16,169 research outputs found
Vitiligo and autoimmune thyroid disorders
Vitiligo represents the most common cause of acquired skin, hair and oral depigmentation, affecting 0.5-1% of the population worldwide. It is clinically characterized by the appearance of disfiguring circumscribed skin macules following melanocyte destruction by autoreactive cytotoxic T lymphocytes. Patients affected by vitiligo usually show a poorer quality of life and are more likely to suffer from depressive symptoms, particularly evident in dark-skinned individuals. Although vitiligo is a non-fatal disease, exposure of affected skin to UV light increases the chance of skin irritation and predisposes to skin cancer. In addition, vitiligo has been associated to other rare systemic disorders due to presence of melanocytes in other body districts, such as in the eyes, auditory, nervous and cardiac tissues, where melanocytes are thought to have roles different from that played in the skin.
Several pathogenetic models have been proposed to explain vitiligo onset and progression, but clinical and experimental findings point mainly to the autoimmune hypothesis as the most qualified one. In this context, it is of relevance the strong association of vitiligo with other autoimmune diseases, in particular with autoimmune thyroid disorders, such as Hashimoto thyroiditis and Graves’ disease. In this review, after a brief overview of vitiligo and its pathogenesis, we will describe the clinical association between vitiligo and autoimmune thyroid disorders and discuss the possible underlying molecular mechanism(s)
Variant of TYR and Autoimmunity Susceptibility Loci in Generalized Vitiligo.
BACKGROUND
Generalized vitiligo is an autoimmune disease characterized by melanocyte loss, which results in patchy depigmentation of skin and hair, and is associated with an elevated risk of other autoimmune diseases.
METHODS
To identify generalized vitiligo susceptibility loci, we conducted a genomewide association study. We genotyped 579,146 single-nucleotide polymorphisms (SNPs) in 1514 patients with generalized vitiligo who were of European-derived white (CEU) ancestry and compared the genotypes with publicly available control genotypes from 2813 CEU persons. We then tested 50 SNPs in two replication sets, one comprising 677 independent CEU patients and 1106 CEU controls and the other comprising 183 CEU simplex trios with generalized vitiligo and 332 CEU multiplex families.
RESULTS
We detected significant associations between generalized vitiligo and SNPs at several loci previously associated with other autoimmune diseases. These included genes encoding major-histocompatibility-complex class I molecules (P=9.05×10−23) and class II molecules (P=4.50×10−34), PTPN22 (P=1.31×10−7), LPP (P=1.01×10−11), IL2RA (P=2.78×10−9), UBASH3A (P=1.26×10−9), and C1QTNF6 (P=2.21×10−16). We also detected associations between generalized vitiligo and SNPs in two additional immune-related loci, RERE (P=7.07×10−15) and GZMB (P=3.44×10−8), and in a locus containing TYR (P=1.60×10−18), encoding tyrosinase.
CONCLUSIONS
We observed associations between generalized vitiligo and markers implicating multiple genes, some associated with other autoimmune diseases and one (TYR) that may mediate target-cell specificity and indicate a mutually exclusive relationship between susceptibility to vitiligo and susceptibility to melanoma
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A case of new-onset vitiligo in a patient on tofacitinib and brief review of paradoxical presentations with other novel targeted therapies
With recent advancements in the understanding of vitiligo pathogenesis, Janus kinase (JAK) inhibitors have emerged as a promising new treatment modality, but their effects remain incompletely elucidated. Tofacitinib, an oral JAK 1/3 inhibitor approved for the treatment of rheumatoid arthritis, has previously been shown to induce significant re-pigmentation in vitiligo. However, as with other novel targeted therapies, cutaneous adverse effects have been observed. We report a 36-year-old woman with a history of rheumatoid arthritis, refractory to multiple pharmacotherapies, who was initiated on tofacitinib and subsequently developed progressive depigmented patches consistent with new-onset vitiligo. Although definitive causation cannot be established in this case without additional studies, it is important to note that many targeted therapies have the potential to induce paradoxical effects, that is, the occurrence or exacerbation of pathologic conditions that have been shown to respond to these medications. Paradoxical findings with other targeted therapies include the occurrence of melanoma during treatment with BRAF inhibitors, keratoacanthomas with PD-1 inhibitors, vitiligo and psoriasis with TNF-alpha inhibitors, and hidradenitis suppurativa with various biologic agents. Although JAK inhibitors hold therapeutic promise in the treatment of inflammatory skin disorders, further research is warranted to more fully comprehend their effects
The effectiveness of oral low_dose corticosteroids and topical corticosteroids together in the treatment of vitiligo patients.
