Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The circulating lupus anticoagulant is a spontaneously acquired immunoglobulin that has been associated in vivo with an increased risk of thrombotic episodes. We describe the case of a young woman with central retinal-artery occlusion associated with circulating lupus anticoagulant in the absence of systemic lupus erythematosus or any other autoimmune or collagen vascular disease. In cases of central retinal-artery occlusion without apparent cause, the presence of the lupus anticoagulant should be excluded especially in cases that have been exposed to the human immunodeficiency virus.
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PMID:Central retinal-artery occlusion in a patient with circulating lupus anticoagulant. 250 58

Beyond routine hematoxylin-eosin histologic examinations, specialized diagnostic techniques allow examination of biopsy material for subtle morphological and functional alterations. Morphological analytic techniques (1-micron section analysis, transmission electron microscopy, x-ray probe microanalysis, and digital image analysis) and functional analytic techniques (immunofluorescence, immunohistochemistry, and molecular biologic techniques) are valuable diagnostic tools. These techniques have applications in evaluating cutaneous T-cell lymphoma and atypical lymphocytic infiltrates, vesiculobullous disorders, lupus erythematosus and collagen vascular diseases, vasculitis, poorly differentiated tumors, storage diseases, and infections.
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PMID:Special techniques in dermatology. 266 12

Exaggerated acute and late effects were observed in three of four women with pre-existing collagen vascular disease (CVD) within 2 years after definitive megavoltage radiation therapy for breast carcinoma. Five women with breast carcinoma, who developed CVD 3 months to 10 years after radiation therapy, had no complications. An abnormally severe reaction was observed during treatment of one patient with discoid lupus. The patient developed moist desquamation that persisted for a month, requiring early termination of treatment. One year after treatment, the patient developed paresthesias in the ipsilateral arm. A planned reduction of the prescribed dose in a second patient with progressive systemic sclerosis did not prevent intense erythema at the end of treatment, followed 14 months later by chest wall necrosis, which eventually required multiple surgeries including chest wall resections. The third patient, who had systemic lupus erythematosis, developed necrosis 2 years after treatment, which progressed over 12 years to osteoradionecrosis of the clavicle, sternum and rib cage. Multiple surgeries to repair the defect were complicated by flap necrosis and pleurocutaneous fistulas. The fourth patient died 6 months after radiotherapy without apparent sequelae. None of the patients had evidence of recurrent carcinoma. A history of collagen vascular disease appears to be a contraindication to breast conservation or for elective irradiation for breast cancer.
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PMID:Consequences of breast irradiation in patients with pre-existing collagen vascular diseases. 277 73

Lyme disease is capable of producing a wide variety of clinical pathologic conditions and lesions having in common histologic features of collagen-vascular disease. The plasma cell is an omnipotent inflammatory responder in most tissues involved by Lyme disease, ranging from relatively acute to lesions that have gone on for years. Vascular thickening also seems to be prominent, and in the dermis is accompanied by scleroderma-like collagen expansion. The disease in some ways resembles the responses seen in lupus erythematosus such as mild cerebritis with lymphocytes and plasma cells in the leptomeninges. Lymphoplasmacytic panniculitis of Lyme disease resembles lupus profundus, both in the infiltrate and the plasma cell-blood vessel relationship. The onion skin thickened vessels of the synovia resemble the vessels of lupus spleens, while the scleradermoid thickening of the dermis and various skin lesions of stage III Lyme disease suggest a collagen-vascular disorder. Finally, the perivascular lymphoid infiltrate in clinical myositis does not differ from that seen in polymyositis or dermatomyositis. All of these histologic derangements suggest immunologic damage in response to persistence of the spirochete, however few in number.
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PMID:Clinical pathologic correlations of Lyme disease by stage. 284 22

10 consecutive patients fulfilled the diagnostic criteria for lupus anticoagulant. 4 had concomitant systemic lupus erythematosus, 1 Waldenstrom's disease and 5 had no apparent underlying disease. Only the case with Waldenstrom's disease presented a bleeding tendency, with bleeding time greater than 20 min; the others had a history of thrombotic complications. A defect of platelet aggregation induced by ADP, epinephrine, collagen and arachidonic acid was documented in the Waldenstrom's disease case whose lupus anticoagulant was an IgM. In the others, lupus anticoagulant, identified as IgG immunoglobulins, produced no aggregation abnormalities. However, beta-thromboglobulin levels in platelets, plasma and urine were consistent with a pattern of platelet activation in all cases. IgG immunoglobulins separated from sera of 6 patients showed lupus anticoagulant activity, with no effects on platelet aggregation of normal platelet-rich plasma, but they induced secretion of beta-thromboglobulin from normal platelets.
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PMID:Interaction between platelets and lupus anticoagulant. 296 26

