Calcitonin and vitamin

PTH works with two other primary hormones— calcitonin and vitamin D—in regulating calcium homeostasis. These three hormones, as well as several other endocrine factors, are all involved in controlling calcium levels for various physiologic needs. How these hormones interact in controlling normal bone formation and resorption is of particular interest to rehabilitation specialists. Regulation of bone mineral homeostasis and the principal hormones involved in this process are presented in the following section. 

Know the effects of parathyroid hormone, calcitonin, and vitamin D in controlling calcium and phosphate metabolism. Know what controls the levels of such hormones in the bloodstream. 

The parathyroid hormone (PTH), calcitonin, and vitamin D regulate calcium. 

Arnaud (7) has developed a butterfly model that provides a diagrammatic view of the complex interrelationships among the three hormones (parathyroid, calcitonin, and vitamin D) that control calcium homeostasis (serum concentrations of ionic calcium) and their target organs (bone, kidney, and intestine) (Fig. 35.1). The right side (B loops) of the butterfly model describes the processes that increase the serum calcium concentration in response to hypocalcemia the left side (A loops) depicts the events that occur in response to hypercalcemia. 

A more positive control of calcium ion concentration is brought about by the cell-mediated resorption or deposition of stable bone material. These adjustments are slower, but quantitatively greater, than the simple exchange reaction. They take place with great precision with regard to the sites in the bone where resorption and deposition occur, their timing and the constancy of plasma ion concentration achieved. The process thus provides for both the continuous remodelling of bone and for the calcium-phosphorus homoeostasis of the blood and tissue fluids. The former depends on the position on the bone surface of various stimulated cells and the latter on the net result of stimulation of cells in bone, intestine and kidney by parathyroid hormone, calcitonin and vitamin D. The mode of action of these substances and the interplay of their various effects are complex. 

Osteoporosis Encourage patients to ingest adequate amounts of calcium and vitamin D, encourage smokers to discontinue tobacco use, and consider initiation of medications for osteoporosis (e.g., bisphosphonates, calcitonin, and parathyroid hormone) if the patient is taking glucocorticoids for an extended period of time or if the patient has evidence of low bone mineral density.15,41... 

Marcus, R., Agents affecting calcification and bone turnover calcium, phosphate, parathyroid hormone, vitamin D, calcitonin, and other compounds, in Goodman and Gilman s The Pharmacological Basis of Therapeutics, 9th ed., Hardman, J.G. and Limbird, L.E., Eds., McGraw-Hill, New York, 1996, chap. 61. 

Alternatives to steroid hormone therapy for osteoporosis include raloxifene, bisphosphonates, sodium fluoride, vitamin D and calcium supplementation, calcitonin, and parathyroid hormone. Tamoxifen has estrogenic effects on bone and delays bone loss in postmenopausal women. However as a result of estrogenic activity in the uterus, long-term tamoxifen administration has been associated with an increased risk of... 

Clinical trials have demonstrated that the use of the bisphosphonates, nasal calcitonin, or human rPTH combined with calcium and vitamin D supplementation is effective in preventing drug-induced osteoporosis. Thus, individuals receiving over the long term any medication that can induce osteomalacia should also take one of these compounds and have periodic bone density determinations. 

With the exception of the possible development of a hypervitaminosis associated with high-dose administration of vitamin D2 or D3, the compounds discussed in this chapter are relatively safe. Allergic reactions to the injection of calcitonin and PTH have occurred and chronic use of some bisphosphonates has been associated with the development of osteomalacia. The principal side effects of intravenous bisphosphonates are mild and include low-grade fever and transient increases in serum creatinine and phosphate levels. Oral bisphosphonates are poorly absorbed and can cause esophageal and gastric ulceration. They should be taken on an empty stomach the individual must remain upright for 30 minutes after ingestion. 

Plasma calcium level is precisely regulated by three hormones e.g. parathormone, calcitonin and calciferol (which is a active form of vitamin D). They control its absorption, exchange with bone and excretion. 

The main features of hypocalcemia are neuromuscular—tetany, paresthesias, laryngospasm, muscle cramps, and convulsions. The major causes of hypocalcemia in the adult are hypoparathyroidism, vitamin D deficiency, chronic kidney disease, and malabsorption. Neonatal hypocalcemia is a common disorder that usually resolves without therapy. The roles of PTH, vitamin D, and calcitonin in the neonatal syndrome are under active investigation. Large infusions of citrated blood can produce hypocalcemia by the formation of citrate-calcium complexes. Calcium and vitamin D (or its metabolites) form the mainstay of treatment of hypocalcemia. 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

Kaskani E, Lyritis GP, Kosmidis C, et al. Effect of intermittent administration of 200 IU intranasal salmon calcitonin and low doses of 1 alpha(OH) vitamin D3 on bone mineral density of the lumbar spine and hip region and biochemical bone markers in women with postmenopausal osteoporosis a pilot study. Clin Rheumatol. 2005 24 232-238. 

