It has been previously shown that the level of circulating undercarboxylated osteocalcin (ucOC) is elevated in elderly women in comparison with young, healthy, premenopausal ones. To understand the mechanism of the increase in the ucOC in the elderly and to assess its potential consequences on bone fragility, we have measured ucOC in the sera of 195 elderly institutionalized women 70-101 yr of age. In 45 women (23%) serum ucOC was above the upper limit of the normal range for young women. The level of ucOC was negatively correlated with 25OHD (r = -0.32, P < 0.001) even after excluding the effect of age, parathyroid hormone (PTH), and creatinine by partial correlation (r = -0.24, P < 0.002). During an 18-mo follow-up, 15 women sustained a hip fracture and their baseline ucOC level was higher (P < 0.01) in women who subsequently sustained hip fracture than in the nonfracture group contrasting with no significant differences for serum calcium, phosphate, alkaline phosphatase, creatinine, PTH, 250HD, and total and carboxylated OC. The risk of hip fracture was increased in women with elevated ucOC (relative ratio 5.9, 99.9% Cl 1.5-22.7, P < 0.001). During 1 yr of calcium/vitamin D2 treatment, ucOC decreased (P < 0.05), especially in those with the initially increased values (from 2.22 +/- 0.35 to 1.41 +/- 0.29 ng/ml, P <0.005) contrasting with an increase in the placebo group (P < 0.05). In conclusion, the increase in ucOC in the elderly reflects not only some degree of vitamin K deficiency but also their poor vitamin D status, suggesting that vitamin D may be important, either directly or indirectly through its effect on bone turnover, for achieving a normal gamma-carboxylation of OC. The ucOC, but not conventional calcium metabolism parameters, predicts the subsequent risk of hip fracture, suggesting that serum ucOC reflects some changes in bone matrix associated with increased fragility.

/pdf/serum-undercarboxylated-osteocalcin-is-a-marker-of-the-risk-1gx0bw4byb.pdf

Serum undercarboxylated osteocalcin is a marker of the risk of hip fracture in elderly women.

Experimental, epidemiological, and clinical data indicate that progesterone is active in bone metabolism. Progesterone appears to act directly on bone by engaging an osteoblast receptor or indirectly through competition for a glucocorticoid osteoblast receptor. Progesterone seems to promote bone formation and/or increase bone turnover. It is possible, through estrogen-stimulated increased progesterone binding to the osteoblast receptor, that progesterone plays a role in the coupling of bone resorption with bone formation. A model of the interdependent actions of progesterone and estrogen on appropriately-"ready" cells in each bone multicellular unit can be tied into the integrated secretions of these hormones within the ovulatory cycle. Figure 5 is an illustration of this concept. It shows the phases of the bone remodeling cycle in parallel with temporal changes in gonadal steroids across a stylized ovulatory cycle. Increasing estrogen production before ovulation may reverse the resorption occurring in a "sensitive" bone multicellular unit while gonadal steroid levels are low at the time of menstrual flow. The bone remodeling unit would then be ready to begin a phase of formation as progesterone levels peaked in the midluteal phase. From this perspective, the normal ovulatory cycle looks like a natural bone-activating, coherence cycle. Critical analysis of the reviewed data indicate that progesterone meets the necessary criteria to play a causal role in mineral metabolism. This review provides the preliminary basis for further molecular, genetic, experimental, and clinical investigation of the role(s) of progesterone in bone remodeling. Much further data are needed about the interrelationships between gonadal steroids and the "life cycle" of bone. Feldman et al., however, may have been prophetic when he commented; "If this anti-glucocorticoid effect of progesterone also holds true in bone, then postmenopausal osteoporosis may be, in part, a progesterone deficiency disease."

Progesterone as a bone-trophic hormone.

Vitamin K is a cofactor required for the formation of gamma-carboxyglutamate (Gla) residues in proteins. Osteoblasts produce at least three different Gla-containing proteins: osteocalcin, matrix Gla-protein, and protein S. After cellular secretion of these proteins, the main part of each remains bound to the hydroxyapatite matrix in bone, but their function remains unclear. Part of the newly synthesized osteocalcin is also set free into the bloodstream, where it may be used as a diagnostic marker for bone formation. Several studies have demonstrated that a poor vitamin K status is associated with an increased risk of osteoporotic bone fractures. Whether vitamin K supplementation will reduce the rate of bone loss in postmenopausal women remains a matter of debate.

