Think Zinc Deficiency: Acquired Acrodermatitis Enteropathica Due to Poor Diet and Common Medications

Macdonald, James B.; Connolly, Suzanne M.; DiCaudo, David J.

doi:10.1001/archdermatol.2012.435

Cited by 13 publications

(3 citation statements)

References 6 publications

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“…Skin manifestations of zinc deficiency include symmetric, eczematous dermatitis that favors a periorificial or acral distribution, but often spares the vermilion border. Other areas of involvement may include skin folds and mucocutaneous areas such as the vulvovaginal region as seen in this case (6,7). These areas are subjected to both mechanical and chemical trauma.…”

Section: Discussionmentioning

confidence: 95%

Intravenous zinc therapy for acquired zinc deficiency secondary to gastric bypass surgery: a case report

Vick

Mahmoudizad

Fiala

2015

Dermatologic Therapy

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Zinc deficiency may result from either a congenitally inherited defect of zinc absorption or is acquired secondarily from a variety of factors affecting dietary zinc intake, absorption, or loss. We report a case of acquired zinc deficiency secondary to gastric bypass surgery that resulted in vulvar cutaneous manifestations of delayed onset, with failure to clear after oral supplementation with zinc. The patient experienced improvement of symptoms only after administration of intravenous zinc supplementation. Upon review of the current literature, it is thought that the patient's original suboptimal response to oral supplementation and improvement after receiving intravenous zinc were related to the intentional surgical alteration and bypass of the absorptive capacity of the duodenum and jejunum. With the current prevalence of obesity and availability of surgical weight loss therapies, it is important to be mindful of the resulting nutritional deficiencies, their clinical manifestations, and factors affecting the efficacy of therapeutic approaches as seen in this case.

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Section: Discussionmentioning

confidence: 95%

Intravenous zinc therapy for acquired zinc deficiency secondary to gastric bypass surgery: a case report

Vick

Mahmoudizad

Fiala

2015

Dermatologic Therapy

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“…Incompletely absorbed Zn 2+ -binding drugs and common diuretics can also cause medically significant Zn 2+ deficiency, e.g. the angiotensin receptor blocking drugs and thiazide diuretics (Macdonald et al 2012 ). Valsartan has a zinc-binding thiazole ring, and absorption from the gut is less than one third.…”

Section: Can the Independent Benefits Of Metformin And Zn 2...mentioning

confidence: 99%

Coordination chemistry suggests that independently observed benefits of metformin and Zn2+ against COVID-19 are not independent

Lockwood

2024

Biometals

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Independent trials indicate that either oral Zn2+ or metformin can separately improve COVID-19 outcomes by approximately 40%. Coordination chemistry predicts a mechanistic relationship and therapeutic synergy. Zn2+ deficit is a known risk factor for both COVID-19 and non-infectious inflammation. Most dietary Zn2+ is not absorbed. Metformin is a naked ligand that presumably increases intestinal Zn2+ bioavailability and active absorption by cation transporters known to transport metformin. Intracellular Zn2+ provides a natural buffer of many protease reactions; the variable “set point” is determined by Zn2+ regulation or availability. A Zn2+-interactive protease network is suggested here. The two viral cysteine proteases are therapeutic targets against COVID-19. Viral and many host proteases are submaximally inhibited by exchangeable cell Zn2+. Inhibition of cysteine proteases can improve COVID-19 outcomes and non-infectious inflammation. Metformin reportedly enhances the natural moderating effect of Zn2+ on bioassayed proteome degradation. Firstly, the dissociable metformin–Zn2+ complex could be actively transported by intestinal cation transporters; thereby creating artificial pathways of absorption and increased body Zn2+ content. Secondly, metformin Zn2+ coordination can create a non-natural protease inhibitor independent of cell Zn2+ content. Moderation of peptidolytic reactions by either or both mechanisms could slow (a) viral multiplication (b) viral invasion and (c) the pathogenic host inflammatory response. These combined actions could allow development of acquired immunity to clear the infection before life-threatening inflammation. Nirmatrelvir (Paxlovid®) opposes COVID-19 by selective inhibition the viral main protease by a Zn2+-independent mechanism. Pending safety evaluation, predictable synergistic benefits of metformin and Zn2+, and perhaps metformin/Zn2+/Paxlovid® co-administration should be investigated.

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“…Zinc (Zn) is the second most abundant trace element in the body that is capable of interacting with more than 300 proteins involved in almost all aspects of cell function [11][12][13] , including a well-established role in immune health [14][15][16] . Much of what we know about the effect of Zn on immune function comes from studies where dietary Zn has been deficient, either due to reduced intake as a result of malnourishment, or via genetic means such as loss of function of ZIP4, a Zn transporter, which clinically leads to the condition Acrodermatitis enteropathica [17][18][19][20] . In all of these settings of Zn deficiency, widespread immune effects can be seen, including defective B cell development, atrophy of the thymus, and disrupted T cell function 14,[21][22][23][24][25] .…”

Section: Introductionmentioning

confidence: 99%

Activation of the Zinc-sensing receptor GPR39 promotes T cell reconstitution after hematopoietic stem cell transplant

Iovino

Cooper

deRoos

et al. 2021

Preprint

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Prolonged lymphopenia represents a major clinical problem after cytoreductive therapies such as chemotherapy and the conditioning required for hematopoietic stem cell transplant (HCT), contributing toward the risk of infections and malignant relapse. Restoration of T cell immunity is dependent on tissue regeneration in the thymus, the primary site of T cell development; although the capacity of the thymus to repair itself diminishes over lifespan. However, although boosting thymic function and T cell reconstitution is of considerable clinical importance, there are currently no approved therapies for treating lymphopenia. Here we found that Zinc (Zn), is critically important for both normal T cell development as well as repair after acute damage. Accumulated Zn in thymocytes during development was released into the extracellular milieu after HCT conditioning, where it triggered regeneration by stimulating endothelial cell-production of BMP4 via the cell surface receptor GPR39. Dietary supplementation of Zn was sufficient to promote thymic function in a mouse model of allogeneic HCT, including enhancing the number of recent thymic emigrants in circulation; although direct targeting of GPR39 with a small molecule agonist enhanced thymic function without the need for prior Zn accumulation in thymocytes. Together, these findings not only define an important pathway underlying tissue regeneration, but also offer an innovative preclinical approach to treat lymphopenia in HCT recipients.

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Think Zinc Deficiency: Acquired Acrodermatitis Enteropathica Due to Poor Diet and Common Medications

Cited by 13 publications

References 6 publications

Intravenous zinc therapy for acquired zinc deficiency secondary to gastric bypass surgery: a case report

Intravenous zinc therapy for acquired zinc deficiency secondary to gastric bypass surgery: a case report

Coordination chemistry suggests that independently observed benefits of metformin and Zn2+ against COVID-19 are not independent

Activation of the Zinc-sensing receptor GPR39 promotes T cell reconstitution after hematopoietic stem cell transplant

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