Early scurvy complicating anorexia nervosa.
Scurvy is an extremely rare complication of anorexia nervosa. Despite the poor intake of nutrients, anorexia nervosa is not commonly associated with vitamin deficiencies. We report a case of early scurvy complicating long-standing anorexia nervosa. Anorexia nervosa appears to be increasing in incidence. Although scurvy is unusual, this case shows the importance of its recognition as a nutritional consequence of anorexia nervosa.
SCURVY develops after 1 to 3 months of ascorbic acid deficiency. The duration of the ascorbic acid deficiency determines the severity of the clinical manifestations. In general, anorexia nervosa is not characterized by vitamin deficiency. We describe a case of early scurvy complicating anorexia nervosa.
A 46-year-old 1-lispanic woman was admitted to the hospital because of cachexia. The patient had had a long history of early satiety, epigastric pain, constipation, and progressive weight loss over the past several years. Two weeks before admission, the patient noticed easy bruising anti a nonpruritic rash on the lower extremities. Her medical history included nephrolithiasis, malnutrition, and normocytic anemia. The surgical history inclues a hysterectomy with bilateral salpingo-oophorectomy. On review of systems, the patient reported fatigue, lethargy, epigastric discomfort, and constipation. There was no history of trauma, fevers, chills, dyspnea, insomnia, or psychiatric illness.
On physical examination, the patient was withdrawn and cachectic. At presentation, the vital signs were normal. Weight was 85 lb, height 65 inches. Palpable perifollicular papules and nonpalpable purpuric macules and papules extended from the ankle to the knee bilaterally. Hemorrhages and ecchymoses surrounded the knees and elbows bilaterally, but hemarthroses were absent. Lanugo was present over the arms. No lesions were noted on the hands, feet, nail beds, arms, or back. Petechiae were noted on the hard palate. The patient had few teeth, poor oral hygiene, and periodontal disease. Temporal wasting was present. No lymphadenopathy was noted. The neck, lungs, and heart were normal. Mild epigastric tenderness was elicited with palpation. There was no peripheral edema. Rectal examination showed scant occult blood. Psychomotor retardation was evident.
Laboratory data showed normocytic anemia with a reticulocyte index of 0.2, transthyretin value 5.2 mg/dL, morning cortisol level 4.7 [micro]g/dL, thyrotropin (TSH) value 7.49 [micro]U/mL, prothrombin time 12.1 sec, activated partial thromboplastin time 31 sec, and platelet count 140,000/[mm.sup.3]. Results of a cosyntropin stimulation test were normal, as were prolactin, thyroxine, liver enzyme and serum chemistry values, and erythrocyte sedimentation rate. A platelet ascorbic acid level was not obtained. Abdominal and pelvic CT scans showed small amounts of ascites, periportal edema, and a resolved left hydronephrosis. Findings on esophogastroduo-denoscopy and colonoscopy were normal. A skin punch biopsy of a perifollicular lesion showed hyperkeratotic perifollicular plugging, extravasation of red blood cells, hemosiderin in dermis, and lymphocytic inflammation.
Further dietary and social history revealed that the patient had lost 10 kg over the past 3 years. Her diet included small portions of boiled chicken and white rice. She ate canned vegetables rarely. She described herself as reclusive and fully dependent on family members for her care. While hospitalized, she refused house meals, liquid nutritional supplements, and the majority of oral medications. When questioned about her refusals, the patient was concerned about the size of her stomach and appeared fearful of weight gain. Each new medication or food was negotiated with the patient. She denied the seriousness of her weight loss. There was no evidence of binge eating, self-induced vomiting, or misuse of laxatives.
The patient was treated with ascorbic acid therapy via vitamin supplements and enteral supplements. The ecchymoses and petechiae resolved over the course of 7 days. The palpable perifollicular papules persisted. The patient was discharged to home but was readmitted 6 months later because of constipation and abdominal pain. Fever and leukopenia quickly developed, associated with hypotension. The patient died of refractory septic shock likely due to ischemic colitis.
We describe a malnourished patient with early scurvy and anorexia nervosa. Two other cases of scurvy associated with anorexia nervosa have been reported. (1,2) In our case, the early manifestations of scurvy were present in the form of petechiae and ecchymoses. Follicular hyperkeratosis on skin biopsy supports the clinical diagnosis of early scurvy. The patient met the DSMIV criteria for restricting type of anorexia nervosa.