Role of vitamin K in bone metabolism.

Vitamin K and bone health

Although several observational studies have demonstrated an association between vitamin K status and bone mineral density (BMD) in postmenopausal women, no placebo-controlled intervention trials of the effect of vitamin K1 supplementation on bone loss have been reported thus far. In the trial presented here we have investigated the potential complementary effect of vitamin K1 (1 mg/day) and a mineral + vitamin D supplement (8 µg/day) on postmenopausal bone loss. The design of our study was a randomized, double-blind, placebo-controlled intervention study; 181 healthy postmenopausal women between 50 and 60 years old were recruited, 155 of whom completed the study. During the 3-year treatment period, participants received a daily supplement containing either placebo, or calcium, magnesium, zinc, and vitamin D (MD group), or the same formulation with additional vitamin K1 (MDK group). The main outcome was the change in BMD of the femoral neck and lumbar spine after 3 years, as measured by DXA. The group receiving the supplement containing additional vitamin K1 showed reduced bone loss of the femoral neck: after 3 years the difference between the MDK and the placebo group was 1.7% (95% Cl: 0.35–3.44) and that between the MDK and MD group was 1.3% (95% Cl: 0.10–3.41). No significant differences were observed among the three groups with respect to change of BMD at the site of the lumbar spine. If co-administered with minerals and vitamin D, vitamin K1 may substantially contribute to reducing postmenopausal bone loss at the site of the femoral neck.

Vitamin K1 supplementation retards bone loss in postmenopausal women between 50 and 60 years of age.

Cardiac hydatid cyst with clinical features resembling subaortic stenosis.

In recent years, the cardiovascular manifestations of systemic lupus erythematosus have became more apparent as a consequence of both prolonged survival and improvement in diagnostic modalities. We report the case of a 16-year old woman with systemic lupus erythematosus in whom the presence of cardiomyopathy was characterized by endomyocardial biopsy. This diagnostic technique also showed that the histologic hall-mark of lupus myocardiopathy persisted despite corticosteroid and plasmapheresis, suggesting the need of a careful cardiac follow-up in these patients.

Endomyocardial biopsy in diagnosis and management of cardiovascular manifestations of systemic lupus erythematosus (SLE).

To further investigate the relationship between oophorectomy (OF) and mineral bone loss, 15 women who underwent total hysterectomy and bilateral oophorectomy were studied for 12 months after surgery. Mineralometric and metabolic data were obtained before and after 3, 6, and 12 months. The women lost bone mineral content (measured by single photon absorptiometry) at the same rate they lost cortical and trabecular bone, suggesting that bone loss after OF is a generalized phenomenon. Our data also show that in increase in bone resorption takes place only in the first period after OF; the persistency of a negative bone balance up to 12 months, accompanied by a reduction of osteocalcin serum levels, may be dependent on a reduced bone formation, probably due to osteoblastic insufficiency.

Postoophorectomy bone loss is associated with reduced bone Gla protein serum levels: a possible effect of osteoblastic insufficiency.

Estrogen deficiency after ovariectomy in the rat is followed by an increase of bone turnover and bone loss. Estrogens are thought to modulate the sensitivity of skeleton to Parathyroid Hormone; according to the recently reported evidence of estrogen receptors on osteoblasts, however, a direct effect on bone cells should not be ruled out. We studied the behaviour of Bone Gla Protein (Osteocalcin), a reliable marker of osteoblast function, in growing rats after ovariectomy and treatment with 17 beta-estradiol. Results indicate that ovariectomy stimulates, as expected, bone turnover, and that estrogen induces a further increase of osteoblast activity revealed by the rise of Bone Gla Protein plasma levels. This data may have clinical implications in humans, where estrogens are currently suggested for prevention and therapy of post menopausal osteoporosis.

Effects of Ovariectomy and 17β-Estradiol on Bone GLA Protein in Growing Rats: An Indirect Evidence for Estrogen Receptors in Bone Cells

Alternating Wolff-Parkinson-White syndrome associated with attack of angina.

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