Human beta-defensin 1 circulating level and gene polymorphism in non-segmental vitiligo Egyptian patients

Abstract Background: Vitiligo is an acquired depigmented skin disorder. It has a genetic and autoimmune background. Human beta defensin-1(HBD-1) plus its gene polymorphism were linked to some autoimmune disorders. Objectives: To elucidate the possible role of HBD-1 in the pathogenesis of non-segmental vitiligo (NSV) through evaluation of HBD-1 serum levels and its single nucleotide polymorphism (SNP) in patients having NSV, in addition, to correlating the results with the extent of vitiligo in those patients. Methods: A current case-control study included 50 patients having NSV and 50 controls. The authors used Vitiligo Area Scoring Index (VASI) score to assess vitiligo severity and laboratory investigations to assess serum HBD-1 level using ELISA and defensin-beta1 (DEFB1) SNP using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: There were significantly lower HBD-1 serum levels in NSV cases than in controls (p < 0.001). There was a significant predominance of GG DEFB1 genotype and G allele in NSV patients in comparison to controls (p < 0.001). The levels of serum HBD-1 and DEFB1 genotypes were not associated or correlated significantly with any of the personal and clinical parameters of vitiligo patients. Study limitations: The small sample size. Conclusions: DEFB1 gene polymorphism (GG genotype and G allele) may modulate vitiligo risk and contribute to vitiligo development in Egyptian populations. Decreased circulating HBD-1 levels might have an active role in vitiligo etiopathogenesis that could be mediated through its possible anti-inflammatory effects.

Study of purine derivatives and their relation to renal disorders in patients with psoriasis.

BACKGROUND: Psoriasis (Pso) is a chronic proliferative skin condition associated with hyperuricemia that may impair renal function. OBJECTIVES: The current study investigates the correlation between purine derivatives (PDs) and renal function in patients with Pso. PATIENTS/METHODS: This case-control study comprises 30 psoriatic patients and 30 age- and sex-matched healthy controls. The enzyme-linked immunosorbent assay (ELISA) was used to assess serum xanthine oxidase (XO) and urine albumin levels. Serum uric acid (SUA) and urinary creatinine were measured using the colorimetric method. RESULTS: There was a rise in the related PDs levels in patients with Pso compared to controls, as evidenced by the enhanced SUA levels (p < 0.001) and XO levels (p < 0.001). The presence of the related PDs in the serum was linked to the severity of Pso, and there was also a connection between the related PDs levels in the blood and indicators of renal dysfunction. Moreover, SUA and urinary albumin creatinine ratio (UACR) were found to be significantly correlated (r = 0.371 and p = 0.044), as were XO and UACR (r = 0.422 and p = 0.020). In psoriatic patients with itching and palmoplantar affection, mean SUA levels were considerably more significant than those in other instances (p = 0.005 and p = 0.018, respectively). CONCLUSION: Pso, being a hyperproliferative disease, is associated with hyperuricemia, which has a harmful effect on kidney function. The related PDs may be unique serological biomarkers for patients with Pso who are at high risk of developing renal abnormalities, especially with higher severity scores.

Human beta-defensin 1 circulating level and gene polymorphism in non-segmental vitiligo Egyptian patients.

BACKGROUND: Vitiligo is an acquired depigmented skin disorder. It has a genetic and autoimmune background. Human beta defensin-1(HBD-1) plus its gene polymorphism were linked to some autoimmune disorders. OBJECTIVE: To elucidate the possible role of HBD-1 in the pathogenesis of non-segmental vitiligo (NSV) through evaluation of HBD-1 serum levels and its single nucleotide polymorphism (SNP) in patients having NSV, in addition, to correlating the results with the extent of vitiligo in those patients. METHODS: A current case-control study included 50 patients having NSV and 50 controls. The authors used Vitiligo Area Scoring Index (VASI) score to assess vitiligo severity and laboratory investigations to assess serum HBD-1 level using ELISA and defensin-beta1 (DEFB1) SNP using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: There were significantly lower HBD-1 serum levels in NSV cases than in controls (p < 0.001). There was a significant predominance of GG DEFB1 genotype and G allele in NSV patients in comparison to controls (p < 0.001). The levels of serum HBD-1 and DEFB1 genotypes were not associated or correlated significantly with any of the personal and clinical parameters of vitiligo patients. STUDY LIMITATION: The small sample size. CONCLUSIONS: DEFB1 gene polymorphism (GG genotype and G allele) may modulate vitiligo risk and contribute to vitiligo development in Egyptian populations. Decreased circulating HBD-1 levels might have an active role in vitiligo etiopathogenesis that could be mediated through its possible anti-inflammatory effects.

