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Biomedical subjects

B McConkey

Publications and source records attributed to B McConkey.

At least 37 records · Page 2Linked to original sources
PubMed1986

Sulphasalazine for rheumatoid arthritis: toxicity in 774 patients monitored for one to 11 years.

Sulphasalazine is being used increasingly to treat rheumatoid arthritis, though its long term safety profile has not been established in this condition. The incidence and nature of adverse effects occurring in 774 patients with rheumatoid arthritis treated with sulphasalazine for periods ranging from one to 11 years were therefore noted. Altogether 205 of the patients stopped treatment permanently due to an adverse effect. One hundred and fifty six (76%) of these events occurred within three months and few beyond the first year. Most events were trivial and were self limiting after withdrawal of the drug; of the potentially more serious adverse effects, 33 (66%) occurred within three months of treatment. None of the patients died or suffered lasting ill effects. It is concluded that adverse effects of treatment with sulphasalazine are generally seen within three months; though regular monitoring is desirable during that period, thereafter few worrying problems occur.

Adolescent↗
PubMed1986

Non-steroidal anti-inflammatory drugs and renal failure.

In 3 years seventeen patients presented to one unit with renal failure associated with the use of non-steroidal anti-inflammatory drugs (NSAID). Seven patients presented with acute renal failure, in four due to acute tubular necrosis and in three to acute interstitial nephritis; all recovered when NSAID treatment was stopped. Four patients presented with symptomless renal impairment discovered during routine follow-up in a rheumatology clinic; again all improved on withdrawal of NSAID. The remaining six patients presented with chronic renal failure, a disorder not previously associated with NSAID treatment. The pattern of renal disease associated with NSAID may be more extensive than has previously been recognised. A history of NSAID use should be sought in all patients presenting with unexplained renal failure.

Acute Kidney Injury↗
PubMed1986

The effect of antirheumatic drugs on circulating immune complexes in rheumatoid arthritis.

The relationship between antirheumatic drug treatment and levels of circulating immune complexes (125I-C1q binding activity) has been investigated in a prospective two-year study of patients with rheumatoid arthritis using the erythrocyte sedimentation rate (ESR) and serum C-reactive protein concentration as indices of disease activity. Twenty-eight patients were treated with non-steroid anti-inflammatory drugs, 14 patients had 'second line' drugs and 13 patients were treated with adrenal corticosteroids. Serum 125I-C1q binding activity did not change during non-steroid anti-inflammatory drug treatment; however, immune complex levels did fall during treatment with new (ICI 55,897, sulphasalazine) and established (gold, penicillamine) second line drugs. Serum 125I-C1q binding activity reflected the response to treatment shown by serum C-reactive protein and ESR. Serum C-reactive protein concentration and ESR fell with all doses of adrenal corticosteroids. In contrast, immune complex levels did not fall when doses of adrenal corticosteroids were below 20 mg/day prednisolone. 125I-C1q binding activity fell during high dose adrenal corticosteroid therapy (greater than 40 mg/day prednisolone; 1 g methylprednisolone infusions). Serial measurements of 125I-C1q binding activity correspond to ESR and the serum C-reactive protein concentration in distinguishing between anti-inflammatory drugs, which provide symptomatic relief only, and second line drugs which may retard disease progression. The fall in circulating immune complex levels during 'high' dose corticosteroid treatment, but not during 'low' dose treatment, suggests that corticosteroids have a dose-dependent effect on the immune system in addition to their anti-inflammatory properties.

Adult↗
PubMed1985

Serum amyloid A protein during the treatment of rheumatoid arthritis with second-line drugs.

Serum amyloid A protein (SAA), serum C-reactive protein (CRP) and the ESR were measured in 19 patients with rheumatoid arthritis before treatment and during therapy with gold, penicillamine or sulphasalazine for a mean period of 14.8 months (range 6-23 months). All three measurements decreased significantly; however, only 7% of SAA values fell to within the normal range (18-44 mg/l), compared to 38% measurements of serum CRP (less than 10 mg/l) and 32% of the ESR (less than 25 mm/h). In 8 (42%) of the 19 patients, SAA remained high (greater than 400 mg/l) for 3 months or more whilst serum CRP was depressed below 20 mg/l; this discrepancy was not related to particular drugs. We conclude that during treatment of rheumatoid arthritis with gold, penicillamine or sulphasalazine, SAA concentrations can be high when serum CRP and ESR are suppressed. SAA may be a more sensitive index of disease activity.

Adult↗
PubMed1985

Does sulphasalazine cause folate deficiency in rheumatoid arthritis?

