TOBACCO SMOKE AND CHEWING – GENERAL CHARACTERISTICS AND TREATMENT

Man has started using tobacco from very ancient times. At present tobacco is consumed for smoking (beedi, cigarette, pipe, cigar, hookah, etc.) or for chewing with or without other constituents such as betel, arecanut, and lime or as snuff applied to the nasal or oral mucosa. All

these habits are very much prevalent in all societies in India.

GENERAL CHARACTERISTICS

Tobacco smoke contains several constituents, which irritate the respiratory tract and inhibit ciliary action. The tar that is produced is carcinogenic to the respiratory tract. Depending upon the brand of cigarette and the manner of smoking the level of carbon monoxide in the smoke may vary from 1-5%. Nicotine present in tobacco is responsible for the addiction. Sympathomimetic effects of nicotine give rise to higher heart rate, elevation of systolic and diastolic blood pressure, increase in cardiac output and peripheral vasoconstriction. The threshold for ventricular tachycardia and ventricular fibrillation is lowered. By increasing platelet aggregation, platelet adhesion, plasma fibrinogen and viscosity of blood, nicotine favors intravascular thrombosis. There is reduction in platelet survival and clotting time. Atherogenesis is favored by the rise in total cholesterol, low density lipoproteins and free fatty acids, and also fall in high density lipoproteins (HDL) brought about by nicotine. Blood levels of carboxyhemoglobin are elevated. Oxygen carrying capacity of blood is reduced. Rise in blood carbon monoxide leads to intimal hypoxia, increase in the permeability of arterial intima and lipid deposition.

Cigarette smoking is associated with mild airway obstruction and impairment of lung function in adolescents. Females are affected more. Heavy smokers suffer from tachycardia, palpitation, cardiac arrhythmias, hypertension, tremors, anorexia, agitation and insomnia. In those who practice the chewing habit, in addition to absorption of nicotine from the buccal mucosa the local irritation caused by the cud leads to precancerous and cancerous changes.

SMOKING

Tobacco is a highly habit forming agent. Several studies have been shown that the first cigarette exposes the individual and the addiction will occur even with the second or third ‘smoke’. Children of smoking parents acquire this habit more freely. The harmful ingredients taken up by the smoker and exhaled by him depend upon several factors such as the number of cigarettes smoked and their frequency, depth of inhalation, smoking the cigarette only partially or fully and the environment in which the smoker smokes – whether open or confined space. Inhalation of the exhaled smoke by others nearby is termed passive smoking, which is also associated with adverse effects in various degrees.

There is irrefutable evidence that smoking is a major risk factor for chronic bronchitis, emphysema and cancers of lung, larynx, esophagus, bladder, kidney, pancreas and cervix uteri. Coronary heart disease, hypertension, strokes, peripheral vascular occlusions, thromboangitis obliterans, peptic ulcers and several other conditions are directly or indirectly attributable to tobacco. Tobacco is the most important cause of cancer and cancer death, affecting several organ systems. Both main stream and second hand smoke are group-1 carcinogens, i.e. included among the highest cancer causing agents in humans. Lung cancer is several times more common in smokers compared to nonsmokers. 90% of bronchogenic carcinoma is related to smoking, either direct or passive. Smoking contributes to 50% of the death of cigarette smokers, with half of these deaths occurring in middle life. Smokers lose 10 years of their life expectancy, compared to non-smokers.

Smoking by parents has an adverse effect on their children. Smoking mothers have an increased risk of spontaneous abortion and their children have lower birth weights, higher perinatal mortality and a greater risk of sudden infant death syndrome. Medical associations of several countries have urged their governments to undertake measures to restrict the spread of tobacco habit. These include restriction of sales of tobacco to those below the age of 18 years, ban on advertisement, education in schools and through public media, prohibition of smoking in public places and public transport, heavy taxation on cigarettes and withdrawal of aids to tobacco industry.

