Background-A double blind, placebo controlled study was undertaken to determine the eVects of 104 weeks of intermittent cyclical etidronate therapy on bone mineral density (BMD) in patients undergoing long term oral corticosteroid therapy. Methods-Forty nine patients of mean age 59 years on long term (>6 months) corticosteroid treatment were randomised to receive either 400 mg/day etidronate or placebo for 14 days followed in both groups by calcium (equivalent to 97 mg elemental Ca/day) with vitamin D (400 IU) for 76 days. The cycle was repeated a total of eight times over a period of two years. Dual energy x ray absorptiometry (DEXA) measurements of the lumbar spine and hip BMD and biochemical bone marker analyses were performed at baseline and every six months. Results-Twenty six patients (10 men) received cyclical etidronate and 23 (nine men) received placebo. The mean (SD) dose of corticosteroid (prednisone or equivalent) at baseline in the etidronate group was 8 (4) mg/day and in the placebo group was 7 (4) mg/day. Most of the patients (43%) suVered from asthma. Forty one patients completed the study (22 in the etidronate group and 19 in the placebo group). All had a low BMD at entry and with treatment a significant difference was observed between groups in the mean (SE) percentage change from baseline in lumbar spine BMD at week 104 of 4.5 (1.65)% (p = 0.007) with a 95% confidence interval (CI) of 1.12 to 7.87%. No clinically or statistically significant treatment diVerences were observed at the hip or with bone markers. The incidence of adverse events was similar in the two groups. Conclusions-The results show that intermittent cyclical etidronate therapy with calcium and vitamin D supplementation significantly increases lumbar spine BMD in patients with osteoporosis resulting from long term treatment with corticosteroids. (Thorax 1998;53:351-356) Keywords: osteoporosis; corticosteroids; etidronate It is well established that high dose corticosteroids can result in marked bone loss, especially during the early part of treatment. The exact dose at which this occurs is yet to be clearly defined although the general consensus indicates that 7.5-10 mg/day of prednisone or its equivalent is associated with bone loss. These doses of corticosteroid are frequently indicated in patients with a wide range of chronic inflammatory, autoimmune and hypersensitivity conditions such as asthma, rheumatoid arthritis, polymyalgia rheumatica, and systemic lupus erythematosus. It is not uncommon for these patients to be treated with high (>10 mg/day) doses for the first year and then a lower dose subsequently. The available evidence suggests that bone loss, although reversible, is greatest during the first six months 1 and that up to 50% of patients taking corticosteroids long term will develop osteoporosis and experience vertebral crush fractures due to the associated decrease in bone mass. 2The aetiology of corticosteriod induced bone loss may be complex but is thought to involve the direct inhibition of the bone...
SUMMARY We report a family with some of the features of both types B and E Julia Bell brachydactyly. We feel therefore that this family may constitute a new syndrome and we would like to name this after the family involved, the Ballard syndrome.Brachydactyly, the shortening of digits due to anomalous development of any of the phalanges or metacarpals, was the first inherited disorder recognised in man as showing dominant Mendelian inheritance.' In 1951, Julia Bell classified these abnormalities into five groups.2We report here a family with an unusual type of brachydactyly which shows similarities to Julia Bell types B and E. In type B, the basic digital malformation pattern involves a symmetrical deformity with absence or hypoplasia of the terminal phalanges in the index to little fingers, with complete or nearly complete absence of the finger nails. The thumbs often show changes in the distal phalanges and digits on the radial side of the hand are less severely affected than on the ulnar side. In type E brachydactyly, there is shortening of one or more of the metacarpals with or without shortening of the metatarsals.3 Case reportsThe proband was a 46 year old white male, initially seen in the Rheumatology Department with a torn medial meniscus. During the physical examination it was noted that he had abnormally short ring and little fingers on both hands with marked concavity of the nails on these fingers. In addition to this, his thumbs were broadened and again the nail growth was abnormal, as shown in fig 1. Otherwise his physical examination was normal. X-ray of his hands (fig 2) showed short metacarpals in the ring and little fingers. The terminal phalanges of the thumbs were broader than usual. X-ray of his feet (fig 3) showed shortened fourth and fifth metatarsals.The proband's brother and his brother's daughter HIG2 X-rav of probhand'shn Ittds.
Objectives-To document the variety of liver diseases and the clinical picture of hepatic hypertrophic osteoarthropathy
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