Literature

Clinical Pearls & Morning Reports

Posted by Carla Rothaus, MD

Published January 31, 2024

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What is the link between vitamin A deficiency and keratinizing desquamative squamous metaplasia?

Squamous metaplasia of the urothelium usually arises from chronic infection (e.g., schistosomiasis) or mechanical irritation (e.g., a long-term indwelling urinary catheter). If the urothelium is replaced by keratinizing squamous cells that are then shed into the urine, the condition is called keratinizing desquamative squamous metaplasia. Read the NEJM Clinical Problem-Solving Article here.

Clinical Pearls

Q: Is keratinizing desquamative squamous metaplasia associated with urinary tract obstruction?

A: Keratinizing desquamative squamous metaplasia is a pathologic adaptation of the urinary tract in which the native urothelial lining transforms to squamous epithelium with prominent keratin deposition. This form of metaplasia impairs urothelial integrity, leading to mucosal sloughing. The resulting keratinaceous debris (plaques) can lead to urinary stasis or obstruction.

Q: What is the link between vitamin A deficiency and keratinizing desquamative squamous metaplasia?

A: Vitamin A has an essential role in epithelial integrity. Vitamin A deficiency has been shown to induce keratinizing desquamative squamous metaplasia in the urothelial tracts of animal models; the authors are aware of one case of urothelial keratinizing desquamative squamous metaplasia in a human that resulted from vitamin A deficiency and resolved with vitamin A treatment.

Morning Report Questions

Q: What are some other manifestations of vitamin A deficiency?

A: Vitamin A is a fat-soluble vitamin that occurs in multiple chemical forms. It is a transcription factor ligand with roles in gene regulation for morphogenesis, differentiation, and proliferation, which collectively are responsible for the integrity of epithelial tissue. Vitamin A deficiency causes metaplasia and keratinization of the corneal and conjunctival epithelium, leading to ulceration, scarring, and blindness. Vitamin A is essential for the formation and maturation of keratinocytes, which are epithelial cells that produce the structural protein keratin; deficiency leads to abnormal keratin protein differentiation and skin hyperkeratosis (thickening of the outermost layer) and dryness.

Q: What measures are recommended to avoid vitamin deficiencies in persons who have undergone bariatric surgery?

A: Patients who undergo operations that induce malabsorption by means of anatomical alterations, such as the biliopancreatic diversion with duodenal switch and Roux-en-Y gastric bypass, are at higher risk for nutritional deficiencies than those who undergo restrictive bariatric procedures, such as sleeve gastrectomy or gastric banding. Vitamin A deficiency after biliopancreatic diversion with duodenal switch often coexists with deficiencies of zinc, copper, iron, and other fat-soluble vitamins. At least one nutritional deficiency develops within 4 years after the procedure in 70% of patients, and in one retrospective study, reoperation (usually a lengthening of the common limb) occurred in approximately 10% of patients because of protein-calorie malnutrition. Guidelines advise that patients who undergo bariatric surgery should undergo laboratory monitoring for deficiencies in vitamin B12, folic acid, iron, 25-hydroxyvitamin D, and vitamin A; symptoms or examination findings that are compatible with deficiencies of copper, zinc, selenium, or thiamine should trigger relevant laboratory testing.

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