Tobacco Chewing

There are recent reports from India that chewing tobacco is also associated with increased risk of cardiovascular morbidity. Further studies are needed. Betel chewing as a cause of oral cancer is well known. Several brands of such proprietary preparations (Pan Masalas) are available in the Indian market. These are being used by a large number of persons, especially the youth. Their role in the genesis of oral cancer and other systemic diseases is not yet fully assessed.

OCCUPATIONAL HEALTH PROBLEMS AMONG TOBACCO WORKERS

The varieties of tobacco include Virginia tobacco (cigarette tobacco) and non-virginia tobacco. Persons may be exposed to tobacco during agricultural operations or curing processes. Ill effects of tobacco are considered to be due to absorption of nicotine through the skin or respiratory tract. The levels of nicotine and its metabolic product cotinine are increased in urine.

The symptom complex occurring in the exposed workers is collectively known as green symptoms. These consist of neurological symptoms like headache, giddiness, nausea, vomiting, prostration and respiratory symptoms such as cough and dyspnea. Usually, these symptoms are transient. The occurrence of green symptoms is associated with raised urinary levels of nicotine and cotinine. Virginia tobacco is less toxic than the non-virginia variety. The respiratory symptoms may be aggravated by aero-allergens such as pollen and fungi belonging to the species Gladosporium and Altemaria. The nature of contact with tobacco also partly determines the clinical manifestations. Persons who pluck the leaves generally get headache and giddiness, while those carrying the leaves for curing get nausea and vomiting. In agricultural workers engaged in curing, entry of tobacco is through the respiratory tract.

Treatment

Since the symptoms are usually mild, and last only for a few hours, removal from the surroundings is itself curative. The local practice among the workers is to take tea and jaggery followed by rest.

STARVATION  – General Characteristics, Clinical Features and Treatment

GENERAL CHARACTERISTICS

Severe starvation on a mass scale occurs during special situations like prolonged war, drought, and other natural or political calamities. Chronic starvation of different grades affects large number of people in the developing countries, even during normal times. Several famines have occurred during the 19th and early part of the 20^th centuries. Famines were a regular occurrence in Bengal during the colonial rule. Though acute and chronic food shortage occur from time to time in various parts of India as a result of floods, drought or earthquakes, widespread famine has not occurred in the latter part of this century.

In addition to food shortage, inability to ingest or digest and absorb food also results in starvation. Individuals may resort to starvation voluntarily or this may result from psychiatric abnormalities.

Loss of weight amounting even up to 50% of body weight is the most prominent feature. The weight loss is initially caused by the loss of fluid. Later on it is owing to catabolism of tissues to meet energy needs. The body stores of carbohydrate (liver and muscle glycogen) are depleted within two to three days and fat is mobilized in the form of free fatty acids which is used as fuel by the muscles. Glucose is spared for the brain. Tissue proteins are also broken down in order to meet the energy needs. Protein synthesis is diminished and alanine is released by the muscles to the liver for conversion to glucose, which is made available to the brain. During prolonged starvation, brain metabolism can adapt to use betahydroxybutyrate and acetoacetate also as fuel. Generalized emaciation results. Liver and intestines are the first to lose

tissue, and this is followed by muscles and skin. The brain is preserved right till the end.

CLINICAL FEATURES

The patient is apathetic and irritable. The loss of fat around the buttocks, thighs, back, and buccal region gives the characteristic appearance with prominence of bones and dry, thin, inelastic, loose skin. A brownish, patchy pigmentation is generally encountered. The hair becomes characteristically dry and easily pluckable. During cold weather cyanosis of extremities may develop. Systemic disturbances Cardiovascular changes include bradycardia, lowered systolic and diastolic pressure, and reduction in venous pressure and cardiac output. The heart size is also reduced. Respiratory rate is lowered, so also the vital capacity. Growth hormone level is decreased.

Basal metabolism is lowered. Corticosteroid is normal. In both sexes sexual function is diminished leading to loss of libido in males and amenorrhea in females. Hypothermia may develop on exposure to cold. Though personality changes may be manifest, the intellect usually remains clear till the end. Capacity for work is reduced due to loss of muscle mass. Mild normocytic normochromic anemia is not uncommon.

