Drug Eruptions From Anticonvulsant Drugs

Goldstein, Norman

doi:10.1001/archderm.1963.01590170070012

Cited by 15 publications

(4 citation statements)

References 8 publications

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“…The clinical picture of pseudolymphoma consists of generalized lymphadenopathy, malaise, fever and a skin rash, with the frequent association of pain and swelling in the joints as well as hepatosplenomegaly [1,2,[5][6][7][8][9]. In some cases diarrhea may be a part of this picture [10,11].…”

Section: Discussionmentioning

confidence: 99%

Pseudolymphoma Syndrome

Halevy¹,

Feuerman²

1977

Dermatology

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A transient dermatologic abnormality which gave a histologic picture compatible with malignant lymphoma is described. The clinical manifestations included diarrhea, hepatosplenomegaly, moderate lymph node enlargement without histopathological changes and evidence of involvement of the reticulo-endothelial system. Both the dermatologic and gastrointestinal disorders appeared approximately 1 year after discontinuation of treatment with diphenylhydantoin, which the patient had taken for 2 years. The possible association between the transient abnormality and the previous diphenylhydantoin therapy justifies the classification of this case as ‘pseudolymphoma syndrome’.

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Section: Discussionmentioning

confidence: 99%

Pseudolymphoma Syndrome

Halevy¹,

Feuerman²

1977

Dermatology

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“…Increased L1 transcripts and ORF1p protein have been detected in kidney biopsies from patients with lupus nephritis and in salivary gland biopsies from Sjögren's syndrome patients [98]. In healthy individuals, L1 transcripts are low or undetectable, but can be induced by demethylating drugs like 5-aza-deoxycytosine [99], including those known to cause drug-induced lupus [100,101], e.g., hydralazine and Alu elements have also gained interest in lupus research due to the association of Aluderived RNA with Ro60 [95][96][97], a well-recognized SLE autoantigen. In a 2015 paper [97], immune complexes formed by anti-Ro60 autoantibodies where isolated from SLE patients and the bound RNA sequenced, revealing that much of it was Alu-and L1-derived.…”

Section: How L1 Retrotransposons May Trigger Ifn-positive Slementioning

confidence: 99%

“…Increased L1 transcripts and ORF1p protein have been detected in kidney biopsies from patients with lupus nephritis and in salivary gland biopsies from Sjögren's syndrome patients [98]. In healthy individuals, L1 transcripts are low or undetectable, but can be induced by demethylating drugs like 5-aza-deoxycytosine [99], including those known to cause drug-induced lupus [100,101], e.g., hydralazine and procainamide. Reduced methylation of the 5 regulatory ("promoter") region of L1 has been reported in both adult and pediatric lupus patients [102].…”

Section: How L1 Retrotransposons May Trigger Ifn-positive Slementioning

confidence: 99%

Implications of Endogenous Retroelements in the Etiopathogenesis of Systemic Lupus Erythematosus

Ukadike

Mustelin

2021

JCM

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Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease. While its etiology remains elusive, current understanding suggests a multifactorial process with contributions by genetic, immunologic, hormonal, and environmental factors. A hypothesis that combines several of these factors proposes that genomic elements, the L1 retrotransposons, are instrumental in SLE pathogenesis. L1 retroelements are transcriptionally activated in SLE and produce two proteins, ORF1p and ORF2p, which are immunogenic and can drive type I interferon (IFN) production by producing DNA species that activate cytosolic DNA sensors. In addition, these two proteins reside in RNA-rich macromolecular assemblies that also contain well-known SLE autoantigens like Ro60. We surmise that cells expressing L1 will exhibit all the hallmarks of cells infected by a virus, resulting in a cellular and humoral immune response similar to those in chronic viral infections. However, unlike exogenous viruses, L1 retroelements cannot be eliminated from the host genome. Hence, dysregulated L1 will cause a chronic, but perhaps episodic, challenge for the immune system. The clinical and immunological features of SLE can be at least partly explained by this model. Here we review the support for, and the gaps in, this hypothesis of SLE and its potential for new diagnostic, prognostic, and therapeutic options in SLE.

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“…Wegen der weitverbreiteten An wendung von Hydantoinen und Phénobarbital ist ein Fall von Kreuzsen sibilisierung zwischen diesen beiden Mitteln erwähnenswert [173], Die Häufigkeitsangaben für die bekannte Gingivahyperplasie unter Hydantointherapie schwanken zwischen 20 und 60% (cf. Tabelle, Diverses 6.2).…”

Section: Hydantoineunclassified

Hautnebenwirkungen interner Arzneimittel

Widmer¹,

Zürcher²,

Krebs³

1976

Dermatology

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This, the fourth part of a synopsis of cutaneous side effects of drugs, covers the drugs affecting the central nervous system: antiepileptics, hypnotics, narcotics and psychopharmaceutics; the myorelaxants and antiallergics follow, and lastly there is a section on drug addiction and placebo. The various cutaneous side effects are listed in chart form referring to more than 500 sources. A drug index is attached for handy reference. The reviews of certain drug induced skin disorders are continued with tables covering photosensitivity and changes in skin colour. Phototoxicity, photoallergy and light sensitivity by porphyria are differentiated. The various pigmentation disorders, colour changes due to metal deposits as well as different localisations are included.

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Drug Eruptions From Anticonvulsant Drugs

Cited by 15 publications

References 8 publications

Pseudolymphoma Syndrome

Pseudolymphoma Syndrome

Implications of Endogenous Retroelements in the Etiopathogenesis of Systemic Lupus Erythematosus

Hautnebenwirkungen interner Arzneimittel

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