Etiology and Key Pathogenetic Mechanisms
The onset of PEM is driven by the complex interaction of multiple exogenous and endogenous factors. Based on the leading mechanism of action, all causes are classified into three major groups:
- Factors causing eating and intake disorders (malnutrition). This group includes conditions in which food physically does not enter the body or cannot be swallowed. These are general or isolated protein starvation, anorexia nervosa, intractable vomiting, as well as various disorders of swallowing and propulsion of the food bolus through the gastrointestinal tract.
- Factors leading to digestive disorders (maldigestion). These include secretory, enzymatic, and motor insufficiency of the gastrointestinal organs. This also includes inflammatory diseases (gastritis, enteritis, colitis), peptic ulcers of the stomach and intestine, and irritable bowel syndrome.
- Factors disrupting nutrient absorption mechanisms (malabsorption). These develop due to a deficiency of specific enzymes responsible for protein transport in the villi of the small intestine. Other causes can include lymph stasis in intestinal capillaries, Crohn's disease, and short bowel syndrome.
Kwashiorkor — Unbalanced Malnutrition
Kwashiorkor is a form of PEM that occurs with acute dietary lack of protein and essential amino acids. The pathology often manifests against the background of a pronounced predominance of carbohydrates in the daily diet. The prognosis for this condition is extremely unfavorable, which is associated with significant hypotrophy of the intestinal mucosa and the development of achylia.
The clinical presentation is based on a characteristic tetrad of symptoms:
- Generalized edema. Forms as a consequence of a critical drop in blood albumin levels, leading to a decrease in oncotic pressure (hypo-oncquia).
- Hypotrophy and atrophy of skeletal muscles due to a lack of building material.
- Developmental delay (both physical and neuropsychiatric).
- Severe immunodeficiency states (combined T- and B-dependent), which are frequently complicated by secondary infections leading to death.
Additionally, patients exhibit a negative nitrogen balance, gastrointestinal disturbances, and anemia. Regarding the endocrine system, secondary hyperaldosteronism caused by hypovolemia is observed, along with severe dysionia (hypernatremia, hypokalemia, hypomagnesemia, and hypophosphatemia).
Nutritional Marasmus
Unlike kwashiorkor, nutritional marasmus is a combined form of PEM resulting from a total and severe deficit of not only proteins, but also energy (calories), vitamins, and minerals. The main cause is a meager, monotonous diet or prolonged absolute starvation. Despite the severity of the condition, with timely and proper treatment, the prognosis remains favorable.
Key manifestations of nutritional marasmus:
- Extreme emaciation of the body with a weight loss of more than 60%.
- Significant hypotrophy of all structures: skeletal musculature, internal organs, bone tissue, and complete disappearance of subcutaneous adipose tissue.
- Growth retardation and delayed neuropsychiatric development.
- Negative nitrogen balance (15–25% below normal).
Important distinguishing feature: unlike patients with kwashiorkor, patients with nutritional marasmus have a fully preserved appetite.
With a prolonged course of the pathology, polyhypovitaminosis and immunodeficiency develop (predominantly T-cell mediated against the background of thymic hypotrophy). Catabolic processes dominate metabolism: hypoglycemia, ketonemia, and ketoacidosis occur (resulting from lipid breakdown), and in severe cases, hyperkalemia. The hormonal profile is characterized by stably elevated levels of glucagon and somatostatin.
Marasmic Kwashiorkor and Changes in Protein Pools
Marasmic kwashiorkor is a severe mixed variant of protein starvation that often develops against the background of a superimposed infection. It combines features of nutritional marasmus (pronounced tissue hypotrophy) and kwashiorkor (generalized hypoproteinemic edema).
| Indicator | Kwashiorkor | Nutritional Marasmus | Marasmus + Kwashiorkor |
|---|---|---|---|
| Body weight | Normal or increased (edema) | Sharply decreased | Decreased |
| Adipose tissue | Preserved | Depleted | Depleted |
| Visceral protein pool | Depleted | Preserved | Depleted |
| Somatic protein pool | Preserved | Depleted | Depleted |
States with a Positive Nitrogen Balance
The opposite of protein deficiency are conditions accompanied by persistent hyperproteinemia and a prolonged positive nitrogen balance. Their etiology includes simple overeating (polyphagia), an unbalanced diet with an excess of protein foods, as well as pathological activation of protein synthesis (for example, in diabetes mellitus or growth hormone hyperproduction).