In some individuals dependent edema appears even without lowering of plasma albumin. Nocturnal polyuria is common though the renal function is not grossly affected.

TREATMENT

The course of treatment should depend upon the severity of the disorder. Mild cases of starvation require only oral feeds. Overzealous dietary supplementation may lead to diarrhea and death. In the early stages, gradual introduction of easily absorbable and predigested food may be necessary till the alimentary functions return to normal. Fats and fatty foods have to be avoided to prevent diarrhea. Skimmed milk is superior to whole milk.

Skimmed milk powder reconstituted to give 10-15% strength is well tolerated if given as small feeds (up to 100 mL) frequently. A daily intake of about 3,000 kcal and 100 g proteins should be aimed at. Severely debilitated patients should be fed using an intragastric tube in order to ensure adequate intake. After the initial rapid gain in weight due to correction of dehydration, a steady increase of 1-1.5 kg/week can be considered as adequate response. In all cases of severe starvation especially if complicated by intercurrent illnesses and diarrhea, parenteral nutrition should be resorted to without delay.

If starvation occurs on a wide scale, relief camps have to be organized to provide shelter, food, potable water and general sanitation. Community kitchens may have to be set up to provide food. In these endeavours, the medical personnel have to work in close liaison with social service organizations and governmental agencies.

ROAD ACCIDENTS – General Considerations, Injuries Caused by Road Accident and Management At the Site of Accident

General Considerations

In modern times mortality and morbidity caused by road accidents is on the rise. This is common in all countries of the world where fast traffic on the road is increasing.

The accidents may involve the vehicles or the pedestrians using the road. The major types of accidents are collision between vehicles, loss of control of the vehicle and collision with hard objects or overturning. The other type of accidents involves knocking down pedestrians or occupants of lighter vehicles such as two wheelers and light motor vehicles. In general the major damage and passenger injury occurs to the lighter vehicle.

The major factors contributing to road accidents can be classified as given below:

A. Causes attributable to the vehicles

1. Speed of the vehicle- The rate and severity of the accident increases with increasing speed of either vehicle. With the introduction of modern highways speed-related injuries have become much more common

2. Mechanical defects in the vehicle, which lead to failure of the controls.

3. Exceeding the safety limits prescribed for the vehicle in terms of speed, loading and maintenance.

B. Causes attributable to the driver

1. Fatigue and sleep- long driving exceeding 6 hours of continuous driving leads to driver fatigue, delay in the reflexes and tendency to sleep.

2. Drunkenness: Consumption of alcohol and less commonly other narcotic drugs impairs the efficiency of the driver

3. Inattention, non-compliance with signals and rash driving

4. Inexperience of the driver

Most of the major collision accidents occur on highways, especially in the early hours of the morning when driver fatigue and somnolence are maximal. Rarely accidents may occur due to organic disease in the driver such as epilepsy, cardiovascular disease, strokes and others.

Injuries to Pedestrians

Walking on highways and fast traffic roads is associated with injury to the pedestrians. Elderly people, obese individuals, persons with movement disorders, alcoholics and children are involved more.

INJURIES CAUSED BY ROAD ACCIDENTS

Vehicular Accidents

Trauma to the driver and passengers due to the impact and damage and deformation to the vehicle are usually serious. This leads to injuries which may be instantaneously fatal. In motor car accidents, the luggage kept unsecured in the passenger compartment fly out and cause further missile- like injuries to the passengers. Trauma to vital parts such as head, chest cage, spine, bones, abdomen and major blood vessels, intracranial injuries, intracranial bleeding, tension pneumothorax, rupture of major blood vessels like aorta, injuries to the heart, rupture of solid organs and hollow viscera in the abdomen and pelvis and exsanguinating bleeding ( both external and internal ) are the causes of death at the site of accident or within a few hours. Pedestrian injuries cause death due to damage to vital structures, especially intracranial bleeding, chest injuries, intra abdominal injuries and exsanguination.

