BackgroundPemphigus vulgaris (PV) is an autoimmune bullous disease caused by acantholysis of keratinocytes due to pathogenic desmoglein-3 autoantibodies. Role of vitamin D has been recently implicated in various autoimmune conditions due to its immunomodulatory effects on innate and adaptive immune responses. One of the key mechanisms of the immune regulation by vitamin D is through its anti-inflammatory effects by suppression of Th17 functions. Thus, vitamin D may be involved in pathogenesis of PV. In this study, the serum vitamin D, IL-17 and TGF-β levels in PV patients as well as healthy controls were estimated in order to understand the underlying immune mechanism involved in disease pathogenesis.ResultsThis retrospective study included 30 biopsy proven PV patients’ sera. Ten age matched volunteers without any cutaneous or autoimmune conditions were recruited as healthy control (HC). Serum Vitamin D levels were measured using chemiluminescence, whereas IL-17 and TGF-β levels were determined using ELISA. All patients showed deficient vitamin D levels (11.1 ± 5.8 ng/ml). Moreover, all the PV patients had elevated serum IL-17 levels (210.7 ± 105.3), whereas it was not detectable in any (n = 10) of the healthy controls sera (ELISA sensitivity ≥ 8 pg/ml). The mean serum TGF-β concentration was also lower in patient sera as compared to healthy control, and the TGF-β/IL-17 ratio was drastically reduced in patients (30.30 ± 28), as compared to healthy controls (1363.34 ± 559.52).ConclusionsHypovitaminosis is common in North India, as ascertained by deficient levels in healthy controls, and was also consistently observed in PV patient. These low levels were not related to age or gender. The increased serum IL-17 and dramatic reduction in TGF-β/IL-17 ratio in diseased patients further indicate that dysregulation of the Treg/Th-17 axis of T effector cells may be of significance in pathogenesis of PV. Thus, the study indicates that vitamin D insufficiency may be a predisposing factor in PV, contributing through its role in any of the various adaptive immune mechanisms that regulate T cell functions in vivo. Thus, there is a need to further evaluate the Treg/Th-17 axis, as it may have an important role in disease progression.
Widespread cutaneous small vessel vasculitis secondary to COVID-19 infection Dear Editor, Since the beginning of the coronavirus disease (COVID)-19 pandemic, various dermatological manifestations including chilblain-like lesions, livedo reticularis, urticaria, varicella-like, petechial, and maculopapular exanthems have been reported. 1-4 COVID-19-induced cutaneous small vessel vasculitis (CSVV) has also been recently described. 5 CSVV refers to a subgroup of vasculitis localized to the skin. Drugs and infections are chief causes of CSVV. A 47-year-old otherwise healthy male presented to our emergency department with a 6-day history of skin and oral lesions, low grade fever, malaise, and polyarthralgia. The rash started as small red to violaceous plaques on the legs and extended to the arms and trunk. He simultaneously developed a painful tongue sore and gum bleeding. On the third day, a persistent dry cough developed. He denied a history of recent travel, sick contacts, insect bites, medication use, and family history of autoimmune disorders. On examination, temperature was 37.5°C (99.5°F).
Kindler syndrome (KS) is an inherited dermatosis linked to the FERMT1 gene, and is characterized clinically by trauma-induced acral skin blisters in infancy and childhood, photosensitivity, and progressive poikiloderma. We report a case of KS in a 7-year-old Indian girl with severe mucosal involvement of the oral cavity and genitourinary tract. Mutation analysis in the girl showed a homozygous FERMT1 mutation, c.862C>T, p.R288*. The clinical manifestations in patients with KS show significant inter individual variation, even with the same type of mutations and within members of the same family. Our case highlights the role of environmental modifiers in regulating the clinical features of KS.
This study demonstrates that serial GA peels in combination with a MKF are efficacious and safe in the treatment of facial PIH in dark-skinned patients.
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