The Hypocalcemia is a relatively frequent finding in medical practice, and its clinical presentation is variable and is defined as the decrease in total calcium concentration below its reference value, which is usually 8.5 mg/dl. The clinical signs of hypocalcemia are mainly due to neuromuscular irritability and are more evident and intense when the onset of hypocalcemia is acute.

It should be noted that it was Sydney Ringer in the year 1883, more than 135 years ago, who showed for the first time that calcium was an essential element for myocardial contraction, through experiments done in frogs. Currently, its participation as a second intracellular messenger and intervention in intracellular proteolysis, apoptosis, enzymatic activation / deactivation, secretion of neurotransmitters, muscle contraction, platelet aggregation, cellular bioenergetics and gene transcription is demonstrated.

But how does hypocalcemia appear?

In general, the hypocalcemia is the result of both an increase in the loss of ionized calcium in the blood, deposition in the tissues, renal elimination or an increase in its binding to circulating proteins, and a decrease in the supply of calcium to the circulation due to intestinal malabsorption or decreased bone resorption.

The concentration of serum calcium is tightly regulated to maintain its physiological functions. The main factors that can influence calcemia are the concentration of phosphates (acute), the concentration of parathormone (PTH) (subacute) and the concentration of metabolites of vitamin D (chronic).

The main causes of hypocalcemia in adults can be grouped, according to the physiopathological mechanism that produces them, in hypoalbuminemia, loss of calcium from the circulation and poor supply from the intestine or bone.

Diagnosis of hypocalcemia

In the initial approach of a hypocalcemic patient it is convenient to confirm the presence of a real hypocalcemia. In case of doubt, ionized calcium can be measured directly. Before diagnosing hypocalcemia, it is necessary to ensure the existence of normal figures of albumin, which, as already mentioned, is accompanied by a decrease in total calcium values.

In the initial assessment of hypocalcemia, the clinical context is important. Sometimes the diagnosis is obvious, as occurs in hypocalcemia due to drugs, in hypomagnesemia, in renal failure, after thyroid surgery or in critical situations. In the rest of the patients it is necessary to resort to complementary tests, fundamentally determination of creatinine, phosphorus, magnesium, intact PTH and metabolites of vitamin D.

Once hypocalcaemia is ascertained, the measurement of magnesium and creatinine makes it possible to exclude hypomagnesemia and renal failure, respectively. Then, once the intake of calcium chelators or the exaggerated contribution of phosphorus is excluded, the serum concentrations of phosphorus, PTH and vitamin D metabolites should be measured. The increase of phosphorus in the absence of renal insufficiency, of exogenous contribution or of destruction tissue suggests a hypoparathyroidism or a pseudohypoparathyroidism. On the contrary, the decrease in phosphorus suggests the existence of a secondary hyperparathyroidism or a reduced phosphorus intake and, in the latter case, the fractional excretion of phosphorus is less than 5%.

What is the use of PTH measurement?

Differentiates hypocalcemia due to PTH deficiency from other causes. An increase in PTH reflects a secretory response of the normal parathyroid glands to hypocalcemia. Therefore, it suggests that hypocalcemia is due to other causes, in general an absence or a lack of action of vitamin D. PTH is also increased in pseudohypoparathyroidism and in hypomagnesemia, situations in which there is hypocalcemia due to a poor response from peripheral tissues to PTH.

In vitamin D deficiency, PTH is elevated and there is a tendency to hypophosphatemia. As a general rule, patients with vitamin D deficiency have mild or moderate hypocalcemia and hypophosphatemia.

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