HLA antigens and toxic reactions to sodium aurothiopropanol sulphonate and D-penicillamine in patients with rheumatoid arthritis.

Perrier, P.; Raffoux, C; Thomas, P.; Tamisier, J. N.; Busson, M; Gaucher, A; Streiff, F

doi:10.1136/ard.44.9.621

Cited by 27 publications

(6 citation statements)

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“…Several studies have shown that HLA polymorphism contributes to susceptibility to adverse drug reactions 4,5,20. To the best of our knowledge, the present report is the first to show an association of DRB1*08:02 with BI-Pro in Japanese RA patients.…”

Section: Discussionsupporting

confidence: 59%

HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

et al. 2014

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BACKGROUNDDrug-induced proteinuria can occur in rheumatoid arthritis (RA) patients treated with d-penicillamine, gold salts, or bucillamine (Buc), and represents a drug hypersensitivity reaction. Striking associations of human leukocyte antigen (HLA) alleles with adverse reactions have recently been reported for many drugs.METHODSWe investigated the association of HLA class II with Buc-induced proteinuria (BI-Pro) in 485 Japanese RA patients treated with Buc, of whom 25 had developed BI-Pro.RESULTS AND CONCLUSIONThis preliminary study showed a highly significant association of DRB1*08:02 with BI-Pro (P = 1.09 × 10−6, corrected P [Pc] = 1.96 × 10−5, odds ratio [OR] 25.17, 95% confidence interval [CI] 7.98–79.38). DQB1*04:02 was also significantly associated with increased risk of BI-Pro (P = 2.44 × 10−5, Pc = 2.69 × 10−4, OR 10.35, 95%CI 3.99–26.83). These findings provide useful information for promoting personalized medicine for RA.

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Section: Discussionsupporting

confidence: 59%

HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

et al. 2014

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“…DNA typing of HLA-DR alleles from patients with RA confirmed the shared epitope hypothesis, because HLA-DRB1*0401, 0404, 0405, 0408, HLA-DRB1*0101 and DRB1*1402 share the same sequence at positions 70–74 in the third exon, but DRB1*0402 and others do not [7, 14]. HLA antigens have also been reported to be associated with the reactive side effects of drugs to RA [15, 16, 17, 18, 19, 20, 21]and also with the severity of the disease [22, 23, 24, 25, 26, 27, 28, 29, 30]as well as with the susceptibility to RA with extra-articular manifestations [25, 31, 32, 33, 34, 35]. …”

Section: Introductionmentioning

confidence: 62%

“…These nephropathies, especially toxic nephropathy and secondary amyloidosis, could determine the prognosis of patients [36, 40]. HLA-DR3 has been reported to be associated with proteinuria after treatment with D -penicillamine and sodium aurothiomalate in Caucasian patients [16, 17]. Panayi et al [15]described that serological HLA-DR3 and/or serological HLA-DR15 were associated with a toxic reaction against kidney under gold therapy.…”

Section: Discussionmentioning

confidence: 99%

“…However, a considerable number of patients with RA develop such kidney diseases as renal amyloidosis and/or toxic or allergic reactions to prescribed drugs [36, 37, 38, 39, 40]. A significant association of the presence of serological HLA-DR3 with the development of proteinuria during the treatment with aurothiomalate and D -penicillamine has been reported in Caucasian patients with RA [16, 17]. We herein report the findings of analyses of the immunogenetic backgrounds of Japanese patients with RA and RI.…”

Section: Introductionmentioning

confidence: 99%

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Association between HLA-DRB1*15 and Japanese Patients with Rheumatoid Arthritis Complicated by Renal Involvement

Tokunaga¹,

Noda²,

Kaneoka³

et al. 1999

Nephron

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We performed serological phenotyping of HLA antigens in 175 patients with rheumatoid arthritis (RA) with (n = 41) and without (n = 134) renal involvement (RI), and DNA typing of HLA class II alleles in 75 patients. Among the patients with RA, the frequency of serologically determined HLA-DR4 was found to be significantly increased (odds ratio: 1.8, confidence interval: 1.3–2.5, p = 2.4×10^–4). In the patients without RI, the frequency of serological DR4 significantly increased (odds ratio: 2.2, confidence interval: 1.6–3.3, p = 2.6×10^–5). On the other hand, among the patients with RI, a serological determinant, DR15, did significantly increase (odds ratio: 2.7, confidence interval: 0.9–8.4, p = 1.2×10^–3) in comparison to the controls. At the DNA level, we found that the association of Japanese RA patients with serological HLA-DR4 was based on that with a genotype of HLA-DRB1*0405 (odds ratio: 2.4, confidence interval: 1.5–4.0, p = 4.4×10^–4) and also found an association of HLA-DRB1*1501 (odds ratio: 2.8, confidence interval: 1.2–6.6, p = 0.017) with RA patients having RI. Our results confirmed the association of HLA-DRB1*04 with RA over the ethnic barrier at the DNA level. Our results also suggested a distinct genetic effect of HLA-DRB1*1501 in the aspect of the susceptibility of RI in RA.

