7. Zinc Deficiency-Related Skin Disorders
Approximately one-third of the world’s population suffers from zinc deficiency following a consequence of low zinc consumption, malabsorption, or increased loss. Low consumption of zinc is endemic to Southeast Asia, sub-Saharan Africa, rural Iran, Turkey, and Egypt [101,102]. Other zinc deficiency predisposing factors include a low-protein diet, a vegetarian diet, eating disorders such as anorexia nervosa or bulimia nervosa, parenteral nutrition, hookworm infection, AE, formula milk low in zinc, and other gastrointestinal and renal dysfunctions. Other zinc deficiency-related skin disorders include necrolytic migratory erythema [103,104], pellagra [105], and pressure ulcers [106].
In infants, zinc deficiency is attributed to either classic acrodermatitis enteropathica (AE), maternal milk low on zinc, or premature infants with prolonged parenteral nutrition, all of which can be reversed upon zinc supplementation [107,108].
7.1. Acrodermatitis Enteropathica (AE)
Acrodermatitis is a zinc deficiency skin disease that is either hereditary or acquired [109]. It is attributed to zinc malabsorption in the duodenum or maldistribution of zinc to bodily tissues [110,111]. The latter can be diagnosed by identifying lower-than-normal ALP levels in blood serumzinc-binding ligands that transport zinc [112,113]. [82]. Some studies suggested that the malabsorption of zinc is caused by a defect in the pancreatic
AE is characterized by the presence of cutaneous lesions that vary from mild to severe and are located around body openings and nails, with mild or severe diarrhea and alopecia [110,114]. Secondary infections due to immunosuppression are common and if AE is left untreated it can lead to death. Another form of AE showing zinc deficiency symptoms is observed in infants before weaning occurring as a result of reduced zinc secretion into the mother’s milk [115,116]. The identification of AE is performed by detecting low plasma zinc levels and it can be reversed with proper zinc supplementation [109].
7.2. Pathogenesis of AE
Zinc deficiency leads to elevating ATP and ADP levels and reducing adenosine levels in all cells due to extracellular adenine-nucleotide hydrolysis suppression in addition to causing a decrease in the activity of four major ectoenzymes (ENPP1, ENPP3, NT5E/CD73, and TNAP involved in the hydrolysis of extracellular ATP to adenosine (A) through ADP and AMP).
As a result, zinc affects extracellular adenine-nucleotide metabolism, and its deficiency slows both extracellular ATP clearance and adenosine (A) production [117,118].
ZnT zinc transporters ZnT5 and ZnT6 heterodimers and ZnT7 homodimers may also increase vulnerability to zinc deficiencies as they are both required for TNAP and NT5E/CD73 activity [117,119].
It is also suggested that zinc deficiency causes a decrease in Langerhans cells that express ENTPD1/CD39, leading to severe acrodermatitis [120,121,122,123].
four major ectoenzymes (ENPP1, ENPP3, NT5E/CD73, and TNAP
Geeni ENPP1 ectonukleaarinen pyrofofataasi 1
https://www.genecards.org/cgi-bin/carddisp.pl?gene=ENPP1&keywords=ENPP1
Geeni ENPP3
https://www.genecards.org/cgi-bin/carddisp.pl?gene=ENPP3&keywords=ENPP3
Geeni NT5E/CD73
https://www.genecards.org/cgi-bin/carddisp.pl?gene=NT5E&keywords=CD73
Geeni TNAP , ALPL
https://www.genecards.org/cgi-bin/carddisp.pl?gene=ALPL&keywords=TNAP
ENTPD1
https://www.genecards.org/cgi-bin/carddisp.pl?gene=ENTPD1&keywords=ENTPD1
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