Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inbred MRL, NZB and BXSB strains of mice spontaneously develop a systemic, lupus-like autoimmune disease. The progress of autoimmunity is accompanied with a cascade of behavioral changes, most consistently observed in tasks reflective of emotional reactivity and the two-way avoidance learning task. Given the possibility that behavioral alterations may reflect a detrimental consequence of autoimmune-inflammatory processes and/or an adaptive response to chronic malaise, they are tentatively labeled as autoimmunity-associated behavioral syndrome (AABS). It is hypothesized that neuroactive immune factors (pro-inflammatory cytokines, brain-reactive antibodies) together with endocrine mediators (corticotropin-releasing factor, glucocorticoids) participate in the etiology of AABS. Since AABS develops natively, and has a considerable face and predictive validity, and since the principal pathway to autoimmunity is known, AABS may be a useful model for the study of CNS involvement in human autoimmune diseases and by extension, for testing autoimmune hypotheses of several mental disorders (major depression, schizophrenia, Alzheimer's disease, autism and AIDS-related dementia).
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PMID:Neurobehavioral alterations in autoimmune mice. 916 68

We report a case of Yersinia enterocolitica 0.9 septicaemia complicating systemic lupus erythematosus in an elderly male patient. The infection gave rise to digital vasculitis, fevers and general malaise on top of pre-existing articular symptoms. Features of Yersinia septicaemia may mimic some of the signs of lupus.
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PMID:Vasculitis and bacteraemia with Yersinia enterocolitica in late-onset systemic lupus erythematosus. 937 33

Urticarial vasculitis (UV) is a primary syndrome or a cutaneous vasculitic lesion occurring in the course of a collagen disease, as the systemic lupus erythematosus (LE). UV is a recently recognized disorder which affects most exclusively the female sex and may be differentiated from common (nonvasculitic) urticaria because it is characterized by inflammation and necrosis of blood vessels (vasculitis). UV and common urticaria may be induced by a variety of factors and pathogenetic mechanisms. It seems that a continuum exists, ranging from benign cutaneous lesions of urticaria to vasculitis with strong immunological involvement. On the basis of the clinical evaluation, two major groups of UV have been classified, the normocomplementemic, with a less severe clinical course, and the hypocomplementemic UV, a rare immune complex-mediated disorder related to LE as for as the similar pathogenesis and systemic involvement are concerned. A case of a young female patient with a unique syndrome characterized by crises of urticarial recurrent painful lesions of unknown origin, associated with angioedema of the tongue and soft palate, severe malaise, arthralgias and abdominal pain is reported. Dyspnea and cough were sometimes present, but fever was absent. Symptoms were caused by physical stress, heat or pressure and were little responsive to corticosteroids. Although skin biopsy did not prove with certainty the occurrence of vasculitis, clinical data and laboratory findings (normal levels of complement fractions, raised erythrocyte sedimentation rate, presence of cryoglobulins and ASMA, nDNA and AMA autoantibodies and absence of ANA autoantibodies and LE cells) suggest a normocomplementemic UV, excluding a classic LE. The family doctors and the internist must become familiar with the "lupus-like" syndromes, which include UV. In fact, a correct diagnosis of this syndrome is important because, although prognosis of UV may not be severe, the possibility exists of a systemic involvement (mainly renal) with progression to LE.
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PMID:[Urticarial vasculitis syndrome. A case report and review of the literature]. 945 98

The major initial clinical manifestations of systemic lupus erythematousus (SLE) were skin and mucous membrane involvement (52%), fever and malaise (48%), arthritis and arthralgias (44%). Lupus nephritis was diagnosed in 74% of patients and diffuse proliferative nephritis was the commonest histologic picture encountered. Except for a higher prevalence of anti-SS-A (Ro) (63%), other autoantibodies were within the normal range reported from Western countries. There was no significant association between HLA-A, B or DR specificities in 51 Chinese patients, nor was there any differences seen in the polymorphism of tumour necrosis factor alpha gene (TNF-alpha). Arthritis was less commonly seen in males with SLE. Prevalences of leukopenia and antibodies to anti-SS-A (Ro) and anti-La (SS-B) antigens were lower in men. Late onset lupus patients (> 50 years of age) tended to have more insidious onset of disease, lower female predominance and less frequent complaints of fever, alopecia, arthritis and malar rash at presentation. The causes of death were often treatment related. Survival studies among 183 SLE patients during the period from 1970 to 1980 revealed a 5- and 10-year survival rate of 70% and 60%, respectively. Infections and active lupus disease were 2 major causes of death. Research into SLE is targeted at increasing our understanding of the disease process and improving outcome and prognosis.
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PMID:Systemic lupus erythematosus in Singapore. 958 73

