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)

A systemic lupus erythematosus-like syndrome developed simultaneously with pulmonary reactions of the chronic type in three female patients after treatment with nitrofurantoin for 12, 27 and 38 months, respectively. The syndrome was characterized by elevated ESR, polyclonal hypergammaglobulinaemia, the presence of IgG antinuclear antibodies and a positive latex-fixation test. Two patients had severe arthralgia and one of them peripheral lymphadenopathy. Pleural effusion and a chronic active hepatitis were present in the third patient, in whom interstitial cystitis also developed. All signs and symptoms of the lupus-like syndrome disappeared, without corticosteroid or other medication, when nitrofurantoin was omitted. The diminution of pulmonary infiltrates and the reversal of interstitial cystitis also appeared to be directly related to cessation of nitrofurantoin therapy. Our findings indicate that long-term medication with nitrofurantoin may cause, in addition to pulmonary changes, a simultaneous lupus-like syndrome our data also raise the possibility that interstitial cystitis may occur as an adverse reaction to nitrofurantoin therapy.
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PMID:Lupus-like syndrome associated with pulmonary reaction to nitrofurantoin. Report of three cases. 107 7

A 40-yr-old Caucasian woman who had been suffering from systemic lupus erythematosus (SLE) since five years developed vague abdominal complaints whilst under treatment with a low dose of steroids. She had been admitted because of vomiting and abdominal tenderness. The ESR and CRP levels were rising and the C4 level had been persistently low in the preceding months. Normal non-invasive procedures did not allow a diagnosis to be made. Therefore exploratory laparotomy was performed and revealed a non-bacterial peritonitis and an oedematous jejunum. She responded well to a high dose of prednisone. Serositis of the peritoneum as well as bowel vasculitis may be a rare manifestation of SLE despite apparent control of other lupus manifestations. In this patient serositis flares were associated with a rise in CRP level.
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PMID:Lupus peritonitis presented as vague abdominal complaints in a SLE patient. 143 59

A 51-year-old woman had been suffering from blood-stained purulent sinusitis and antibiotic-resistant bouts of fever for 4 months. She had microhematuria and serological evidence of inflammation (erythrocyte sedimentation rate [ESR] 92/135 mm, C-reactive protein 5.0 mg/dl). When she was admitted to hospital suspected of having postinfectious glomerulonephritis she complained of spontaneous colic-like pains in the left flank. Within one day the haemoglobin concentration fell from 10 to 6.5 g/dl. Ultrasound and computed tomography demonstrated a large space-occupying lesion around the left kidney. At operation this was found to be a rupture of the kidney with perirenal bleeding which was treated without removing the kidney. No biopsy was taken, but serological tests showed antineutrophil cytoplasmatic antibodies (cANCA), indicating Wegener's granulomatosis as the cause of the compensated renal insufficiency and spontaneous renal rupture. Under immunosuppressive treatment the inflammatory signs (ESR 18/44 mm), fever, chronic maxillary sinusitis, raised serum creatinine concentration and the ANCA titre all regressed, while proteinuria of about 4 g/24 h persisted. There was no recurrence during a follow-up period of 15 months. Serological signs of marked inflammatory activity, urinary sediments of nephritis and spontaneous retroperitoneal bleeding should suggest that, in addition to lupus erythematodes and panarteritis nodosa, Wegener's granulomatosis be included in the differential diagnosis.
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PMID:[Spontaneous kidney rupture as an early complication of Wegener's granulomatosis]. 154 1

Inflammatory aneurysms are characterised by a peculiar clinical (i.e. abdominal-lumbar pain, weight loss and increased ESR) and morphological picture (whitish wall, adhesion to the surrounding organs and thickness greater than 0.5 cm). The lymphomonoplasmacellular infiltrate and the interstitial deposits of collagen define the histological picture of these lesions. The authors describe three abdominal aortic aneurysms macroscopically characterised by parietal edema, hyperemia and hypertrophy of the preaortic lymphnodes. Histological study revealed a conspicuous and widespread lymphomonoplasmacellular infiltrate and interstitial edema. The abdominal-lumbar pain, the increase in ESR and the reactive C protein defined the clinical and laboratory aspects. Serological tests for syphilis, rheumatoid arthritis and lupus erythematosis were negative. The question which arises from these observations is whether these forms represent separate entities or an early stage in the evolution of inflammatory abdominal aortic aneurysms with fibrosis.
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PMID:Inflammatory abdominal aortic aneurysms: does an early stage exist? 175 89

