Background Reduced bone mass predisposes patients to the development of vertebral fractures. Measurement of bone mass by non-invasive methods is used to detect patients with involutional osteoporosis at risk from fractures. These methods have not been assessed in patients with steroid dependent osteoporosis. The objective of this study was to assess the value of a predictive fracture threshold value of bone density in patients with steroid dependent asthma. Methods Three groups of patients were studied. Group 1 (67 patients) had steroid dependent asthma (mean daily dose of prednisone 11-7 mg) and no vertebral fractures, group 2 (32 patients) had steroid dependent asthma (mean daily dose of prednisone 12 mg) and vertebral fractures, and group 3 (55 patients) were not taking steroids but had involutional osteoporosis and a recent non-traumatic vertebral fracture. Bone mineral density was measured by dual photon absorptiometry and vertebral fractures by radiography of the lumbar spine. A fracture threshold was determined in the two groups with fractures as the 90th percentile of the mean bone mineral density measured in the lumbar spine. Results Bone mineral density was significantly higher in the steroid dependent group with fractures (group 2) than in group 3 patients, who had involutional

Background -Injectable calcitonin is effective in reducing spinal bone loss in steroid-dependent asthma but side effects are frequent. In contrast, a nasal spray presentation has been shown to be effective and well tolerated in involutional osteoporosis. To test the efficacy of nasal calcitonin a two year prospective trial was conducted in 44 steroid-dependent asthmatic patients. Methods -All patients received a calcium supplement of 1000 mg and were allocated randomly into two groups treated with either salmon calcitonin nasal spray (200 IU every other day, n=22) or calcium alone (n=22) for two years. All patients completed the first year of the study. Five patients in each group dropped out during the second year. In the calcitonin group one patient developed generalised pruritus and four lost steroid dependence, and in the calcium alone group five were no longer dependent on steroids. The efficacy oftreatment was evaluated as follows: bone turnover assessed by biochemical markers, bone loss assessed by serial measurement oflumbar spine density, and rates of bone fractures. Results -The bone mass in the calcitonin group increased by 2*7% in the first year while in the group receiving calcium alone it decreased by 2-8%; this difference was significant. Calcitonin prevented more bone loss during the second year while the calcium alone group continued losing bone mass (-7-8%

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Respiratory and skeletal (deltoid) muscle strength were evaluated in 34 oral steroid-dependent asthmatics by use of maximal inspiratory and expiratory pressures and a myometer. The patients were compared to age- and sex-matched asthmatics who had never been on continuous oral steroid treatment. Endurance time was also studied in ten steroid-dependent asthmatics and ten controls using a pressure threshold breathing device. Nutritional status was assessed from body weight, midarm circumference, triceps skinfold (TSF), prealbumin, albumin, and total protein. An open biopsy from deltoid muscle was taken from nine steroid-dependent asthmatics and the diameter of type 1 and type 2 fibers was measured by a morphometric study. No differences were found between study and control groups either in respiratory and skeletal muscle strength or in endurance time. Steroid-dependent asthmatics showed a decrease in TSF, total protein, albumin, and potassium serum levels when compared with the control group but differences were not statistically significant after Bonferroni's adjustment for multiple comparison studies. Transversal diameter of type 2 fibers was significantly correlated with the percentage of ideal weight (r = 0.75 p less than 0.05), but not with average daily dose of steroids nor with the length of steroid treatment. Our results support the clinical impression that steroids, at the doses usually administered in chronic severe asthma, do not cause muscular weakness. We also found that malnutrition rather than corticosteroids is the most important contributory factor to type 2 muscle fiber atrophy in steroid-dependent asthma.

Recent studies suggest that inhaled corticosteroids can adversely affect bone metabolism. The objective of this study was to evaluate the importance of these adverse effects in a case-control study.Bone mineral density (BMD) was measured in 48 asthmatic adults (15 males and 33 females) treated with inhaled steroids (beclomethasone or budesonide) and in 48 gender and age-matched healthy subjects at baseline and at 2 yrs. Vertebral BMD was measured by dual energy X-ray densitometry.Patients had been treated with a dose of 662±278 µg (range 300-1,000 µg) of beclomethasone dipropionate or budesonide for more than 1 yr (mean duration of treatment 10.6 yrs, range 1-16 yrs). Twenty four patients had needed 1-6 short courses of oral steroids and seven had received oral corticosteroids (mean daily dose 6.2 mg prednisone) for 2-15 yrs more than 4 yrs prior to the BMD measurements. During the follow-up, 14 patients required 1-3 short courses of oral steroids. There was no correlation either between inhaled corticosteroid doses or duration of treatment and BMD values. There were no significant differences in BMD baseline values between patients and healthy controls. BMD significantly decreased in both groups at 2 yrs, from 1.08±0.19 to 1.05±0.19 g·cm -2 (p=0.002) in asthmatics versus 1.12±0.17 to 1.09±0.18 g·cm -2 (p=0.008) in controls. There were no significant differences in BMD loss between patients and healthy controls. Furthermore, no differences were found in bone loss when pre-and postmenopausal women were compared with their healthy control counterparts. No differences in baseline BMD were found between patients who had received regular oral corticosteroid therapy or booster courses of oral corticosteroids and those who had not.Inhaled corticosteroid treatment at a mean dose of 662 µg·day -1 and sporadic booster courses of oral corticosteroids do not further increase bone mass loss with respect to that expected from natural bone mass loss.