Secondary hypocalcemia

Soluble oxalates in the leaves are absorbed via the gastrointestinal tract. Once absorbed, oxalates bind with calcium producing secondary hypocalcemia. 

Liebscher and Liebscher 2000, Meij etal. 2002). Meanwhile, four primary hereditary hypomagnesemia disorders have been identified (i) hypomagnesemia with secondary hypocalcemia (HSH) (ii) familial hypermagnesemia, hypercalciuria and neph-rocalcinesis (HHN) and (iii) dominant hypo-magnesemia/hypocalciuria and (iv) recessive hypomagnesemia (Meij et al. 2002). 

Hypomagnesemia has been associated with more than 50 drugs, especially those that are nephrotoxic, including cisplatin, aminoglycoside antibiotics, cyclosporine, and amphotericin B. Secondary hypocalcemia and hypokalemia may result with myasthenia and tetany (Swaminathan 2003). 

Renal osteodystrophy Altered bone turnover that results from sustained metabolic conditions that occur in chronic kidney disease, including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. 

Secondary hyperparathyroidism Increased secretion of parathyroid hormone from the parathyroid glands caused by hyperphosphatemia, hypocalcemia, and vitamin D deficiency that result from decreased kidney function. It can lead to bone disease (renal osteodystrophy). 

Symptomatic hypocalcemia commonly occurs because of parathyroid gland dysfunction secondary to surgical procedures involving the thyroid, parathyroid, and neck. 

Hypocalcemia with signs of tetany secondary to magnesium sulfate therapy for eclampsia has occurred. 

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. 

Calcium play vital role in excitation - contraction coupling in myocardium. Calcium mediates contraction in vascular and other smooth muscles. Calcium is required for exocytosis and also involved in neurotransmitters release. Calcium also help in maintaining integrity of mucosal membranes and mediating cell adhesions. Hypercalcemia may occur in hyperthyroidism, vitamin D intoxication and renal insufficiency, which can be treated by administration of calcitonin, edetate sodium, oral phosphate etc. Hypocalcemia may occur in hypothyroidism, malabsorption, osteomalacia secondary to leak of vitamin D or vitamin D resistance, pancreatitis and renal failure. Hypocalcemia can be treated by chloride, gluconate, gluceptate, lactate and carbonate salts of calcium. 

In contrast to the hypocalcemia that is more often associated with chronic kidney disease, some patients may become hypercalcemic from two other possible causes (in addition to overzealous treatment with calcium). The most common cause of hypercalcemia is the development of severe secondary (sometimes referred to as tertiary) hyperparathyroidism. In such cases, the PTH level in blood is very high. Serum alkaline phosphatase levels also tend to be high. Treatment often requires parathyroidectomy. 

Secondary> hyperparathyroidism 30 mg PO daily Parathyroid carcinoma 30 mg PO bid titrate q2—4wk based on Ca PTH levels swallow whole take w/ food Caution [C, /—] w/ Szs Disp Tabs SE N/V/D, myalgia, dizziness, 4- Ca2+ Interactions T Effects W/ CYP3A4 inhibitors such as ketoconazole, itraconazole, erythromycin T effects OF drugs metabolized at CYP2D6 such as TCA, thioridazine, flecainide, vinblastine EMS Monitor ECG for signs of hypocalcemia (T QT interval) OD May cause severe hypocalcemia calcium salts can be given... 

The major problems of chronic renal failure that impact on bone mineral homeostasis are the loss of l,25(OH)2D and 24,25(OH)2D production, the retention of phosphate that reduces ionized calcium levels, and the secondary hyperparathyroidism that results. With the loss of l,25(OH)2D production, less calcium is absorbed from the intestine and less bone is resorbed under the influence of PTH. As a result hypocalcemia usually develops, furthering the development of hyperparathyroidism. The bones show a mixture of osteomalacia and osteitis fibrosa. 

The choice of vitamin D preparation to be used in the setting of chronic renal failure in the dialysis patient depends on the type and extent of bone disease and hyperparathyroidism. No consensus has been reached regarding the advisability of using any vitamin D metabolite in the predialysis patient. l,25(OH)2D3 (calcitriol) will rapidly correct hypocalcemia and at least partially reverse the secondary hyperparathyroidism and osteitis fibrosa. Many patients with muscle weakness and bone pain gain an improved sense of well-being. 

