Study of calprotectin gene polymorphism and serum level in acne vulgaris patients.

BACKGROUND: Acne vulgaris (AV) is an inflammatory skin disease of the pilosebaceous unit. S100A8 and S100A9 (the light subunits of calprotectin) gene polymorphisms have been known to be associated with inflammatory disorder. Until now, no study investigated calprotectin gene polymorphism in acne patients. OBJECTIVE: This study was designed to investigate calprotectin serum levels and gene polymorphism (rs3806232) in acne vulgaris patients and to correlate them with different clinical aspects of them. METHODS: This case-control study included 50 patients having variable degrees of acne vulgaris (AV) severity, in addition to a control group of 26 age- and gender-matched seemingly healthy volunteers. RESULTS: Acne vulgaris patients had considerably greater (P < 0.001) mean serum calprotectin levels than the control group (3.86 ± 2.58 pg/ml vs. 0.29 ± 0.14). AA genotype of calprotectin S100 A8 (rs3806232) was significantly predominant over AG or GG genotypes in patients compared to the controls, and the A allele was significantly (P < 0.001) predominant in patients (80%), while A and G alleles were equally distributed in controls; also, there was a significantly higher serum calprotectin level in calprotectin AA genotype than in AG or GG (P < 0.001) in acne vulgaris patients. CONCLUSION: The serum levels of calprotectin were considerably greater in AV patients than in controls. AA genotype and A allele of the S100 A8 gene were significantly higher in patients, which was associated with significantly higher calprotectin serum levels. Thus, calprotectin, both gene and serum level, might participate in disease pathogenesis, which needs further studies.

Relationship of steroid sex hormones with female sexual dysfunction in female patients having urinary incontinence.

To investigate serum estradiol, progesterone and dehydroepiandrosterone levels on FSD in females having urinary incontinence (UI), we studied 150 females [100 having UI (50 with FSD and 50 without FSD) and 50 controls]. There were significant lower estradiol and progesterone and higher DHEA serum levels in patients than controls (P = 0.001for all). In UI patients, females having sexual disruption had significantly low levels of estradiol (p = 0.001). Low estradiol serum level represented an isolated predictive factor for sexual dysfunction in incontinent female patients (p = 0.001). A low estradiol serum level might be a possible risk factor for FSD in women having UI.

Neuronal Precursor Cell Expressed Developmentally Down Regulated 4 (NEDD4) Gene Polymorphism Contributes to Keloid Development in Egyptian Population.

BACKGROUND: Keloids represent chronic fibroproliferative skin disorders in which there is deposition of extracellular components, especially type 1 collagen, fibronectin and elastin, in excessive amounts. NEDD4 is associated with fibrosis found in abnormal wound healing through increased fibroblast proliferation and regulation of type 1 collagen expression. The exact etiology of keloid formation is undefined, but the role of genetic factors was demonstrated. OBJECTIVE: To investigate the polymorphism of the NEDD4 gene rs8032158 in a sample of Egyptian patients who have keloids. METHODS: The current case-control study was conducted in 160 unrelated subjects; 100 keloid patients and 60 ages and sex coincided with apparently healthy controls. All subjects underwent a complete history, and weight and length were measured to calculate body mass index (BMI). The Vancouver Scar Scale (VSS) was used to assess keloid severity. An analysis of the polymorphism of the NEDD4 gene rs8032158 T/C was performed using taqman allelic discrimination (real-time PCR). RESULTS: The rs8032158 CC genotype was observed significantly in keloid patients and increased the risk of keloid development by approximately 2 times (p = 0.003, OR = 1.80). The C allele significantly increased the risk of keloid development by approximately 2 times (P = 0.002, OR = 2.08). The carriers of the CC genotype were significantly associated with severe keloid form and with the highest VSS values. CONCLUSION: The polymorphism of the NEDD4 gene rs8032158 could participate in the formation of keloids in the Egyptian population. The NEDD4 rs8032158 CC genotype may have a role in keloid severity.

Resistin adipokin in atopic dermatitis patients: A clinical, biochemical, and genetic study.

BACKGROUND/OBJECTIVES: Atopic dermatitis (AD) is an inflammatory chronic skin disorder. The etiology of AD is not fully understood. Therefore, we aimed by this study to shed light on the potential role of resistin in an etiopathogenesis of AD through investigation of resistin rs3745367 single nucleotide polymorphism (SNP) and resistin serum levels, and their relation to leukocytic count in a sample of Egyptian patients having atopic dermatitis. METHODS: This case-control study included 45 patients having AD and 40 controls. SCORAD index was assessed to evaluate the severity of AD. CBC, ELISA, and PCR-RFLP were performed to detect leukocytic count, resistin serum level, and resistin rs3745367 SNP, respectively. RESULTS: Atopic dermatitis patients had significant low serum resistin concentrations (P = .036) and a significantly high frequency of leukocytosis (P = .003). Low resistin serum levels were significantly related to AD disease severity (P < .001) and the presence of leukocytosis (P < .001). Resistin rs3745367 GG genotype (P = .030), as well as its G allele (P = .019), was expressively associated with AD development, and both increased the risk of AD by 3- and 2-fold, respectively. Resistin rs3745367 GG genotype was significantly linked to low resistin serum levels (P < .001), AD-positive family history (P = .015), and the presence of leukocytosis (P < .001). CONCLUSIONS: Resistin rs3745367 gene polymorphism may contribute to the development of AD. Resistin may have an immune-modulating active character in the AD etiopathogenesis that could be mediated through its anti-inflammatory effect. From this piece of work, we may suggest resistin as a new therapy to mitigate the pro-inflammatory environment found in AD.

