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The aim of the study was to assess risedronate's effect on bone mineral density in postmenopausal women with rheumatoid arthritis receiving glucocorticoids. We carried out a two center, 2 year, double-masked, placebo-controlled trial with a third year of nontreatment follow-up. We studied 120 women requiring long-term glucocorticoid therapy at > 2.5 mg/day prednisolone randomized to treatment with daily placebo; daily 2.5 mg risedronate; or cyclical 15 mg risedronate (2 out of 12 weeks). At 97 weeks, bone mineral density was maintained at the lumbar spine (+1.4%) and trochanter (+0.4%) in the daily 2.5 mg risedronate group, while significant bone loss occurred in the placebo group (-1.6%, p = 0.03; and 4.0%, p < 0.005, respectively). At the femoral neck, there was a nonsignificant bone loss in the daily 2.5 mg risedronate group (-1.0%) while in the placebo group bone mass decreased significantly (-3.6%, p < 0.001). The difference between placebo and daily 2.5 mg risedronate groups was significant at the lumbar spine (p = 0.009) and trochanter (p = 0.02) but did not reach statistical significance at the femoral neck. Although not significantly different from placebo at the lumbar spine, the overall effect of the cyclical regimen was similar to that of the daily 2.5 mg risedronate regimen. Treatment withdrawal led to bone loss in the risedronate groups that was significant at the lumbar spine. A similar number of patients experienced adverse events (including upper gastrointestinal events) across treatment groups and risedronate was generally well tolerated. Thus risedronate preserves bone mass in postmenopausal women with rheumatoid arthritis receiving glucocorticoids while patients receiving a placebo have significant bone loss.

OBJECTIVE: To determine whether percutaneous estradiol (pE2) (1.5 mg/day) is able to counteract the postmenopausal bone loss in postmenopausal hysterectomized women, in a double-blind study versus oral estriol (E3) (2 mg/day). METHODS: The bone mineral density of the lumbar spine (LS) and of the proximal femur (PF) was measured every 3 months by dual energy X-ray absorptiometry for 2 years in 43 hysterectomized postmenopausal women (21 in the E2 group and 22 in the E3 control group), and in a subset of patients for a 3rd year. The statistical analyses were performed on Macintosh using Stat View II. RESULTS: A significant bone loss of 1.2 (0.4%)% and of 1.3 (0.3)% per year was observed in the control group, respectively at LS and at PF, versus a significant gain of 1.2 (0.5)% per year in the treated group at the LS. No significant change at PF occurred in the treated group. In the 20 patients followed up for a 3rd year on pE2, an increase of 1.2 (0.9) and 2.5 (1.4)% at LS in the 12 former active group patients and the eight formerly control patients, respectively was seen. The same trend was observed at the proximal femur. CONCLUSION: pE2 (1.5 mg E2) is able to counteract the postmenopausal bone loss in hysterectomized women, whereas E3 (2 mg/day administered orally) is unable to maintain bone mass.

Paget's disease of bone is characterized by a high bone turnover. Therefore, antiresorbing agents such as bisphosphonates are clearly indicated. However, as they accumulate in the pagetic lesions, they could produce some focal defects of bone mineralization. In a double-blind study, we have had the opportunity to compare the effects of tiludronate and of etidronate (both at a fixed dose of 400 mg/day orally) on the radiological changes of 12 patients suffering from Paget's disease of bone. After breaking the code, good agreement was observed between the radiological evaluations and the applied therapy: All positive bone balances were observed in the tiludronate group, except for three questionable densifications in the etidronate group, and the negative bone balances in the etidronate group. This confirms our previous experience with etidronate in Paget's disease when X-ray films of the lesions are followed sequentially during therapy.

The case of a 49-year-old woman suffering from generalized skeletal pain and multiple fractures accompanied by severe hypophosphataemia and low urinary phosphorus excretion is reported. She had been taking large amounts of antacids containing aluminum hydroxide for many years. A diagnosis of antacid-induced osteomalacia was made. It was confirmed by biological work-up, radiographs and bone biopsy. A dramatic biological, osteodensitometric, and clinical improvement was achieved by withdrawal of antacids and phosphorus administration. The literature concerning this unusual condition has been reviewed.

