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Fulltext The Role of Combination Calcipotriol plus Betamethasone Dipropionate Gel in the Treatment of Moderate-to-Severe Scalp Seborrhoeic Dermatitis

Yap FB

Sultan Qaboos Univ Med J, 2018 Nov;18(4):e520-e523.
PMID: 30988973 DOI: 10.18295/squmj.2018.18.04.015

Objectives: This study aimed to investigate the off-label use of a combination calcipotriol plus betamethasone dipropionate (CBD) gel in the treatment of moderate-to-severe scalp seborrhoeic dermatitis (SSD).
Methods: This retrospective study involved 32 patients with SSD who were prescribed CBD gel at the Subang Jaya Medical Centre, Selangor, Malaysia, between January 2016 and December 2017. The Physician Global Assessment Scale was used to assess disease severity. Itching/discomfort was evaluated using a visual analogue scale.
Results: The mean age was 35.8 ± 6.9 years. Severe disease was seen in 53.1%. Complete clearance was recorded in 15.6%, 40.6% and 59.4% of patients at weeks two, six and 10, respectively. By week 10, 87.5% had achieved marked improvement. Both mean itching and discomfort scores significantly improved at weeks two, six and 10 (P <0.001). Better outcomes were significantly associated with disease duration and itching intensity and discomfort at presentation (P <0.050).
Conclusion: CBD gel should be considered as an option for SSD cases not adequately controlled by prior conventional treatment.

Matched MeSH terms: Calcitriol/pharmacology
Vitamin D deficiency attenuates endothelial function by reducing antioxidant activity and vascular eNOS expression in the rat microcirculation

Wee CL, Mokhtar SS, Banga Singh KK, Rasool AHG

Microvasc Res, 2021 Nov;138:104227.
PMID: 34324883 DOI: 10.1016/j.mvr.2021.104227

This study examined the effects of vitamin D deficiency on vascular function and tissue oxidative status in the microcirculation; and whether or not these effects can be ameliorated with calcitriol, the active vitamin D metabolite. Three groups (n = 10 each) of male Sprague Dawley rats were fed for 10 weeks with control diet (CR), vitamin D-deficient diet without (DR), or with oral calcitriol supplementation (0.15 μg/kg) for the last four weeks (DSR). After 10 weeks, rats were sacrificed; mesenteric arterial rings were studied using wire myograph. Oxidative stress biomarkers malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were measured in the mesenteric arterial tissue. Vascular protein expression of endothelial nitric oxide synthase (eNOS) was determined by Western blotting. Acetylcholine-induced endothelium-dependent relaxation of DR was lower than CR. eNOS expression and SOD activity were lower in mesenteric arterial tissue of DR compared to CR. Calcitriol supplementation to DSR did not ameliorate the above parameters; in fact, augmented endothelium-dependent contraction was observed. Serum calcium was higher in DSR compared to CR and DR. In conclusion, vitamin D deficiency impaired microvascular vasodilation, associated with eNOS downregulation and reduced antioxidant activity. Calcitriol supplementation to vitamin D-deficient rats at the dosage used augmented endothelium-dependent contraction, possibly due to hypercalcaemia.

Matched MeSH terms: Calcitriol/pharmacology
Oral paricalcitol versus oral calcitriol in continuous ambulatory peritoneal dialysis patients with secondary hyperparathyroidism

Jamaluddin EJ, Gafor AH, Yean LC, Cader R, Mohd R, Kong NC, et al.

Clin Exp Nephrol, 2014 Jun;18(3):507-14.
PMID: 23903802 DOI: 10.1007/s10157-013-0844-2

Secondary hyperparathyroidism (SHPT) is common in end-stage renal disease. Our primary objective was to evaluate the efficacy of oral paricalcitol versus oral calcitriol on serum intact parathyroid hormone (iPTH) and mineral bone parameters in continuous ambulatory peritoneal dialysis (CAPD) patients with SHPT. The secondary objective was to analyze highly sensitive C-reactive protein (hsCRP) and peritoneal membrane function in both groups.

Matched MeSH terms: Calcitriol/pharmacology
Fulltext Calcitriol Supplementation Ameliorates Microvascular Endothelial Dysfunction in Vitamin D-Deficient Diabetic Rats by Upregulating the Vascular eNOS Protein Expression and Reducing Oxidative Stress

Wee CL, Mokhtar SS, Singh KKB, Yahaya S, Leung SWS, Rasool AHG

Oxid Med Cell Longev, 2021;2021:3109294.
PMID: 33623633 DOI: 10.1155/2021/3109294

Diabetes mellitus contributes to macro- and microvascular complications, leading to adverse cardiovascular events. This study examined the effects of vitamin D deficiency on the vascular function and tissue oxidative status in the microcirculation of diabetic rats and to determine whether these effects can be reversed with calcitriol (active vitamin D metabolite) supplementation. Streptozotocin-induced diabetic rats were fed for 10 weeks with control diet (DC) or vitamin D-deficient diet without (DD) or with oral calcitriol supplementation (0.15 μg/kg) in the last four weeks (DDS) (10 rats each group). A nondiabetic rat group that received control diet was also included (NR). After 10 weeks, rats were sacrificed; mesenteric arterial rings with and without endothelium were studied using wire myograph. Western blotting of the mesenteric arterial tissue was performed to determine the protein expression of endothelial nitric oxide synthase (eNOS) enzyme. Antioxidant enzyme superoxide dismutase (SOD) activity and oxidative stress marker malondialdehyde (MDA) levels in the mesenteric arterial tissue were also measured. The DC group had significantly lower acetylcholine-induced relaxation and augmented endothelium-dependent contraction, with reduced eNOS expression, compared to NR rats. In mesenteric arteries of DD, acetylcholine-induced endothelium-dependent and sodium nitroprusside-induced endothelium-independent relaxations were lower than those in DC. Calcitriol supplementation in DDS restored endothelium-dependent relaxation. Mesenteric artery endothelium-dependent contraction of DD was greater than DC; it was not affected by calcitriol supplementation. The eNOS protein expression and SOD activity were significantly lower while MDA levels were greater in DD compared to DC; these effects were not observed in DDS that received calcitriol supplementation. In conclusion, vitamin D deficiency causes eNOS downregulation and oxidative stress, thereby impairing the vascular function and posing an additional risk for microvascular complications in diabetes. Calcitriol supplementation to diabetics with vitamin D deficiency could potentially be useful in the management of or as an adjunct to diabetes-related cardiovascular complications.

Matched MeSH terms: Calcitriol/pharmacology*