Previous Page Table Of ContentsNext Page



Part III. Disorders of malnutrition

Chapter 22. Other micronutrient deficiencies and minor nutritional disorders

Nutritional neuropathies

The nervous system is the communications system within the body, and it is a highly complicated mechanism. If it does not function properly there can be important consequences. The nervous system needs oxygen and nutrients and obtains its energy from carbohydrates. A range of complex enzymes controls its functioning. These enzymes are proteins, and their activities require the participation of a number of vitamins. It is not surprising therefore that dietary deficiencies can cause symptoms and signs indicating impairment or damage to the nervous system.

The relationship between diet and the nervous system is still not fully understood, and the subject is beyond the scope of this book. Nevertheless it is important for all medical persons to keep in mind that any disease of the nervous system may have a nutritional origin. If it is impossible to obtain a proper diagnosis of a nutritional disease, the sufferer should be advised and helped to eat a balanced diet.

The B group of vitamins has a special place in relation to the nervous system. These vitamins are commonly found in the outer layers of cereal grains. Milling tends to reduce the quantity of B vitamins in cereal flours. Deficiencies of B vitamins are therefore common, and cases of various neuropathies are likely to increase. For example, an outbreak of a neuropathy in a Tanzanian institution was caused by a change in diet from lightly milled to highly milled maize meal as the main source of energy.

Neuropathies may lead to weakness and pins and needles in the feet, severe burning pains, ataxia, nerve deafness, disturbances of vision, absent or exaggerated reflexes and other symptoms. There is much overlap in the causation of many of these conditions, and classification is difficult.

The neurological signs of dry beriberi and of thiamine deficiency in alcoholics (alcoholic polyneuropathy and the so-called Wernicke-korsakoff syndrome) were described in Chapter 16, and the burning feet syndrome in pantothenic acid deficiency was mentioned in Chapter 11. These are all either polyneuropathies affecting the peripheral nerves or are caused by lesions of the central nervous system (in Wernicke's encephalopathy). It is likely that patients with mixed forms are often not correctly diagnosed. It can be difficult to distinguish accurately between neurological complications resulting from nutrient deficiencies and those resulting from toxins (for example, lathyrism, described in Chapter 34) or drugs.

As discussed below, vitamin B6 deficiency secondary to treatment of tuberculosis with isoniazid leads to a polyneuritis. The cause of a recent outbreak of optic neuritis and an epidemic neuropathy in Cuba has not been definitively determined. The outbreak has subsided but was almost certainly the result of a nutrient deficiency, most probably a dietary deficiency of thiamine. Konzo, an epidemic neurological disease, occurs as a result of excessive cyanide intake in those eating toxic cassava (see Chapters 26 and 34).

Riboflavin deficiency (ariboflavinosis)

A dietary deficiency of riboflavin resulting in clinical signs is very prevalent worldwide, in both industrialized and non-industrialized countries. In the United States a ten-state nutrition survey showed poor riboflavin status in over 12 percent of all subjects and in 27 percent of black people examined. In most studies in poor countries riboflavin deficiency is found to be much more prevalent, often affecting 40 percent of the people. As described below, the main clinical features are lesions of the mouth. A deficiency does not cause either life-threatening disease or serious morbidity.

The most frequently seen abnormalities in riboflavin deficiency are angular stomatitis and cheilosis of the lips. Angular stomatitis consists of fissures or cracks in the skin radiating from the angles of the mouth. Sometimes the lesions extend to the mucous membrane inside the mouth. The cracks have a raw appearance but may become yellowish as a result of secondary infection. In cheilosis there are painful cracks on the upper and lower lips. The lips may be swollen and denuded at the line of closure. The lesions may be red and sore or dry and healing.

Glossitis (inflammation of the tongue) occasionally develops involving a patchy denudation, papillary atrophy and so-called magenta tongue. These conditions are not caused exclusively by riboflavin deficiency.

Scrotal dermatitis in males and vulval dermatitis in females have been particularly well described in experimentally induced riboflavin deficiency. The affected skin is usually intensely itchy and tends to desquamate.

Abnormalities in the eyes including redness and vascularization (visible blood vessels), photophobia and lacrimation have been associated with riboflavin deficiency.

A skin condition named dyssebacia may occur near the nose.

Affected persons often have several signs of deficiency at the same time (Figure 14).

In surveys laboratory assessment of riboflavin status has usually been based (as with other water-soluble vitamins) on urinary excretion of the vitamin. A level below 30 g of riboflavin per gram of creatinine is considered low. Riboflavin status in the individual is better determined by measuring the increased activation of red blood cell (erythrocyte) gluta-thione reductase. Few hospital laboratories in developing countries are able to do these tests.

Treatment consists of large oral doses of riboflavin for a few days, followed by lower doses which may need to be taken for a long time unless a diet rich in riboflavin is consumed. A dose of 10 mg riboflavin twice a day for one week, followed by 4 mg daily for several weeks, is recommended. Dietary intakes of around 1 to 1.5 mg daily will be protective. Milk is a particularly rich source of riboflavin.