Expression of cold-inducible RNA binding protein in psoriasis.

Psoriasis is an immune-mediated skin disease with a potential morbidity in patients. Cold-inducible RNA binding protein (CIRP) is a stress responsive protein having diverse roles in cancer and inflammation. This study aimed to evaluate the expression of CIRP, (serum and tissue), in psoriasis patients and to correlate this expression to the clinico-pathological data of the patients. The serum level and tissue expression of CIRP were compared between 20 patients and 20 healthy controls. Additionally, the association between CIRP level and various clinicopathological parameters was done. The serum level of CIRP was measured by enzyme-linked immunosorbent assay (ELISA) while its tissue expression was detected via immunohistochemistry. CIRP was expressed in the epidermis of all studied cases and controls with nuclear localization. A significant difference in its epidermal expression between lesional, perilesional cases and controls was observed. It was higher in control epidermis than perilesional skin and the lowest in lesional skin. Conversely, the serum CIRP level was significantly higher in psoriasis patients compared to healthy subjects. CIRP seemed to have a significant pathologic role in psoriasis patients with evident difference in its intracellular and extracellular expression levels suggesting a potential difference it its function.

Nucleotide binding and oligomerization domain 2 in psoriasis: a clinical and immunohistochemical study.

Psoriasis is a chronic immune-mediated inflammatory disease, affecting about 2 to 3% of the population worldwide. Nucleotide-binding and oligomerization domain 2-like receptor has been implicated in the pathogenesis of different inflammatory diseases. The current work aims to investigate the expression of nucleotide-binding and oligomerization domain 2-like receptor in psoriatic skin through an immunohistochemical study. This cross-sectional case-control study included 20 patients with chronic plaque psoriasis and 20 age- and sex-matched normal subjects as controls. Psoriasis severity was assessed through the use of Psoriasis Area Severity Index (PASI) score. Skin biopsies were taken under local anesthesia from cases and from matched sites of controls. Expression of nucleotide-binding and oligomerization domain 2 in epidermis of studied cases and controls showed positive epidermal expression of nucleotide-binding and oligomerization domain 2 in all cases (100%) versus 6 (30%) controls with a significant increase (χ2 = 21.54, P˂0.001). Moreover, dermal expression of nucleotide-binding and oligomerization domain 2 was higher in psoriatic skin lesion (95%) compared to controls (15%) with a significant difference (χ2 = 25.86, P˂0.001). We concluded that nucleotide-binding and oligomerization domain 2 may be implicated in psoriasis pathogenesis being higher in cases in comparison to controls.

Serum lipocalin-2 levels are decreased in patients with leprosy.

Background Leprosy is an infectious disease caused by Mycobacterium leprae affecting the skin, peripheral nerves and mucosae. Lipocalin-2 is a key component of the immune system's antimicrobial defence - it prevents iron uptake by binding and sequestering iron-scavenging siderophores and thus inhibits bacterial growth. Aim We evaluated serum lipocalin-2 levels in leprosy patients and its relationship to the pathogenesis and prognosis of the disease. Materials and methods In this case-control study, serum lipocalin-2 levels were measured by ELISA in 20 patients with leprosy and 20 healthy controls. Results Serum levels of lipocalin-2 were significantly reduced (P < 0.001) in leprosy patients as compared to controls. The levels were significantly higher (P < 0.014) in patients with multibacillary leprosy than in those with paucibacillary leprosy. Although the levels of lipocalin-2 were higher in patients with multiple nerve involvement as compared to those with involvement of 1 or 2 nerves, the results were not statistically significant. Limitation of the study The small sample size and the lack of different ethnic groups in the study were the major limitations of this study. Conclusion The lower lipocalin-2 concentrations in leprosy patients point to the importance of the protective functions of lipocalin-2. The elevated levels of lipocalin-2 observed in leprosy patients with neural involvement may be related to the reported neurodegenerative role of lipocalin-2.

Pneumatocele formation following COVID-19 pneumonia. Is there a role for surgical intervention?

COVID-19 mainly causes a lower respiratory tract illness, meaning there has been great interest in the chest and lung radiological findings seen during the course of the disease. Most of this interest has centred around the computed tomographic findings. Most commonly, computed tomographic images report ground-glass opacities but a less common finding, and potential complication associated with COVID-19, is pneumatocele formation. In this case series, we describe the presentation and management of three patients with large pneumatoceles that developed during the recovery phase of COVID-19. A conservative approach is most recommended, with surgical intervention reserved for complicated cases that cause cardiorespiratory compromise.

