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)

Steroid induced psychosis in SLE is rare but clinically important, and often difficult to distinguish from lupus cerebritis. We report a patient with SLE who became depressed following an increase in her steroid dosage. Based on her clinical presentation and high levels of antibodies to P ribosomal proteins (both in CSF and serum) a diagnosis of lupus cerebritis was made. Steroid dosage, time intervals, and the duration of mental changes may help in differentiating steroid psychosis from lupus cerebritis. No single laboratory test sufficient to establish a definitive diagnosis of lupus cerebritis is available at the present time. However, elevated levels of antibodies to P ribosomal proteins may assist in confirming the diagnosis of this condition.
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PMID:Lupus psychosis: differentiation from the steroid-induced state. 835 89

In the present study, the authors reported a case of systemic lupus erythematosus (SLE) with central nervous system involvement (CNS lupus). The authors also longitudinally investigated plasma levels of brain-derived neurotrophic factor (BDNF) and catecholamine metabolites in the patient, and found that plasma levels of BDNF, 3-methoxy-4-hydroxyphenylglycol (MHPG), and homovanillic acid (HVA) were raised in accordance with the severity of psychotic symptoms in this case of CNS lupus. These results suggest that it is useful to measure plasma levels of BDNF and the catecholamine metabolites in order to predict the severity of psychotic symptoms in CNS lupus and to provide a differential diagnosis from that of steroid-induced psychosis.
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PMID:Plasma levels of brain derived-neurotrophic factor and catecholamine metabolites are increased during active phase of psychotic symptoms in CNS lupus: a case report. 1662 41

To evaluate the frequency and risk factors of acute psychosis in a large cohort of patients with systemic lupus erythematosous (SLE). To identify clinical and laboratory variables useful in differentiating acute psychosis as a primary manifestation of central nervous system (CNS) from corticosteroid induced psychosis. Five hundred and thirty seven consecutive patients with SLE were studied, with follow-up ranging from 4 to 8.8 years. A standardized medical history, neurological, rheumatologic, and psychiatric examinations and serologic testing were performed in all patients. The type and frequency of risk factors associated with acute psychosis as a primary manifestation of CNS system and corticosteroid induced psychosis was determined using multivariate regression with automatic backward stepwise selection. We identified acute psychosis in 89 of 520 (17.1%) SLE patients. Psychosis primary to CNS involvement was diagnosed in 59 of these patients, corticosteroid induced psychosis in 28 and primary psychotic disorder not related to SLE or medication in two patients. Psychosis secondary to SLE at disease onset occurred in 19 patients and was associated with disease activity (p = 0.001; OR = 2.4; CI = 1.5-6.2). Psychosis during follow-up of SLE was observed in 40 patients and associated with positive antiphospholipid antibodies (p = 0.004; OR = 3.2; CI = 1.9-4.5) and less frequently with renal (p = 0.002; OR = 1.9; CI = 0.0-0.6) and cutaneous (p = 0.04; OR = 1.1; CI = 0.0-0.8) involvement. We identified 28 patients with 38 episodes of psychosis associated with corticosteroid therapy. All the patients had severe active disease and ten of these patients had hypoalbuminemia when psychosis developed. At the time of psychotic event, all the patients were taking prednisone in doses varying from 0.75 to 1 mg/kg day(-1). Psychosis resolved after tapering prednisone down in all patients. Acute psychosis related to SLE was observed in 11.3% of our cohort. Recurrence of primary psychosis was associated with other CNS manifestations related to SLE.
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PMID:Acute psychosis in systemic lupus erythematosus. 1763 2

Neurological manifestations in lupus can be due to active lupus disease affecting the brain or to other reasons. Reversible posterior leucoencephalopathy syndrome, primary lymphoma of the central nervous system, cerebral infections by bacteria (e.g. mycobacteria), viruses (e.g. JC virus), fungi (e.g. Cryptococcus) and parasites (e.g. Acanthamoeba), steroid-induced psychosis and reactive depression need to be excluded. Brain-reactive autoantibodies have been described as associating with neuropsychiatric lupus. The strongest associations described to date are with antiribosomal P protein and antiphospholipid antibodies. However these autoantibodies have not been shown to play significant roles in the pathogenesis. Treatment strategy for severe neuropsychiatric lupus include establishing definitive diagnosis, early identification and treatment of aggravating factors, appropriate symptomatic treatment, adequate immunosuppression, selective B-cell depletion and autologous haematopoietic stem cell transplant. Systematic reviews have shown that cyclophosphamide administration is superior to pulse methylprednisolone as a maintenance therapy. Mycophenolate mofetil has been shown to have modest effect and should only be considered if cyclophosphamide cannot be administered.
Lupus 2010 Oct
PMID:Neuropsychiatric lupus: clinical challenges, brain-reactive autoantibodies and treatment strategies. 2094 48

Despite precise definitions and exclusions for 19 syndromes of neuropsychiatric systemic lupus erythematosus (NPSLE), under some circumstances it appears to be difficult to differentiate whether neuropsychiatric symptoms are caused by SLE or by other reasons such as primary mental disorders or substance-induced mood disorders, especially induced by glucocorticoids or antimalarials. We report the case of a male patient with SLE who presented with an exacerbation of bipolar disorder triggered by chloroquine. Firstly, when the patient was diagnosed with SLE, he underwent six months of therapy with chloroquine without any psychiatric symptoms. Later, the SLE returned and the patient was prescribed chloroquine again, without any mental illness. When the third exacerbation of SLE occurred, it coincided with a severe depressive episode with psychotic features that became aggravated for the first time after the administration of chloroquine. The chloroquine was subsequently replaced with hydroxychloroquine for the next six months without any behavioral problems, following which, the SLE and mood disorder were in remission. Later, a bipolar disorder relapse occurred, manifested by a manic episode, and in the following three months, despite psychiatric treatment, a manic episode with psychotic features developed four days after chloroquine was prescribed for arthritis. It was the second time that the mood disorder was exacerbated by chloroquine. Since that time, chloroquine has been withdrawn. Currently the patient is undergoing treatment with hydroxychloroquine and psychiatric drugs with good response. Our case points out that although chloroquine-induced psychosis is rare, patients presenting with behavioral changes need physicians' attention in order to diagnose early and efficiently treat encountered mood disorders.
Lupus 2014 Feb
PMID:Exacerbations of bipolar disorder triggered by chloroquine in systemic lupus erythematosus--a case report. 2537 39

Abstract A 55-year-old woman with well-controlled systemic lupus erythematosus (SLE) suffered from the abrupt onset of massive intractable ascites, which did not respond to conventional diuretic therapy. While treatment with methylprednisolone pulse therapy ameliorated this lupus peritonitis, neuropsychiatric symptoms then appeared. After a diagnosis of the central nervous system (CNS) lupus, pulse therapy was continued and the patient recovered from the lupus psychosis. We discuss the differential diagnosis between CNS lupus and steroid-induced psychosis with particular references to recent diagnostic methods for CNS lupus.
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PMID:A case of central nervous system lupus in succession to lupus peritonitis: a difficulty in the differential diagnosis between lupus psychosis and steroid-induced psychosis. 2438 54