Celiac disease is the result of the development of inflammatory-allergic condition due to gluten intolerance. The disease occurs both in adults and in children in a number of countries all over the world. Its occurrence is fairly frequent, it is estimated that approximately 1% of the population suffers from it. Patients manifest not only gastrointestinal symptoms, but also symptoms which are the consequence of malabsorption syndrome, such as osteoporosis, hypochromic anemia, hypoproteinaemia, hypocalcemia, short stature in children, vitamin deficiency, secondary polysensibilization, and emotional disturbances. Moreover, it has been observed that the occurrence of autoimmunological diseases and neoplasms in patients who are not treated with gluten-free diet doubles (Swinson et al., 1983 Ventura et al., 1999). 

For symptomatic hypocalcemia, calcium may be administered intravenously. If hypocalcemia is secondary to hypoparathyroidism or pseudohypoparathyroidism, vitamin D and oral calcium supplements are administered. 

Because magnesium deficiency is usually secondary to another disease process or to a therapeutic agent, the features of the primary disease process may complicate or mask magnesium deficiency. Neuromuscular hyperexcitabihty with tetany and seizures may be present. These symptoms and signs may also be due to hypocalcemia, and magnesium deficiency is a common cause of hypocalcemia. Magnesium deficiency impairs PTH secretion and causes resistance to PTH in the kidneys and bone. 

Osteitis fibrosa (hyperparathyroid bone disease) is the most common high-turnover bone disease. This disorder is caused by the high concentrations of serum PTH in secondary hyperparathyroidism. Secondary hyperparathyroidism is a consequence of the hypocalcemia associated with hyperphosphatemia and l,25(OH)2D deficiency. Hyperphosphatemia is a result of the kidneys inability to excrete phosphate. l,25(OH)2D deficiency results from the inability of the kidneys to synthesize l,25(OH)2 because of decreased renal mass and suppression of 25(OH)D-la-hydroxylase activity by high concentrations of phosphate. Deficiency of l,25(OH)2D leads to reduced intestinal absorption of calcium and reduced inhibition of PTH secretion by l,25(OH)2D. Skeletal resistance to PTH also contributes to the hypocalcemia and secondary hyperparathyroidism. 

An increased risk of cataracts secondary to lactose and galactose ingestion is present in subpopulations with a deficiency in galactokinase activity (Couet et al. 1991). In addition, people with hyperparathyroidism, hypocalcemia, or hypoglycemia are predisposed to cataracts (Lloyd et al. 

Kenny and Heiskell (Kl) regard the phosphaturic effect of thyrocalcitonin as possibly due to secondary stimulation of parathormone release by hypocalcemia this is not, however, supported by the findings of Robinson et al. (R4) and Milhaud and Moukhtar (M9) that the phosphaturic effect of thyrocalcitonin was present in parathyroid-ectomized and thyroparathyroidectomized rats, respectively. It has been... 

Vitamin D and its metabolites play an important role in the maintenance of extracellular calcium concentrations and in normal skeletal structure and mineralization. Vitamin D is necessary for the optimal absorption of calcium and phosphorus. On a worldwide basis, the most common cause of hypocalcemia is nutritional vitamin D deficiency. In malnourished populations, manifestations include rickets and osteomalacia. Nutritional vitamin D deficiency is uncommon in Western societies because of the fortification of miUc with ergocalciferol. " The most common cause of vitamin D deficiency in Western societies is gastrointestinal disease. Gastric surgery, chronic pancreatitis, small-bowel disease, intestinal resection, and bypass surgery are associated with decreased concentrations of vitamin D and its metabolites. Vitamin D replacement therapy may need to be administered by the intravenous route if poor oral bioavailability is noted. Decreased production of 1,25-dihydroxyvitamin D3 may occur as a result of a hereditary defect resulting in vitamin D-dependent rickets. It also can occur secondary to chronic renal insufficiency if there is insufficient production of the 1 -a -hydroxylase enzyme for the... 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

Hyperphosphatemia is not uncommonly observed in patients undergoing treatment for acute leukemia and lymphomas. Chemotherapeutic treatment of acute lymphoblastic leukemia may result in the release of large amounts of phosphorus into the systemic circulation secondary to lysis of lymphoblasts. Initiation of chemotherapy for Burkitt s lymphoma results in a rapid lysis of malignant cells, resulting in hyperphosphatemia, hyperuricemia, hyperkalemia, and hypocalcemia. This syndrome is commonly referred to as tumor lysis syndrome. ... 

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