The Role of TROP2 in BCC and Cutaneous SCC: A Clinical and Immunohistochemical Study.

BACKGROUND: Nonmelanoma skin cancer (NMSC) mainly includes basal (BCC) and squamous (SCC) cell carcinoma. Trophoblast cell-surface antigen2 (TROP2), a cell-signal transduction, is one of the tumor-related calcium signal transducer gene family. TROP2 was highly expressed in many cancers, however, its role in BCC and SCC has not yet been studied. OBJECTIVE: To investigate TROP2 immunohistochemical expression in BCC and SCC (lesional and peri-lesional) skin compared to controls and correlates its expression with the clinicopathologic parameters of the studied cases. METHODS: This case-control study included 17 BCC and 15 SCC patients as well as 12 age and sex matched controls. History and clinical examination were completed. Histological examination of skin biopsies was done together with TROP2 immune-staining. RESULTS: In the studied BCC and SCC cases, there was a significant stepwise up-regulation of TROP2 H score from control to peri-lesional, ended by lesional epidermis in one hand (p=0.003 for BCC and p<0.001 for SCC) and tumor island in another hand (p=0.001 for BCC and p=0.003 for SCC). TROP2 expression in both BCC and SCC tumor tissues was not affected by any of the studied clinicopathological parameters of the investigated cases. CONCLUSION: TROP2 could have an important role in BCC and SCC pathogenesis. TROP2 targeting may have appraising effect in clinical application in BCC and SCC management.

Neutrophil Cytosolic Factor-1 Genotyping in Acne Vulgaris.

Acne vulgaris (AV) is a very common inflammatory dermatosis. It has a complex pathogenesis in which oxidative stress plays an important role. Neutrophil cytosolic factor (NCF)-1 gene encodes for NCF1 protein which shares in reactive oxygen species (ROS) production. Copy number variation (CNV) is a type of genetic variance in which gene copies are duplicated or deleted. The current work aimed to detect the association between NCF1 CNV and NCF-1 genotypes and AV to explore their possible role in increased disease risk or influencing its clinical presentation. Twenty-five cases with AV and 25 age- and gender-matched healthy volunteers were selected. NCF1 CNV and genotypes were determined using quantitative real-time polymerase chain reaction. NCF1 copy number was significantly increased in patients compared to the control group (p = 0.02). Higher copy number increased the risk of occurrence of AV by about 4-fold. The NCF1 genotype was more prevalent in patients (72%) compared to NCF1B (24%) and NCF1C (4%) variants, while NCF1B and NCF1C variants (68%) were more prevalent in the control group. The NCF1B genotype decreased the risk of occurrence of AV by 0.2-fold. NCF1 was significantly associated with cases more than controls (p = 0.005). It increased the risk of occurrence of acne by 5.4-fold. There was significant association between NCF1 copy number and disease duration where higher number was associated with long disease duration (p = 0.03). Higher copy number was also associated with the NCF1 genotype (p = 0.01). This study suggests that increased copy number of NCF1 gene may be a predisposing factor for AV development. However, the presence of NCF1B and NCF1C variants lowers ROS production and subsequently decreases the risk of development of AV.

Re-appraisal of Keratinocytes' Role in Vitiligo Pathogenesis.

BACKGROUND: Vitiligo is a common pigmentary disorder. Studies on its pathogenesis extensively investigated melanocytes' abnormalities and few studies searched for keratinocytes' role in disease development. Liver X receptor-α (LXR-α) is a member of nuclear hormone receptors that acts as a transcription factor. Its target genes are the main regulators of melanocyte functions. AIM: The aim of this study is to investigate keratinocytes' role in vitiligo pathogenesis through immunohistochemical expression of LXR-α in lesional, perilesional, and distant nonlesional vitiligo skin. MATERIALS AND METHODS: This case-control study was carried out on 44 participants. These included 24 patients with vitiligo and 20 age- and sex-matched normal individuals as a control group. Biopsies, from cases, were taken from lesional, perilesional, and distant nonlesional areas. Evaluation was done using immunohistochemical technique. RESULTS: Keratinocyte LXR-α expression was upregulated in the lesional and perilesional skin (follicular and interfollicular epidermis) compared with control skin (P <0.001 for all). There was significant association between higher histoscore (H-score) in lesional epidermis (P <0.001) and in hair follicle (P =0.001) and the presence of angiogenesis. There was significant association between higher H-score in lesional epidermis and suprabasal vacuolization (P =0.02). No significant association was found between H-score or expression percentage and clinical data of selected cases. CONCLUSION: LXR-α upregulation is associated with keratinocyte damage in vitiligo lesional skin that leads to decreased keratinocyte-derived mediators and growth factors supporting the growth and/or melanization of surrounding melanocytes. Therefore, melanocyte function and survival are affected.

