Effect of salt restriction on urine hydroxyproline excretion in postmenopausal women

Article Abstract:

When a woman reaches menopause, the amount of a substance known as hydroxyproline in her urine increases, indicating that more of it is being excreted or removed through the kidneys. This increased excretion of hydroxyproline is thought to reflect an increase in bone turnover, as occurs after menopause from osteoporosis (bone loss that increases the risk of fracture). The level of calcium in the urine is also elevated after menopause, and this increased loss of calcium in the urine may be what incites the increased rate of bone turnover, as the body attempts to maintain a normal level of calcium in the blood in the face of increased losses in the urine. The amount of calcium in the urine is directly related to the amount of sodium in the urine. The amount of sodium in the urine in turn is related to a number of factors, one of which is the amount of sodium taken in. Theoretically, those women who take in too much sodium, as in a high salt diet, may have increased sodium levels in their urine, giving increased calcium levels in their urine, causing increased bone turnover and osteoporosis, and resulting in increased levels of hydroxyproline in the urine. A study was done in which dietary salt intake was restricted, which resulted in decreased levels of urinary hydroxyproline, thereby implying less bone turnover and therefore less osteoporosis. These results were seen in approximately 25 percent of the patients studied, suggesting that salt restriction is one factor to be considered in the treatment and prevention of osteoporosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Food and nutrition, Fluid-electrolyte balance, Osteoporosis, Osmoregulation, Salt, Salt (Food)

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Relationship between forearm and vertebral mineral density in postmenopausal women with primary hyperparathyroidism

Article Abstract:

The majority of patients with hyperparathyroidism are postmenopausal women without symptoms. These women have only mildly elevated levels of calcium in their blood, resulting from the increased activity of the parathyroid gland. There is a difference of opinion regarding which treatment, if any, is appropriate for these patients. Since the condition causes a depletion of calcium in the bones, which can lead to fractures, it is worthy of further investigation. Bone mineral density was measured in 28 postmenopausal women with mild hypercalcemia (elevated blood calcium), which was presumably due to hyperparathyroidism. Bone mineral density of the spine was measured using single-energy computed tomography, and bone mineral density of the forearm was determined using gamma rays. The results indicated that the mineral loss from the forearm was significantly greater than that from the spine. Indeed, eight of the patients had already experienced one or more fractures in peripheral bones such as the forearm. Other studies have found a different distribution of mineral density loss, but these studies also evaluated a different spectrum of patients, including those with hypercalcemia. It may be, therefore, that these results only apply to postmenopausal women with mild hypercalcemia. The results of this study suggest that even mild hypercalcemia should be treated, either with estrogen or norethisterone, or by surgical removal of the parathyroids. (Consumer Summary produced by Reliance Medical Information, Inc.)

Usage, Risk factors, Bone diseases, Fractures (Injuries), Fractures, Bone densitometry

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Treatment of postmenopausal hyperparathyroidism with norethindrone

Article Abstract:

The long-term effect of the steroid drug norethindrone on the mineral content of the forearm bone was assessed in 15 women. These women were postmenopausal, or past the stage of menopause, and also had mild hyperparathyroidism, or increased activity of the parathyroid gland. This gland regulates calcium and phosphorus metabolism. The forearm bone mineral content (FMC) increased from 810 milligrams per centimeter (mg/cm) to 841 mg/cm after two years of treatment. This corresponded to an increase in bone mineral content of 1.9 percent per year. Most of the increase in bone occurred in the first six months of treatment. FMC values were corrected for body fat content to determine whether the increase in FMC was due to a real bone gain or a decrease in fat mass. After correction for fat content, FMC was shown to increase from 885 mg/cm to 909 mg/cm. Norethindrone treatment was also associated with a decrease in the subcutaneous (under the skin) fat layer. These findings show that norethindrone treatment causes an increase in bone mass in postmenopausal women with mild hyperparathyroidism, which is maintained for at least two years. (Consumer Summary produced by Reliance Medical Information, Inc.)

Bones, Drug therapy, Norethindrone

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