MANAGEMENT AT THE SITE OF ACCIDENT

Effective first aid helps to save life and reduce morbidity and delayed mortality. Mainly this consists of maintenance of the airway and attention to ventilation, tourniquets to arrest external hemorrhage, immobilization of parts of the body such as the neck and spine to avoid further damage to the vital neural structures, covering open chest injuries which interfere with ventilation and rapid transport to the nearest hospital with adequate facilities. It is the duty of all medical men to give first aid in such a situation. It is to be remembered that an obvious injury may distract the attention of the doctor from other invisible injuries such as internal bleeding or rupture of viscera which can cause death.

When major accidents involving buses occur, a large member of persons will be simultaneously affected and this may cause a heavy strain on the medical facilities. In this situation, a senior medical officer has to inspect the victims and using the principles of ‘triage’, arrange for appropriate management. In such an emergency all medical personnel have to participate in the emergency management.

All road traffic accidents invite legal procedures which have to be complied with. General guidelines to reduce road traffic accidents and their consequences

1. Education of the public on the safe use of roads and motor vehicles

2. Strict compliance with road traffic rules

3. Avoidance of alcohol and drugs before driving

4. Avoid driver fatigue and somnolence

5. Avoid the presence of unsecured luggage in the passenger compartment

6. Use the seat belts as prescribed.

7. Enforcement of traffic regulations by the appropriate authorities

RIBOFLAVIN (VITAMIN – B2)

Riboflavin is essentially required in all oxidation reduction reactions involving the coenzymes flavin mononucleotide and flavin adenine dinucleotide which take part in tissue oxidation and respiration. It is moderately heat resistant, but boiling in alkaline media or exposure to sunlight destroys this vitamin.

Good dietary sources include liver, meat, eggs, kidney, milk, other dairy products, green leafy vegetables, and sprouted cereals and pulses. Daily requirement is 0.60 mg/1000 kcal, i.e. a total of 1.5-2 mg.

1. Signs of deficiency Angulostomatitis, cheilosis, nasolabial seborrhea, and possibly vascularization of the cornea are the characteristic features. Angulostomatitis may also occur in deficiencies of niacin and folic acid. Mucosa of the lips appears red and denuded in cheilosis. On taking hot and spicy food there may be soreness. Vascularization of the cornea has been described in some surveys. In glossitis the mucosa over the tongue is red, swollen and painful. This responds to riboflavin therapy. Some cases show lesions in the oral mucosa, eyes, and genitals (oculooro-genital syndrome). The oculo-orogenital syndrome presents as blepharo-conjunctivitis, angular stomatitis, bright red atrophic tongue and dermatitis of the pubic region. This syndrome may occur in pyridoxine deficiency as well.

2. Treatment Riboflavin in a dose of 2-5 mg thrice a day cures the condition in a few days. The drug can be given orally as tablets or syrup or by injections. Treatment of oculo-orogenital syndrome is to give riboflavin up to 100 mg/day and pyridoxine 150 mg/day. The lesions clear within 7-10 days.

Q FEVER – Forms, Acute Q fever, Chronic Q Fever, Diagnosis, Treatment and Prevention

It is a zoonosis caused by coxicella burnetii- It is a gram negative pleomorphic coccobacillus which is having homology with Legionella pneumophilia

Two forms exist

1. A small cell variant (SCV) and

2. A large cell variant (LCV)

The SCV exists in nature and it is resistant to environmental factors. The LCV develops in the host’s monocytes and multiplies. It is the pathogenic form. The disease exists an Australia, India, USA and other areas. Animal reservoirs include cows, goats, sheep, dogs, cats and others. Organisms are shed in milk, feces, urine and products of conception. Humans become infected by ingestion of infective material or droplet infection through the respiratory tract. Incubation period is 12 to 30 days.

Acute Q Fever

This resembles influenza clinically, with varying degrees of pneumonia and hepatitis. Fever lasts for an average of 10 days (range 10-57 days).

Chronic Q Fever

This occurs in 60-70% of infected persons. It leads to endocarditis which supervenes on pre-existing valvular lesions. Untreated, the condition is fatal. Q fever may recrudesce during pregnancy and lead to abortion. Other manifestations include osteo-articular infections and hepatitis.

