 Abstract | | |
Zinc deficiency is an uncommon condition, known to occur in two forms: inherited type, known as Acrodermatitis enteropathies and the acquired type. Cutaneous clinical manifestations observed include characteristic dermatitis on acral, periorificial, and anogenital areas through an unknown mechanism. The patient had a combination of causes which lead to a state of zinc deficiency. We are presenting it due to the rarity of acquired acrodermatitis in patients of gastrointestinal tuberculosis and renal transplant recipients. We emphasize the awareness about this condition, especially in resource-poor settings, where serum zinc levels may not be available, and a trial of oral zinc may be given.
How to cite this article:
Ghuge P, Karia R, Malkani RH. Acquired zinc deficiency in a renal transplant recipient with gastrointestinal tuberculosis responding promptly to oral correction. Saudi J Kidney Dis Transpl 2018;29:1199-202 |
How to cite this URL:
Ghuge P, Karia R, Malkani RH. Acquired zinc deficiency in a renal transplant recipient with gastrointestinal tuberculosis responding promptly to oral correction. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2021 Mar 4];29:1199-202. Available from: https://www.sjkdt.org/text.asp?2018/29/5/1199/243962 |
| Introduction | |  |
Acrodermatitis enteropathica (AE) is an uncommon autosomal recessive genetic disorder of zinc malabsorption. Acquired zinc deficiency has multiple etiologies such as low nutritional intake, malabsorption, excessive loss of zinc, chronic diseases, or a combination of all these factors. Intestinal tuberculosis (TB) is the most common cause of malabsorption in India. Treatment with oral zinc gives prompt relief to the patient.
| Case Report | | |
A 46-year-old female patient presented with multiple, dark colored, itchy, scaly lesions involving both her upper and the lower limbs for one month. The lesions on the thigh were painful. She did not have a history of similar lesions in the past or in her family. She was a diagnosed with a case of ileocecal TB and was on anti-TB therapy for the past seven months. She was also a renal transplant recipient. The patient preferred a mixed diet (vegetarian and nonvegetarian), did not report any weight loss recently and did not show any features of malnutrition. There was no history of chronic diarrhea, decreased appetite, loss of hair, or alcohol abuse. On cutaneous examination, there was evidence of multiple, well-defined, hyperpigmented, scaly plaques, measuring of 3–7 cm [Figure 1]a and [Figure 1]b. A differential diagnosis of atypical dermatophytic infection, psoriasis, seborrhoeic dermatitis and acquired Acrodermatitis enteropathica was considered. The laboratory investigations were as follows hemoglobin: 9.6 g%, packed cell volume: 28.3%, mean corpuscular hemoglobin concentration: 33.9%, red blood cell count: 2.95 millions/L, mean corpuscular volume: 95.9 fL, mean corpuscular hemoglobin: 32.5 pg, erythrocyte sedimentation rate: 103 mm/h, white blood cell count: 6150/mm3 (neutrophils: 74.7%, lymphocytes: 18.3%, eosinophils: 1.0%, monocytes: 6.0%), and platelet count: 297,000/μL. The other investigations were as follows: blood urea nitrogen: 16.8 mg/dL, serum creatinine: 1.2 mg/dL, serum sodium: 133.2 mmol/L, serum potassium: 4.4 mmol/L, serum chloride: 98.3 mmol/L, serum bicarbonate: 22.5 mmol/L, serum cholesterol: 1.43 mcg%, and dehydroepiandrosterone sulfate: 0.04 mcg/mL. She was negative for Hepatitis B virus and hepatitis C virus. Histopathological evaluation of the skin lesions revealed hyperkeratosis, epidermal pallor, and psoriasiform hyperplasia suggestive of nutritional dermatosis [Figure 2]a and [Figure 2]b. The patient was treated with 3 mg/kg/day of elemental zinc (50 mg of elemental zinc per 220 mg zinc sulfate) along with topical emollients. The plaques showed reduced erythema and scaling by the end of one week, with decrease in their thickness by two weeks. There was complete clearance of the plaques by the end of three months [Figure 3]. | Figure 3: Clearance of hyperpigmented and scaly lesions on the thighs after zinc treatment.
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| Discussion | | |
Zinc deficiency is known to occur in two forms. The inherited type, known as Acrodermatitis enteropathica or acquired by low nutritional intake (including parenteral alimentation, plant-based diets, alcoholism), malabsorption (including bariatric surgery, celiac sprue, and intestinal TB), excessive loss of zinc through the alimentary tract (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 all these factors.[1]
Zinc absorption mainly occurs through the apical membrane of enterocytes with the help of diet-derived luminal factors. Malabsorption and possibly intestinal microbiota limit this zinc availability. The transporter ZIP4 present throughout the gastrointestinal tract is the main processor of dietary zinc for loading into enterocytes from the apical membrane.[2] TB of the intestine is a common cause of malabsorption in India, next only to tropical sprue.[3]
Intestinal TB is a common condition. Next, to tropical sprue, it is the most important cause of malabsorption in India.[4] The other causes of malabsorption are: bacterial overgrowth proximal to a stricture, bile salt deconjugation, diminished absorptive surface, involvement of lymphatics, and lymph nodes.[5]
The causes of Zn deficiency in kidney disease are not clear. Serum zinc levels are commonly found to be low in chronic kidney disease. After the renal transplant, the loss of zinc increases further, and the deficiency may become clinically apparent.[6] The results of a study by Mahajan et al, suggested that zinc deficiency persist up to one-year posttransplant and may be related to increased urinary zinc losses.
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.[8] Alkaline phosphatase is a zinc-dependent enzyme. Its levels can be used as an indicator of zinc deficiency.[9]
Treatment for zinc deficiency starts at 3 mg/kg/day of elemental zinc (50 mg of elemental zinc per 220 mg zinc sulfate) with rapid clinical improvement, even before changes in the serum zinc level are seem.[10]
| Acknowledgment | | |
We would like to thank Dr. B. V. Gandhi for his support for submitting the present case.
Conflict of interest: None declared.
| References | | |
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| 3. | Ranjan P, Ghoshal UC, Aggarwal R, et al. Etiological spectrum of sporadic malabsorption syndrome in Northern Indian adults at a tertiary hospital. Indian J Gastroenterol 2004; 23:94-8. [ PUBMED] [Full text] |
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| 6. | Mahajan SK. Zinc in kidney disease. J Am Coll Nutr 1989;8:296-304. |
| 7. | Mahajan SK, Abraham J, Migdal SD, Abu-Hamdan DK, McDonald FD. Effect of renal transplantation on zinc metabolism and taste acuity in uremia. A prospective study. Transplantation 1984;38:599-602. |
| 8. | Maret W, Sandstead HH. Zinc requirements and the risks and benefits of zinc supplementation. J Trace Elem Med Biol 2006;20:3-18. |
| 9. | Glover MT, Atherton DJ. Transient zinc deficiency in two full-term breast-fed siblings associated with low maternal breast milk zinc concentration. Pediatr Dermatol 1988;5:10-3. |
| 10. | Maverakis E, Fung MA, Lynch PJ, Draznin M, Michael DJ, Ruben B, et al. Acrodermatitis enteropathica and an overview of zinc metabolism. J Am Acad Dermatol 2007;56: 116-24. |
Correspondence Address:
Dr. Ram H Malkani
Department of Dermatology, Jaslok Hospital and Research Center, Mumbai, Maharashtra
India
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DOI: 10.4103/1319-2442.243962 PMID: 30381519 
[Figure 1], [Figure 2], [Figure 3] |
