... food-intake and weight- loss of about 10 kilograms over the ... on face; dry skin; stained lower incisors; bilateral salivary ... a diagnosis of AN binge-eating type.
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Journal of The Association of Physicians of India ■ Vol. 63 ■ September 2015
Anorexia Nervosa with Obsessive-Compulsive Disorder Adyapad Pani1, Gouranga Santra2, Kali Das Biswas3
Abstract We report the case of an adolescent female, previously nonobese, belonging to educated average socioeconomic Muslim family. She stopped taking food, developed a perception of distorted body image with occasional episodes of binge eating and forced vomiting. She became amenorrheic and emaciated with loss of secondary sexual characters. She satisfied the criteria for anorexia nervosa with obsessive-compulsive disorder.
Introduction
A
norexia nervosa (AN), an eating disorder, common in adolescent females of developed countries, is more prevalent in the upper socio-economic c l a s s e s . A n o r e x i a h a s a n a ve r a g e prevalence of 0.3-1% in women and 0.1% in men in developed countries. 1 It is declared to be rare in non-Western countries.2 Though there are few published reports, a qualitative study probing the clinical form is lacking in the Indian literature. We intend to focus on the clinical pattern of AN in India by providing a descriptive analysis of one case, attending the medical gastroenterology out-patient department.
Case Report A 14 year old adolescent female, belonging to an urban Muslim family o f a ve r a g e s o c i o e c o n o m i c s t a t u s , wa s b r o u g h t b y h e r p a r e n t s w i t h the chief complaints of pain upper abdomen associated with grossly r e d u c e d f o o d - i n t a k e a n d we i g h t loss of about 10 kilograms over the past year and amenorrhoea for the past six months. The pain abdomen subsided with conventional therapy. Her menarche was at twelve years of age but menstruation stopped for the last six months. The anorexia, vomiting and amenorrhoea persisted. History suggestive of any systemic disease, depression or mood-swing was absent. Her birth history and developmental history were unremarkable and immunisation history was appropriate for age. At the time of presentation, s h e wa s i n V I I I t h s t a n d a r d , o f t e n obsessed with her studies. Her school-
performance was satisfactory. She was a little bit perfectionist. On examination, her body weight was 25 kilogram, height-four feet ten inches, Quetelet’s index-11.5; she was grossly emaciated. There was bilateral pedal edema, mild pallor, pulse rate-54 per minute and blood pressure-92/60 mm Hg. She had alopecia, lanugo hair on face; dry skin; stained lower incisors; bilateral salivary gland enlargement; atrophied breasts (Tanner III), and sparse pubic and axillary hairs (Tanner II). Systemic examinations were normal. Laboratory parameters were hemoglobin- 9.8 g/dL with normochromic normocytic as well as microcytic hypochromic anemia, total count- 3600/cumm, ESR- 15 mm/hour, aspartate aminotransferase (AST)58 IU/L, alanine aminotransferase (ALT)- 54 IU/L, serum albumin- 2.9 g/dL, fasting blood sugar - 70 mg/ dl, urea- 62 mg/dL, Creatinine- 1.5 mg/dL, serum potassium - 3 meq/L, calcium- 8.4 mg/L. Endocrine work up revealed low estrogen, low luteinizing hormone (LH), low follicle stimulating hormone (FSH), increased serum cortisol, low normal thyroxine and a normal thyroid stimulating hormone (TSH). Skeletal X-ray showed osteopenia. Electrocardiogram showed bradycardia and non-specific ST-T changes. However, sputum for acid fast bacilli, chest X-ray, ELISA for HIV, routine urine and stool examination, two-dimensional echocardiography with Doppler, ultrasonography
abdomen, upper gastro-intestinal endoscopy, colonoscopy, magnetic resonance imaging of brain were all non-contributory. On repeated interrogation, she a d m i t t e d t h a t o n e ye a r b a c k , s h e gradually started having intense fear of weight-gain with perception of distortion of her body-image without any noticeable psychosocial precipitating incident either at home or in school. She preferred isolation in her room and avoided socialising except attending school. Since then she started self-imposed dietary restrictions, avoided fried foods and other calorierich foods and preferred eating raw vegetables. There was also history of alopecia, cold intolerance, occasional ‘binge-eating’ followed by self-induced vomiting, and occasional constipation. There was no history of any anorectic drug or purgative intake. She enjoyed sketching which she could never