Main Causes of Development
The concentration of magnesium in the blood can critically decrease through three main pathogenetic scenarios.
- Inadequate intake. Occurs with a basic dietary deficiency of the element 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 laxative abuse.
- Increased excretion. Most commonly associated with the kidneys. This can be primary renal tubular defects or secondary suppression of Mg²⁺ ion reabsorption. Secondary losses are provoked by endocrine shifts (hyperaldosteronism, hypoparathyroidism), electrolyte imbalance (hypercalcemia, hypophosphatemia), and the use 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.
- Intracellular redistribution. Magnesium can rapidly leave the bloodstream and enter cells. Such a shift is characteristic of hyperinsulinemia, respiratory alkalosis, alcohol withdrawal syndrome, and conditions following the correction of hyperparathyroidism.
Pathogenesis of Clinical Manifestations
The key and most significant manifestation of magnesium deficiency is increased neuromuscular excitability.
At the cellular level, this is explained by a decrease in the excitation threshold of nerve and muscle fiber membranes, as well as an increase in their conductivity. The situation is additionally 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).
In the cardiovascular system, magnesium deficiency in the blood and extracellular fluid, along with concomitant calcium deficiency, provokes tachycardia, various cardiac arrhythmias, and a sustained increase in blood pressure.
Metabolic and Tissue Disorders
Hypomagnesemia rarely occurs in isolation. Patients consistently exhibit combined electrolyte disorders:
- Hypocalcemia develops because low magnesium levels suppress the secretion of parathyroid hormone (PTH).
- Hypokalemia occurs against the background of inhibited renal K⁺ reabsorption driven by low magnesium concentrations.
At the tissue level, the deficiency of the element impairs the activity of magnesium-dependent enzymes (specifically, phosphatases and transferases). The reduction of their kinetic properties disrupts protein and carbohydrate metabolism. This leads to tissue dystrophy—erosions and trophic ulcers may form on the skin. Simultaneously, a process of generalized calcification is triggered: due to a lack of magnesium in the extracellular fluid, calcium begins to actively transport into tissues, depositing in cartilage, kidneys, and blood vessel walls.
This condition is particularly severe in pediatric patients. The reduction of magnesium effects on enzyme activation disrupts membrane digestion and cellular metabolism. Clinically, this is manifested by hypothermia, poor intestinal food absorption, and marked growth retardation.
Principles of Correction
To normalize magnesium levels and eliminate symptoms, a comprehensive approach is applied, including three main therapeutic directions:
- Etiotropic treatment — identifying and eliminating the underlying pathology that served as the primary cause of the decreased electrolyte level in the blood.
- Pharmacological correction — intravenous infusions of specialized preparations (e.g., magnesium sulfate or magnesium oxide solution).
- Diet therapy — a targeted increase in the daily diet proportion of magnesium-rich foods (millet, peas, beans).