The Use of Meshed Dermal Autograft in Breast Reconstruction.

The advantages and disadvantages of acellular dermal matrix (ADM) in breast reconstruction have been well documented. ADM is commonly used in breast reconstruction, but it adds cost to the procedure and has been associated with an increased risk of seroma, flap necrosis and infectious complications. A dermal autograft may be a useful alternative to matrices, and it has a lot of advantages: more biocompatible and more likely to be retained as a free graft, low cost, well tolerated, readily available and integrated. This report discusses a new surgical technique that uses an autologous dermis, which was harvested from the controlateral breast in patients having simultaneous breast reduction/mastopexy. Before the insertion, the autologous dermal matrix was meshed at a ratio of 3:1 to increase the graft surface area, to provide additional draining and to improve the engraftment of the autologous dermal matrix. Consequently, the resulting meshed graft allows for the cover of the inferior pole of a larger breast size implant and decreases the complication rate. In our clinic, this method was used on five women; there was one limited necrosis of the mastectomy flaps. The described technique is straightforward and reliable, it adds minimally to the operative time, and it eliminates costs and covers a bigger part of the prosthesis and promises good results. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Unusually very late-onset new growth of intraocular retinoblastoma: A case report and review of literature.

PURPOSE: To report a patient who presented with a very late-onset new growth of intraocular retinoblastoma, which occurred 11 years after the initial combined treatment. OBSERVATIONS: A 12-year-old monoophthalmic female patient presented with bilateral familial retinoblastoma showing new growth of intraocular tumor after 11 years of complete regression following combined local and systemic treatments. The new tumor growth was treated with diode laser transpupillary thermotherapy, ruthenium-106 plaque radiotherapy and adjuvant intravenous chemotherapy and the tumor regressed. CONCLUSIONS AND IMPORTANCE: Despite initial satisfactory treatment and complete regression of the tumor, very late-onset new growth of intraocular retinoblastoma can occur. Hence, life-long follow-up in all patients with retinoblastoma is warranted, given the risk for new tumor formation even later in life. To our knowledge, this is the first report of new growth of intraocular retinoblastoma after regression for more than a decade.

Serum Vitamin D and Facial Aging: Is There a Link?

BACKGROUND: The vitamin D endocrine system, besides multiple other functions, regulates aging in many tissues, including the skin. It protects the skin against the hazardous effects of many skin age-inducing agents, including ultraviolet radiation. Thus, in the present study we aimed to investigate the relationship between facial skin aging and 25-hydroxyvitamin D [25(OH)D] serum levels in healthy Egyptian adults. METHODS: Sixty-one healthy adult subjects were included. Photodamage scores (erythema/telangiectasias, lentigines, hyperpigmentation and coarse wrinkling) were assessed and graded. Serum vitamin D was measured using enzyme immunoassay and subjects were classified as sufficient, insufficient or deficient according to the vitamin level. RESULTS: The mean 25(OH)D serum level was 43.90 nmol/l. A high prevalence of vitamin D deficiency was detected in the studied subjects regardless of their age or gender. Also, vitamin D levels were not correlated with photodamage scores and were not affected by the Fitzpatrick skin phototype, duration of sun exposure per day or the use of sunscreens (p > 0.05 for all). CONCLUSIONS: Aging is a complex process that is influenced by many genetic and environmental factors. Facial aging is not correlated with serum vitamin D level, and clinical trials using oral or topical vitamin D to combat aging are better predictors of its effects rather than in vivo studies.

Nuclear factor kappa B and cyclo-oxygenase-2: two concordant players in psoriasis pathogenesis.

