Protein-energy malnutrition

Etiology and key mechanisms of development

The onset of PEM is caused by the complex impact of multiple exogenous and endogenous factors. Based on the leading mechanism of action, all causes are classified into three major groups:

1. Factors causing nutritional disorders (malnutrition). This group includes conditions where food physically does not enter the body or cannot be swallowed. This is general or isolated protein starvation, anorexia nervosa, intractable vomiting, as well as various disorders of swallowing and food bolus transit through the gastrointestinal tract.
2. 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, as well as irritable bowel syndrome.
3. Factors disrupting nutrient absorption mechanisms (malabsorption). These develop when there is a deficiency of specific enzymes responsible for protein transport in the villi of the small intestine. Other causes may include lymphostasis in intestinal capillaries, Crohn's disease, and short bowel syndrome.

Kwashiorkor — unbalanced deficiency

Kwashiorkor is a form of PEM that occurs due to acute nutritional deficiency of protein and essential amino acids. Often, the pathology manifests against the background of a pronounced predominance of carbohydrates in the daily diet. The prognosis for this disease is extremely unfavorable, which is associated with significant hypotrophy of the intestinal mucosa and the development of achylia.

The clinical picture is based on a characteristic tetrad of symptoms:

• Generalized edema. Formed as a consequence of a critical decrease in blood albumin levels, leading to a drop in oncotic pressure (hypooncquia).
• Hypotrophy and atrophy of skeletal muscles due to a lack of building material.
• Developmental delay (both physical and neuropsychological).
• Severe immunodeficiency states (combined T- and B-dependent), which are often complicated by secondary infections leading to a fatal outcome.

Additionally, patients exhibit a negative nitrogen balance, gastrointestinal disorders, and anemia. From the endocrine system, secondary hyperaldosteronism caused by hypovolemia is observed, as well as severe dysionia (hypernatremia, hypokalemia, hypomagnesemia, and hypophosphatemia).

Alimentary dystrophy (alimentary marasmus)

Unlike kwashiorkor, nutritional marasmus is a combined form of PEM resulting from a total and severe deficiency of not only proteins, but also energy (calories), as well as vitamins and minerals. The main cause is poor, monotonous nutrition 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 neuropsychological 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 predominate in metabolism: hypoglycemia, ketonemia, and ketoacidosis occur (as a result of 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 an superimposed infection. It combines signs of nutritional marasmus (pronounced tissue hypotrophy) and kwashiorkor (total hypoproteinemic edema).

Conditions with a positive nitrogen balance

The opposite of protein deficiency is 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, and pathological activation of protein synthesis (for example, in diabetes mellitus or growth hormone hyperproduction).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis of secondary hyperaldosteronism in protein starvation
• Mechanisms of development of ketonemia and ketoacidosis in nutritional marasmus
• Impact of protein-energy malnutrition on T- and B-cell immunity
• Conditions associated with a positive nitrogen balance and hyperproteinemia

Other topics in "Chapter 9. Nucleic Acid and Protein Metabolism Disorders"

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