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)

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

Seven patients who developed a syndrome of eosinophilia, connective-tissue disease, and cutaneous abnormalities while ingesting tryptophan were examined. Other clinical manifestations commonly seen were pulmonary symptoms, fever, lymphadenopathy, and the development of myopathy. Laboratory features included mild elevations of aldolase and lactate dehydrogenase levels, with essentially normal creatine kinase levels, erythrocyte sedimentation rates, and C-reactive protein levels. Biopsy findings included features of scleroderma, small-vessel vasculitis, fasciitis, and myopathy. Discontinuation of tryptophan administration and implementation of corticosteroid therapy were of some benefit in relieving the intense myalgias and cutaneous findings that developed. Although temporally related to tryptophan ingestion, it is unclear whether this substance, a metabolite, or a contaminant were causal. We speculate that the pathogenesis of this syndrome may relate to abnormalities in tryptophan metabolism.
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PMID:Tryptophan-associated eosinophilic connective-tissue disease. A new clinical entity? 230 82

Infectious bursal disease in 35-day-old specific-pathogen-free (SPF) chickens was characterized clinically by its acute onset and brief duration. Clinical signs included depression, anorexia, diarrhea, and polyuria. A detectable precipitin antibody response occurred between 3 and 5 days postinoculation. Evaluation of pooled serum samples obtained from infectious bursal disease virus (IBDV)-infected chickens revealed transient changes in potassium, cholesterol, uric acid, lactate dehydrogenase, serum glutamic-oxalic transaminase, and serum proteins. Individual serum samples analyzed for uric acid concentration indicated that several IBDV-infected chickens had serum uric acid concentrations above the normal comparison range. Histopathologic examination of lymphoid and nonlymphoid tissues from IBDV-infected SPF chickens affirmed that the predominant lesion was lymphoid necrosis in the bursa of Fabricius. Other lymphoid organs were much less severely affected and possessed greater regenerative potential. Nonspecific and relatively mild changes were found in the liver and kidney: hepatic lipidosis and necrosis, renal intratubular crystalline deposits (probably urates), and increased ectopic lymphoid foci. There was no evidence of immune-complex-mediated arteritis/vasculitis in the sartorius muscle or any other tissue examined. Histopathologic and ultrastructural evidence of glomerulonephritis was rare but compatible with acute immune complexemia.
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PMID:The pathogenesis of infectious bursal disease: serologic, histopathologic, and clinical chemical observations. 631 94

Seven patients with systemic lupus erythematosus (SLE) or SLE-like disease developed thrombotic microangiopathy. Prominent features of their acute illnesses were microangiopathic hemolytic anemia (7), thrombocytopenia (7), fever (1), nervous system disease (4), and renal dysfunction (5). Laboratory data were significant for antinuclear antibody (ANA) (7), DNA (5), low C3 level (3), low C4 level (2), antiphospholipid antibody (6), schistocytes (7), and lactate dehydrogenase > 500 (7). All seven patients received treatment that initially included steroids but later included cyclophosphamide (4), plasma infusion (1), plasmapheresis (5), intravenous gamma-globulin (2), anti-platelet agents (2), or vincristine (3). Six patients improved, and one patient expired during treatment. Of the six patients who survived this complication, three expired within the year following their acute illnesses. Histology, available in two cases, showed vascular changes consistent with a microangiopathic process. We conclude that the spectrum of vascular diseases in SLE extends beyond vasculitis to include noninflammatory vascular processes that can cause equally devastating complications.
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PMID:Systemic lupus erythematosus complicated by thrombotic microangiopathy. 789 75