Diagnosis

Antibodies can be detected by indirect immunofluorescence.

Treatment

Acute Q fever —doxycycline 100 mg bid po for 14 days. Chronic Q fever—life long doxycycline therapy may be necessary. Addition of hydroxycloroquine 200 mg tds po given for 18 months favours recovery. It acts synergistically with doxycycline.

Prevention

Pasteurization of milk is partly protective. Occupational risk can be reduced by vaccination in persons exposed to the risk.

PYRIDOXINE – Normal Daily Requirement, Clinical Features

The active form of this vitamin is pyridoxal. Pyridoxal phosphate acts as a coenzyme in several reactions, especially in the metabolism of amino acids and biological amines such as catecholamines and 5-hydroxytryptamine. It takes part in the biosynthesis of gamma-amino-butyric acid in the brain. Yeast, liver, meat, whole grain cereals, peanuts, bananas and legumes are good dietary sources.

Normal daily requirement is 1.25 mg and it is present in the ordinary Indian diets and hence nutritional deficiency is rare. Drugs like INH, oral contraceptives and hydralazine may interfere with the metabolism of this vitamin and produce conditioned deficiencies.

Clinical features include dermatitis, cheilosis, angulostomatitis, glossitis, dizziness, vomiting and peripheral neuropathy. Infantile convulsions have been attributed to nutritional pyridoxine deficiency. Pyridoxine deficiency is known to produce one form of sideroblastic anemia which responds to high doses of this vitamin.

Concurrent administration of 6 mg of pyridoxine prevents the development of neuritis in subjects treated with INH.

PROTEIN ENERGY MALNUTRITION – General Characteristics, Etiology and Pathogenesis, Clinical Features (Kwashiorkor and Marasmus)

GENERAL CHARACTERISTICS

Protein-energy malnutrition (PEM) has been defined by WHO and FAO (1973) as “a range of pathological conditions arises from coincident lack of protein and calories in varying proportions occurring most frequently in infants and young children and commonly associated with infections”.

The clinical spectrum includes a variety of clinical syndromes, with ‘marasmus’ and ‘kwashiorkor’ at the two extremes and the intermediate forms (marasmic kwashiorkor) and nutritional dwarfism in between. Mild cases may present only with apathy and retardation of growth. Childhood malnutrition has been graded taking the weight for age as the criteria.

Etiology and pathogenesis:

Protein-energy malnutrition is an environmental disease, caused by deficient intake of protein and calories. It results from the combined influences of low food availability, poverty, ignorance, illiteracy and cultural taboos, frequent infections and poor environmental sanitation.

CLINICAL FEATURES

Marasmus

Severe restriction of food in an infant, as in cases of gross inadequacy of breast milk, leads to arrest of growth. Due to starvation the subcutaneous fat and muscles are used up as energy sources. The baby becomes emaciated. Unlike as in kwashiorkor, there is no edema. Loss of the buccal pads of fat give the infant a withered and ‘old man’s’ look. The weight is below the sixtieth percentile. The height depends upon the onset and duration of undernutrition. In the early stages the infant eats well but appetite is lost as the condition progresses. Initially, inadequacy of food leads to constipation, but later on diarrhea sets in with green stools containing mucus. In the well-established form the baby is apathetic.

Moderate anemia may develop. The skin and hair are usually normal.

KWASHIORKOR

This name was coined by Dr Cicely Williams in 1933, to denote ‘disease of the child deposed from the breast by the conception of a new fetus’. Children between the ages of 1 and 3 years are affected more. The disease starts when the baby is weaned from the breast.

Pathology

Main changes are seen in the small intestines, liver, pancreas and thymus. Small intestinal mucosa shows blunting of villi and atrophy of brush border, so that the columnar epithelium appears to become cuboidal. The total absorbing surface is reduced. Lactose intolerance is common because of disaccharidase deficiency. Liver shows fatty infiltration of the parenchymal cells. The pancreatic acini are atrophic and enzyme activity is reduced. Thymus is markedly atrophied and this may contribute to deficiency of cell mediated immunity.

