Phenothiazine‐induced systemic lupus erythematosus with superior vena cava syndrome: case report and review of the literature

Steen, Virginia D.; Ramsey‐Goldman, Rosalind

doi:10.1002/art.1780310716

Cited by 25 publications

(10 citation statements)

References 15 publications

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“…Nevertheless, clozapine serum levels were associated with increased APL levels in patients with schizophrenia [79]. Still, increased APL levels induced by antipsychotics seldom seem to be associated with VTE [74,75], although a few cases have been reported [76,78,82].…”

Section: Biological Mechanismsmentioning

confidence: 99%

Risk of venous thromboembolism due to antipsychotic drug therapy

Hägg

Jönsson

Spigset

2009

Expert Opinion on Drug Safety

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An increasing number of reports suggest a link between venous thromboembolism (VTE) and the use of antipsychotics. To better understand this association the available body of evidence has been critically scrutinised. Relevant articles were identified in the databases Scopus and PubMed. Several observational studies using different methodologies show an increased risk of VTE in psychiatric patients. This elevated risk seems to be related to the use of antipsychotic medication and in particular to the use of clozapine and low-potency firstgeneration drugs. Many studies investigating the association have, however, methodological limitations. The biological mechanisms involved in the pathogenesis of this possible adverse reaction are largely unknown but several hypotheses have been suggested such as druginduced sedation, obesity, increased levels of antiphospholipid antibodies, enhanced platelet aggregation, hyperhomocysteinemia and hyperprolactinemia. The association may also be related to underlying risk factors present in psychotic patients. Physicians need to be aware of this possible adverse drug reaction. Although supporting evidence has not been published they should consider discontinuing or switching the antipsychotic treatment in patients experiencing VTE. In addition, although data is lacking, the threshold for considering prophylactic antithrombotic treatment should be low when risk situations for VTE arise, such as immobilisation, surgery and so on.

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Section: Biological Mechanismsmentioning

confidence: 99%

Risk of venous thromboembolism due to antipsychotic drug therapy

Hägg

Jönsson

Spigset

2009

Expert Opinion on Drug Safety

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“…The patient also showed a reduction in her ESR from high 70s to 43 as her symptoms decreased. There was some thought that she could have had a drug-induced lupus as a result of her treatment with perphenazine, which has been documented in the literature, 19 but, in retrospect, a review of her symptoms shows that she likely met diagnostic criteria for lupus based on the following symptoms: thrombocytopenia (not necessarily antibiotic-induced), hemolytic anemia, arthritis, CNS manifestations, anti dsDNA, and positive ANA. The patient also had a truncal rash for several weeks of her admission, which was thought to be fungal, but did not respond to nystatin.…”

Section: Case Reportmentioning

confidence: 99%

Catatonia as the Presenting Symptom in Systemic Lupus Erythematosus

Pustilnik

Trutia²

2011

Journal of Psychiatric Practice

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Catatonia is a syndrome of physical and behavioral abnormalities that can result from psychiatric, neurological, or medical illness. Although systemic lupus erythematosus (SLE) is commonly known to cause neurological and psychiatric manifestations, it has only rarely been reported to cause the catatonic syndrome. In nearly all previously reported cases, the diagnosis of catatonia was reported in patients with an established diagnosis of lupus. We report a case in which a woman with no known medical history presented with catatonia that did not respond to standard treatment with benzodiazepines, suffered a long and complicated hospital course, and was eventually diagnosed with lupus. With initiation of treatment for lupus, her symptoms of catatonia remitted. This case illustrates the importance of considering medical causes in the diagnosis and treatment of psychiatric disorders, especially the catatonic syndrome.

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“…Chlorpromazine is the most frequent culprit with over 300 cases reported [14,18,31,32,[39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55]. The first report of a phenothiazine-induced LA (PZILA) was published in 1977 by Canoso and Hutton [39].…”

Section: Phenothiazinesmentioning

confidence: 99%

“…Experiments with ultraviolet light have demonstrated the induction of stable chlorpromazine-ssDNA complexes [60]. Reports of Coombs-positive studies, false-positive syphilis tests, and thrombocytopenia have been made, but are few in number [14,39,41,43,47,48].…”

Section: Phenothiazinesmentioning

confidence: 99%

“…The tables includes examples of drugs that have been shown to induce both a hemolytic anemia and a lupus anticoagulant. While this classification conceptually explains how drug-related antibodies may be induced, relatively few studies of DILA actually performed a direct Coombs test [12,15,16,21,24,41,47]. Of those tested, the highest reported incidence was 67% (n024) in a group treated for >2.5 years with antipsychotic agents that included CPZ [41].…”

Section: Potential Mechanismsmentioning

confidence: 99%

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Drug-Induced Lupus Anticoagulants and Antiphospholipid Antibodies

Dlott

Roubey

2011

Curr Rheumatol Rep

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Lupus anticoagulants (LA) are immunoglobulins (IgG, IgM, and/or IgA) which interfere with one or more of phospholipid-dependent in vitro coagulation tests, eg, activated partial thromboplastin time (aPTT), kaolin clotting time (KCT), dilute Russell viper venom time (dRVVT), and dilute prothrombin time (dPT). LAs may be seen in a variety of clinical settings including the primary antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE), other autoimmune diseases, secondary to infections, malignancies, and in association with certain drugs. LAs associated with the antiphospholipid syndrome and other autoimmune disease recognize certain phospholipid-binding proteins (β(2)-glycoprotein I [β(2)GPI] or prothrombin). Many drugs have been implicated as possibly causing LAs, although the majority of such cases are limited to a select few. Drug-induced LAs are heterogeneous, differing in laboratory findings as well as related clinical complications. This paper reviews the English medical literature on drug-induced LA and potential mechanisms of induction.

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Phenothiazine‐induced systemic lupus erythematosus with superior vena cava syndrome: case report and review of the literature

Cited by 25 publications

References 15 publications

Risk of venous thromboembolism due to antipsychotic drug therapy

Risk of venous thromboembolism due to antipsychotic drug therapy

Catatonia as the Presenting Symptom in Systemic Lupus Erythematosus

Drug-Induced Lupus Anticoagulants and Antiphospholipid Antibodies

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