Sulphasalazine impairs folic acid absorption and metabolism but rarely leads to folate deficiency in inflammatory bowel disease (IBD). In rheumatoid arthritis (RA), however, serum and red cell folate concentrations are often low and sulphasalazine might stress folate metabolism. In a prospective study, 2 g sulphasalazine was compared with 500 mg penicillamine daily in 30 patients over 24 weeks. Pre-treatment serum and red cell folate concentrations were low-normal. Improvements in disease activity and haemoglobin occurred in both treatment groups, but MCV increased only in patients taking sulphasalazine. Serum and red cell folate concentrations did not change in either group. Increased MCV with sulphasalazine might therefore reflect reticulocytosis secondary to drug-induced haemolysis. The mechanisms by which sulphasalazine antagonizes folate metabolism are dose-dependent and, consequently, higher doses might precipitate folate deficiency.

Arthritis, Rheumatoid↗
PubMed1984

Outcome of attempts to treat rheumatoid arthritis with gold, penicillamine, sulphasalazine, or dapsone.

The outcome of attempts to continue treatment indefinitely with either gold, penicillamine, sulphasalazine, or dapsone was studied in 240 patients with rheumatoid arthritis (RA). The usual reason for discontinuing treatment was the occurrence of an adverse effect. This led to 53% of patients stopping gold, 33% sulphasalazine, 32% penicillamine, and 17% dapsone. The next most frequent reason was that the drug was ineffective, leading to discontinuation in 37% of patients having dapsone, 24% sulphasalazine, 19% penicillamine, and 16% gold. Other reasons for stopping treatment were infrequent. The high discontinuation rate of these drugs over 2 years in part accounts for the conflict of opinion on whether they can alter the course of RA; their efficacy must to a large extent be governed by their acceptability.

Adolescent↗
PubMed1984

Rheumatoid arthritis: the effects of treatment with dapsone on hemoglobin.

Hemoglobin concentration (Hb) was measured at 6 week intervals for up to a year in 84 patients with rheumatoid arthritis treated with dapsone. During the first 6 weeks, mean Hb decreased from 12.0 to 11.0 g/dl (p less than 0.001). Falls in Hb occurred in 81% of patients but exceeded 2 g/dl in only 10%. After more than 6 weeks of treatment mean Hb increased, though a few individuals became anemic during this period. Anemia led to discontinuation of dapsone in 5 (6%) patients. Men and patients receiving corticosteroids had higher pretreatment Hb values; after falls in mean Hb at 6 weeks, recovery was more rapid in these 2 subgroups. Changes in Hb produced by 100 mg and 150 mg dapsone daily were similar.

Adult↗
PubMed1983

Comparison between penicillamine and sulphasalazine in rheumatoid arthritis: Leeds-Birmingham trial.

Sulphasalazine was first formulated by Svartz in the early 1940s, specifically for use as a remission inducing drug in rheumatoid arthritis. After the publication of an unfavourable trial, however, the drug was restricted to patients with ulcerative colitis. In the late 1970s sulphasalazine was re-examined in rheumatoid arthritis and favourable results reported in "open" trials. A double blind controlled trial was therefore conducted comparing enteric coated sulphasalazine and D-penicillamine in patients with active rheumatoid arthritis. A total of 63 patients were recruited in two centres; 31 were treated with sulphasalazine and 32 received penicillamine. After 16 weeks' treatment both drugs had produced significant improvements in clinical score, pain score measured on a visual analogue scale, grip strength, Ritchie articular index, erythrocyte sedimentation rate, and serum C reactive protein concentration. Nausea was the major side effect in the sulphasalazine treated group. No potentially dangerous effects of sulphasalazine were encountered in contrast with those seen in the penicillamine group. The results suggest that sulphasalazine is an effective and safe drug capable of producing remissions in active rheumatoid arthritis. They also lend confidence to the use of preliminary "open" trials as a means of screening for remission inducing drugs in rheumatoid arthritis.

Adult↗
PubMed1983

A comparison between clinical and laboratory tests in rheumatoid arthritis.

Five clinical measurements (clinical score, articular index, visual analogue pain score, visual analogue function score, grip strength) were compared with two laboratory tests (the erythrocyte sedimentation rate and serum C-reactive protein concentration) in 68 patients with rheumatoid arthritis (RA). Patients treated with nonsteroid anti-inflammatory drugs showed clinical deterioration when treatment was interrupted, followed by improvement on resumption; there was no change in the laboratory tests. Patients treated with remission-inducing drugs (RIDs) had improved clinical measurements and also reduced erythrocyte sedimentation rate and serum C-reactive protein levels. Treatment with RID's led to similar trends in both clinical and laboratory tests, but correlation coefficients between the tests at intervals rarely attained statistical significance. The different response times for each test and probably also errors inherent in clinical measurements introduced sufficient variability to account for the discrepancy. Of the clinical tests, 'clinical score' appeared the most satisfactory.

Adult↗