Drug-Related Lupus

Adams, Louis E.; Hess, Evelyn V.

doi:10.2165/00002018-199106060-00004

Cited by 38 publications

(5 citation statements)

References 128 publications

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“…Our findings of minocycline-induced lupus are mostly consistent with the features of DIL associated with other drugs such as procainamide, isoniazid or hydralazine [6, 7, 8]. The main clinical features in the analysed cases were polyarthritis/polyarthralgia often with evidence of synovitis.…”

Section: Discussionsupporting

confidence: 86%

“…While the age of the patients represents the age of the population at risk for both the underlying diseases and the drugs used in treatment, the gender of a patient mainly reflects the disease for which they are receiving drugs. In contrast to idiopathic SLE, with a female-to-male ratio of 8:1, DIL typically occurs only slightly more often in females [8]. However, with respect to gender distribution, minocycline-induced lupus shows a completely different pattern.…”

Section: Discussionmentioning

confidence: 99%

“…chlorpromazine, hydralazine, isoniazid, procainamide) have been reported to cause symptoms and laboratory findings which closely resemble SLE [5, 6, 7, 8]. However, drug-induced lupus (DIL) is a less well-defined syndrome, and a generally accepted definition for this disease does not exist [6, 7].…”

Section: Introductionmentioning

confidence: 99%

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Minocycline-Induced Lupus

Bircher²,

2000

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Background: Minocycline has increasingly been associated with different adverse auto-immune reactions including drug-induced lupus. Objective: To identify the scope of minocycline-induced lupus and to characterise its typical features. Methods: Comprehensive Medline and Embase search of the English and non-English literature for case reports of minocycline-induced lupus. Results: We included 57 cases of minocycline-induced lupus (mean age ± SD at onset: 21.6 ± 8.6 years, median time of exposure: 19 months, range 3 days to 6 years). All patients showed the clinical features of polyarthralgia/polyarthritis often accompanied by liver abnormalities. Twelve patients had evidence of dermatological manifestations (i.e rash, livedo reticularis, oral ulceration, subcutaneous nodules, alopecia). The ANA test was positive in all patients. Conclusion: Long-term exposure to minocycline may be associated with drug-induced lupus. Baseline and periodic liver function and ANA tests accompanied by appropriate clinical monitoring are suggested for patients receiving long-term minocycline therapy.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

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Minocycline-Induced Lupus

Bircher²,

2000

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“…Hydralazine (Figure 1) is a prototype of 'lupus-inducing drugs' that elicit anti-nuclear antibodies and a syndrome resembling systemic lupus erythematosus in recipients [1][2][3]. This adverse effect has reduced its usage as an antihypertensive drug, at least with larger doses.…”

Section: Introductionmentioning

confidence: 99%

Triplex-DNA stabilization by hydralazine and the presence of anti-(triplex DNA) antibodies in patients treated with hydralazine

Thomas¹,

Seibold²,

Adams

et al. 1995

Biochemical Journal

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Hydralazine is an antihypertensive drug that elicits andti-nuclear antibodies in patients as an adverse effect. We investigated the ability of hydralazine to promote/stabilize the triplex DNA form of poly(dA).2poly(dT). Under conditions of low ionic strength, the polynucleotide melted as a double helix with a melting temperature (Tm) of 55.3 degrees C. Hydralazine destabilized this duplex form by reducing its Tm to 52.5 degrees C. Spermidine (2.5 microM), a natural polyamine, provoked the triplex form of poly(dA)-.2poly(dT) with two melting transitions, Tm1 of 42.8 degrees C corresponding to triplex-->duplex+single-stranded DNA and Tm2 of 65.4 degrees C, corresponding to duplex melting. Triplex DNA thus formed in the presence of spermidine was further stabilized by hydralazine (250 microM) with a Tm1 of 53.6 degrees C. A similar stabilization effect of hydralazine was found on triplex DNA formed in the presence of 5 mM Mg2+. CD spectra revealed conformational perturbations of DNA in the presence of spermidine and hydralazine. These results support the hypothesis that hydralazine is capable of stabilizing unusual forms of DNA. In contrast with the weak immunogenicity of DNA in its right-handed B-DNA conformation, these unusual forms are immunogenic and have the potential to elicit anti-DNA antibodies. To test this possibility, we analysed sera from a panel of 25 hydralazine-treated patients for anti-(triplex DNA) antibodies using an ELISA. Our results showed that 72% of sera from hydralazine-treated patients contained antibodies reacting toward the triplex DNA. In contrast, there was no significant binding of normal human sera to triplex DNA. Taken together our data indicate that hydralazine and related drugs might exert their action by interacting with DNA and stabilizing higher-order structures such as the triplex DNA.

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“…It is estimated that up to 10% of cases of SLE and SCLE might be drug induced [1, 2]. Three conditions are usually required to assess the diagnosis of drug-induced LE: no sign of LE before drug administration; presence of antinuclear antibodies and at least one clinical feature of LE while under treatment with the offending drug, and rapid improvement of clinical symptoms together with a gradual decrease in antinuclear antibodies serum titer following causal drug withdrawal [3].…”

Section: Introductionmentioning

confidence: 99%

Terbinafine-Induced Subacute Cutaneous Lupus Erythematosus

Farhi¹,

Viguier²,

Cosnes

et al. 2006

Dermatology

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Background: Nearly 10% of lupus erythematosus (LE) are drug induced. More than 60 different drugs are involved in iatrogenic LE. We report herein 3 cases of terbinafine-induced LE. Observations: Three patients receiving terbinafine for a suspected dermatophytic infection developed a subacute cutaneous LE, within 7 weeks following terbinafine introduction. The patients’ medical history included sicca syndrome, lung carcinoma and Kikuchi disease, respectively. Clinical remission occurred within 15 weeks following terbinafine withdrawal. Discussion: Sixteen cases of terbinafine-induced LE have been previously reported, including 13 women. The median age was 54 years. Prior autoimmunity was reported in 10 cases, including 5 pre-existing LE. The median delay between terbinafine introduction and LE onset was 5 weeks. The median time until clinical recovery following terbinafine withdrawal was 8 weeks. Conclusion: Terbinafine should be prescribed only in patients with proven dermatophytosis. We recommend cautious monitoring in patients with pre-existing autoimmunity. The diagnosis of terbinafine-induced LE should lead to the immediate and definitive withdrawal of the drug.

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Drug-Related Lupus

Cited by 38 publications

References 128 publications

Minocycline-Induced Lupus

Minocycline-Induced Lupus

Triplex-DNA stabilization by hydralazine and the presence of anti-(triplex DNA) antibodies in patients treated with hydralazine

Terbinafine-Induced Subacute Cutaneous Lupus Erythematosus

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