Nuclear factor kappa B (NFκB) is a key regulatory element in a variety of immune and inflammatory pathways, cellular proliferation, differentiation and apoptosis. Cyclo-oxygenase 2 (COX2) is one of the downstream targets of NFκB. The current work aimed to explore the possible role of NFκB and COX2 in psoriasis pathogenesis through their immunohistochemical (IHC) expression in skin biopsies of this disease and correlating this expression with clinico-pathological parameters of studied cases. 103 subjects were studied; including 58 cases with psoriasis vulgaris (lesional and perilesional skin) and 45 normal, age- and gender-matched subjects, as a control group. NFκB and COX2 expressions were evaluated using standard IHC techniques. NFκB and COX2 were upregulated in psoriasis lesional skin compared to perilesional (p < 0.001 for both) and control skin (p < 0.001 for both). Higher NFκB and COX2 H scores were significantly associated with absent granular cell layer (p = 0.02 for both), severe degree of perivascular inflammatory infiltrate (p = 0.03 and 0.002, respectively) and thin suprapapillary epidermis (p = 0.003 and 0.006, respectively). Significant positive correlation was noted between NFκB and COX2 H scores in epidermis (r = 0.41, p = 0.02) and dermis (r = 0.6, p = 0.04) of lesional skin. Significant positive correlation between NFκB H score and PASI score (r = 0.38, p = 0.04) and between COX2 H score and PASI score (r = 0.52, p < 0.001) were detected in lesional epidermis. In conclusion, both NFκB and COX2 play a role in the pathogenesis of chronic plaque psoriasis. This may open an avenue for research for new therapeutic modalities based on their inhibition.

Immunolocalization of glioma-associated oncogene homolog 1 in non melanoma skin cancer.

Glioma-associated oncogene homolog (GLI)1 is involved in controlling cell proliferation and angiogenesis. The aim of this work was to explore its possible role in non-melanoma skin cancer pathogenesis through its immunohistochemical (IHC) expression in skin biopsies of these diseases and correlating this expression with the clinico-pathological parameters of the studied cases. Seventy-six cutaneous specimens were studied; 30 cases with basal cell carcinoma (BCC), 30 cases with squamous cell carcinoma (SCC) and 16 normal skin samples, from age- and gender-matched subjects, as a control group. GLI1 was expressed in all BCC cases and in 60% of SCC cases. All SCC cases showed cytoplasmic, while 70% of BCC cases showed nucleocytoplasmic immunoreactivity. It was over expressed in BCC and SCC compared to normal skin (p = 0.01 and 0.0006, respectively). Higher Histo (H) score in BCC cases was significantly associated with female gender (p = 0.04), multiple lesions, desmoplastic stromal reaction and stromal angiogenesis (p < 0.001 for all). Higher H score in SCC cases was significantly associated with scalp location, nodular type, recurrent lesions, high tumor grade, lymphovascular invasion (p = 0.004 for all), inflammatory stromal reaction (p = 0.01), lymph node involvement and absence of calcification (p = 0.001 for both). In conclusion, GLI1 may play a role in BCC pathogenesis through its role in cell proliferation, migration, and angiogenesis. Its upregulation and cytoplasmic localization in SCC may suggest that its role in tumor pathogenesis is through mechanisms other than Hedgehog pathway activation. Further studies are needed to clarify the exact molecular basis of its oncogenic action.

Androgenetic alopecia, metabolic syndrome, and insulin resistance: Is there any association? A case-control study.

CONTEXT: Although several previous studies have investigated the association of metabolic syndrome (MS) and insulin resistance (IR) with androgenetic alopecia (AGA), the results have been inconsistent. AIM: We attempted to assess the presence of MS and IR in patients with AGA. This may help to detect if AGA can be considered as a clue for underlying serious systemic diseases. MATERIALS AND METHODS: One hundred male patients with stages III-VII AGA, in Hamilton-Norwood classification, and 100 normal, gender- and age-matched control subjects were included. Anthropometric measures, blood pressure, fasting glucose, fasting insulin, high-density lipoprotein cholesterol, and triglycerides were measured for the all participants. The presence of MS and IR was evaluated. RESULTS: There were statistically significant differences regarding mean values of body weight (P < 0.001), height (P = 0.002), waist circumference (P < 0.001), body mass index (P < 0.001), systolic (P < 0.001), and diastolic blood pressure (P < 0.001), fasting glucose (P < 0.001), triglycerides (P < 0.001), high-density lipoprotein cholesterol (P < 0.01), fasting insulin (P = 0.02) and homeostasis model assessment of insulin resistance (P < 0.001) between cases and controls. A statistically significant association was found between AGA and MS (P = 0.002) and between AGA and IR (P < 0.001). Multiple logistic regression analysis revealed that waist circumference (>102 cm) was the most significant risk factor for developing MS. It increased the risk of MS by 1.25-folds (95% CI = 1.10-1.42, P < 0.001). CONCLUSION: Our results support the recommendation for assessing MS and IR in all young males with stage III or higher AGA. Early intervention is critical to reduce the risk and complications of cardiovascular disease and type 2 diabetes mellitus later in life.

