The role of anemia and vitamin D levels in acute and chronic telogen effluvium
Telogen effluvium (TE) is an abnormality of hair cycling. Vitamin D promotes hair follicle differentiation. The importance of vitamin D in hair growth is evident in patients with hereditary vitamin D receptor deficiency. The role of vitamin D in the pathogenesis of TE has not been investigated before. We investigated the role of vitamin D, ferritin, and zinc in the pathogenesis of TE. Materials and methods: We measured serum hemoglobin, ferritin, zinc, calcium, phosphate, parathormone, magnesium, 25 and 1,25-hydroxyvitamin D3, and bone alkaline phosphatase and thyroid stimulating hormone levels in 63 female patients and 50 control subjects. Twenty-nine of the TE patients were classified in the acute TE group and 34 were classified in the chronic TE groups. Results: Ferritin (acute TE; 17.0 ± 12.8, chronic TE; 19.6 ± 15.2, control; 35.5 ± 31.8, P < 0.001) and hemoglobin (acute TE; 12.7 ± 1.7, chronic TE; 13.3 ± 1.0, control; 14.2 ± 1.2, P < 0.0001) levels were significantly lower in the TE group than in the control group. However, 25-hydroxyvitamin D3 levels were significantly higher in the TE group than in the control group (acute TE; 18.5 ± 9.2, chronic TE; 24.4 ± 11.2, control; 15.6 ± 15.8, P < 0.01). Vitamin D levels increased gradually from control groups to acute and chronic TE groups. However, active D vitamin levels (1,25-hydroxyvitamin D3) were similar. Conclusion: Iron deficiency anemia seems to be the main triggering factor for the development of TE and the increase in serum 25-hydroxyvitamin D3 levels may be related to increased exposure to UV light due to TE.
The role of anemia and vitamin D levels in acute and chronic telogen effluvium
Telogen effluvium (TE) is an abnormality of hair cycling. Vitamin D promotes hair follicle differentiation. The importance of vitamin D in hair growth is evident in patients with hereditary vitamin D receptor deficiency. The role of vitamin D in the pathogenesis of TE has not been investigated before. We investigated the role of vitamin D, ferritin, and zinc in the pathogenesis of TE. Materials and methods: We measured serum hemoglobin, ferritin, zinc, calcium, phosphate, parathormone, magnesium, 25 and 1,25-hydroxyvitamin D3, and bone alkaline phosphatase and thyroid stimulating hormone levels in 63 female patients and 50 control subjects. Twenty-nine of the TE patients were classified in the acute TE group and 34 were classified in the chronic TE groups. Results: Ferritin (acute TE; 17.0 ± 12.8, chronic TE; 19.6 ± 15.2, control; 35.5 ± 31.8, P < 0.001) and hemoglobin (acute TE; 12.7 ± 1.7, chronic TE; 13.3 ± 1.0, control; 14.2 ± 1.2, P < 0.0001) levels were significantly lower in the TE group than in the control group. However, 25-hydroxyvitamin D3 levels were significantly higher in the TE group than in the control group (acute TE; 18.5 ± 9.2, chronic TE; 24.4 ± 11.2, control; 15.6 ± 15.8, P < 0.01). Vitamin D levels increased gradually from control groups to acute and chronic TE groups. However, active D vitamin levels (1,25-hydroxyvitamin D3) were similar. Conclusion: Iron deficiency anemia seems to be the main triggering factor for the development of TE and the increase in serum 25-hydroxyvitamin D3 levels may be related to increased exposure to UV light due to TE.
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