The history of antiarrhythmic therapy reveals these agents to be associated with a high incidence of toxicity. Although several agents have ocular effects, amiodarone is the most widely recognized for producing adverse effects in the eyes. Corneal microdeposits are almost ubiquitous in patients being treated with amiodarone. However, they are, for the most part, benign and produce no changes in visual acuity. Lack of microdeposits should prompt the physician to investigate whether there is a problem with drug absorption or adherence to therapy. Other effects on the eye have been reported including optic neuropathy, but no causal link has been proved with amiodarone. The population of patients treated with amiodarone often have ischemic disease and/or diabetes, which affect retinal and optic nerve health. Many antiarrhythmic agents also affect lung function. The frequent association of procainamide with a lupus-like syndrome, where half the cases develop pleural-pericardial involvement, may require discontinuation of that drug. Although beta blockers and to a lesser degree, calcium antagonists, may cause bronchospasm in some patients, this is not usually a major clinical problem. Again, it is amiodarone that has the most widespread reputation for causing pulmonary toxicity. Although infrequent (< 1% incidence), it generates the most fear as it is sometimes fatal. Because of the lack of a diagnostic "gold standard," it is often overdiagnosed, placing patients at risk from overlooked congestive heart failure and infections and from recurrent arrhythmias after drug withdrawal. Patients with pre-existing pulmonary disease appear to be more at risk. Common features include indolent onset of cough, malaise and fever associated with patchy peripheral infiltrates, and severely decreased diffusion capacity. Several cases of pulmonary toxicity have had inordinately high serum desethylamiodarone to amiodarone ratios. Most cases recover with cessation of amiodarone therapy. Steroids are commonly used, but are of unproved efficacy. In terms of its toxicity, amiodarone remains the most feared of the antiarrhythmic agents. In the future, a better understanding of its pharmacokinetics, mechanisms of toxicity, and optimal dosing regimens should provide a possibility of better strategies for avoidance, early diagnosis, and more directed therapy of toxicities associated with amiodarone.
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PMID:Clinical organ toxicity of antiarrhythmic compounds: ocular and pulmonary manifestations. 1056 58

We report a case of a 31-year-old woman with common variable immunodeficiency (CVID) complicated with intractable diarrhea and the functional disorder of renal tubules. The patient became hypogammaglobulinemic after she suffered from measles at 6 years of age. She also suffered from lupus-like syndrome at 7 years of age. The complete remission was obtained by glucocorticosteroid treatment. An intravenous immunoglobulin replacement therapy was introduced at 11 years of age, since then her general condition was stable for more than 20 years. When she was 29 years old, she suffered from generalized malaise, anorexia with body weight loss, and numbness of face. The intractable diarrhea as protein loosing syndrome, and the severe abnormality of electrolyte balance with metabolic acidosis as the functional disorder of renal tubules were found. Her condition was not improved by the electrolytes or alkali replacement therapy. She was admitted for further evaluation and treatment. The intractable diarrhea and the functional disorder of renal tubules were dramatically improved after absolute restriction of food intake under hyperalimentation. When she began to take food, the symptom and sign became worse again. The interstitial nephritis and nonspecific inflammation of intestine were found by the tissue biopsy. The most characteristic finding was the infiltration of lymphocytes (predominantly CD 8 + T lymphocytes) in both intestinal mucosa and renal interstitium. The introduction of glucocorticosteroids improved her general condition and biochemical findings. This CVID case is complicated with intractable diarrhea and the functional disorder of renal tubules which is associated with the infiltration of CD 8 + lymphocytes in intestine and kidney. We consider that such case is very rare and valuable to report.
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PMID:[A case of common variable immunodeficiency with intractable diarrhea and the functional disorder of renal tubules]. 1086 33

Kikuchi's disease (KD) can occur in association with systemic lupus erythematosus (SLE). The treatment of concomitant diseases, however, is unclear. We describe a case of a 45-y-old man who presented with generalized histiocytic necrotizing lymphadenitis, fever, malaise and weight loss. Ten months later he also developed arthritis, serositis, anemia, leukopenia and lymphopenia. ANA, anti-Smith, anti-snRNP and anti-Ro antibodies were positive. He responded rapidly and favorably to mid-dose prednisone. Hydroxychloroquine, added 5 months later, allowed tapering down and discontinuation of prednisone treatment. He has remained in complete remission for 5 years.
Lupus 2001
PMID:Therapeutic response and long-term follow-up in a systemic lupus erythematosus patient presenting with Kikuchi's disease. 1123 25