Immunolocalization of androgen receptor and estrogen receptors in skin tags.

Skin tags (STs) are benign connective tissue tumors of the dermis. Several clinical observations suggested the involvement of sex steroids in their development. This study aimed at investigating the possible role of androgen receptor (AR) and estrogen receptors (ERs) in STs pathogenesis through their immunohistochemical (IHC) localization in skin biopsies of this disease and to correlate their expression with different clinical and histopathological parameters. Using IHC techniques, we examined 62 cases with STs and 30 gender- and age-matched, healthy subjects, representing the control group. ERα, ERß, and AR were upregulated in STs compared to normal skin in epidermis and dermis (p < .001 for all). Higher AR H score was significantly associated with axillary STs (p = .02), skin colored tags (p = .03), acanthosis, and papillomatosis (p = .04 for both). Higher ERα H score was significantly associated with hyperpigmented tags (p < .001) and positive family history (p = .003). Higher ERß H score was significantly associated with female gender and obesity (p = .004 for both). Higher ERα and AR H scores were significantly associated with loose collagen arrangement (p = .02, p = .004, respectively). Higher AR, ERα, and ERß H scores were significantly associated with the presence of mast cells (p = .01, p = .04, p = .002, respectively) and dilated blood vessels (p = .006, p = .04, p = .04, respectively). In conclusion, AR and ERs may share in STs pathogenesis through their effect on keratinocytes, fibroblasts, and mast cells.

Expression of iNOS and NF-κB in melasma: an immunohistochemical study.

OBJECTIVE: To investigate the role of inducible nitric oxide synthases (iNOS) and nuclear factor-kappa B (NF-κB) in the pathogenesis of melasma through their immunohistochemical (IHC) co-localization in skin of melasma and to correlate their expression with the clinical and the histopathological data. STUDY DESIGN: This prospective case-control study was conducted on 34 female patients with melasma and 30 age- and gender-matched healthy subjects as a control group for evaluation of IHC expression of iNOS and NF-κB in melasma. RESULTS: There were significant differences between lesional and perilesional skin regarding iNOS intensity, iNOS histo-score (H-score), NF-κB intensity, and NF-κB H-score (p < 0.001 for all). There were significant associations between the higher values of H-scores for both iNOS and NF-κB and positive family history (p = 0.002 and p = 0.001, respectively) and very severe melasma areas and severity index score (p < 0.001 and p = 0.001, respectively). There was a positive correlation between H-score values of both iNOS and NF-κB (r = +0.604 and p < 0.001). CONCLUSION: The IHC co-localization and direct correlation of both iNOS and NF-κB in melasma could provide evidence about their role as co-players in melanogenesis and might provide new targets for a more efficient treatment for melasma.

Oxidative stress in alopecia areata: a case-control study.

BACKGROUND: Increased reactive oxygen species (ROS) and lipid peroxidation are seen in many dermatologic disorders, including atopic dermatitis, psoriasis, vitiligo, acne vulgaris, pemphigus vulgaris, and lichen planus. In alopecia areata (AA), there is increased production of ROS from perifollicular inflammatory cells. OBJECTIVE: The aim of this study was to determine the oxidative stress index (OSI) and lipid peroxidation by studying serum total oxidant capacity (TOC), total antioxidant capacity (TAC), and malondialdehyde (MDA) values in AA patients. METHODS: The study included 35 AA patients and a control group consisting of 30 age- and sex-matched healthy volunteers. The serum TOC, TAC, and MDA values were measured, and the OSIs were calculated and compared in both groups. RESULTS: The mean serum TOC (p < 0.001), MDA (p < 0.001), and OSI (p < 0.001) values were found to be significantly higher in AA patients than in the control group. The mean serum TAC value was significantly lower (p < 0.05) in cases than in controls. Significantly higher MDA (p < 0.001), TOC (p < 0.001), and OSI values (p < 0.001) and lower TAC values (p < 0.01) were found in severe AA than in mild or moderate AA. CONCLUSION: The demonstrated results confirmed the presence of oxidative stress and lipid peroxidation in AA. Whether these changes play a role in disease pathogenesis or result from the inflammatory process requires further investigation.