Sodium Fluoride (NaF) is the only medication so far clinically available with a bone formation stimulating property, through its peculiar mitogenic dose-dependent action on the osteoblast cell line. Bone strength is commensurate to bone mass, and in a condition with fragility fractures, like osteoporosis, it seems logical to restore bone mass without weakening bone strength. However, as with any active drug. NaF therapy requires adhesion to elementary rules if drawbacks are to be prevented. A first mandatory rule is not to prescribe NaF without calcium supplementation, if bone loss at the appendicular skeleton is to be avoided; to prevent this, the availability of monofluorophosphate (MFP), containing the fluoride and calcium salts in the same preparation has enhanced the compliance to calcium supplementation. A second rule is not to give supraphysiological doses of vitamin D, for the same reason. Third, if one wants to avoid a calcium shift from cortical to trabecular bone and osteomalacia, one should use small doses of NaF, of the order of 50 mg/day. With this in mind, the bioavailability of the drug has to be taken into account, particularly its gastrointestinal absorption which is dramatically enhanced if a plain non entericoated (EC) capsule is used, as compared to that of an EC tablet with the same face value. Too much NaF is deleterious to bone, a fact known for years. Already in 1972, it was noted that in all patients receiving 60 mg or more of NEC NaF, daily, morphologically abnormal bone developed and which appeared irregular and contained areas of incompletely mineralized bone. The bone was histologically and microradiographically normal in patients receiving 45 mg or less of NEC NaF/day. Fourth, NaF therapy is contraindicated in renal insufficiency owing to an enhanced retention in the skeleton. NaF is, however, by no means the ideal medication, because its therapeutic window is narrow. It has many bothersome drawbacks, and notably it is irritating for t

OBJECTIVE. To measure serum levels of tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) in patients with rheumatoid arthritis (RA) and age-matched control subjects and to study how these correlate with serum levels of hyaluronan (HA) and antigenic keratan sulfate (KS) and other biochemical as well as clinical indicators of disease activity. METHODS. Immunoassays were used to measure levels of TNF alpha, IL-6, HA, and antigenic KS in the serum of 35 patients with RA and a group of age- and sex-matched control subjects. Clinical disease activity in the RA group was assessed using the Lansbury index. Drug intake was recorded and the erythrocyte sedimentation rate, and levels of fibrinogen, creatinine, bilirubin, alkaline phosphatase, lactate dehydrogenase, and aminotransferase were measured. RESULTS. Serum levels of TNF alpha, IL-6, and HA were significantly higher in the RA population than in the control group. In patients with RA, serum levels of HA correlated positively with serum levels of TNF alpha and with clinical joint scores, but only weakly with other laboratory parameters of inflammation. Serum levels of antigenic KS correlated negatively with levels of circulating TNF alpha, but much more weakly with other clinical and biochemical parameters of disease activity. CONCLUSION. These in vivo data support in vitro studies which have shown that TNF alpha is a potent stimulator of HA synthesis by synovial lining cells. The results strengthen the contention that serum HA may be a unique marker of synovial involvement and inflammation, rather than of only inflammation, in RA.

Osteoporosis constitutes a major financial burden for society, which will increase in the near future owing to the ageing of the population. Women are the most common victims of involutional osteoporosis because of post-menopausal bone loss induced by oestrogenic deficit. Men are nevertheless not completely untouched by osteoporosis, however, compared to women, they are under less threat. Every effort should be made to curtail the financial burden on society and to improve the quality of life of sufferers. The first steps should be to increase the calcium intake, the level of exercise and to decrease the risk of falls. A preventive therapy with oestroprogestogens should be instituted at the time of the menopause, provided there is no contraindication. In the absence of fracture data, the modalities of alternative therapies like calcitonin and bisphosphonates are still debated. For people already suffering from fractures, restorative therapy should be considered. Sodium fluoride therapy is able to provoke a decrease in vertebral fracture frequency without compromising cortical bone strength provided elementary rules for its use are respected. Whether bisphosphonates can protect against fractures is still unsettled. Vitamin D has a physiological role, particularly in institutionalized elderly patients deprived of any exposure to the sun. Anabolic steroids are not devoid of side effects, and furthermore, no fracture data are so far available.

