BMTs. Engraftment occurred in 12 of 17 attempts. The addition of monoclonal antibodies to lymphocyte function-associated antigen-1 and CD2 molecules appeared to improve engraftment. Six patients were long-term survivors, whereas others died of viral infections (n = 7), among which Epstein-Barr virus-induced B-lymphocyte proliferative disorder was predominant. Delay in development of full T- and B-cell functions accounted for severe infectious complications. These results confirm the excellent outcome of HLA genetically identical BMT in WAS, whereas BMT from HLA partially incompatible donors should be strictly restricted to patients with severe complications of WAS.
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PMID:Bone marrow transplantation in 26 patients with Wiskott-Aldrich syndrome from a single center. 876 21

A 52-year-old female was admitted to our hospital in August 1988, for evaluation of purpura and gingival bleeding. Hematologic examination showed mild leukocytosis (12,400/microliter) and severe thrombocytopenia (1,000/microliter). On bone marrow examination, megakaryocyte count was normal and the number of myeloblasts was increased (7.2%). Serological examination was positive for anti-nuclear antibody and anti-DNA antibody. She was diagnosed as having idiopathic or autoimmune thrombocytopenia, and received thrombocyte transfusion and gamma-globulin administration. Hematologic values improved temporarily, but leukocytosis and thrombocytopenia recurred. On the 22nd hospital day, leukocytes increased to 49,300/microliter and thrombocytes decreased to 10,000/microliter. Bone marrow myeloblasts were also increased to 18.8%, and she was suspected of having myelodysplastic syndrome. Then, hematologic values improved simultaneously, and she was discharged in November 1988. After the discharge, leukocyte count ranged from 6,000 to 16,500/microliter, but the number of bone marrow myeloblasts was normal. However, transient thrombocytopenia appeared in association with decrease or absence of bone marrow megakaryocytes and rise of platelet associated-IgG, (PA-IgG) to 99.6 ng/10(7) cells. From September to December 1989, she complained of fever, morning stiffness, multiple arthralgia, and oral ulcer. On serological findings, she was positive for LE cell. Therefore, she was diagnosed as having systemic lupus erythematosus (SLE). In January 1990, she had a high grade fever and dyspnea. Bilateral pleuritis and interstitial pneumonitis were shown on the chest roentgenogram. She received gamma-globulin administration, methylprednisolone pulse therapy, and mechanical ventilation. However, hypoxia developed rapidly, and she died of respiratory failure. Autopsy revealed severe interstitial pneumonitis, fibrinous pleuritis, fibrinous pericarditis, and vasculitis in the arcuate artery of the kidney. This is the first report of SLE complicating thrombocytopenia associated with decrease of megakaryocytes and rise of the PA-IgG, and severe leukocytosis associated with increased bone marrow myeloblasts.
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PMID:[An autopsy case of systemic lupus erythematosus complicating leukocytosis, amegakaryocytic thrombocytopenia, interstitial pneumonitis, and pleulitis]. 881 May 48

The actual efficacy and applicability of high dose intravenous immunoglobulin (IVIG) therapy in the rheumatic disorders is still being debated. In the last few years clinical results have become available on a large number of patients, and efforts have been devoted to experimental studies of the mechanism of action of IVIG. However, the results of controlled clinical trials will be crucial to indicate stricter guidelines and directions for future clinical and experimental research. IVIG is of major value in Kawasaki disease and in severe lupus-associated thrombocytopenia. Its possible benefits are also remarkable in refractory dermatomyositis and probably in some patients with the antiphospholipid syndrome and recurrent miscarriages despite standard treatment. At present, the role of IVIG therapy remains controversial in lupus nephritis and in systemic vasculitis, while it does not seem to be effective in rheumatoid arthritis.
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PMID:High dose intravenous immunoglobulin therapy for rheumatic diseases: clinical relevance and personal experience. 882 53

Thyroid hormone preparations, especially thyroxine, are widely used either at replacement doses to correct hypothyroidism or at suppressive doses to abolish thyrotropin (thyroid-stimulating hormone) secretion in patients with differentiated thyroid carcinoma after total thyroidectomy or with diffuse/ nodular nontoxic goitre. In order to suppress thyrotropin secretion, it is necessary to administer slightly supraphysiological doses of thyroxine. Possible adverse effects of this therapy include cardiovascular changes (shortening of systolic time intervals, increased frequency of atrial premature beats and, possibly, left ventricular hypertrophy) and bone changes (reduced bone density and bone mass), but the risk of these adverse effects can be minimised by carefully monitoring serum free thyroxine and free liothyronine (triiodothyronine) measurements and adjusting the dosage accordingly. Thionamides [thiamazole (methimazole), carbimazole, propylthiouracil] are the most widely used antithyroid drugs. They are given for long periods of time and cause adverse effects in 3 to 5% of patients. In most cases, adverse effects are minor and transient (e.g. skin rash, itching, mild leucopenia). The most dangerous effect is agranulocytosis, which occurs in 0.1 to 0.5% of patients. This life-threatening condition can now be effectively treated by granulocyte colony-stimulating factor administration. Other major adverse effects (aplastic anaemia, thrombocytopenia, lupus erythematosus-like syndrome, vasculitis) are exceedingly rare.
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PMID:Adverse effects of thyroid hormone preparations and antithyroid drugs. 886 63

We describe a 6-year-old female patient with systemic lupus erythematosus (SLE) manifested mainly as steroid-dependent thrombocytopenia who developed a vasculitic appearing rash on her palms and soles following treatment with intravenous immunoglobulin (IVIg) (1 gm/kg/infusion x 2, 1 day apart). Vascular occlusion resulting in ischemic gangrene of the fore and midfeet eventually developed, necessitating bilateral amputation. This and other side effects described in SLE indicate that exacerbation of SLE, with the possibility of vasculitis, may occur following IVIg therapy.
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PMID:Vasculitis in systemic lupus erythematosus following intravenous immunoglobulin therapy. 897 66

Thrombocytopenia is often found in patients with liver diseases, especially due to congestive splenomegaly caused by portal hypertension. Immune thrombocytopenia has been described rarely, and it seems to be especially associated with hepatitis C virus, which has been described as having a particular interaction with the immune system contributing to the induction of autoimmunity. Interferons, on the other hand, because of their immunomodulatory properties, are able to induce or exacerbate autoimmune diseases. Mild thrombocytopenia is a common adverse effect of interferon therapy. Severe life-threatening thrombocytopenia is extremely rare. We report two cases of severe immune thrombocytopenia in patients with chronic hepatitis C, probably induced by alpha-interferon. Bone marrow aspirate and elevated platelet-associated IgG antibodies, determined by indirect immunofluorescence, were suggestive of immune thrombocytopenia. None of the patients had any clinical sign of autoimmune syndrome, including arthritis, serositis, Sicca syndrome, vasculitis, thyroid abnormalities and others. Cryoglobulins and rheumatoid factor were tested and were undetectable. The patients' histories of exposure to alpha-interferon and the exclusion of other causes are most consistent with drug-induced immune thrombocytopenia. After alpha-interferon withdrawal, thrombocytopenia was treated successfully with prednisolone and immunoglobulins. Response to treatment was consistent with the diagnosis of alpha-interferon-induced immune thrombocytopenia and peripheral consumption of platelets.
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PMID:Immune thrombocytopenia and alpha-interferon therapy. 900 28


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