Comparison of the single dose pharmacokinetics of sulphasalazine in rheumatoid arthritis and inflammatory bowel disease.

Astbury, Carol; Taggart, A J; Juby, L. D.; Zebouni, L; Bird, H. A.

doi:10.1136/ard.49.8.587

Cited by 18 publications

(10 citation statements)

References 23 publications

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“…Plasma concentrations of sulphapyridine may be highly variable in patients with rheumatoid arthritis. Maximum concentrations ranged from 8 to 22 mglL after single 2g doses of sulphasalazine in 1 study (Astbury et al 1990). Mean (± SD) steady-state concentrations of 18 ± 20 mglL were reported in 12 older patients, and 15 ± 8 mglLin 8 younger patients after 17 days' administration of sulphasalazine 2 g/day .…”

Section: Concentration-effect Relationshipsmentioning

confidence: 89%

“…Estimates of about 10 to 30% absorption in the small intestine, with extensive enterohepatic recycling, have been reported (Khan & Truelove 1982;Lewkonia et al 1973;Pinals 1988). The terminal elimination half-life of sulphasalazine in groups of patients with rheumatoid arthritis and with inflammatory bowel disease ranged from 3 to 9 hours (Astbury et al 1990). Elimination half-life was prolonged in the elderly (Taggart et al , 1992.…”

Section: Overview Of Dispositionmentioning

confidence: 92%

“…The bioavailability of sulphapyridine from sulphasalazine in patients with rheumatoid arthritis may be greater than from those with inflammatory bowel disease (Astbury et al 1990). Higher sulphapyridine concentrations may explain the apparently higher incidence of adverse effects reported in people with rheumatoid arthritis.…”

Section: Absorptionmentioning

confidence: 98%

“…Minor toxic effects are thought to be related to higher plasma sulphapyridine concentrations (Astbury et al 1990). Plasma concentrations of sulphapyridine may be highly variable in patients with rheumatoid arthritis.…”

Section: Concentration-effect Relationshipsmentioning

confidence: 99%

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Clinical Pharmacokinetics of Slow-Acting Antirheumatic Drugs

Tett

1993

Clinical Pharmacokinetics

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The pharmacokinetics of the slow acting antirheumatic drugs (SAARDs), hydroxychloroquine, chloroquine, penicillamine, the gold complexes and sulphasalazine, in humans have been studied. For all these drugs, both in controlled clinical trials and in empirical observations from rheumatological practice, delays of several months are reported before full clinical effects are achieved. Variability in response is also characteristic of these agents. Pharmacokinetic factors may partially explain these clinical observations. Delays in the achievement of steady-state concentrations or of concentrations likely to have a therapeutic benefit may occur because of slow drug accumulation. Variable concentrations may arise after standard administered doses because of interindividual pharmacokinetic variability. These factors are likely to contribute to the delay in response and the variable response, respectively. Pharmacokinetics of the antimalarials, hydroxychloroquine and chloroquine, are characterised by extensive tissue sequestration with reported volumes of distribution in the thousands of litres. Both drugs have reported elimination half-lives of greater than 1 month. A 2- to 3-fold range occurs in the fraction of an oral dose absorbed from a tablet formulation. Variable interindividual clearance is also reported. Hydroxychloroquine and chloroquine are administered as racemates. Enantioselective disposition of both compounds occurs, again with notable interindividual variability. Sulphasalazine is split in the large intestine into sulphapyridine, proposed to be the active compound in rheumatoid arthritis, and mesalazine (5-aminosalicylic acid). Sulphapyridine is metabolised partly by acetylation, the rate of which is under genetic control. A wide range of sulphapyridine steady-state concentrations are reported after standard doses of sulphasalazine. The gold complexes are administered either intramuscularly or in an oral form (auranofin). Gold is widely distributed in the body. Very long terminal elimination half-lives and slow accumulation rates are reported. Penicillamine is administered orally. Its bioavailability is variable and may decrease by as much as 70% in the presence of food, antacids and iron salts. Penicillamine forms disulphide bonds with many proteins in the blood and tissues, creating potential slow release reservoirs of the drug. Like the other SAARDs, gold complexes and penicillamine are found in a wide range of blood concentrations after administration in standard doses to different individuals. More research must be conducted into the concentration-effect relationships of the SAARDs before the pharmacokinetic characteristics of these drugs can be used effectively to optimise patient therapy.

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Section: Concentration-effect Relationshipsmentioning

confidence: 89%

Section: Overview Of Dispositionmentioning

confidence: 92%

Section: Absorptionmentioning

confidence: 98%

Section: Concentration-effect Relationshipsmentioning

confidence: 99%

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Clinical Pharmacokinetics of Slow-Acting Antirheumatic Drugs

Tett

1993

Clinical Pharmacokinetics

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“…A higher incidence of adverse reaction has been noted after treatment with sulfasalazine in adult rheumatoid arthritis than in inflammatory bowel disease (Astbury et al 1990; references therein). A comparative single-dose (sulfasalazine 2g) pharmacokinetic study by Astbury et al (1990) revealed significantly higher plasma concentrations of sulfapyridine but lower values for sulfasalazine in rheumatoid arthritis than in inflammatory bowel disease.…”

Section: Suljasalazinementioning

confidence: 97%

Clinical Pharmacokinetics of Drugs Used in Juvenile Arthritis

Skeith

Jamali

1991

Clinical Pharmacokinetics

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Juvenile arthritis is defined as the occurrence of objective evidence of arthritis for a minimum of 6 weeks, in a child 16 years of age or younger. With a reported incidence of 9 to 19.6 per 100,000 children, juvenile arthritis is considered to be a rare disease. There is no known cure; however, up to 75% of patients will undergo remission by late adolescence. Drugs used in the treatment of juvenile arthritis are divided into 2 major classes: (a) the nonsteroidal anti-inflammatory drugs (NSAIDs) including salicylates, naproxen, ibuprofen, fenoprofen, ketoprofen, flurbiprofen, indomethacin, sulindac, tolmetin and diclofenac, and (b) disease modifying agents which encompass drugs such as antimalarial agents, gold, methotrexate, penicillamine and sulfasalazine. In almost all the reports dealing with the pharmacokinetics of NSAIDs, the level of disease activity has not been noted. The level of activity is important since, during a flare, the plasma albumin may fall to the point that it causes a substantial and clinically significant increase in the unbound serum concentration of highly bound drugs. The relationship between the concentration of these drugs in the systemic circulation and their efficacy is not clear. However, for many of them, therapeutic drug monitoring is recommended as a means of reducing the possibility of toxic reactions. Further pharmacokinetic and -dynamic evaluations are needed for many of these drugs in juvenile arthritis.

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Sulfasalazine

Haagsma¹

2005

Antirheumatic Therapy: Actions and Outcomes

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Comparison of the single dose pharmacokinetics of sulphasalazine in rheumatoid arthritis and inflammatory bowel disease.

Cited by 18 publications

References 23 publications

Clinical Pharmacokinetics of Slow-Acting Antirheumatic Drugs

Clinical Pharmacokinetics of Slow-Acting Antirheumatic Drugs

Clinical Pharmacokinetics of Drugs Used in Juvenile Arthritis

Sulfasalazine

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