The case of a 75-year-old Japanese woman with adult-onset Still's disease who presented with cerebral haemorrhage is described. She had been in clinical remission for 2 years, after induction therapy including non-steroidal anti-inflammatory drugs, prednisolone, cyclophosphamide and mizoribine followed by auranofin, until her cerebral haemorrhage occurred, although her serum level of ferritin had gradually increased. After the onset of cerebral haemorrhage, the patient's serum level of thrombomodulin was elevated although c-reactive protein and lactate dehydrogenase were not increased. Anti-cardiolipin antibody and lupus anti-coagulant were not detected. Patients with adult-onset Still's disease are rarely reported to develop cerebral vascular disease, possibly because the disease is most frequent in young adults. The cerebral haemorrhage may have been caused by the vasculitis due to Still's disease.
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PMID:Cerebral haemorrhage complicating adult-onset Still's disease: a case report. 895 35

Alteration of redox balance in the serum of patients with systemic lupus erythematosus (SLE) and systemic vasculitis (SV) was investigated. Excess in oxidative processes has been measured through concentration of lipid peroxides which was found to increase by 26% in SLE and 32% in SV. Antioxidant protection capacity against this oxidative aggression has been assessed both by determining the level of activity of the enzymes participating in this process (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase GSH-Px) and by determining the total antioxidant serum activity. The results have shown that, within antioxidant protection of the body against oxidative stress, glutathione peroxidase plays the most important role and its activity is significantly affected by the great concentration of lipidic peroxides. We have also shown that there is positive correlation (r = 0.91) between the level of lipidic peroxides and the extent to which the tissue is affected. The latter is assessed by studying the serum activity of lactate dehydrogenase. Therefore, these two biologic parameters are shown to be very useful when the study of the development of the diseases is undertaken.
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PMID:Antioxidant protection in collagen-vascular diseases. 1082 21

Twenty-four dogs with a parasitologically and serologically established diagnosis of leishmaniasis were studied to investigate the atrophy of the masticatory muscles which commonly occurs in this disease, and to compare the lesions in the masticatory muscles with those in the cranial tibial muscles. The 24 animals were divided into three groups of eight, group A dogs with no muscular atrophy, group B dogs with different degrees of atrophy in the masticatory and skeletal muscles, and group C dogs with similar degrees of atrophy in the masticatory and skeletal muscles. Increased activities of creatine phosphokinase and lactate dehydrogenase were recorded in only some of the dogs in groups B and C, but there were no significant differences between the mean activities in the three groups. Electromyographic changes indicating myopathy and involving both the temporalis and cranial tibial muscles, were observed in two of the dogs in group A, seven of those in group B, and in all the dogs in group C. Muscle histopathology revealed a variable degree of muscle fibre necrosis and atrophy, mononuclear infiltrates and neutrophilic vasculitis in all the dogs except two in group A. Leishmanial amastigotes were found within macrophages and myofibres in 16 of the dogs, some in each group. IgG immune complexes were detected in muscle samples, and circulating antibodies against myofibres were detected in serum samples from all the 24 dogs.
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PMID:Masticatory and skeletal muscle myositis in canine leishmaniasis (Leishmania infantum). 1088 83

Intravascular lymphomatosis (IVL) is a rare malignancy characterized by a proliferation of atypical lymphoid cells occluding small blood vessels (venules, capillaries and small arteries). The symptoms are caused by embolisms due to massive proliferation. Nervous system and skin are the most common sites of involvement but all organs may be involved, although it is typified by the absence of malignant cells in lymphoid tissues. We describe three cases of IVL: first patient was a 57 years old man with rapidly progressive dementia and neurological involvements and second case of a 69 years old man hospitalised with predominant symptoms in the lung (cough, dyspnea and fever), and a woman presenting as fever of unknown origin (FUO) with systemic inflammatory response syndrome. In all cases that we reported have been diagnosed post-mortem because of rapid progression of a multisystem disease and the absence of pathognomonic clinical manifestations. Diagnosis can be made using biopsy of one of the involved organs. In conclusion, we propose that IVL should be included in the differential diagnosis of acute confusional state, dementia or other unexplained neurological manifestations, fever of unknown origin, vasculitis, occult neoplasia or infections with signs of a systemic disease and marked elevation of serum lactate dehydrogenase (LDH).
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PMID:[Intravascular lymphomatosis. A report of three cases]. 1577 21