Moderate deficiency of ascorbic acid is associated with petechial hemorrhage and ecchymosis. Severe ascorbic acid deficiency results in gingival hemorrhage, hemarthroses, and subperiosteal hemorrhage. Follicular hyperkeratosis with corkscrew hairs is present on skin examination in moderate to severe cases. Nonspecific complaints include weakness, fatigue, dyspnea, and muscle aches. A normocytic anemia can develop, and poor wound healing develops due to decreased collagen synthesis. (3-6)
Ascorbic acid is required for the synthesis of collagen, dopamine, and carnitine. Unlike most mammals, humans cannot synthesize ascorbic acid. Without intake of ascorbic acid, body stores are depleted in 1 to 3 months. (5-7) In the United States, scurvy is most commonly observed in the homebound elderly, food faddists, and patients with malnutrition associated with malignancy.
According to dietary history in anorexic patients, intake of calcium, iron, niacin, riboflavin, and ascorbic acid is significantly lower than in normal subjects. (8) Despite near starvation, anorexia nervosa is not commonly associated with vitamin deficiencies. In a study comparing 20 anorexic female subjects with 20 control subjects, no significant differences were found in serum levels of thiamin, pyridoxine, ascorbic acid, folate, vitamin E, or vitamin D. (9)
Anorexia nervosa usually develops during adolescence, with a small percentage of cases developing after age 25. Multiple studies of anorexia nervosa confirm that 90% to 95% of the cases involve women. The lifetime prevalence rate of anorexia nervosa is 0.5%. An increase in the age-adjusted incidence rate of anorexia nervosa from 7.0 per 100,000 in 1950 to 1954 to 26.3 in 1980 to 1984 has been reported. (10) In females 15 to 24 years of age, a significant linear increase in age-adjusted incidence of anorexia nervosa between 1935 and 1984 is noted. (10) The mean annual increase of age-standardized rates of anorexia nervosa from 1965 to 1991 was 5.3%. (11) From these studies, it appears that the incidence of anorexia nervosa is increasing.
With the common use of nutritional supplementation of ascorbic acid, scurvy has gone from an omnipresent distemper at sea to a curiosity. In our case, early scurvy presented itself as a complication of anorexia nervosa, a common disease that appears to be increasing in incidence. Although scurvy is unusual, this case illustrates the importance of its recognition as a nutritional consequence of anorexia nervosa.
(1.) George GCW, Zabow T, Beaumont PJV: Scurvy in anorexia nervosa. S Afr Med J l975; 49:1420
(2.) Metha CL, Cripps D, Bridges AJ: Systemic pseudovasculitis from scurvy in anorexia nervosa. Arthritis Rheum 1996; 39:532-533
(3.) Barthelemy H, Chouvet B, Cambazard F: Skin and mucosal manifestations in vitamin deficiency. J Am Acad Dermatol 1986; 15:1263-1274
(4.) Hodges RE, Hood J, Canham JE, et al: Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr 1971; 24:432-443
(5.) Levine M: New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med 1986; 314:892-902
(6.) Miller SJ: Nutritional deficiency and the skin. J Am Acad Dermatol 1989; 21:1-30
(7.) Greene HL, Hambidge KM, Schanler R, et al: Guidelines for the use of vitamins, trace elements, calcium, magnesium, and phosphorus in infants and children receiving total parenteral nutrition. Am J Clin Nutr 1988; 48:1324-1342
(8.) Thibault L, Roberge AG: The nutritional status of subjects with anorexia nervosa. Int J Vitamin Nutr Res 1987; 57:447-452
(9.) Van Binsbergen CJ, Odink J, Van den Berg H, et al: Nutritional status in anorexia nervosa: clinical chemistry, vitamins, iron and zinc. Eur J Clin Nutr 1988; 42:929-937
(10.) Lucas AR, Beard CM, O'Fallon WM, et al: Fifty-year trends in the incidence of anorexia nervosa in Rochester, Minn. Am J Psychiatry 1991; 148:917-922
(11.) Eagles JM, Johnston MI, Hunter D, et al: Increasing incidence of anorexia nervosa in the female population of northeast Scotland. Am J Psychiatry 1995; 152:1266-1271
RELATED ARTICLE: KEY POINTS
* Anorexia nervosa is not commonly associated with vitamin deficiencies.
* Anorexia nervosa appears to be increasing in incidence.
* Stores of ascorbic acid deplete in 1 to 3 months.
* The duration of ascorbic acid deficiency determines the severity of scurvy.
* Scurvy is an unusual nutritional consequence of anorexia nervosa.
From the Division of Critical Care Medicine, Miriam Hospital; the Department of Medicine, Division of General Internal Medicine, Rhode Island Hospital; and Brown University School of Medicine, Providence, RI.
Reprint requests to Kenneth Christopher, MD, Miriam Hospital, Division of Critical Care Medicine, 164 Summit Ave, Providence, RI 02906.
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|Author:||Wing, Edward J.|
|Publication:||Southern Medical Journal|
|Date:||Sep 1, 2002|
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