FIGURE 14. Characteristics of riboflavin deficiency (ariboflavinosis)

Pyridoxine or vitamin B6 deficiency

A primary dietary deficiency of vitamin B6 resulting in symptoms of disease is very rare, because even poor diets contain adequate quantities of this vitamin.

Pyridoxine deficiency occurs in developing countries mainly secondary to treatment of tuberculosis with the medicine isoniazid. This drug, which is highly effective and can be taken by mouth, was introduced as a treatment for tuberculosis in the early 1950s and became widely used, in part replacing injection of streptomycin which was until then the most common treatment. Despite the development of other medicines, isoniazid is still widely used. Tuberculosis, largely controlled in industrialized countries in the 1970s, is now in resurgence, with drug-resistant cases and cases related to acquired immunodeficiency syndrome (AIDS) worrying public health officials. In many African and Asian countries tuberculosis has remained prevalent and is an important cause of morbidity and mortality.

Isoniazid taken in large doses over long periods is very likely to precipitate vitamin B6 deficiency. It is said to increase vitamin B6 needs.

The deficiency is usually manifested by neurological abnormalities, including a peripheral neuritis which may involve severe pain in the extremities, including the legs. Experience in East Africa showed that because of the pain rural patients were often unable to walk to health centres for examination or to obtain their medicine.

It is strongly recommended that tuberculosis patients being treated with isoniazid be given 10 to 20 mg pyridoxine by mouth daily. Unfortunately, pyridoxine is much more expensive than isoniazid, so providing the vitamin greatly increases the cost of treatment.

It has been suggested that in certain parts of the world, particularly in Thailand, low intakes of vitamin B6 may be responsible for bladder stones. It is known that vitamin B6 increases oxalate excretion in urine and that vitamin B6 deficiency leads to an increased risk of oxalate stone formation in the kidney or bladder.

Hormonal contraceptive pills have been associated with both folate and vitamin B6 deficiencies. However, the newer birth control pills have not been shown to result in vitamin B6 deficiency. Oral vitamin B6 tablets have been claimed to reduce the nausea of some women in the first months of pregnancy.

An extremely rare congenital disease called pyridoxine-responsive genetic disease leads to hyperirritability, convulsions and anaemia in the first few days of life. Unless treated very early with vitamin B6 the child develops serious permanent mental retardation.

Minor nutritional disorders and clinical signs

The most important and serious diseases resulting from nutritional deficiencies have already been covered. They have been described in terms of syndromes or disease entities and have not been classified according to their aetiology. Other clinical conditions may also arise from dietary

deficiencies, and some of them may lead to the diseases described earlier. Some have physical signs that can be observed but cause little disfigurement or disability. Some conditions have a specific, known aetiology. Other conditions, although they may occur commonly in malnourished persons, may not have had their exact cause elucidated. All are of some importance and should be looked for because they can lead a medical worker into an investigation of the diet of a patient and can thus serve to prevent the onset of more serious disease. They should especially be sought in routine examinations of groups of persons, such as those carried out in schools, prisons and institutions, or during medical surveys of a community. These minor disorders can serve as indicators of the dietary status of the community as a whole.

Dry scaly skin or xerosis

Normal skin is smooth and slightly oily and has a healthy sheen. In xerosis the skin loses these characteristics and becomes dry, scaly and rather rough to the touch. Pieces of the skin tend to flake off much as in dandruff of the scalp. This condition is thought to be caused mainly by vitamin A deficiency. However, lack of protein and fat may also have a part.

Crazy-pavement or cracked skin

(mosaic dermatosis)

This condition is commonly found on the lower leg. The skin resembles a paved walk or the sun-baked and cracked bed of a dried-up mud swamp. There are islands of fairly normal skin, each surrounded by a shallow crack. The edges may be scaly or desquamating. Protein and vitamin A deficiencies may have a part in causing the disorder; dirt and alternate exposure to dryness and moisture under hot conditions may also be causative factors.

Follicular hyperkeratosis

Type I follicular hyperkeratosis consists of lesions that feel spiky to the touch, consisting of multiple horny dry papules. They are most commonly seen on the backs of the arms. On close inspection they are seen to arise from the hair follicles. This condition is associated with a deficiency of vitamin A and possibly also of riboflavin.

Type II follicular hyperkeratosis is similar in appearance and occurs commonly on the trunk or thighs. The surrounding skin is less dry, and the mouths of the hair follicles are seen to contain brown-pigmented denatured blood. This condition is possibly caused by vitamin C deficiency.

Dyssebacia (naso-labial seborrhoea)

This condition, in which plugs of yellowish keratin stand out from the follicles, is usually seen on each side of the nose but sometimes extends to other parts of the face. It is believed to be caused by riboflavin deficiency.