Case 1. A 23-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and limbs, particularly over the dorsum of the hands and fingers; diffuse alopecia; and an inability to climb stairs and get up from a low seat. The clinical examination showed red to violaceous well-demarcated plaques on sun-exposed areas on the dorsum of the fingers and hands, with periungual erythema and telangiectasia; facial erythema; and heliotrope rash. There was also symmetric involvement of proximal muscles of the limbs. Laboratory examination showed hypergammaglobulinemia, elevated serum aspartate aminotransferase, and serum alanine aminotransferase; normal activities of creatinokinase, lactate dehydrogenase, and aldolase; an antinuclear antibody titer of 1:40 with a speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Skin biopsy histopathology showed hyperkeratosis, edema of the upper epidermis, scattered inflammatory infiltrate, and focal accumulation of mucin in the form of acid mucopolysaccharides. Deep asymptomatic nodules on the inner upper limbs appeared later. Histopathology of these lesions showed focal areas of lobular panniculitis in the subcutaneous tissue, with lymphoplasmocytic inflammatory infiltrate without vasculitis (Figure 1 and Figure 2). Case 2. A 29-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and lower extremities. Clinical examination showed red to violaceous well-demarcated aching plaques on the internal surface of the thighs and tips of the fingers; periungual erythema and digital petechiae; Raynaud's phenomenon; and bilateral ulnar and cervical enlarged lymph nodes. Laboratory examination showed elevated serum aspartate aminotransferase, alanine aminotransferase, creatinokinase, lactate dehydrogenase, and aldolase; negative venereal disease research test results; an antinuclear antibody titer of 1:1024 with speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Histopathology of the deep asymptomatic nodule on the inner left thigh showed lobular panniculitis with a scattered inflammatory infiltrate and diffuse fat necrosis, in addition to calcium deposition between the lipocytes and microcysts without vasculitis (Figure 3).
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PMID:Dermatomyositis with panniculitis. 1721 24

We retrospectively analyzed 77 patients with pathologically diagnosed angioimmunoblastic T-cell lymphoma from a single city. There were 43 men and 34 women; the median age was 64.5 years (range, 30-91 yr). Average time between first symptoms of the disease and diagnosis was 3.6 months. At diagnosis, peripheral nodes were present in all but 1 patient, and were generalized in 90% of cases. Constitutional symptoms were reported in 77% of cases and spleen enlargement in 51%. A cutaneous eruption--morbilliform, urticarial, or more polymorphic--was present in 45% of patients; in one-third of them, the eruption occurred after drug administration. Other clinical manifestations included pleuritis (22%); arthralgia or arthritis (17%); ear, nose, and throat involvement (14%); central or peripheral neurologic manifestations (10%); and ascites (5%). Most patients presented with advanced disease at diagnosis (bone marrow involvement in 60% of cases). The main laboratory abnormalities were elevated lactate dehydrogenase levels (71%), inflammatory syndrome (67%), hypergammaglobulinemia (50%), anemia (51%), and lymphopenia (52%). Auto- or disimmune manifestations were reported in one-third of patients: autoimmune hemolytic anemia was present at diagnosis in 19% of patients and thrombocytopenic purpura in 7%. Documented vasculitis was described in 12% of cases. Clonality was analyzed in lymph nodes in 47 patients: T-cell and B-cell clones were found in 45 (96%) and 20 (45%) patients, respectively. Chromosomal abnormalities were identified in 62% of cases: trisomies 3, 5, 18, 19, additional X chromosome, and deletion of chromosome 7 were the most common abnormalities. The current study underlines the diversity of presenting manifestations of angioimmunoblastic T-cell lymphoma.
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PMID:Angioimmunoblastic T-cell lymphoma: clinical and laboratory features at diagnosis in 77 patients. 1787 58


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