This report describes a new method for detecting and quantitating those immunoglobulins G (IgG) in serum that are related to Graves' disease. The method is based on previous observations which indicate that the guinea pig fat cell membrane (FCM) is capable of binding Graves'-specific IgG, but does not bind the IgG common to Graves' disease and Hashimoto's disease, such as antimicrosomal antibodies. Crude FCM preparations were iodinated by a lactoperoxidase technique and were then treated with Triton X-100 to yield a solubilized radioiodinated FCM (SFCM) preparation. SFCM, which retained bovine (b) TSH binding and Graves'-IgG binding properties, provided a radioactively labeled receptor with which to test for the presence of fat cell-binding IgG (FBI) in immunoprecipitates prepared by reacting these IgG with antibody against the Fc fragment of human IgG. FBI values (percentage of added SFCM bound to immunoprecipitate; mean + SD) in IgG from 16 patients with thyrotoxicosis caused by Graves' disease (6.0 +/- 1.7) were completely separated from those in IgG from 16 normal subjects (0.4 +/- 0.3). IgG from 2 hypothyroid patients with Hashimoto's disease, which were strongly positive in the TSH binding inhibition (TBI) assay, yielded FBI values within the range in Graves' disease, but values in TBI-negative IgG from 15 other patients with Hashimoto's disease were normal (0.0 +/- 0.9). Moderately false positive FBI values were found in the IgG of 15 patients with rheumatoid arthritis or systemic lupus erythematosis, all rheumatoid factor positive, 3 of which were also TBI positive. In IgG from Graves' disease and those from patients with TBI-positive collagen-vascular disease, binding of SFCM was inhibited by bTSH in a dose-dependent manner. As with binding of TSH to thyroid plasma membranes, similar but less potent inhibition of binding of IgG to SFCM was produced by LH, FSH, and hCG, but not by insulin, glucagon, PRL, or ACTH. FBI values in TBI-negative IgG from patients with collagen-vascular disease were also decreased by TSH, but higher concentrations of bTSH were required. In 40 IgG from among the various clinical groups tested, a significant correlation was found between FBI values and TBI activity (r = 0.48; P less than 0.01). In addition, among 10 IgG from Graves' disease and 6 from collagen-vascular disease patients, a very close correlation (r = 0.89; P less than 0.001) was noted between their TBI activity and the extent to which their FBI values were decreased by a standard concentration of bTSH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Detection and measurement of fat cell-binding immunoglobulins: a new method applicable to the diagnosis and study of Graves' disease. 299 73

Symptoms and signs in four patients with thalidomide-induced neuropathy developing during treatment of discoid lupus were limited for long period to distal paresthesiae with altered sensory conduction velocities. Semi-thin biopsy specimens of the distal sural nerve showed depopulation of myelinized fibers, mainly affecting those of large caliber, and signs of axonal degeneration. Study of dissociated fibers showed a high proportion of E fibers. Morphometry confirmed the axonal lesion. Ultrastructural examination demonstrated anomalies of axons of amyelinic fibers (vacuoles, lamellar figures) and of Schwann cells (stacked cytoplasmic prolongations), together with numerous collagen pockets, all non-specific lesions. The disease course was slow, with disappearance of sensory symptoms in a few weeks in 3 of the 4 cases and normal clinical findings in one of the four patients one year after cessation of treatment. Definite correlations between the dose administered and the severity of the neuropathy could not be established. The still poorly understood mechanism of action is discussed.
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PMID:[Neuropathies caused by thalidomide]. 300 71

D-penicillamine (DPA) leads to side effects in different ways: collagen and elastin crosslinking are inhibited, which results in thin and vulnerable skin, cutis laxa, elastosis perforans serpiginosa, wound healing defects and embryopathy. Toxic influences effect thrombo- and leukocytopenia (incidence 5-15%), gastrointestinal disturbances (10-30%), changes or loss of taste (5-30%), loss of hair (1-2%), and partly proteinuria (5-20%). Acute hypersensitive reactions include DPA-allergy (2-10%). Severe adverse effects are autoimmune phenomena such as pemphigus, DPA-induced lupus erythematosus, polymyositis/dermatomyositis, membranous glomerulopathy and hypersensitivity pneumonitis (like Good-pasture's syndrome) and myasthenia (all less than 1%). In addition there are a number of rare side effects, often single observations. Risk factors include a genetic disposition (especially HLA-B8 and -DR3), poor sulphoxidizers and, to a certain degree, higher age. During pregnancy and in clinically relevant disturbances of bone marrow, liver and renal function DPA is contraindicated. The total incidence of side effects amounts to 30-60%, the withdrawal rate is 20-30%; therefore clear indications and a regular survey of DPA therapy are necessary.
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PMID:[D-penicillamine--side effects, pathogenesis and decreasing the risks]. 306 3

A brief overview is presented of the different antinuclear autoantibodies most frequently mentioned in the literature at the present time. The relationship between these autoantibodies and collagen diseases is described in terms of their usefulness in diagnosis and follow-up. Lupus anticoagulant is also mentioned in view of its possible relationship with anti-DNA autoantibodies.
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PMID:[Antinuclear antibodies: the classical and the new]. 311 55

Circulating lupus anticoagulant occurs in 5-37% of all patients with systemic lupus erythematosus. Its occurrence is not restricted to collagen vascular disease states. Lupus anticoagulant causes a prolongation of certain laboratory coagulation studies yet it is associated in vivo with a history of systemic intravascular thromboses. Placental vessels are also affected. Less than one in six pregnancies complicated by the presence of this auto-antibody is successful. Treatment of afflicted parturients with anti-platelet therapy has increased perinatal survival rates. Derangements in the coagulation profile and concomitant anti-platelet therapy confound the rational use of regional anaesthesia in the management of labour and delivery in these high-risk pregnancies.
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PMID:Lupus anticoagulant. Implications for obstetric anaesthetists. 312 65


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