Clinical features

This child is stunted and skeletal muscles are wasted. The presence of fairly normal amounts of subcutaneous fat and edema give a deceptively plump appearance. Pitting edema is a prominent feature.

The child is apathetic, irritable and drowsy. Characteristic skin changes occur in many and when present; these are diagnostic. These include flaky paint dermatosis seen over areas of pressure and trauma, fissuring and ulceration at the flexures and a mosaic like appearance (crazy pavement appearance). The hair becomes thin, sparse, brownish and lusterless. They may fall off. Regrowth of normal pigmented hair heralds nutritional recovery. Since periods of nutritional deprivation and partial correction of nutrition alternate in many cases, the hair shows alternate bands of pigmentation and depigmentation (flag sign). The appetite is poor. Diarrhea is a frequent feature. There may be concomitant deficiencies of iron, folate, fat soluble vitamins and B complex factors. Hepatomegaly occurs in a third of the cases. This is due to fatty infiltration. With recovery the liver reverts to normal without sequelae.

MARASMIC KWASHIORKOR

In this condition, features of marasmus and kwashiorkor are present simultaneously. The body weight is less than 60% of the normal. Dependent edema is present. Mental changes, skin and hair changes and hepatomegaly are evident.

Secondary infection is very common in protein energy malnutrition. This is due to the fact that both humoral and cellular immunity are defective. The intestinal flora is altered and this may account for the diarrhea. Episodes of infection further jeopardize the nutritional status.

Laboratory investigations

The total protein content of the body is reduced, and this is reflected most prominently as hypoalbuminemia. The plasma levels of essential aminoacids are low, but the non-essential amino acids remain normal or even elevated. Basal metabolic rate is reduced. Hypoglycemia occurs commonly. Total body water is increased and all the compartments show increase of fluid. The plasma osmolality is reduced. Renal plasma flow is diminished and this results in impairment of renal function. Plasma sodium is increased with reduction in potassium and magnesium. Gross reduction of serum sodium is associated with a poor prognosis.

Prognosis depends on the severity of the disease at diagnosis and promptness of treatment. Marked weight loss, severe infections, fluid and electrolyte imbalance, hypoglycemia, hypothermia, cardiac failure, elevation of serum bilirubin and liver enzymes, drowsiness and xerophthalmia indicate poor prognosis. In severe cases mortality goes up to 20%. The disease is entirely preventable by ensuring adequate caloric and protein intake to the growing child in the first three years of life. Proper management in the established case gives rise to full recovery, catch up growth and restoration of normal parameters. Recurrence is likely if the adverse environment is not corrected.

Treatment

Treatment is aimed to supply a diet rich in calories, proteins and other essential nutrients. For success of treatment supplementation should be with natural foods available locally. 150 Kcal/kg of energy and 3.3 g/kg of proteins are optimally required for catch-up growth. Fats are administered to supply adequate calories without increasing the bulk. Children with lactose intolerance do not tolerate carbohydrates, but they tolerate fats. As the child gains appetite the frequency of feeding is increased. If there is severe anorexia, forced feeding has to be

resorted to. Salt should be restricted to avoid congestive cardiac failure. The National Institute of Nutrition, Hyderabad has formulated an energy-protein rich mixture to treat PEM at home. It consists of whole wheat 40 g, Bengal gram 16 g, groundnut 10 g, Jaggery 20 g (total 86 g). This supplies 330 calories and 11.3 g proteins. Skimmed milk, eggs and cereals are added as the condition improves. In addition to nutritional correction, intercurrent infections have to be controlled simultaneously. Initial recovery is heralded by the disappearance of edema. The major biochemical abnormalities are corrected within 2-3 weeks. Complete correction of all reversible changes, referred to as ‘clinical recovery’ occurs only in 2-3 months.