Scrotal (or genital) dermatitis

The skin of the scrotum (or the genital region in females) is affected, becoming dry and irritated. There may be desquamation, intense itching and secondary infection. Riboflavin deficiency (and possibly deficiency of other B vitamins) seems to be the cause.

Oedema of the tongue

The tongue is swollen, with notches on the sides corresponding to the teeth. The papillae are usually prominent. This condition is associated with deficiency of riboflavin and niacin.

Atrophic tongue

The tongue is much smoother than normal, usually reddened (magenta-coloured) and denuded of normal papillae. It may be painful. This condition may be caused by a lack of niacin and other B vitamins.

Patchy glossitis

In patchy glossitis the tongue shows patchy desquamation; the patches are often red and inflamed oval areas. This condition is usually the result of riboflavin deficiency and may sometimes be accompanied by oedema of the tongue.

Parotid swelling

Swelling of the parotid gland can be felt as a firm area just in front of and slightly below the meatus (hole) of the ear. The swelling is usually bilateral. It may disappear completely after a balanced diet is consumed for six to 12 months. The condition is possibly associated with protein deficiency.

Tropical ulcers

Tropical ulcers affect the lower leg and may be single or multiple. They are chronic, sometimes large and often grossly infected. The cause has not been fully elucidated but is possibly nutritional. Tropical ulcers are rare in well-nourished persons.

The nutrition examination

At the nutrition examination, the name, sex and age of the individual should be recorded. If the subject is female, it should be noted if she is pregnant or lactating. Table 29 summarizes the signs to look for in the examination. The following measurements should also be taken:

It is also important to note other observations that may have a bearing on the case, e.g. parasitic infection or scarred cornea.

A list of deficiency disorders is given in Table 30.

TABLE 29

Signs to look for in a nutrition examination

Part of body examined

Possible changes or disorders

Hair

Colour change

 

Texture change

Eyes

Bitot's spots

 

Xerosis and xerophthalmia

 

Keratomalacia

 

Pallor of the conjunctiva of the lower lid

 

Vascularization of the cornea

Mouth

Angular stomatitis

 

Cheilosis

 

Glossitis

 

Atrophic tongue

 

Oedema of tongue

 

Mottled teeth

 

Carious teeth

 

Swollen or bleeding gums

 

Pallor of tongue

Skin

Oedema

 

Follicular hyperkeratosis

 

Crazy-pavement skin

 

Dry scaly skin

 

Hyperpigmentation

 

Ulcers

 

Haemorrhages

 

Pallor beneath nails

Central nervous system

Apathy

 

Irritability

 

Anaesthesia or sensory changes

 

Calf tenderness

 

Abnormal gait

 

Loss of reflexes

 

Poor mental development

 

Dementia

Skeleton

Deformity (e.g. knock-knees)

 

Rickety rosary

 

Bony swelling

 

Skeletal fluorosis

Other

Thyroid enlargement

TABLE 30

Deficiencies and associated signs

Deficiency

Associated disorder

Vitamin A

Follicular hyperkeratosis, Type I

 

Night blindness

 

Bitot's spots

 

Conjunctival xerosis

 

Corneal xerosis

 

Keratomalacia

 

Possibly also dry scaly skin and crazy-pavement skin

Riboflavin

Angular stomatitis

(ariboflavinosis)

Cheilosis of lips

 

Scrotal or genital dermatitis

 

Possibly also follicular

 

hyperkeratosis, oedema of the

 

tongue, magenta tongue and

 

patchy glossitis

 

Vascularization of the cornea

Thiamine

Oedema

 

Anaesthesia

 

Calf tenderness

 

Abnormal gait

 

Various central nervous system signs

Niacin

Hyperpigmentation

 

Pellagrous dermatitis

 

Atrophic tongue

 

Diarrhoea

 

Mental signs

Vitamin C

Swollen or bleeding gums

 

Petechial or other skin haemorrhages

 

Other haemorrhages

 

Follicular hyperkeratosis, Type II

 

Tender subperiosteal swellings

Vitamin D

Deformity

 

Rickety rosary

 

Bony swelling

 

Bow-legs

 

Knock-knees

Protein-energy

Muscle wasting

 

Apathy

 

Irritability

 

Oedema

 

Dermatosis

 

Hair changes

 

Weight reduction

 

Height reduction

 

Small arm circumference

 

Reduced skinfold thickness

Iodine

Enlargement of thyroid

 

Cretinism

 

Deaf-mutism

 

Mental retardation

Fluorine

Dental caries

 

Mottled teetha

 

Bone changesa

Iron

Anaemia

 

Pale conjunctiva of lower lid

 

Pallor of tongue

 

Pallor of nailbed

 

Poor growth

 

Poor appetite

a From excess, not deficiency, of fluorine.

Previous PageTop Of Page Table Of ContentsNext Page