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“…Calin (1980) suggested that genetic predisposition plays a role. Adverse effects, especially renal, with D-penicillamine have been found to be more frequent in patients with rheumatoid arthritis who belong to the HLA-Bs (Dequeker et al 1984) or DR3 (Perrier et al 1985) groups. Other studies, however, have shown that adverse effects with D-penicillamine are completely unpredictable, even if the patient has previously suffered toxicity with gold salts (Kean et al 1982).…”

Section: Pharmacokinetic Drug Interactionsmentioning

confidence: 97%

Clinical Pharmacokinetics of D-Penicillamine

Netter

Bannwarth

Pere

et al. 1987

Clinical Pharmacokinetics

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Penicillamine exists as 2 stereoisomers, but only the D-isomer is used therapeutically. Its chemical reactivity derives from its functional groups, of which the thiol group seems the most important. It is difficult to determine penicillamine in biological fluids because of its instability, the presence of endogenous compounds with a thiol function, and the various chemical forms in which it occurs, namely reduced free penicillamine, penicillamine bound to proteins, and internal (P-S-S-P) and mixed (P-S-S-C) disulphides. The earliest assay methods (colourimetry, isotopic methods, gas-phase chromatography) were neither sensitive nor specific. High performance liquid chromatography with electrochemical detection has led to a more specific assay for D-penicillamine, with detection based on either derivatisation reactions or on electro-oxidisation of the thiol function. With dual-electrode detectors (Au/Hg) disulphides can be assayed directly. D-penicillamine is absorbed rapidly but incompletely (40 to 70%) in the intestine, with wide interindividual variations. Food, antacids and, in particular, iron reduce absorption of the drug. Its bioavailability is also dramatically decreased in patients with malabsorption states. The peak plasma concentration occurs at 1 to 3 hours after ingestion, regardless of dose, and is of the order of 1 to 2 mg/L after an oral dose of 250 mg; some investigators have reported a double peak in plasma, which is probably not due to an enterohepatic cycle. The concentration in plasma then decreases rapidly, generally following a biphasic curve. When long term treatment is discontinued, there is a slow elimination phase lasting 4 to 6 days, which suggests that there is a 'deep compartment' or 'slow pool of the drug reversibly bound to tissues', particularly the skin. This may explain the persistence of its therapeutic effect and the occurrence of undesirable side effects after treatment has been stopped. During long term treatment plasma concentrations are highly variable between individuals. They do not seem to be correlated with the activity or the toxicity of D-penicillamine in patients with rheumatoid arthritis. More than 80% of plasma D-penicillamine is bound to proteins, particularly albumin. The rest is mainly in the free reduced form or as disulphides. Only a small portion of the dose is metabolised in the liver to S-methyl-D-penicillamine. The route of elimination is mainly renal; disulphides represent the main compounds found in the urine. Faecal excretion corresponds mainly to the non-absorbed fraction of the drug.

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HLA antigens and toxic reactions to sodium aurothiopropanol sulphonate and D-penicillamine in patients with rheumatoid arthritis.

Cited by 27 publications

References 10 publications

HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

Association between HLA-DRB1*15 and Japanese Patients with Rheumatoid Arthritis Complicated by Renal Involvement

Clinical Pharmacokinetics of D-Penicillamine

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HLA antigens and toxic reactions to sodium aurothiopropanol sulphonate and D-penicillamine in patients with rheumatoid arthritis.

Cited by 27 publications

References 10 publications

HLA-DRB1*08:02 Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

HLA-DRB1*08:02 Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

Association between HLA-DRB1*15 and Japanese Patients with Rheumatoid Arthritis Complicated by Renal Involvement

Clinical Pharmacokinetics of D-Penicillamine

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HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients

HLA-DRB108:02* Is Associated with Bucillamine-Induced Proteinuria in Japanese Rheumatoid Arthritis Patients