Prevention and Rehabilitation

PEM is a preventable disease. Three levels of prevention have been formulated. Primary prevention is achieved by nutrition education to prevent occurrence of PEM. Secondary prevention is aimed at early detection and proper treatment. Tertiary prevention consists of nutritional rehabilitation of an established case. The importance of breast feeding as a prophylactic against protein calorie malnutrition cannot be overemphasized. Correct feeding practices, both during health and disease, proper sanitation, deworming and family planning methods have to be employed simultaneously to achieve lasting benefit. Nutrition rehabilitation is employed to prevent residual nutritional handicap and prevent recurrence of protein energy malnutrition. Even at the initial stages of treatment the mother should be made to participate in the selection, preparation and administration of food. This measure helps to impart nutritional education to her, prevent recurrence and detect relapse early.

PELLAGRA – General Features, Pathology, Clinical Features, Skin Changes, Course and Prognosis, Treatment and Prevention

General Features

This disease was widely prevalent in India among the maize eating communities in all states, especially Andhra Pradesh, Tamil Nadu and Rajasthan. Consumption of sorghum or jowar also predisposes to this tendency. Newer varieties of maize and sorghum with better nutritive value have helped to reduce the incidence of pellagra.

Alcoholism and malabsorption states precipitate pellagra. Inborn disorders of metabolism such as Hartnup disease in which the absorption of tryptophan is impaired lead to pellagra in rare cases.

Pathology

Dermatitis, changes in the oral and intestinal mucosa and degenerative changes in the central nervous system are seen. Ulcers may develop in the intestines. Chromatolysis of ganglion cells occurs in the central nervous system. Patchy demyelination occurs in the spinal cord.

Clinical features

Generalized malnutrition is evident in most cases. The most well-known features are the three Ds—dermatitis, diarrhea and dementia, but these characterize the very advanced stage of the disease. Pellagra should be diagnosed much before this classical picture develops, since the advanced stage is associated with high mortality.

Skin changes

These are seen over areas exposed to sunlight. These start with erythema which may resemble sunburn. This progresses to vesiculation, ulceration, secondary infection, and crusting. In chronic pellagra the skin becomes rough, thickened, scaly and pigmented. In

home-bound patients not exposed to the sun, pellagra may develop without the skin changes—“Pellagra sine pellagra”.

Mucous membrane changes are evident in the mouth and vulva. Skin of the perianal region shows degenerative and inflammatory lesions. The tongue is raw and beefy in appearance. Angulostomatitis may be present.

Alimentary symptoms

Vague alimentary symptoms like anorexia, nausea, vomiting, and dyspepsia are invariably seen. Diarrhea is common but not always present. The stools may be watery or rarely dysenteric.

Neurological features

Anxiety, depression, irritability and failure to concentrate are early symptoms. Advanced cases show delirium, dementia and psychiatric manifestation. Mental symptoms may be mistaken for primary psychiatric disorders.

Course and prognosis

Advanced cases are fatal due to diarrhea, secondary infections, or other associated nutritional disorders. Early treatment reverses the symptoms completely.

Treatment

Well-balanced diet containing adequate supply of proteins should be instituted. Nicotinamide is well absorbed if given orally. It is given in a dose of 100 mg every 6 h for 2-3 weeks. In the advanced cases 50-100 mg may be given intramuscularly or intravenously.

Supplements such as the other B complex vitamins and iron should be concurrently administered. Local application of antihistamine creams and protective clothing gives relief to the skin lesions.

Prevention

In maize eating communities other sources of niacin should be provided along with. In non-endemic areas pellagra may develop in the elderly, inmates of mental homes, etc. Such groups require vitamin supplementation.

PANTOTHENIC ACID AND BIOTIN

PANTOTHENIC ACID

Pantothenic acid is converted to coenzyme A in the body. This vitamin is widely distributed in animal and vegetable foods and hence dietary deficiency is very rare. Though the exact requirement is not clearly known, 10 mg may represent an adequate daily intake. Deficiency in experimental animals leads to dermal and hair changes, neuromuscular degeneration and fatal adrenal hemorrhage.

Calcium pantothenate has been used for other conditions like paralytic ileus, and streptomycin toxicity based on empirical findings. There is no conclusive proof to support these claims.