Osteopathy Prevention or improvement in osteopathy typical in PBC can be achieved by means of UDCA. In addition, sodium fluoride (50 mg/day), calcium (1,500 mg/day), alendronate (10 mg/day orally), and vitamin D, e.g. 1.25 (0H)2 Ds (500-5000 units/day orally) should be administered. Calcitonin (50 units 3x/week i.m.) has also been used. (113) Substitution of oestrogens is advisable for postmenopausal women. (228) Daily muscular activity is considered to be the most important measure (e. g. regular physical exercise, stretching exercises, purposeful swimming). Every patient should engage in physical exercise as a daily must , because this is very effective for the activation of the muscular system (s. pp 536, 732) ... 

Calcium is essential for the normal growth and development of the body, especially (in the form of calcium phosphate) of the bones and teeth. Its level in the blood is regulated by the opposing actions of the thyroid hormone calcitonin, and the parathyroid hormone parathormone. Its uptake from food is enhanced by vitamin D (calciferol). Forms of calcium used therapeutically include the folinic acid supplement calcium foiinate, and the mineral supplements calcium bicarbonate, calcium carbonate, calcium gluconate and calcium lactate. 

The plasma concentration of calcium is kept remarkably constant throughout life at about 8.8-10.3 mg/dL (2.20-2.58 mmol/L). The normal serum calcium concentration is maintained by the integrated actions of parathyroid hormone (PTH) vitamin D metabolites, calcitonin, and cytokines such as transforming growth factor and interleukin-6. The principal target sites for these hormones... 

Interaction of PTH, calcitonin, and serum concentrations of calcium and phosphate in calcium and phosphate homeostasis. [Modified and reproduced, with permission, from A. W. Norman, Vitamin D The Calcium Homeostatic Hormone. Academic Press, New York, 1979.]... 

B. Hyperparathyroidism is the likely cause of all of the patient s symptoms. Increased parathyroid hormone leads to bone demineralization, increased calcium uptake from the intestine, increased blood levels of calcium, decreased calcium ion excretion by the kidney, and increased phosphate excretion in the urine. Increased blood calcium levels caused renal stones, while bone demineralization progressed to osteopenia. The patient s intake of calcium and vitamin D are not excessive. Calcitonin acts to decrease bone demineralization. Muscle weakness and depression reflect the widespread role of calcium ion in many physiologic processes. 

The parathyroids are small, but important, glands involved in regulation of blood calcium levels together with calcitonin secreted by the thyroid gland and vitamin D. Calcitonin has a use in treating Paget s disease and osteoporosis (see Chapter 7). 

Much evidence exists to support the contention that boron has beneficial effects on bone. The effects of boron, however, are most evident in the presence of suboptimal status of another nutrient important in bone formation or remodeling. In chicks, boron deprivation (0.465 mgkg diet) exacerbates the distortion of marrow sprouts (location of calcified scaffold erosion and new bone formation) and delay in imtiation of cartilage calcification in bones during marginal vitamin D deficiency (Hunt 1996). In humans, estrogen therapy to maintain bones increases serum 17P-estra-diol this increase is depressed when dietary boron intake is low (0.25-0.35 g per day) (Nielsen 1996, 1997). Boron deprivation also can exacerbate the increase in serum calcitonin and osteocalcin caused by low dietary copper and magnesium in humans. 

This active vitamin D metabolite (1,25 dihydroxycholecalciferol) is an important cofactor for intestinal calcium absorption, which involves calbindins (calcium binding proteins) in the intestine and kidney. Calcitriol is produced in the kidneys by the conversion of 25-hydroxycholecalciferol (calcidiol) and its formation is stimulated by a reduction of plasma calcium and/or phosphate and increased production of parathyroid hormone and prolactin (Figure 6.3). Calcitriol also inhibits the release of calcitonin and, together with PTH, increases the absorption of calcium and phosphate from the gastrointestinal tract and the kidneys. Growth hormone, glucocorticoids, estrogens, testosterone, and the thyroid hormones also influence calcium metabolism. 

Describe the therapeutic and toxic effects of vitamin D. calcitonin, and bisphosphonates. 

Calcitonin therapy requires the concomitant oral administration of elemental calcium (500 mg/day). Clinical studies have shown that the combination of intranasal calcitonin salmon (200 lU/day), oral calcium supplementation (>1,000 mg/day of elemental calcium), and vitamin D (400 lU/day) has decreased the rate of new fractures by more than 75% and has improved vertebral BMD by as much as 3% annually (3). Calcitonin prevents the abnormal bone turnover characteristic of Paget s disease of the bone and has antiresorptive activity. In the presence of calcitonin, the osteoclast brush borders disappear, and the osteoclasts move away from the bone surface undergoing remodeling (36). Side effects are significantly more pronounced when calcitonin-salmon Is administered by injection and can include nausea, vomiting, anorexia, and flushing. Because calcitonin-salmon Is protein in nature, the possibility of a systemic allergic reaction should be considered. 

The efficiency of Ca absorption is much lower at around 30%. The P and Ca concentration in the blood is regulated by three substances vitamin D, calcitonin and parathyroid hormone (Chapter 10.2). These substances, the latter two being polypeptides, between them control the absorption of the two elements from the intestine, their deposition and resorption in bone, and... 

---