Tacalcitol 4micrograms/g ointment

Vitamin D is one significant prohormone substance in human organ systems. It is a steroidal hormone produced in the skin upon exposure to UVB rays. This paper presents a systematic review of the utilization of topical vitamin D, specifically cholecalciferol, calcipotriol, and tacalcitol, in the treatment of vitiligo. It considers the role of vitamin D in stimulating the synthesis of melanin and melanogenesis, which can help with the process of repigmentation. The inclusion of calcipotriol or tacalcitol in Narrowband Ultraviolet Phototherapy (NB-UVB) has shown the potential to enhance therapeutic outcomes for vitiligo. However, their effectiveness in combination with Psoralens Long Wave Ultraviolet Radiation (PUVA) and Monochromatic Excimer Light (MEL) treatment for vitiligo is limited. In contrast, combining topical corticosteroids with vitamin D analogues has demonstrated superior efficacy in treating vitiligo compared to using vitamin D analogues alone, while also providing the added benefit of reducing corticosteroid-related adverse effects. In addition, treating stable vitiligo with topical cholecalciferol and microneedling has shown success. Future studies are needed to ascertain an efficient method of administering vitamin D topically as an anti-vitiligo agent.

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Purpose: Beyond its direct anticancer effects in breast cancer (BC), vitamin D 3 (VD 3 ) also modulates tumor progression and metastasis through immune mechanisms. T-helper 17 (Th17) cells may play a key role in these effects. This study investigates how VD 3 influences Th17 differentiation in 4T1 and 67NR murine BC models. Methods: Calcitriol or tacalcitol was administered to young and aged mice bearing 4T1 or 67NR tumors. Tumor growth, angiogenesis, and metastasis were evaluated. CD4 + lymphocytes isolated from tumors and other tissues were analyzed by flow cytometry for IL-17 and osteopontin (OPN, Spp1 ) receptors. CD4 + splenocytes were separated; gene expression was assessed using qPCR, and protein levels by Western blotting, ELISA. CD3 + CD4 + splenocytes were ex vivo differentiated into Th17 cells with blockade of CD29, CD51, and CD44, followed by flow cytometric analysis of IL-17 and IFNγ expression. Results: Tacalcitol increased metastasis in young mice but decreased it in aged mice with 4T1 tumors. Th17 cell levels in the lungs increased in young mice treated with tacalcitol but declined in aged counterparts. IL-17 + and IFNγ + Th17 cells increased upon differentiation from splenocytes of treated mice. CD29 promoted IL-17 expression in tacalcitol-treated mice, while CD51 and CD44 had opposing effects. CD51 blockade reduced IFNγ + Th17 cells in both treatment groups. Spp1 expression increased in CD4 + lymphocytes, and OPN levels were elevated in induced Th17 cells from tacalcitol-treated young mice, suggesting a role in Th17 activation. Conclusion: CD29 stimulates IL-17 expression in response to tacalcitol, while CD51 and CD44 exert opposing effects. CD51 also mediates IFNγ expression. VD 3 -induced modulation of IL-17 and IFNγ in Th17 cells may influence their pro- or anticancer function. Keywords: 4T1, metastasis, angiogenesis, vitamin D, IL-17, IFNγ

