Osteoporosis primary

The most common form of osteoporosis is primary osteoporosis. Primary osteoporosis is seen in postmenopausal women and is also caused by advancing age. In some cases it may be idiopathic with no identifiable cause. 

Alendronate should be considered hrst-line treatment for primary osteoporosis in men owing to its proven benefit in reducing fractures and relative safety. 

Osteoporosis can be classified as either primary (no known cause) or secondary (caused by drugs or other diseases). Primary osteoporosis is found most often in postmenopausal women and aging men, but it can occur in other age groups as well. 

Compared with postmenopausal osteoporosis, few clinical trials have been conducted evaluating therapies in men. Although alendronate and calcitonin have both been studied, only alendronate reduces fracture rates in men. Teriparatide also has been studied, but no data are available yet on fracture rates. At this time, alendronate and teriparatide are approved by the FDA for the treatment of osteoporosis in men. Owing to proven benefit in reducing fractures and relative safety, alendronate should be considered first-line treatment for primary osteoporosis in men. Teriparatide should be reserved as alternate therapy in this population. 

Osteoporosis associated with RA follows a multifaceted pathogenesis, but the primary mechanism likely is mediated by osteoclast activity.12 The cytokines involved in the inflammatory process directly stimulate osteoclast and inhibit osteoblast activity. Additionally, arthritis medications can lead to increased bone loss. Bone mineral density should be evaluated at baseline and routinely using dual-energy x-ray absorptiometry.11,12... 

Anastrozole is a selective nonsteroidal aromatase inhibitor that lowers estrogen levels. The pharmacokinetics of anastrozole demonstrate good absorption, with hepatic metabolism the primary route of elimination and only 10% excreted unchanged by the kidney. The elimination half-life is approximately 50 hours. Anastrozole is used for the adjuvant treatment of postmenopausal women with hormone-positive breast cancer and in breast cancer patients who have had disease progression following tamoxifen. Side effects include hot flashes, arthralgias, osteoporosis/bone fractures, and thrombophlebitis. 

Half-life increases as the dose and serum concentration increases Volume of distribution Adults 0.7 L/kg Children 0.8 L/kg Neonates 1.2 L/kg Protein binding Adults, children 88-92% Neonates 65% Primary elimination route Hepatic (4-8 pmol/L) unbound concentration osteoporosis, rash... 

The primary goal of osteoporosis management is prevention. Optimizing skeletal development and peak bone mass accrual in childhood, adolescence, and early adulthood will reduce the future incidence of osteoporosis. 

This drug class has an enormous potential in the primary and secondary prevention of several types of estrogen-dependent tumors, postmenopausal osteoporosis, and cardiovascular and neurodegenerative diseases. 

Bazedoxifene s primary indication is the treatment and prevention of postmenopausal osteoporosis (Miller et al. 2002). In animal models bazedoxifene displays estrogenhke agonistic activity on bone loss and significantly reduces total cholesterol levels with doses as low as 0.1 mg/kg (Miller et al. 2002). Also in these models, there is no evidence of an estrogenic stimulatory effect on the endometrial epithelial cell (Miller et al. 2001). 

In preclinical models of postmenopausal osteoporosis, lasofoxifene inhibited bone turnover and prevented bone loss throughout the skeleton (Maeda et al. 2004). The primary indication of lasofoxifene is the treatment and prevention of postmenopausal osteoporosis. In preclinical models, lasofoxifene inhibited breast tumor formation and reduced serum cholesterol (Maeda et al. 2004). Lasofoxifene-treated animals did not differ from ovariectomized controls with respect to endometrial thickness and superficial and basal endometrial gladular epithelial luminal area (Maeda et al. 2004 Ke et al. 2004). 

The study of osteoclast differentiation is important for understanding potential new treatments for osteoporosis. Such therapies are typically explored in tissue culture models such as the Raw264 mouse monocytic cell line, which is capable of differentiation into functional multinuclear osteoclasts after treatment with the cytokine Rankl. Use of transformed cell lines raises the concern that results may not be extrapolated to normal tissue. To address this question, the transcriptional responses for Rankl treatment of the Raw264 cell line, and of two ex vivo primary cell systems (bone marrow macrophages, and hematopoetic stem cells) were compared using Affymetrix GeneChips [23]. The models proved to... 

Primary osteoporosis is the most common form of the condition. The secondary form of osteoporosis is diagnosed when an illness and/or medications are present with a negative impact on BMD. Examples of common chronic conditions in old people that can cause secondary osteoporosis are seen in Box 5.14. Examples of drugs that can cause secondary osteoporosis are glucocorticoids, too high doses of thyroid hormone, anticonvulsants, and heparin. Especially the use of glucocorticoids has been known to cause severe osteoporosis even within a short period of treatment. Depending on the doses the development of osteoporosis can occur within a few weeks or months. 

Qassification Idiopathic osteoporosis type 1, occurring in postmenopausal females type 11, occurring in senescent males and females (>70 y). Secondary osteoporosis associated with primary disorders such as Cushing s disease, or induced by drugs, e.g chronic therapy with glucocorticoids or heparin. In these forms, the cause can be eliminated. 

Estrogens are most commonly used as a component of combination contraceptives or as hormone replacement therapy in postmenopausal women. Benefits in postmenopausal women include relief of moderate to severe vasomotor symptoms and decreased risk of osteoporosis. Hormone replacement therapy also may be used in vaginal and vulvar atrophy and in hypoestrogenism caused by hypogonadism, castration, or primary ovarian failure. Less commonly, select breast or prostate cancer... 

Osteoporosis is a metabolic bone disease characterized by low bone mass and micro-architectural deterioration of bone tissue. This will lead to bone fragility and consequent increase in bone fracture risk. Mean bone mineral density (BMD) is measured with dual X-ray absorptiometry (DEXA) and expressed in Tsc (Tscore). WHO standards are a Tsc that is 1 standard deviation (SD) below mean BMD is graded as normal bone, Tsc between 1 and 1.5 SD below mean BMD is graded as osteopenia and a Tsc of more than 2.5 SD below mean BMD is graded as osteoporosis. When the Tsc is below 1.5 SD mean BMD prevention of osteoporosis must be initiated. Primary osteoporosis is caused mainly by hormone deflciency in both women and men. Secondary osteoporosis may result from endocrine, metabolic, nutritional and autoimmune causes or from immobility because of trauma. Also the use of medicaments such as corticosteroids may be contributing. 

Non-compliance is a serious problem in the prevention of osteoporosis and osteoporotic fractures. This is due to adverse effects, lack of noticeable benefit and ignorance. It is difficult to convince regular intake of oral calcium, biphosphonates, vitamin D and in post-menopausal women hormone replacement. Long-term compliance to hormone replacement is worse in developing countries. The most cost-effective therapy for osteoporosis is primary prevention. 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Female hypogonadism, castration, primary ovarian failure PO 1 25-7 5 mg/day for 21 days then off for 8-10 days. Repeat if bleeding does not occur by end of off cycle. Prevention of osteoporosis PO 0.625 mg/day (25 days of 31-day cycle/mo). 

---