Pathophysiology of malnutrition

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Malnutrition can be classified as either primary or secondary [1]. Primary malnutrition is caused by inadequate calorie and nutrient intake. In developed societies, calorie intake is usually presumed to be adequate. However, inadequate intake of micronutrients including vitamins A and E, calcium, iron and zinc are prevalent among children of 1-10 years of age and often unrecognized, especially in minority populations [2]. Primary malnutrition in infants can also occur through child neglect or accidental nutrient insufficiency [3, 4]. For example, a genetic defect impairing zinc transport into breast milk from maternal blood can lead to zinc deficiency in infancy [5]. Eating disorders associated with psychosocial disorder are a common cause for primary failure-to-thrive in children [6]. Other causes include inadequate diet due to food intolerance or imposition of special diets unsuited to growing children. Vegetarian, macrobiotic or vegan diets in children may be associated with low vitamin D, reduced cobalamin, and perhaps iron. However, lacto-ovo-vegetarian children may consume diets closer to expert recommendations than omnivores and their pre-pubertal growth is at least as good [7, 8]. The presentation of malnutrition is outlined in Table 1.

Malnutrition and infection in industrialized countries Table 1. Presentation of malnutrition

Protein calorie malnutrition: marasmus

Protein calorie malnutrition: kwashiorkor


Chronic wasting, underweight

Low weight for height, stunting, short stature

Peripheral edema, depigmenation, hepatomegaly

Often develops at weaning

Iron: (J,) anemia, infections, pica

Zinc: (|) skin lesions, diarrhea, alopecia, infections

Copper: (f) infections, e.g., protozoal infections

Zinc and copper: (J,) hypoproteinemia, anemia

Selenium: (J,) muscle aches, pains, cardiomyopathy, infections

Vitamin A: (J,) keratomalacia, night blindness, infections

Vitamin C: (J,) leg pain, bleeding gums, petechial hemorrhage

Secondary malnutrition can be caused by reduced intake of food, malabsorption, impaired nutrient utilization, and nutrient losses associated with chronic infection and many other clinical conditions as well. Examples include inflammatory bowel disorders, celiac disease, chronic anemia, renal disorders, and cystic fibrosis (CF).

In both primary and secondary malnutrition, understanding of the relevant genetic mechanisms can be helpful in approaching the clinical manifestations. Genetic mechanisms of malnutrition that affect susceptibility to infectious disease include mutations affecting metabolism of the trace elements zinc, iron, and copper, and several vitamins as well as those underlying complex, inherited disorders such as CF and celiac disease. Primary malnutrition impairs immunity impeding host response to infection, but these effects are reversible with nutrient repletion. However, calorie and nutritional supplement alone cannot resolve the secondary malnutrition with organic etiology.

Protein-calorie malnutrition (PCM), sometimes termed protein-energy malnutrition (PEM), is the most common cause of secondary immune deficiency in the world because of wide spread chronic and seasonal food shortages, as well as chronic poverty, the deprivations of war, and maternal malnutrition [9]. The deficiencies associated with PCM usually are multiple, involving varying degrees of calorie, protein, vitamin, and mineral deficits. Classically, PCM is divided into two types - marasmus and kwashiorkor. Marasmus occurs in total calorie deficiency, with chronic wasting and gross underweight. Kwashiorkor occurs due to protein deficiency in the diet, which may be high in calories. The growth retardation is moderate, but these children often appear apathetic and miserable, with various problems such as characteristic dermatitis, brittle reddish tinged hair, edema, moon faces, hepatosplenomegaly, anemia, and hypoalbuminemia. Both marasmus and kwashiorkor often have concomitant vitamin and mineral deficiencies. In industrialized countries, the edematous presentation of kwashiorkor often delays or prevents recognition of this form of protein malnutrition. The causes of protein deficiency include use of low protein milk substitutes such as rice "milk", which contains no milk product, and other beverages, which may be provided by caregivers in response to perceived food intolerance or food aversion [10-12].

Selective micronutrient deficiencies can occur when food and calorie intake is adequate. Iron, copper and zinc deficiencies are the most common due to dietary insufficiency. Results from a large double-blind trial of fortified milk in preschool children show that this intervention can reduce morbidity from diarrhea, respiratory infections and other illnesses, as well as improve iron status and growth. [13] Selenium deficiency occurs primarily in parts of the world where selenium levels are low in the soil. As a constituent of selenoproteins, selenium is needed for the functioning of neutrophils, macrophages, NK cells, and T lymphocytes. Mild selenium deficiency is relatively widespread and appears to worsen viral infection [14]. Selenium and vitamin E deficiency in the mouse have been shown to promote the virulence of Coxsackie B3 virus and influenza by inducing genetic changes in the genomes of the viruses [15]. Selective micronutrient deficiency frequently occurs in patients with underlying systemic illnesses, chronic viral infection and in low birth weight infants [16, 17]. In some cases, the adverse effects have long-term effects [18].

Obesity is a specialized form of malnutrition that is becoming increasingly common in children, raising concerns about type 1 diabetes, cardiovascular disease, and risk of cancer. A recent study has reported that low-grade inflammation, as determined by serum levels of high-sensitivity C-reactive protein, while significantly increased in children with type 1 diabetes, a high level was even more pronounced in apparently healthy juveniles with primary obesity [19]. Uncomplicated morbid obesity in adolescents may be accompanied by alterations in the levels of circulating T cells and cytokine response [20]. Other studies show that regulation of natural killer (NK) function and proliferative response to mitogens in vitro are affected [21, 22]. Leptin, the product of the ob gene, is a pleiotropic molecule that regulates food intake through metabolic and neuro-endocrine functions, has cyto-kine-like activities and is a major regulator of immune function [23]. Leptin is acutely increased during infection and inflammation [24]. Primary leptin deficiency is associated with obesity and altered immune function [25]. Although the relationship between obesity and susceptibility to infections is not well defined, there is consensus that postoperative infections, other nosocomial infections, and risk of serious complications of common infections are enhanced in obesity [26]. A role for fetal programming that links early growth compromise to subsequent development of obesity and the metabolic syndrome has been postulated [27].

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  • lotho
    What is pathophysiology of malnutrition?
    2 years ago
  • layton murphy
    What is pathogenesis in malnutriton?
    2 days ago

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