Introduction: Vitiligo is one of the pigmantary skin disorders, which resulted from melanocyte destruction .vitiligo involved 1% of world population. There are various hypotheses to prove it, such as autoimmunity.vitiligo showed itself by amelonitic white macules in different areas of skin. Although there are a lot of therapeutic modalities for vitiligo but they aren't satisfactory. high_dose corticosteroids is well-established but has a lot of serious side-effects. this study was done to evaluate The effectiveness of oral low_dose corticosteroids and topical corticosteroids together in the treatment of vitiligo patients.
Methods: We used comparative before_after study. we studied the patients who have actively spreading vitiligo. The duration disease was less than 1 year and patient who have more than 15 years old age entered to the study. We used oral and topical corticosteroids together for six months. the patient took daily doses of oral prednisolone(0.3 mg/kg body weight)initially for the first 2 months ,the dosage was then reduced to (0.15 mg/kg body weight)for second 2 months and reduced again to(0.075 mg/kg body weight) for the third 3 months. we used fluocinolone as topical steroids twice a day for all 6 months. The collected data was analyzed by SPSS software.
Results: 12 patients were male and 18 were female, the average of patient's age was 26.511.before starting the study the size of all vitiligo maculs surface was 563.7 cm2, but at the end of study, it reduced to 298.8 cm2. the reduction of lesion size in 27.58% of patient was 80% and more, in 37.93% of patient was between 60_80%and in 33.3% of patients was less than 60%.the most common side _effect was steroidal acne.
Conclusion: The results prove that oral low_dose corticosteroids and topical corticosteroids together is a effective therapeutic way in vitiligo with less than 1 year duration and doesn't lead to serious side effects. And this way is proper for preventing the progression and decreasing the size of vitiligo
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Vitiligo-like lesions located over In-transit metastases of malignant melanoma as a clinical marker of complete response to pembrolizumab.
Anti-programmed cell death (PD)-1 therapies in metastatic tumors have a high incidence of immune adverse events, including cutaneous manifestations such as vitiligo-like lesions. This side effect is associated with increased survival and it is a clinical marker of response to treatment. This case report is a graphic representation of the appearance of vitiligo-like lesions over in-transit metastases of malignant melanoma linked to a complete response to treatment with pembrolizumab
Common variants in FOXP1 are associated with generalized vitiligo
In a recent genome-wide association study of generalized vitiligo, we identified ten confirmed susceptibility loci. By testing additional loci that showed suggestive association in the genome-wide study, using two replication cohorts of European descent, we observed replicated association of generalized vitiligo with variants at 3p13 encompassing FOXP1 (rs17008723, combined P = 1.04 × 10−8) and with variants at 6q27 encompassing CCR6 (rs6902119, combined P = 3.94 × 10−7)
Determining the Characteristic Vocabulary for a Specialized Dictionary using Word2vec and a Directed Crawler
Specialized dictionaries are used to understand concepts in specific domains,
especially where those concepts are not part of the general vocabulary, or
having meanings that differ from ordinary languages. The first step in creating
a specialized dictionary involves detecting the characteristic vocabulary of
the domain in question. Classical methods for detecting this vocabulary involve
gathering a domain corpus, calculating statistics on the terms found there, and
then comparing these statistics to a background or general language corpus.
