A case of acquired zinc deficiency
- Author(s): Bae-Harboe, Yoon-Soo Cindy
- Solky, Ana
- Masterpol, Katherine Szyfelbein
- et al.
Published Web Locationhttps://doi.org/10.5070/D340w733sk
A case of acquired zinc deficiency1. Boston University School of Medicine, Department of Dermatology, Boston, Massachusetts
Yoon-Soo Cindy Bae-Harboe1 MD, Ana Solky2 MD, Katherine Szyfelbein Masterpol1 MD
Dermatology Online Journal 18 (5): 1
2. Tufts University School of Medicine, Department of Dermatology, Boston, Massachusetts
We report a case of adult-onset acquired zinc deficiency after bariatric surgery. Zinc deficiency may be inherited in the form of acrodermatitis enteropathica or acquired by low nutritional intake, malabsorption, excessive loss of zinc, or a combination of these factors .
A 62-year-old man presented with a 4-week history of painful, scaly, and edematous palms and soles. The patient had a longstanding history of eczematous dermatitis of the soles, which never involved the palms in the past. The remainder of the skin examination including body folds and mucosa were normal.
The patient was initially treated with oral prednisone for two weeks without any improvement. Review of systems was negative for constitutional symptoms, joint pains, or diarrhea. The patient’s weight had been stable since significant weight loss from gastric bypass surgery 3 years prior.
|Figure 2||Figure 3|
Cutaneous examination revealed edema, scaly plaques with fissures and desquamation on bilateral palms (Figure 1). Punch biopsy was performed (Figures 2 and 3).
Pertinent laboratory values showed normal zinc level (Serum zinc levels, 88 µg/dL) and erythrocyte sedimentation rate as well as normal complete blood count and basic metabolic panel; tests for cryoglobulins, lupus anticoagulant, and hepatitis panel were negative.
A punch biopsy revealed marked parakeratosis with underlying epidermal hyperplasia and spongiosis. The upper epidermal layers exhibited striking pallor with hypogranulosis. No fungal organisms were identified with Periodic acid-Schiff stain (Figures 2 and 3). Serum zinc levels were within normal limits 88 µg/dL. However, given the patient’s history of gastric bypass, clinical presentation and histological findings, the patient was diagnosed with a nutritional deficiency. Moreover, the patient began supplementation with zinc sulfate 220 mg/day with near resolution of his hand dermatitis in just 6 days, further supporting the diagnosis. Although biotin and essential fatty acid deficiency are in the differential diagnosis, the rapid improvement of the patient’s skin after only zinc supplementation suggested zinc deficiency to be the cause.
Acquired zinc deficiency
Zinc deficiency may be inherited in the form of acrodermatitis enteropathica or acquired by low nutritional intake (including parenteral alimentation, plant based diets, alcoholism), malabsorption (including bariatric surgery, celiac sprue), excessive loss of zinc (such as diarrhea secondary to viral, protozoal, and bacterial pathogens), chronic diseases (liver or renal disease, diabetes, malignancies, sickle-cell disease), or a combination of these factors [1, 2]. Both the inherited and acquired forms can present with similar clinical features. Acrodermatitis enteropathica belongs to the family of necrolytic erythemas that include necrolytic migratory erythema, necrolytic acral erythema, pellagra, and essential fatty acid deficiencies . The entities of acrodermatitis enteropathica and acquired zinc deficiency can resemble one another both clinically and histologically . Female and male adults require 8 mg and 11 mg daily of zinc, respectively; whereas children need 2-11 mg daily of zinc, depending on age and gender . Moderate to severe zinc deficiencies are rare in developed countries .
The clinical presentation of zinc deficiency may vary. Classically, patients present with skin lesions distributed in the perioral, acral, and perineal areas in a symmetric pattern . The hallmarks of acute zinc deficiency can include diarrhea, mental dysfunction, depression, alopecia, and acute dermatitis .
Characteristic histopathologic findings are similar to those described in this patient. Manifestations of zinc deficiency may begin immediately, as evidenced by recurrence of symptoms after supplementation is discontinued . Zinc levels in plasma or serum are the most commonly used tests to evaluate for zinc deficiency. However, those levels do not necessarily reflect cellular zinc status because of tight homeostatic control mechanisms . Because alkaline phosphatase is a zinc-dependent enzyme, low serum levels in the context of normal zinc levels may indicate a zinc deficiency . Zinc levels below 50 mcg/dL may suggest a deficiency , but the clinical effects of zinc deficiency can be present in the absence of abnormal laboratory indices; low levels may be a late indicator of zinc deficiency [8, 11]. It is recommended that clinicians consider risk factors such as alcoholism, inadequate caloric intake, and digestive diseases in addition to symptoms of zinc deficiency, including impaired growth in infants, when determining the need for zinc supplementation. Patients with a recent history of parenteral alimentation or bariatric surgery, as well as patients with chronic diseases, diarrhea, celiac disease, strict plant-based diets may also be vulnerable .
Patients who have undergone bariatric surgery are commonly at risk of developing nutritional deficiencies. Bariatric surgical procedures are described as restrictive or malabsorptive, based on the primary mechanism of action, limiting food intake or affecting nutrient absorption, respectively . In addition, prospective studies on both types of bariatric surgeries have reported multiple nutrient deficiencies, including a zinc deficiency [13, 14]. However, further studies have supported that fewer nutrient deficiencies may occur after restrictive (low intake) versus malabsorptive (designed to induce malabsorption) methods .
Treatment for zinc deficiency should be initiated at 3 mg/kg/day of elemental zinc (50 mg of elemental zinc per 220 mg zinc sulfate). With treatment, prompt clinical improvement ensues, even before any significant changes in the serum zinc level may be observed . In addition to supplementation, any underlying cause for a nutritional deficiency should be investigated if not already evident by history, as in the case of our patient. Given the increase in bariatric surgery over the recent years, clinicians should be wary of the clinical signs of nutritional deficiency in order to optimize diagnosis and treatment.
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