We report an autopsy case of elderly-onset anticentromere antibody-positive pulmonary-renal syndrome. An 84-year-old woman was admitted to our hospital with complaints of leg edema and general malaise. Neither skin rush nor arthritis was seen. Because of hematuria, proteinuria with various casts, renal dysfunction and anemia, a clinically diagnosis of rapidly progressive glomerulonephritis was made. Slight pulmonary hypertension was observed in ultrasonic cardiography. Hypocomplementemia was not seen. Tests for MPO- and PR 3-anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibody were negative, but a high titer of antinuclear antibody with a discrete speckled pattern on immunofluorescent staining was disclosed. Results for anticentromere antibody and anti-Ki antibody were positive, but for anti-Sm antibody and anti-double stranded DNA antibody were both negative. She did not present any clinical features of systemic sclerosis or CREST syndrome. Subsequently, prednisolone was administered, but pulmonary alveolar hemorrhage occurred and the patient died of acute respiratory failure caused by massive pulmonary hemorrhage. Autopsy revealed crescentic glomerulonephritis including glomerular capillaritis and pulmonary capillaritis with positive granular deposits of immunoglobulins and compliment on the glomerular and pulmonary capillary walls. Immunologically mediated crescentic glomerulonephritis and pulmonary capillaritis was then diagnosed histopathologically. The main pathological feature of the case was small-vessel vasculitis with immune-complex deposition. Although this case did not fulfill the clinical criteria for systemic lupus erythematosus (SLE), its histological features resembled those of lupus nephritis and acute lupus pneumonitis. We speculated that anticentromere antibody-positive pulmonary-renal syndrome without any other symptoms or signs of connective tissue disease, such as our case, is a clinical entity distinct from typical SLE or CREST syndrome.
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PMID:[Elderly-onset anticentromere antibody-positive pulmonary-renal syndrome: report of an autopsy case]. 1157 30

Patients with systemic lupus erythematosus (SLE) have increased susceptibility to infection by Pneumocystis carinii, but this condition has rarely been reported in Taiwan. Here, we describe two cases of patients with SLE who developed Pneumocystis carinii pneumonia (PCP). The first patient was a 39-year-old woman presenting with fever and dyspnea that had lasted 2 weeks. Chest roentgenography disclosed bilateral interstitial and alveolar infiltrates. The second patient was a 22-year-old woman presenting with a 4-day history of malaise, cough, dyspnea, and fever. She had concomitant Mycobacterium tuberculosis infection. Both patients had been treated with varying doses of corticosteroids and/or cytotoxic drugs within 4 months before presentation. Diagnosis was established based on the findings of bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB). Both patients received trimethoprim-sulfamethoxazole (20 mg.kg-1.d-1 trimethoprim), but finally died of nosocomial septicemia (Acinetobacter baumanni and Pseudomonas aeruginosa bacteremia in one, P. aeruginosa bacteremia in the other). These two cases demonstrate that PCP should be included in the differential diagnosis of patients with SLE presenting with pneumonic processes. In addition, a second opportunistic pathogen should be suspected. Bronchoscopic examination should be performed if the diagnosis is not clear and should include TBLB and BAL.
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PMID:Pneumocystis carinii pneumonia in systemic lupus erythematosus: a report of two cases. 1176 Mar 77

Solitary dermatofibromas are a common occurrence, especially on the lower limbs of young women, while multiple dermatofibromas (MDF) are rare, accounting for less than 0.3% of all dermatofibromas and may suddenly develop in immunosuppressed patients. We report a patient with systemic lupus erythematosus (SLE) who developed MDF while she was taking oral prednisone. A 46-year-old woman presented in 1989 complaining of photosensitivity, arthralgias, fatigue, malaise and dyspepsia. The patient denied fever, Raynaud's phenomenon, oral ulcer and hair loss. On examination she presented a typical SLE malar rash. Erythrocyte sedimentation rate (ESR) was elevated (54 mm/h). Speckle patterned IgG/IgM antinuclear antibodies were present at 1/1280 titer. Antibodies anti Ro/SSA were detected by counterimmunelectrophoresis up to 1/8 titer. Other laboratory findings were negative or within normal limits. Systemic lupus erythematosus was diagnosed and the patient given 50 mg/day prednisone. After a few months, both clinical symptoms and immunologic parameters improved. Eighteen months later, prednisone was replaced by 500 mg/day hydroxychloroquine. In 1994, she presented again with malar rash, arthralgias and facial hyperpigmentation. Prednisone 15 mg/day was reintroduced and hydroxychloroquine stopped being a possible cause of the facial hyperpigmented macules. In 1996, while she was taking 5 mg/day prednisone, several nodules developed on her limbs within a few months. On examination we observed 16 firm, slightly elevated 3-15-mm wide brown nodules on her arms, legs and trunk. A biopsy specimen of a lesion of the trunk revealed an epidermal seborrheic-keratosis-like hyperplasia with dermal fibrosis and fibroblastic proliferation (Fig. 1). Dermatofibroma was diagnosed.
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PMID:Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus treated with prednisone. 1210 Jul 3


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