The osteoarticular affinity of Streptococcus milleri has only recently been recognized. We report a case of septic prepatellar bursitis caused by this pathogen. The recent literature concerning osteoarticular involvement by S. milleri is reviewed.

OBJECTIVE. We assessed the prevalence, severity, and anatomic distribution of ankylosing spondylitis (AS)-related osteopenia (OP). METHODS. We studied 70 patients (60 males, 10 premenopausal females) with AS (according to the New York criteria) to determine the frequency of OP. Bone mass was measured by plain radiographs of the spine, by single-photon absorptiometry (SPA) of the distal and midshaft of the radius on the nondominant side, by dual-photon absorptiometry (DPA) of the lumbar spine (L2-L4), and by quantitative computed tomography (QCT) of the lumbar spine. RESULTS. SPA values for the radius mass were normal in males and in females, both at the distal and midshaft sites. In contrast, spine radiographs showed diminished density of the vertebral bodies in 69% of the males and 50% of the premenopausal females. Two male patients had had a vertebral compression fracture, and one female patient had had two. DPA values for the spine mass were significantly diminished in the male patients compared with the controls, but not in the female patients. Males with less severe AS also had the largest reduction in lumbar bone mineral content. In patients with more severe disease, lumbar bone mineral content was not statistically different from that in controls. QCT of the lumbar spine performed in 10 patients disclosed low density of the trabecular bone of the vertebral bodies, more so in those with more severe AS and syndesmophyte formation and/or apophyseal joint fusion, which contrasts with the normal values on DPA in these patients. CONCLUSION. Male patients with AS have axial osteopenia. In those who have very severe AS with new bone formation, DPA demonstrates normal values as a result of two opposite trends: central osteopenia (as assessed from QCT) and peripheral new-bone formation, which transforms vertebral bodies into long bones. This could modify the mechanical resistance of the spine and account for the propensity for anteroposterior transvertebral and transdi

We describe a patient with rheumatoid arthritis (RA) who developed hypersensitivity after 3 weeks of therapy with azathioprine with fever, jaundice and renal insufficiency. A percutaneous liver biopsy was compatible with hypersensitivity hepatitis. During azathioprine rechallenge, the symptoms recurred within a few days, consistent with the diagnosis of an acute hypersensitivity reaction. This report is the first to describe the association of an azathioprine induced hypersensitivity simultaneously involving the liver and the kidneys, in the same patient with RA, with resurgence after rechallenge.

Sixteen (16) male patients who were suffering from hypogonadism but who were free from bone symptoms were recruited from the Andrology Clinic. Their bone mineral density (BMD) was assessed by single photon absorptiometry in the non-dominant radius, at both the distal radius (DR) (27% trabecular bone) and the midshaft radius (MR) (90% cortical bone). Measurements were carried out before and during testosterone substitution therapy. BMD was found to be lower in the subjects than in the controls, to a similar extent at both the DR (0.47 +/- 0.02 g/cm2, i.e. 83.1 +/- 4.3% of the value in the controls, or Z score -1.42 +/- 0.39; P less than 0.01) and the MR (0.68 +/- 0.02 g/cm2, i.e. 87.8 +/- 2.4% of the value in the controls, or Z score -1.49 +/- 0.33; P less than 0.01). There was no correlation between testosterone levels and BMD at either the DR or the MR at the beginning of the study. Following testosterone substitution therapy, bone mineral content (BMC) increased significantly at the DR (+5.9 +/- 1.4% per year; P less than 0.01) and at the MR (+1.1 +/- 0.9% per year; P less than 0.01). If the study is limited to the subjects who had achieved full bone age maturity before the start of therapy, the bone gain remains significant only at the DR, a site with a sizeable proportion of trabecular bone.

