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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, roentgenographic, and biochemical features of the dorsal and lumbar spine were reviewed in 72 postmenopausal women. Nineteen women had both osteoporosis (vertebral collapse) and osteoarthrosis. These patients were compared with 26 patients who had only osteoarthrosis of the spine and 27 who had only vertebral collapse. The patients who had both spinal osteoporosis and osteoarthrosis were older, more advanced in menopause, and physically smaller in stature and body weight than the other groups. They also had higher serum parathyroid hormone level, used nonthiazide diuretics more frequently, and had more nulliparity than the other two groups. These patients had osteoarthrosis of the hip to a lesser degree than patients affected by osteoarthrosis alone, and they had fewer fractures of the forearm and other sites than patients with osteoporosis alone. The incidence of femoral neck fractures in both groups, however, was comparable. These results suggest that osteoarthrosis or a related factor might have a protective effect on the progression of osteoporosis. These results confirm earlier observations that postmenopausal osteoporosis and osteoarthrosis are two distinct diseases and not the result of normal aging.
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PMID:Osteoarthrosis retards the development of osteoporosis. Observation of the coexistence of osteoarthrosis and osteoporosis. 199 32

Calcium and phosphorus metabolism was studied in 101 institutionalized subjects over 70 years of age (mean: 82.5 years). The study was performed in serum and urine; it included parathyroid hormone and calcidiol (250HD3) assays and radiological examination of bones with determination of Meunier's index and metacarpal cortical index. Calcidiol concentrations did not vary with age but were higher in people who left the institution and in men. In contrast, there was a significant age-group related increase of parathyroid hormone concentrations. This increase was accompanied by an increase of parathyroid hormone activity, as shown by a parallel fall in phosphorus reabsorption rate. These findings are in agreement with current pathogenetic theories on senile osteoporosis. Invalid subjects had higher urinary calcium and serum parathyroid hormone levels and a lower cortical index. Paradoxically, there was less vertebral collapse as evaluated by Meunier's index, which may suggest that very old patients develop progressive cortical bone hyperresorption entirely independent of sequelae from their former trabecular osteoporosis.
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PMID:[Phosphocalcium metabolism in the elderly. Study of 101 subjects living in an institution]. 340 85

The pathophysiology, clinical presentation, prevention, and treatment of aluminum-related osteomalacia in renal-failure patients are reviewed. Aluminum-related osteomalacia can develop in patients exposed to high concentrations of aluminum either in dialysis solutions or through gastrointestinal aluminum absorption from aluminum-containing antacids used to treat hyperphosphatemia. Although the exact etiology of aluminum-related osteomalacia is unknown, aluminum is believed to inhibit bone mineralization by forming an inhibitory complex with citric acid at physiologic concentrations. The complex is deposited along bone mineralization fronts and in bone marrow. The major symptoms of aluminum-related osteomalacia include skeletal pain, fractures, and vertebral collapse. The disease is difficult to diagnose because patients may have normal or slightly elevated serum concentrations of calcium, phosphate, alkaline phosphatase, and parathyroid hormone. Direct measurement of bone aluminum content (using biopsy) is often needed to confirm diagnosis. The aluminum-chelating agent deferoxamine mesylate can be used to measure bone aluminum content indirectly. Aluminum intoxication can be managed either by preventing exposure to aluminum or by removing deposited aluminum from bone. New standards restrict aluminum content in dialysis solutions, and prevention now focuses on the use of aluminum-free phosphate binders for treatment of hyperphosphatemia. Calcium carbonate may be as effective as aluminum-containing antacids in controlling serum phosphate concentrations, but it should be used cautiously in patients who are hypercalcemic or at risk of developing metastatic calcification. Chelation therapy with deferoxamine has improved the symptoms and bone histology in a small number of patients. Clinical improvements have been seen in patients receiving intravenous deferoxamine 2-6 g per week for 20 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminum-related osteomalacia in renal-failure patients. 389 71

Juvenile osteoporosis is a disease of childhood and adolescence exhibiting marked clinical variability in bone change. The disease usually begins in the prepubertal period or even younger. A case of a Chinese boy suffering from back pain and generalized osteoporosis since 9 yr of age who spontaneously recovered at 14 yr of age when entering puberty is reported. The affected patient was clinically normal (as shown by X rays), until he fractured his left humerus. Metabolic studies indicated a negative calcium balance, but serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcifediol, calcitriol, cortisol and sex hormones were normal. X ray showed typical generalized osteoporosis with vertebral collapse. The disease markedly improved within 5 yr. No family history of inherited skeletal disorders or presenile osteoporosis was noted. The diagnosis of idiopathic juvenile osteoporosis was made.
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PMID:Idiopathic juvenile osteoporosis: five-year case follow-up. 761 64

The onset of idiopathic osteoporosis after delivery is called "Post-Pregnancy Osteoporosis", which was suggested for the syndrome by Nordin in 1955. Back pain and vertebral collapse are the most frequent feature. This disease usually occurs in the first pregnancy and dose not recur, but the mechanisms remains to be elucidated. It is suggested that in patients with post-pregnancy osteoporosis there may have been a transient failure of the usual changes in calciotropic hormones such as 1,25-(OH)2D, calcitonin and parathyroid hormone (PTH) to prepare the maternal skeleton due to the stress of childbirth. The clinical course of these patients accords well with previous reports.
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PMID:[Post-pregnancy osteoporosis]. 796 88

