MINERAL DISORDERS AND TRACE ELEMENTS

Minerals are non-energy yielding micronutrients, which despite contributing lt;5% of body weight, play a vital role in human metabolism, health and disease. Minerals, along with other micronutrients, e.g.

Biologically important minerals may be broadly classified into:

• Macrominerals, which are present in substantial amounts with nutritional requirement usually exceed­ing gt;100 mg#8725;day. Most of them are distributed in tissues as well as function as major electrolytes in body fluids, e.g. sodium, potassium, calcium, magnesium, etc. Important macrominerals have been discussed in Ch 7.

• Microminerals (trace elements), which constitute lt;250 #956;g#8725;gm of body tissue matrix. Minerals present in still smaller amounts (lt;100 ng#8725;gm) are termed as ultra-trace elements.

Role of trace elements in health and disease is being increasing recognized in recent years, which can be broadly divided into three categories, based on current knowledge:

1. Essential trace elements with known biological functions, e.g. iron, iodine, zinc, fluorine, selenium, copper, molybdenum and chromium.

2. Essential trace elements with hitherto ill-identified functions, e.g. manganese, silicon, nickel, boron, cobalt and vanadium.

3. Potentially toxic trace elements with unknown biological functions, e.g. lead, aluminum, tin, cadmium, arsenic, mercury, etc.

Table 6.20 presents an overview of important trace elements in human health and disease. While some of them have been discussed elsewhere, e.g. iron (Ch 19.4.1) and iodine (Ch 22.3.3), other important trace elements are discussed as follows:

Zinc is a component of many enzymes, e.g. carbonic anhydrase, carboxypeptidase, alkaline phosphatase, etc.

Physiology: Zinc is essential trace element for: (a) normal growth, (b) normal chemotaxis and T-cell immunity, (c) normal wound healing, and (d) synthesis of some hormones, e.g. insulin and nucleic acids. Zinc is not well conserved in body as there are no conventional tissue reserves.

RDA for zinc varies from 2.5 mg/day in infancy to ~15 mg#8725;day in adolescents and adults.

Sources: Important sources of zinc include animal foods, e.g. meat, milk and fish, as well as plant foods, e.g. grains, legumes and nuts, though the bioavailability of zinc from plant sources in relatively poor.

Etiologically, zinc deficiency is rarely dietary, usually caused by:

• Increased requirements in early infancy, adolescents and pregnancy

• Decreased intake, e.g. in maternal zinc deficiency, total parenteral nutrition, etc.

TABLE 6.20: Essential trace elements at a glance

RDA: Recommended dietary allowance; ICC: Indian childhood cirrhosis

Treatment: Oral or parenteral supplementation with 5 mg/kg/day (20-40 mg/kg/d in acrodermatitis enteropathica) usually leads to dramatic clinical response within a few days, which should be followed by adequate dietary modification to prevent recurrence. Long-term zinc supplementation is indicated in children with severe growth failure and acrodermatitis enteropathica.

Zinc supplementation is also indicated for 2 weeks in all children with - severe acute malnutrition (2 mg/ kg/day) and diarrheal disorders (20 mg/day or 10 mg/ day in infants lt; 6 months). It is also recommended as adjunct therapy in preterms (2 mg/kg/d for 3 months) and haemolytic anemia, e.g. sickle cell disease or thalassemia.

Fluorine is the most abundant element in nature, though never found in free elemental gaseous form. About 96% of body fluorine is present in bones and teeth.

Physiologically, fluorine is required for formation of apatite—a mineral complex essential for bone mineralization and dental enamel.

Sources: Drinking water is the principle source of fluorine to man apart from sea-food and cheese as other rich sources.

Fluorine deficiency is relatively uncommon, considered to be associated with higher incidence of dental caries and can be prevented by use of fluorinated toothpastes. Fluorine excess (fluorosis) is more important public health problem in India, endemic in areas with high fluoride content in drinking water (gt;0.5-0.8 mg/L or gt;2 ppm).

Prolonged ingestion of high-fluoride water presents with: (a) mottling of teeth, (b) brittle bones with osteosclerosis, (c) calcification of muscles/ tendons, and

(d) failure to thrive, anemia and asthenia. As excess fluorine interferes with calcium metabolism, co-existing calcium deficiency is common and contributes to skeletal changes with osteoporosis/osteomalacia.

Controlling the fluoride content of drinking water is the only method to prevent fluorosis in children.

Copper: Nearly 60% of copper is present within erythro­cytes, rest being in plasma (bound to ceruloplasmin) or tissues (bound to metallothionein).

Physiologically, copper is a constituent of many metabolic enzymes, involved in connective tissue formation, iron metabolism, neuronal myelination, melanin synthesis and cellular energy/oxygen utilization.

Copper deficiency is rarely dietary, presenting as neutropenia, microcytic hypochromic anemia, hypo- pigmented hair, osteoporosis and defective immune function.

Copper toxicity, usually due to use of copper cooking utensils and has been implicated in Indian childhood cirrhosis and hematological malignancies.

Inborn errors of copper metabolism are most important cause of altered copper status in body and include:

• Wilson disease—an autosomal recessive defect in mobilization of hepatic copper, presenting with a triad of chronic liver disease, extra-pyramidal signs and Kayser-Fleischer ring over cornea (Chapter 15.7).

• Menkes-kinky-hair syndrome—a rare X-linked recessive disorder, characterized by fine, brittle and light colored hair, progressive psychomotor retardation and hypopigmented skin.

Selenium is mainly required for: (a) synthesis of gluta­thione peroxidase, an important anti-oxidant enzyme, and (b) conversion of T4 into T3.

Selenium deficiency is definitely associated in two endemic diseases in China— Keshan cardiomyopathy and Kaschin-Beck osteoarthritis. It has been also implicated in higher risk for malignancies and atherosclerosis. Selenium deficiency may affect growth and development due to poor conversion of T4 into T3.

Selenium excess (selenosis) is associated with alopecia and nail deformities.

Molybdenum is a constituent of many enzymes, specially xanthine oxidase and xanthine dehydrogenase­essential for xanthine metabolism.

Molybdenum deficiency is mainly seen in children on prolonged total parenteral nutrition, presenting with renal calculi (due to xanthinuria) and myopathy. It has been also implicated in higher risk of dental caries an esophageal cancers.

Chromium: Major biological role of chromium is to potentiate the action of insulin in carbohydrate, lipid and protein metabolism, probably by acting as a glucose tolerance factor.

Chromium deficiency has been reported only in children on prolonged total parenteral nutrition, leading to impaired glucose tolerance and hyperglycemia. Dietary chromium supplementation may improve glucose tolerance in malnutrition.

6.8