BIOTIN

This is an organic acid functioning as a coenzyme in several carboxylation reactions. It is present in several articles of food and is also synthesized by intestinal bacteria. Daily requirement is about 100 mcg. Naturally occurring deficiency is rare, but conditioned deficiency may develop by overfeeding exclusively with white of egg. This is due to the presence of avidin which antagonizes biotin. Infants who are on parenteral feeding with biotin deficient diets may develop symptoms such as lassitude, irritability, paresthesiae, anorexia, rashes, and hair loss. All these improve with the administration of biotin.

Inherited disorders of biotin metabolism occur rarely. Two types are known. One type may present in the first few weeks of life with metabolic acidosis and a rash. The other presents in the first few months of life with rash, keratocojunctivitis, alopecia, ataxia, hypotonia, and metabolic and lactic acidosis. Both groups respond dramatically to large doses of biotin.

OSTEOMALACIA – Definition, Etiology, Clinical Features and Treatment

Definition

Osteomalacia denotes those disorders where mineralization of newly formed bone matrix (osteoid) is defective.

Etiology

Osteomalacia may be of two different types:

1. Nutritional inadequacy of vitamin D, calcium or both.

2. Vitamin D-resistant osteomalacia. The latter occurs in the following conditions.

a. In renal tubular defects which produce hypophosphatemia

and chronic metabolic acidosis.

b. Chronic administration of diphenylhydantoin which leads to excessive metabolism of vitamin D.

c. Osteoporosis.

d. After parathyroidectomy for osteitis fibrosa or hyperthyroidism in which rapid formation of new bone outstrips bone resorption.

Clinical features

Osteomalacia presents with vague pain which starts as aches and pains insidiously, in the lumbar spine and thighs and spreading later to the arms and ribs.

The pain is frequently felt over the bones themselves, and

not at the joints. The pain is usually symmetrical and nonradiating

and is accompanied by tenderness of involved bones. Proximal muscles are weak and there is difficulty in climbing up stairs and getting up from squatting position. Occasionally, localized acute bone pain develops rapidly. These sites correspond to the development of pseudofractures. Classical radicular pain may develop due to compression fracture of the vertebra.

Physical signs include deformities, which may be missed if not specifically looked for. The usual deformities are triradiate pelvis and spinal kyphosis (due to action of gravity). Pathologic fractures due to weight bearing and avulsion of tendinous attachments may develop. Biochemical features resemble those of rickets.

Characteristic radiological features are the appearance of “pseudofractures” (Milkman’s lines and Loser’s zones). These are linear zones of decalcification which tend to be symmetrical and extend perpendicular to the cortex. The common sites are the pubic rami, ischium, the neck of the femur, the outer edge of the scapula, ribs and vertebrae. Occasionally, Loser’s zones may extend right across a long bone simulating complete fractures. They are called pseudofractures because the gap is bridged by uncalcified osteoid tissue. They do not reveal any discontinuity of bone clinically. The pseudofractures are caused by the decalcification along the course of the major arteries entering the bones especially in areas of muscular attachment, namely the adductor insertion in the pubic ramus and attachment of gluteal muscles to the trochanters of the femur.

Vertebral bodies show compression and widening of intervertebral spaces to produce biconcave or “cod-fish” vertebrae.

However, in patients who develop osteomalacia secondary to renal tubular disorders or chronic renal failure, there is marked cortical thickening and increased density of trabeculae in spongy bone. The reason for this hyperosteosis is not clear. Despite the radiological appearances the bone is abnormally brittle and prone to develop fractures.

Treatment

Nutritional osteomalacia responds well to daily administration of 2000-4000 IU of vitamin D (0.05-0.1 mg) for 6-12 weeks followed by maintenance doses of 400-600 IU daily.

Dietary supplementation of calcium in the form of milk 500 mL per day hastens recovery. Medicinal calcium in the form of calcium gluconate, lactate or carbonate can be given as tablets or suspensions orally in doses of 250 to 500 mg daily. Supplementation has to be continued as long as the diet is deficient in calcium. Adequate supplements of calcium are provided in the form of milk 500-750 mL per day or calcium lactate tablets 1 g along with food.