Hydralazine caused site-specific DNA damage in the presence of Cu(II), Co(II), Fe(III), or peroxidase/H2O2. The order of inducing effect of metal ions on hydralazine-dependent DNA damage [Cu(II) greater than Co(II) greater than Fe(III)] was related to that of accelerating effect on the O2 consumption rate of hydralazine autoxidation. Catalase completely inhibited DNA damage by hydralazine plus Cu(II), but hydroxyl radical (.OH) scavengers and superoxide dismutase did not. On the other hand, DNA damage by hydralazine plus Fe(III) was inhibited by catalase and .OH scavengers. Hydralazine plus Cu(II) induced piperidine-labile sites predominantly at guanine and some adenine residues, whereas hydralazine plus Fe(III) caused cleavages at every nucleotide. Activation of hydralazine by peroxidase/H2O2 caused guanine-specific modification in DNA. ESR-spin trapping experiment showed that .OH and superoxide are generated during the Fe(III)- or Cu(II)-catalysed autoxidation of hydralazine, respectively, and that nitrogen-centered radical is generated during the Cu(II)- or peroxidase-catalysed oxidation. The generation of nitrogen-centered radical was also supported by HPLC-mass spectrometry. The results suggest that the guanine-specific modification by the enzymatic activation of hydralazine is due to the nitrogen-centered hydralazyl radical or derived active species, whereas .OH participates in DNA damage by hydralazine plus Fe(III). The mechanism of hydralazine plus Cu(II)-induced DNA damage is complex. The possible role of the DNA damage induced by hydralazine in the presence of Cu(II) or peroxidase/H2O2 is discussed in relation to hydralazine-induced lupus, mutation, and cancer.
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PMID:Free radical production and site-specific DNA damage induced by hydralazine in the presence of metal ions or peroxidase/hydrogen peroxide. 184 78

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

The clinical and morphological characteristics of drug-induced lupus (DIL) are not unlike those of systemic lupus erythematosus (SLE). However, DIL is characterised by several distinct features: the two sexes are equally affected; onset occurs in advanced middle-age; the black population is seldom affected. Genetic predisposition seems to influence the onset of disease: subjects affected by DIL are prevalently HLA-DR4 haplotypes with a slow acetylator condition. Modifications in humoral immunity include the presence of anti-nuclear antibodies, denatured anti-DNA antibodies, and antihistone antibodies. Likewise, anti-lymphocytotoxic antibodies, increased ESR and hypocomplementemia are often observed. Little is known about alterations in cellular immunity but the dysregulation of lymphocyte T-helper and T-suppressor activity may be an important feature. Drugs most often leading to DIL include hydralazine, beta-blockers, procainamide and hydantoin. Current pathogenetic theories include a possible immune drug-DNA cross-reaction, the induction of new antigenic structures, an interaction between drugs and immunomodulating cells.
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PMID:[Systemic lupus erythematosus induced by drugs]. 197 6

A female newborn of SLE mother developed transient typical discoid-like lupus skin lesions over her face soon after birth and had severe relapse with generalized spreading following an episode of upper respiratory tract infection at 50 days of age. Blood picture showed anemia, transient thrombocytopenia and high ESR. Cardiac echo disclosed small ASD with minimal TR. Both EKG and 24 hrs EKG monitor presented normal findings. Serological studies at the early relapse stage of this disease showed increased serum ANA, IgA and IgM level with normal IgG and decrease of C3 and C4. Both Ro(SSA) and La(SSB) antibody systems were positive in mother but only positive for La(SSB) antibody system in this baby. The alpha-anticardiolipin antibody was negative. We suggest that the Ro(SSA) and/or La(SSB) antibody systems may play a role in the pathogenesis of neonatal lupus erythematosus.
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PMID:Neonatal lupus erythematosus: report of one case. 263 97

Sixty-two cases of systemic lupus erythematous (SLE) treated with Tab. Gentiana macrophylla complex 5 tablets three times per day or 10 tablets twice per day and prednisone 10-30 mg per day were reported. As controls, 19 cases of SLE were treated with prednisone alone at the same time. The results showed complete remission in 86.46% (50/62) cases in the observation group and 31.57% (6/19) cases in the control group. Eight cases of SLE treated with Tab. Gentiana m. complex alone also achieved complete remission in 6 cases and improvement in 2. There was very significant statistical difference between the two groups (P less than 0.001). The Tab. Gentiana m. complex was more effective on the improvement of nephropathy, arthralgia, erythema and restoration of ESR, LE cells and CH50, C3 than prednisone alone. No apparent side effects of Tab. Gentiana m. complex were found in this observation.
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PMID:[Observation on the treatment of systemic lupus erythematous with a Gentiana macrophylla complex tablet and a minimal dose of prednisone]. 273

The finding in a 40-year old and apparently healthy woman of a pseudotumoral lesion of the left arm which had gradually developed over a 9-year period led to a tentative clinical diagnosis of lupus anetoderma. This diagnosis was confirmed on the one hand by histological examination of the skin--which showed almost total disappearance of dermal elastic fibres, while the lympho-histiocytic infiltrate was so discreet that it excluded a deep lupus--and on the other hand by direct immunofluorescence, with lupus band on the lesion and a few abnormalities of the exposed and covered healthy skin. A history of chorea at the age of 13 years raised the problem of a possible relationship between this neurological disease and a systemic lupus erythematosus. This hypothesis was supported by resolutive episodes of arthralgia and abnormal laboratory findings, such as accelerated ESR, leucopenia, decrease of complement and presence of homogeneous antinuclear antibodies. Anticardiolipin antibodies, circulating anticoagulants and VDRL test were negative. Treatment with anti-malarials brought about some degree of cutaneous shrinkage and a significant decrease in ESR. This case is reported because anetoderma as sole manifestation of systemic lupus erythematosus and the occurrence, 17 years previously, of chorea are exceptional events.
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PMID:[Pseudotumoral lupus anetoderma. Child chorea. Development over 28 years]. 305 43


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