Phrynoderma

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Phrynoderma is a type of follicular hyperkeratosis attributed to various nutritional deficiencies, most notably vitamin A. We report a case of a 31-year-old mentally-deficient man who was a resident of a voluntary welfare nursing home. He presented with characteristic hyperkeratotic follicular papules on his trunk in a setting of low serum level of vitamin A and malnutrition. Although commonly seen in South and East Asia, it is rarely reported in Singapore. However, there is still a population at risk here--patients with malabsorption and eating disorders, and institutionalised persons...

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Phrynoderma is a rare form of follicular hyperkeratosis associated with deficiencies in vitamins A or C or essential fatty acids. We report a 6-year-old boy with an unusual presentation of phrynoderma, characterized by multiple minute digitate hyperkeratoses associated with hair casts and related to a severe deficiency in vitamins A and C complicating a chronic intestinal giardiasis. The lesions responded well to oral vitamins A and C combined with albendazole treatment. Vitamin A deficiency-related phrynoderma is rare in western countries and is usually caused by digestive malabsorption resulting from large intestine resection or pancreatic failure...

PURPOSE OF REVIEW: Nutritional deficiency, a global problem, remains uncommon in developed nations. Associated morbidity and mortality make it imperative that clinicians remain familiar with the clinical signs and symptoms of nutritional deficiencies to facilitate diagnosis. This article will review the cutaneous findings and recent literature regarding B12, niacin, zinc, vitamin A, kwashiorkor, biotin and selenium deficiencies, along with the clinical entities of noma and phrynoderma...

Phrynoderma is a distinctive form of follicular hyperkeratosis associated with nutritional deficiency. Although originally thought to represent vitamin A deficiency, several studies have demonstrated multiple etiologies. Characteristic skin lesions are hyperkeratotic papules that first appear on the extensor surfaces of the extremities, shoulders, and buttocks. We report a 14-month-old boy with malnourishment and hyperkeratotic papules and plaques with histologic changes typical of phrynoderma. Despite an extensive evaluation, a specific nutritional deficiency was not identified...

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We describe a patient with vitamin A deficiency phrynoderma caused by a combination of inadequate dietary intake of vitamin A and beta-carotene and malabsorption secondary to primary visceral myopathy and total colectomy.

1. A study was undertaken to investigate the role of vitamin E in the aetiology of phrynoderma (follicular hyperkeratosis). Fifty-six children with the disease and twenty-one normal children were investigated for this purpose. 2. Plasma vitamin E levels (mean +/- SE; mg/l) were found to be low in phrynoderma (3.7 +/- 0.19) in contrast with normal children (6.6 +/- 0.40) and therapy with a combination of vitamin E and B-complex brought about complete cure. 3. The increase in plasma vitamin E levels after the administration of vitamin E at a dose of 100 mg three times daily for 4 weeks was higher than that obtained when vitamin E at the same dose was administered together with vitamin B-complex for 4 weeks, suggesting an interaction between the two vitamins...

The need for safe and effective topical treatments is underlined by several clinical trials over the years treating miscellaneous dermatosis with many and heterologous drugs, sometimes on a simple empirical basis. In a recent study Robinson and Kligman claimed to have obtained satisfactory results treating several cases of actinic keratosis with an alternate regimen of retinoic acid and 5-FU. We wish to report an open-label pilot study using a simple and readily accessible combination of commercially formulated and available agents as 0,05% retinoic acid cream and 5% 5-FU cream over two groups of patients...

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A 41-year-old woman had multiple keratotic papules and nodules on the trunk and extremities four years after a bowel-bypass procedure for morbid obesity. The microscopic features were those of a perforating folliculitis. Serum vitamin A levels were extremely low. Oral vitamin A therapy resulted in dramatic improvement of the cutaneous lesions.

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In 3 dogs, focal, well-circumscribed skin lesions compatible clinically with seborrheic dermatitis responded to oral treatment with vitamin A. Skin biopsy findings were compatible with phrynoderma in man, a disease thought to be associated with vitamin A deficiency. The dogs had been fed commercial dog food and were otherwise healthy. The skin lesions resolved rapidly and completely with vitamin A therapy. Seven other dogs with similar lesions but with histopathologic findings not compatible with phrynoderma or follicular keratosis did not respond to vitamin A therapy...

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