A woman aged 62 developed a septic shock and pulmonary embolism after skin grafting for extensive burns. She was put on anticoagulants. A second shock led to renal insufficiency. Hypercalcaemia developed. A CT scan of the upper abdomen disclosed enlarged adrenal glands. An acute adrenal haemorrhage was suspected. The levels of cortisol were low in the plasma and urine and did not respond to ACTH stimulation. Cortisone replacement therapy improved the condition of the patient and normalized plasma calcium levels. The mechanisms of hypercalcaemia in acute adrenal insufficiency are discussed. Multiple factors have been proposed: haemoconcentration, an increased affinity of plasma proteins for calcium, an increase in the filtrable calcium complexes, and an enhanced calcium mobilization of skeletal origin.

A woman suffering from primary Sjögren's syndrome developed sensitive neuropathy. The disease was further complicated by follicular lymphoma, an unusual albeit already described complication of Sjögren's disease. The clinical data suggest that mononuclear infiltration of the dorsal root ganglions could be at the origin of a sensitive neuropathy, inducing an axonal degeneration of the nerves.

Twenty-five cases of hemochromatosis established on histological grounds were reviewed in order to study their articular complaints. Symptoms relating to articular damage were the first signs of the disease in about one quarter of the cases. More than half of the patients (n = 14) exhibited inflammatory arthritis, usually of the hands and knees. The arthritis was chronic in all the patients. Acute arthritis of the joints of the hands and feet appeared in the course of the disease in two patients. Chondrocalcinosis was present in 20% of cases with X-rays of joints (n = 20). The classical subchondral arthropathy was observed in the metacarpophalangeal joints in 35% of the patients. In two patients chondrocalcinosis and subchondral arthropathy were both present. These data are compared with those of 66 patients suffering from primary hyperparathyroidism and of 229 controls with rheumatic complaints. The severity of the arthropathy in hemochromatosis is stressed.

We describe 3 children with pustulosis palmaris et plantaris associated with chronic recurrent (multifocal) osteomyelitis, located in the clavicle in 2 patients, and in the distal fibula as well as in several metatarsals in the third. The first 2 children also developed inflammatory sacroiliitis, one with chronic peripheral polyarthritis. These 3 cases represent the arthrosteitis and chronic recurrent multifocal osteomyelitis syndrome associated with palmoplantar pustulosis.

A 12-year-old female suffering from osteogenesis imperfecta (OI) was treated with 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (APD) orally, 250 mg daily, for periods of 2 months, alternating with periods of 2 months of abstinence. Total duration of therapy was 1 year. Radiological and clinical improvement was striking. Furthermore, X-rays of the bones showed large, parallel radio-opaque striae, corresponding exactly to the periods of therapy. These were present in all metaphyses.

We report 2 patients with reflex sympathetic dystrophy syndrome (RSDS) associated with renal tubular osteomalacia. In both patients, RSDS was the presenting manifestation. Treatment of the underlying condition with calcitriol resulted in healing in both patients. These cases prompted us to undertake a retrospective study of 24 consecutive patients with osteomalacia (6 of renal tubular origin, 18 related to vitamin D deficiency), and of 259 consecutive patients with RSDS. Among those with osteomalacia, radiologic lesions strongly suggestive of RSDS were found in 5 patients (21%), 4 of whom had renal tubular defects, and only 1 had vitamin D deficiency. In the group with RSDS, 1 patient (0.4%) was found to have osteomalacia of renal tubular origin. Thus, radiologic findings suggestive of RSDS are frequent in patients with osteomalacia, especially that of renal tubular origin. On rare occasions, the full-blown clinical picture of RSDS may obscure the diagnosis of osteomalacia.