The effects of parathyroid hormone (PTH) on 1,4,5-inositol triphosphate (1,4,5-IP3) and intracellular free calcium (Cai2+) in osteoblasts are variable, whereas adenylate cyclase activity is consistently stimulated. Cyclic AMP is considered a mediator in the contractile effects of PTH on osteoblasts, but the regulation and role of Cai2+ remains unclear. Recent studies indicate that protein kinase C (PKC) inhibits PTH-stimulated Cai2+ increases in osteoblastic cells. Therefore, the objectives of this study were to determine the effects of PKC modulators and PTH on UMR 106-H5 rat osteoblastic cell morphology, and the relationship between cell shape and PTH-induced Cai2+ changes. In suspended cells loaded with the calcium indicator dye fura-2, pretreatment with PKC inhibitors calphostin C (100 nM x 1 h) and H-7 (30 microM x 18 h) potentiated the effects of 1 microgram/ml bPTH (1-84) on Cai2+ (83% increase over basal) by 1.4- and 1.65-fold, respectively. In comparison, PTH (10 ng-1 micrograms/ml) was without significant effect on adherent cell Cai2+ as measured by single-cell image analysis, although another in vitro bone resorbing agent, thrombin (10 U/ml), produced an acute 3-fold increase in the ratio (R) of emission (approximately lambda 510 nm) detected and optimized at lambda 348/374 nm (i.e., Ca-bound dye/free dye) in control cells. Phase-contrast microscopy revealed PKC inhibitor-treated cells changed from a spread configuration to a stellate form with retracting processes or cell rounding and a collapse of actin stress fibers. Within 1 h of PTH addition, PKC inhibitor-treated cells continually became extended/respread up to 3 h with an associated increase in actin stress fibers that was preceded by an acute 1.6-fold Cai2+ increase. In contrast, control or PKC activator-treated cells (phorbol 12,13-dibutyrate or 12-O-tetradecanoylphorbol-13-acetate; TPA) contracted/retracted within 5 min in response to PTH. A role for Cai2+ in PTH-induced cell spreading was further indicated by a contractile response to PTH when PKC-inhibitor-treated cells were loaded with the intracellular calcium chelator dimethyl BAPTA (3 microM x 30 min). PTH-induced Cai2+ increases in adherent PKC inhibitor-treated cells were also associated with a 1.8-fold 1,4,5-IP3 increase as measured by mass assay. The data suggest PKC contributes to UMR 106-H5 cell morphology and selectively regulates signal pathways activated by PTH to promote either cell contraction (cAMP) or extension (1,4,5-IP3/Cai2+).
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PMID:Protein kinase C modulator effects on parathyroid hormone-induced intracellular calcium and morphologic changes in UMR 106-H5 osteoblastic cells. 913 85

An 11-year-old neutered male Yorkshire Terrier was presented to the Haemaru Referral Animal Hospital with a history of unresponsive tracheal collapse and an incidental finding of a lung nodule in the left caudal lung lobe on radiography. Thorough physical examination and imaging studies revealed no other masses. Cytologic examination of C-arm mobile fluoroscopy-guided fine-needle aspirates revealed numerous free nuclei and a low number of small round cells with moderate to abundant pale basophilic cytoplasm. Some cells contained indistinct basophilic granules in their cytoplasm, and extracellular pink material was noted. A caudal lung lobectomy was performed, and histologic evaluation of the mass revealed round to polygonal cells with abundant eosinophilic granular cytoplasm and round nuclei with mild anisokaryosis and 0-3 mitotic figures per high-power field. Cells were arranged in packets separated by fine fibrovascular stroma, suggestive of a pulmonary neuroendocrine neoplasm, specifically a carcinoma/carcinoid. The cells were immunoreactive for chromogranin A and neuron-specific enolase, and negative for cytokeratin, synaptophysin, calcitonin, thyroglobulin, parathyroid hormone, CD79a, light lambda, and vimentin. With these findings the tumor was diagnosed as a primary lung carcinoid. Eleven months after resection, there was no evidence of tumor regrowth or metastasis. The absence of necrosis, few mitotic figures, minimal pleomorphism, and benign behavior of this tumor resembled those of a typical carcinoid in humans.
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PMID:Cytologic and immunohistochemical characterization of a lung carcinoid in a dog. 1853 28

Proton pump inhibitor (PPI)-induced hypomagnesemia has been recognized since 2006. Our aim was to further characterize the clinical consequences and possible mechanisms of this electrolyte disorder using 4 cases. Two men (aged 63 and 81 years) and 2 women (aged 73 and 62 years) had been using a PPI (esomeprazole, pantoprazole, omeprazole, and rabeprazole, 20-40 mg) for 1-13 years. They developed severe hypomagnesemia (magnesium, 0.30 +/- 0.28 mEq/L; reference, 1.40-2.10 mEq/L) with hypocalcemia (calcium, 6.4 +/- 1.8 mg/dL), relative hypoparathyroidism (parathyroid hormone, 43 +/- 6 pg/mL), and extremely low urinary calcium and magnesium excretion. One patient was admitted with postanoxic encephalopathy after a collapse likely caused by arrhythmia. The others had electrocardiogram abnormalities (prolonged QT interval, ST depression, and U waves). Concomitant hypokalemia (potassium, 2.8 +/- 0.1 mEq/L) was considered the trigger for these arrhythmias. Hypomagnesemia-induced kaliuresis (potassium excretion, 65 +/- 24 mEq/L) was identified as the cause of hypokalemia. This series of PPI-induced hypomagnesemia shows that this is a generic effect. It also indicates that hypomagnesemia may occur within 1 year of PPI therapy initiation and can have serious clinical consequences, likely triggered by the associated hypokalemia. A high index of suspicion is required in PPI users for unexplained hypomagnesemia, hypocalcemia, hypokalemia, or associated symptoms.
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PMID:A case series of proton pump inhibitor-induced hypomagnesemia. 2018 76