Calcium 4.0

3 min read

By: Dr Ameya Tripathi, Bureau Chief-ICN U.P.

Hypocalcemia part 2

In our previous article we have discussed in detail about physiological results and symptoms of hypocalcemia.

LUCKNOW:Acute hypocalcemia can result in severe symptoms requiring hospitalization, whereas patients who gradually develop hypocalcemia are more likely to be asymptomatic.

1 Symptoms of hypocalcemia most commonly include paresthesia, muscle spasms, cramps, tetany, circumoral numbness, and seizures. Hypocalcemia can also present with laryngospasm, neuromuscular irritability, cognitive impairment, personality disturbances, prolonged QT intervals, electrocardiographic changes that mimic myocardial infarction, or heart failure.

A thorough family history should be taken to rule out any genetic cause. A series of diagnostic test should be carried out which are outlined as below

 Basic investigations

  1. Serum calcium (corrected for albumin)

1 Phosphate

2 Magnesium

Electrolytes

1. Creatinine

1. Alkaline phosphatase

1. Parathyroid hormone

1. 25-hydroxyvitamin D

1. Serum pH

1. Complete blood count

Further investigations

1.Ionized calcium

1. 24-hour urinary phosphate, calcium, magnesium, and creatinine

1. 1,25-dihydroxyvitamin D

1. Renal ultrasonography to assess for nephrolithiasis

1. DNA sequencing to exclude genetic mutations

1. Biochemistry in first-degree family members

Management of hypocalcemia can be divided into management of acute and chronic hypocalcemia

Acute hypocalcemia management-hospitalization and Intravenous calcium is given if serum calcium levels fall below 1.9 mmol/L, or ionized calcium levels are less than 1 mmol/L. Magnesium deficiency or alkalosis should be corrected if present. Acutely, magnesium supplementation therapy will not elevate serum PTH or calcium, as peripheral PTH resistance can last for several days. Rapid correction of hypocalcemia can contribute to cardiac arrhythmia. Cardiac monitoring during intravenous calcium supplementation is necessary, particularly in patients taking digoxin therapy.

Long-term management of chronic hypocalcemia

Oral calcium and vitamin D and its metabolites are essential in management, in addition to correction of hypomagnesemia. Calcium carbonate and calcium citrate have the greatest proportion of elemental calcium (40% and 28%, respectively) and are easily absorbed; they are considered the supplements of choice. Hypercalciuria is a complication of vitamin D therapy, particularly for patients with hypoparathyroidism, as the absence of PTH enhances urinary calcium losses. If hypocalcemia is due to malabsorption of vitamin D, physicians should treat the underlying cause (eg, implementing a gluten-free diet for patients with celiac disease). Magnesium supplementation corrects hypomagnesemia-related hypocalcemia.

Vitamin D inadequacy: Vitamin D inadequacy requires correction with either ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). Ergocalciferol can be given in doses of 50 000 IU weekly or twice a week with assessment of levels 3 months later, titrating up until a normal 25(OH)D level is reached. Alternatively, 300 000 IU of ergocalciferol can be administered intramuscularly, with the first 2 injections spaced 3 months apart, followed by regular injections every 6 months.

Hypoparathyroidism: The treatment of hypoparathyroidism requires careful evaluation of the patient and consideration of the treatment options other than calcium supplementation. The primary goals of management with calcium and vitamin D supplementation include symptom control, maintaining serum calcium in the low-normal range (2.00 to 2.12 mmol/L), maintaining serum phosphorus within a normal range, and maintaining a calcium-phosphate product below 4.4 mmol

Thiazide diuretics decrease urinary calcium excretion by increasing distal renal tubular calcium reabsorption. Combining diuretics with a low-salt, low-phosphate diet and phosphate binders is beneficial. Replacement therapy with PTH is a viable option, as it corrects hypercalciuria and potentially reduces the risk of nephrocalcinosis, nephrolithiasis, and renal insufficiency. It can also reduce the wide fluctuation in serum calcium as well as the need to administer very large doses of calcium and vitamin D metabolites.

Following evaluation and determination of the cause of hypocalcemia, physicians should treat aggressively and closely monitor patients. Management requires identification of the cause of hypocalcemia, followed by calcium and vitamin D metabolite supplementation. Treatment can be further enhanced by introducing thiazide diuretics and other options, which are effective in treating hypocalcemia and preventing symptoms. Conventional therapy for hypoparathyroidism is currently suboptimal and is associated with wide fluctuations in serum calcium, as well as the risks of hypercalciuria, renal impairment, and hypercalcemia.

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