finish due to over-attention to perfection. Her father, a businessman by profession, was the sole earning member, leading to a stressful environment in the family. T h e f a m i l y h i s t o r y wa s d e v o i d o f any psychiatric disorder, or pressure for slimness. Her siblings were also normal. There was no history of childabuse or adolescent problems in the family. We d i a g n o s e d h e r a s A N w i t h obsessive-compulsive disorder. Initial oral nutritional therapy (including supplementation of calcium and vi ta m i n D ora l l y ) , f a m i l y t h e r a py and psychodynamic psychotherapy resulted in six kilogram weight gain in one and a half months. Subsequently, pharmacotherapy with oral fluoxetine and olanzapine lead to a weight of 35 kilograms at the end of three months, though menstruation and development of secondary sexual characters did not resume. This could not be accounted for in view of steady clinical as well
RMO-cum-Clinical Tutor, Dept. of Medicine, Medical College, Kolkata 700073, West Bengal; 2Associate Professor, Dept. of Medicine, Midnapore Medical College, Paschim Medinipur; 3Associate Professor, Dept. of Gastro Medicine, Medical College, Kolkata, West Bengal. Received: 20.12.2011; Accepted: 11.09.2014
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Journal of The Association of Physicians of India ■ Vol. 63 ■ September 2015
as laboratory parameter improvement even after repeated gynaecological as well as psychiatric evaluation.
Discussion Anorexia nervosa (AN) is a psychiatric disorder with the highest mortality among all psychiatric illnesses, 3 characterized by inability or refusal to maintain a minimally normal we i g h t . Pa t i e n t s h a ve p r o f o u n d l y disturbed body-image perception, as well as intense fear of weight gain despite being moderately to severely underweight. A complex interaction between hormonal imbalance, neurotransmitter dysregulation, reduced leptin levels, dietary zinc deficiency and psychosocial, occupational and religious influences in genetically predisposed individuals is thought to mediate its pathogenesis. 4 It is of two types: the binge-eating or purging type, and the restricting type. In AN, remarkable changes may be seen involving endocrine system, gastrointestinal system, fluid and
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electrolyte balance, peripheral blood and bone mineral density. Obsessivecompulsive disorder (OCD) or major depression may be associated. Our patient had most of the above mentioned features, and we established a diagnosis of AN binge-eating type with associated OCD according to both DSM V and ICD 10 criteria. We ruled out conditions like tuberculosis, worm infestation, malignancy, malabsorption, chronic malaria, immunocompromised state and hypopitutirism.
in the absence of any precipitating psychosocial event, AN is a diagnosis of exclusion. But, this case report cautiously points to the fact that due to economic reforms, increased societal pressure and intense influence of media that ‘slim is beautiful’, we are likely to see an increase in the number of Indian patients with AN in the future.
1.
Treasure J, Claudino AM, Zucker N. Eating disorders. Lancet 2010; 375:583–93.
Traditionally, cases of AN from India surmised lack of the fundamental characteristic that AN in India is not accompanied by a ‘fear of fatness’ or desire to be thin, but rather by a desire to fast for religious purposes or eccentric nutritional values. 5 Reports indicate that Western cultural influence might increase the incidence of AN. 6 We have come across only a few case reports of typical AN in the Indian literature. 7,8
2.
Lee S, Chiu H.F, Chen C.N. Anorexia nervosa in Hongkong. Why not more in Chinese. BJ Psychiatry 1989; 154:683-8.
3.
Attia E. Anorexia Nervosa: Current Status and Future Directions. Annual Rev Med 2010; 61:425–35.
4.
Abell TL, Malagelada JR, Lucas AR, et al. Gastric electromechanical and neurohormonal function in anorexia nervosa. Gastroenterology 1987; 93:958–65.
5.
Khandelwal SK, Sharan P, Saxena S. Eating disorders: An Indian perspective. Int J Soc Psychiatry 1995; 41:132–46.
6.
Mumford DB, Whitehouse AM, Platts M. Sociocultural correlates of eating disorders among Asian schoolgirls in Bradford. Br J Psychiatry 1991; 158:222–8.
7.
Chaudhury S., John R. Anorexia nervosa. Indian J Psychiatry 2001; 43:264-98.
In a developing country like India, in a middle class family as this, and
8.
Mendhekar DN, Arora K, Jiloha RC. Anorexia nervosa with binge eating. Indian J Psychiatry 2003; 45:58–9.
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