Terms which are found significantly more often in the specialized corpus than
in the background corpus are candidates for the characteristic vocabulary of
the domain. Here we present two tools, a directed crawler, and a distributional
semantics package, that can be used together, circumventing the need of a
background corpus. Both tools are available on the web
Frontiers in Pigment Cell and Melanoma Research
We identify emerging frontiers in clinical and basic research of melanocyte
biology and its associated biomedical disciplines. We describe challenges and
opportunities in clinical and basic research of normal and diseased melanocytes
that impact current approaches to research in melanoma and the dermatological
sciences. We focus on four themes: (1) clinical melanoma research, (2) basic
melanoma research, (3) clinical dermatology, and (4) basic pigment cell
research, with the goal of outlining current highlights, challenges, and
frontiers associated with pigmentation and melanocyte biology. Significantly,
this document encapsulates important advances in melanocyte and melanoma
research including emerging frontiers in melanoma immunotherapy, medical and
surgical oncology, dermatology, vitiligo, albinism, genomics and systems
biology, epidemiology, pigment biophysics and chemistry, and evolution
Serum thyroid hormone antibodies are frequent in patients with polyglandular autoimmune syndrome type 3, particularly in those who require thyroxine treatment
Polyglandular autoimmune syndrome (PAS) type 3 consists of autoimmune thyroid
disease (AITD) coexisting with ≥1 non-thyroidal autoimmune disease (NTAID) other
than Addison’s disease and hypoparathyroidism. We evaluated the prevalence and
repertoire of thyroid hormones antibodies (THAb) in PAS-3 patients. Using a radioimmunoprecipation technique, we measured THAb (T3IgM, T3IgG, T4IgM, and T4IgG) in
107 PAS-3 patients and 88 controls (patients with AITD without any NTAID). Based
on the selective coexistence of AITD with one NTAID (chronic autoimmune gastritis,
non-segmental vitiligo or celiac disease), patients were divided into group 1 (chronic
autoimmune gastritis positive, n = 64), group 2 (non-segmental vitiligo positive, n = 24),
and group 3 (celiac disease positive, n = 15). At least one of the four THAb was detected
in 45 PAS-3 patients (42.1%) and 28 controls (31.8%, P = 0.14), with similar rates
in the three PAS-3 groups. The rates of T3Ab, T4Ab, and T3 + T4Ab were similar in
groups 1 and 2, while in group 3, T3Ab was undetected (P = 0.02). In PAS-3 patients,
the rate of levothyroxine treatment was greater in THAb-positive patients compared to
THAb-negative patients (76.7 vs. 56.1%, P = 0.03, RR = 1.4, 95% CI 1.03–1.81). Not
unexpectedly, levothyroxine daily dose was significantly higher in group 1 and group 3,
namely in patients with gastrointestinal disorders, compared to group 2 (1.9 ± 0.4 and
1.8 ± 0.3 vs. 1.5 ± 0.2 μg/kg body weight, P = 0.0005 and P = 0.004). Almost half of
PAS-3 patients have THAb, whose repertoire is similar if chronic autoimmune gastritis
or celiac disease is present. A prospective study would confirm whether THAb positivity
predicts greater likelihood of requiring levothyroxine treatment
Aetiology and treatment of epidermal depigmentory disorder in humans
The epidermal depigmentary trigger in humans at post-natal level may occur with the toxification of skin organ with the endogenously produced melanocytotoxic hydrogen peroxide and subsequent formation of hydrogen peroxide- melanolipoprotein conjugate involving the hydrogen bonding of complementary hydroxyl and carbonyl molecular surfaces of these biosignitures respectively. The condition is multifactorial but reversible. The structural and functional degeneration of melanocytes under the acquired condition never occur. The molecular conjugation theory on the aetiology and line of treatment of the epidermal depigmentary disorder (recoined as hepato-epidermal syndrome HES) has been proposed. The inherent sulfoxides of Allium cepa have been found as the renaturant of HES condition with the capacity to dislodge the denaturant hydrogen peroxide forming stronger hydrogen bonding with hydrogen peroxide than that of carbonyl molecular surface of melanolipoprotein, the epidermal colour determinant. The orally and topically defined plant based combined therapy advances the recovery time of HES condition
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