Hypomagnesemia

Main causes of development

Magnesium concentration in the blood can critically decrease via three main pathogenetic scenarios.

1. Inadequate intake into the body. It occurs with a banal deficiency of the element in food or impaired absorption. Since magnesium is absorbed primarily in the small intestine, any problems in this area lead to its shortage. Such factors include prolonged diarrhea, malabsorption syndrome, chronic enteritis, acholia, and abuse of laxatives.
2. Increased excretion. Most often associated with the kidneys. These can be primary defects in the renal tubules or secondary suppression of Mg²⁺ ion reabsorption. Secondary losses are provoked by endocrine shifts (hyperaldosteronism, hypoparathyroidism), electrolyte imbalance (hypercalcemia, hypophosphatemia), and the intake of certain diuretics (furosemide, ethacrynic acid). Stress plays a huge role: the release of adrenaline and cortisol forces the loss of magnesium in the urine.
3. Redistribution into cells. Magnesium can rapidly leave the bloodstream and move inside cells. Such a shift is characteristic of hyperinsulinemia, respiratory alkalosis, alcohol withdrawal syndrome, and states following the correction of hyperparathyroidism.

Pathogenesis of clinical manifestations

The key and most significant manifestation of magnesium deficiency is an increase in neuromuscular excitability.

At the cellular level, this is explained by a decrease in the excitability threshold of nerve and muscle fiber membranes, as well as an increase in their conductivity. The situation is further potentiated by an increase in extracellular potassium levels. Externally, this mechanism manifests as pronounced tremor, motor excitation, impulsivity, attention deficit, and specific muscle contractions — carpopedal spasm (spasm of the hands and feet).

From the cardiovascular system, magnesium deficiency in the blood and intercellular fluid, as well as concomitant calcium shortage, provoke tachycardia, various cardiac arrhythmias, and a persistent increase in blood pressure.

Metabolic and tissue disorders

Hypomagnesemia rarely occurs in isolation. Patients predictably show combined electrolyte disorders:

• Hypocalcemia — develops because low magnesium levels suppress the secretion of parathyroid hormone (PTH).
• Hypokalemia — occurs against the background of the inhibition of renal reabsorption of K⁺ ions under the influence of low magnesium concentration.

At the tissue level, the deficiency of the element affects the activity of magnesium-dependent enzymes (particularly phosphatases and transferases). The reduction of their kinetic properties disrupts protein and carbohydrate metabolism. This leads to tissue dystrophy — erosions and trophic ulcers can form on the skin. In parallel, the process of generalized calcification is triggered: due to the lack of magnesium in the extracellular fluid, calcium begins to be actively transported into tissues, depositing in cartilage, kidneys, and blood vessel walls.

The condition affects the child's body particularly severely. The reduction of magnesium's effects in activating enzymes disrupts membrane digestion and cellular metabolism. Clinically, this is expressed by hypothermia, poor food assimilation in the intestine, and pronounced growth retardation.

Principles of correction

To normalize magnesium levels and eliminate symptoms, a comprehensive approach is used, including three main areas of therapy:

1. Etiotropic treatment — finding and eliminating the main form of pathology that served as the primary cause of the decrease in the electrolyte level in the blood.
2. Drug correction — intravenous infusions of specialized preparations (for example, magnesium sulfate solution or magnesium oxide).
3. Diet therapy — targeted increase in the daily diet of foods rich in magnesium (millet, peas, beans).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of suppression of parathyroid hormone secretion in magnesium deficiency.
• Pathogenesis of carpopedal spasm and changes in the excitability threshold of cell membranes.
• The effect of hypomagnesemia on the kinetics of phosphatases and transferases.
• Features of membrane digestion disorders and growth retardation in children.
• The connection between alcohol withdrawal syndrome and intracellular ion redistribution.

Other topics in section "Chapter 12. Electrolyte Balance Disorders"

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