Low serum calcium

Signs of chronic zinc poisoning evident after 12-14 months. Signs included reduced appetite, emaciation, submandibular edema, diarrhea, moderate anemia, elevated serum zinc (4.3-6.0 mg/L vs. normal 1.8-2.1), liver Zn (420-1600 mg/kg DW vs. normal 72-248), kidney Zn (910-1680 mg/kg DW vs. normal 40-114), and low serum calcium and magnesium. 

Calcium/Vitamin Bq Low serum calcium and low plasma vitamin 85 levels were... 

Conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to l,25(OH)2D3 and 24,25(OH)2D3. Control of the latter step is exerted primarily at the level of the kidney, where low serum phosphorus, low serum calcium, and high parathyroid hormone favor the production of l,25(OH)2D3, whereas fibroblast growth factor 23 inhibits its production. The inset shows the... 

Renal 7 (low serum calcium and 7 (scanty urine, high levels of albumin and bile pigments in urine, increased blood urea) ... 

Calcium determinations in serum are valuable in the diagnosis of a number of pathologic conditions. Hypocalcemia (low serum calcium) is seen in hypopara-... 

The dietary history and laboratory findings for this patient pointed to calcium-deficiency as the cause of her rickets a low serum calcium within the normal range secondary hyperparathyroidism with an elevated serum concentration of PTH and a normal serum concentration of 25-hydroxyvitamin with an elevated serum concentration of 1,25-dihydroxyvitamin D, the active hormone form of vitamin D. The patient s calcium-deficiency was due to the fact that she did not have access to milk because of the expense and the lack of adequate storage facilities for fresh dairy products in the home. 

The relationship of serum calcium and phosphate with rickets was discovered by Howland and Kramer [10]. They found that blood from normal rats could mineralize rachitic rat cartilage, whereas blood from rachitic rats could not. They also provided evidence that a low serum calcium and phosphate status caused rickets. Orr etal. [11] demonstrated that UV irradiation stimulated calcium absorption. This study was largely unappreciated for 30 years until Nicolaysen and Eeg-Larsen [12] and Schachter and Rosen [13] demonstrated evidence for vitamin D-induced intestinal absorption of calcium by an active transport process. 

Low serum phosphate level directly stimulates the enzyme 1-hydroxylase. Low serum calcium level indirectly stimulates the enzyme 1-hydroxylase, via PTH. 

Low serum calcium ion stimulates parathyroid glands to secrete PTH, which in turn stimulates 1-hydroxylase and inhibits 24-hydroxylase reactions in kidney. 

PTH is released in response to low serum calcium zmd induces the production of calcitriol. In contrast, reduced levels of PTH stimulate synthesis of the inactive 24,25-(OH)2D3. 

In patients with renal failure, the occurrence of conditioned zinc deficiency may be the result of a mixture of factors, which at present are ill defined. If 1,25-dihydroxycholecalciferol plays a role in the intestinal absorption of zinc, an impairment in its formation by the diseased kidney would be expected to result in malabsorption of zinc. It seems likely that plasma and soft tissue concentrations of zinc may be "protected in some individuals with renal failure by the dissolution of bone which occurs as a result of increased parathyroid activity in response to low serum calcium. In experimental animals, calcium deficiency has been shown to cause release of zinc from bone. In some patients who are successfully treated for hyperphosphatemia and hypocalcemia, the plama zinc concentration may be expected to decline because of the deposition of zinc along with calcium in bone. Thus, in the latter group in particular, a diet low in protein and high in refined cereal products and fat would be expected to contribute to a conditioned deficiency of zinc. Such a diet would be low in zinc. The patients reported by Mansouri et al. (37), who were treated with a diet containing 20-30 g of protein daily and who had low plasma concentrations of zinc, appear to represent such a clinical instance. Presumably the patients of Halsted and Smith (38) were similarly restricted in dietary protein. In other patients with renal failure whose dietary protein was not restricted, plasma zinc concentration were not decreased. Patients on dialysis had even higher levels, particularly... 

Low serum calcium PTH moves calcium from bone into serum and increases reabsorption of calcium by the kidneys. Absorption of calcium also occurs in the GI tract. 

Other causes of low serum calcium are less common. Hypoparathyroidism is due most commonly to parathyroid gland destruction during neck surgery (90%), and less commonly is idiopathic. Pseudohypoparathyroidism is biochemically similar to hypoparathyroidism however, these patients have inherited resistance to PTH and elevated concentrations of PTH. The molecular basis for the most common form, pseudohypoparathyroidism type I (Albright s hereditary osteodystrophy), is a reduction in guanine nucleotide regulatory complex. Ns, in the adenylate cyclase complex. 

Mechanisms leading to osteomalacia include low serum calcium or phosphorus, chronic acidosis, hypophosphatemia, liver or re-... 

L Low serum calcium and phosphorus ii. High alkaline phosphatase... 

Four parathyroid glands are situated on the lateral lobes of the thyroid. These glands secrete parathyroid hormone in response to low serum calcium levels. Parathyroid hormone then increases the serum calcium levels through the functioning of several mechanisms it stimnlates bone resorption it increases the intestinal absorption of calcium it... 

Parathyroid hormone (PTH), vitamin D and calcitonin work in synchrony to regulate calcium homeostasis (not presented in tables). PTH is an 84 amino acid chain secreted by the parathyroid glands in response to low serum calcium. PTH induces bone resorption, which liberates calcium into the bloodstream. These actions are dependent on adequate serum concentrations of 1,25-dihydroxy cholecalciferol (a derivative of vitamin D). Bone resorption is counterregulated by calcitonin, which inhibits osteoclasts (the cells which degrade bone). 

A new formulation of alendronate, FOSAMAX PLUS D, was approved by the U.S. FDA in April 2005. This formulation includes 70 mg of alendronate and 2,800 lU of vitamin D3 (i.e., a 7-day supply of both the bisphosphonate and vitamin D). This formulation should not be used in patients with severe kidney disease or low serum calcium levels and should not be the only therapy used to correct a vitamin D deficiency. 

Other reports describe patients whose response to usual doses of vitamin D was poor, because of concurrent anticonvulsant treatment with pheny-toin and phenobarbital or primidone. " Other reports clearly show low serum calcium levels,low serum vitamin D levels, osteomalacia, and bone structure alterations in the presence of phenytoin. 

A condition in which there is decalcification of bone tissue. It occurs when there is reduced calcium or vitamin D intake, for instance in malabsorption. Osteomalacia can also occur as a result of treatment with anticonvulsant drugs which are thought to interfere with the metabolism of vitamin D. Low serum calcium levels occur along with high serum alkaline phosphatase levels, the latter being due to a secondary increase in osteoblastic activity. 

Renal disease or toxicosis leading to increased serum phosphorus and low serum calcium levels stimulates secretion of PTH, leading to fibrous osteodystrophy. 

Tetany, characterized by muscle im tching, convulsions, and low serum calcium. 

Tetany—A deficiency of vitamin D may cause tetany, though it is not the only cause. Tetany may also result from insufficient absorption of calcium or from a disturbance of the parathyroid gland. Tetany is characterized by muscle twitching, cramps, convulsions, and low serum calcium—less than 7 mg per 100 ml. 

According to Masironi et al. (1972) (51) calcium could be important in two ways. First it might inhibit - I cite now Masironi the absorption of harmful elements from pipes and soil, or calcium ions might be an addition to dietary calcium . This latter concept is supported by the observation that low serum calcium concentrations were found in soft water areas (Bierenbaum et al. 

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