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Dear Editor, Nevus comedonicus (NC) is a rare hamartoma of the pilosebaceous units.[1] It is a rare type of epidermal nevus clinically characterized by closely arranged, dilated follicular openings with keratinous plugs resembling classical comedones.[2] Lesions may develop at any time from birth to middle age, but are usually present at birth or develop before the age of 10 years.[3] It was first described in 1895 by Kofmann, who used the term “comedo-nevus”.[3] The prevalence of NC has been estimated from 1 in 45,000 to 1 in 100,000, with no gender or racial preference.[2] The most commonly affected sites are the face, neck, upper arms, chest, and abdomen.[4] A 48-year-old male presented with multiple, asymptomatic, grouped, pits filled with black plugs over the trunk and face since birth. The patient gave a history of development of painful cystic swellings on these pits episodically. There was no history of similar complaints among the family members. No history of consanguinity. No history suggestive of any neurological, ocular, and skeletal anomalies. General physical and systemic examination was uneventful. On cutaneous examination, multiple, grouped, comedo-like openings with black, keratinous plugs were distributed over the left malar area, left pre-auricular area, bilateral shoulders, and lateral aspect of the neck on the right side following the lines of Blaschko [Figure 1]. In addition, multiple atrophic plaques with central hypopigmentation were noted over the right side of the back, right lateral chest wall, and right lumbar region [Figure 2]. A dermoscopic examination of the skin lesions over the upper back revealed multiple sharply demarcated keratinous plugs surrounded by dark to light brown structureless homogenous circular areas [Figure 3a]. Histopathological examination of the same lesion showed keratinized stratified squamous epithelium with deep invagination of epidermis filled with keratin. Few of the invaginations contained hair follicles and keratin. Dermis showed fibrocollagenous tissue and scant inflammatory infiltrate [Figure 3b]. These features were consistent with NC. Neurological, ophthalmological, and musculo-skeletal examinations were uneventful. Chest X-ray, X-ray of limbs, USG abdomen and pelvis, Electroencephalogram and CT scan of cranium and spine did not show any abnormality. The patient was treated with oral isotretinoin 20 mg/day for 6 months along with comedone extraction and fractional CO2 laser ablation for a few lesions every month. Although there was a decrease in the occurrence of episodic painful cystic lesions within the NC lesions, the existing NC lesions remained the same.Figure 1: (a) and (b): Multiple, grouped, comedo-like openings with black, keratinous plugs distributed over the left malar area, left pre-auricular area, bilateral shoulders and lateral aspect of neck on the right side following the lines of BlaschkoFigure 2: (a) and (b): Multiple atrophic plaques with central hypopigmentation, noted over the right side of the back, right lateral chest wall and right lumbar regionFigure 3: (a): Dermoscopy (Dermlite 4- 10x polarised contact mode) of the skin lesions over the upper back showing multiple sharply demarcated keratinous plugs surrounded by dark to light brown structureless homogenous circular areas. (Blue arrow). (b): Keratinized stratified squamous epithelium with deep invagination of epidermis filled with keratin. (Red arrow) (H&E, 40X)NC is a rare nevus. It can present as single or multiple lesions. It may be linear, interrupted, unilateral, bilateral, present in a dermatomal distribution, along the lines of Blaschko, or segmental.[3] The exact etiology has not been clarified, considered to be an epidermal nevus developing from the hair follicle. The other opinion is that it is a hamartoma derived from the mesodermal part of the pilosebaceous unit. Genetic mosaicism has been proposed. A mutation of Fibroblast Growth Factor Receptor 2 along with increased expression of interleukin-1-alpha is considered an important factor in the pathogenesis.[4] It can be divided into 2 groups: (1) formation of horny comedone-like plugs occurs without suppurative, acneiform prevalence; and (2) cystic formations, with recurrent infections, fistulas, abscesses, and scars.[1] The histopathological examination evidences an epidermis with dilated follicular openings, filled with horny material with absent or rudimentary sebaceous glands and hair follicles.[1] NC usually occurs by itself but may be linked with a variety of systemic findings such as skeletal or ocular anomalies. The term NC syndrome is used for comedo nevus presenting in association with extra-cutaneous manifestations like the central nervous system, skeletal, ophthalmological, neurological, and spinal abnormality.[5] Clinical presentations include seizures, paresis, mental retardation, ipsilateral cataract, trichilemmal cysts, and developmental delay.[5] Differential diagnoses include atypical acne (e.g., segmental acne and other mosaic acneiform conditions, chloracne), Favre-Racouchot syndrome (large comedones, papules, nodules, and cysts over temporal and periorbital region with dilated pilosebaceous openings and cystic spaces on histopathology) and familial dyskeratotic comedones (widespread comedone-like, hyperkeratotic papules, showing invagination of the epidermis with lamellar keratinous plug and focal evidence of dyskeratosis on histopathology).[4] NC should be treated not only due to cosmetic aspects but also to prevent complications from infections with suppuration and residual scars.[1] Treatment options include topical retinoic acid, 12% ammonium lactate, tacalcitol, and tazarotene 0.05% with calcipotriene 0.005% daily. Surgical excision with tissue expansion can be done for smaller lesions, whereas superficial dermabrasion and regular comedone extraction for extensive lesions. Oral isotretinoin is useful for extensive inflamed acneiform naevi.[5] Bhagwat P V et al.[3] reported a similar case of NC along the lines of Blaschko on the left half of the body with cystic nodule, whereas our patient has an extensive distribution of lesions along the lines of Blaschko. We report this case because of the extreme rarity of extensive NC along Blaschko and face involvement. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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