Immunohistochemical expression HIF1α in chronic plaque psoriasis, an association with angiogenesis and proliferation.

Psoriasis is characterized by excessive cell proliferation, angiogenesis, and regions of hypoxia. Hypoxia stimulates production of hypoxia inducible factors (HIFs) such as HIF1α. The aim of the present study is to investigate the possible role of HIF1α in pathogenesis of psoriasis and to correlate its expression with angiogenesis and proliferation in involved and uninvolved skin in patients with plaque psoriasis using CD34 and Ki-67. The current study was performed on 40 skin specimens of patients presented with chronic plaque psoriasis both involved and uninvolved together with 40 specimens from age- and sex-matched healthy volunteers as a control group. The specimens were submitted for HIF1α, CD34, and Ki-67 immunostaining. HIF1α was expressed in 37.5% of normal skin with mild intensity and cytoplasmic localization instead of its expression in 72.5% and 100% of uninvolved and involved psoriatic skin, respectively. Nucleocytoplasmic pattern of HIF1α was seen in 34.5% and 37.5% of uninvolved and involved psoriatic skin, respectively. Positive and intense expression of HIF1α as well as its nucleocytoplasmic localization were significantly in favor of psoriatic skin either involved or uninvolved in comparison to normal skin (P < 0.05). Intense HIF1α was significantly associated with microvessel density in both involved and uninvolved skin (P < 0.05). Nucleocytoplasmic pattern was significantly associated with epidermal acanthosis (P < 0.05) and tended to be associated with percentage of Ki-67 of psoriatic skin (P = 0.06). The present study demonstrated that HIF1α is upregulated in the skin of psoriatic cases (involved and uninvolved) compared to normal skin indicating its role in pathogenesis of psoriasis especially its active nuclear form that showed an association with angiogenesis and proliferation.

Epidemiology of dermatophyte infections among school children in Menoufia Governorate, Egypt.

Most superficial mycotic infections of human skin are due to dermatophytes. Children are frequently affected due to different predisposing factors, particularly overcrowding in classrooms. This study aimed to estimate the prevalence of dermatophytes infections and their related risk factors among school children in Menoufia Governorate, Egypt. Six public primary and preparatory schools were randomly selected and their pupils (n = 3464) were asked to complete a predesigned questionnaire covering both personal data and suspected risk factors for superficial dermatophyte infections. The children were also examined for dermatological diseases. Any suspected lesions were biopsied for mycological examination. The prevalence of clinically suspected dermatophytes infections was 1.41%, whereas the prevalence of culture confirmed cases was 0.98%. The most common clinical type was tinea capitis with a prevalence of 1.01%. Microsporum canis was the only isolated organism from the suspicious lesions with a 69.4% positivity rate. A higher prevalence was observed among boys, low socio-economic pupils and those with a family history of dermatophyte infections. Pet contact and sharing towels and caps among pupils were significant risk factors. Dermatophyte infection is still prevalent among basic school pupils. Fortunately, it is related to preventable risk factors. We recommend regular screening and use of educational health programmes for kids to control it.

Immunohistochemical Expression of Leptin in Non Melanoma Skin Cancer.

INTRODUCTION: Obesity in adults is associated with numerous health disorders including some forms of cancer. Various epidemiological studies have found a link between excess adiposity and malignant melanoma; however, the association with non melanoma skin cancer is questionable. Leptin is a hormone produced mainly by the adipose tissue and its serum level may reflect body mass index. Leptin is reported to promote proliferation and angiogenesis and deregulate apoptosis, therefore facilitates the process of carcinogenesis. AIM: The current study tried to assess leptin localization and expression in non melanoma skin cancer to verify its possible role in pathogenesis of this cancer. MATERIALS AND METHODS: This study was carried out on 13 Basal Cell Carcinoma (BCC) cases and 14 Squamous Cell Carcinoma (SCC) cases together with 19 normal skin biopsies as a control group using immunohistochemical method. RESULTS: Leptin was expressed in 52.6% of the normal epidermis with pure cytoplasmic and both cytoplasmic and nuclear staining patterns. All cases of SCC (100%) and two cases of BCC (15.4%) showed leptin expression in tumour cells whereas nuclear expression was in favour of SCC. Stromal expression of leptin was seen in both SCC (57.1%) and BCC (38.5%) without significant differences. Percentage of leptin expression by tumour cells in SCC showed positive linear correlation with tumour size (p=0.02) and microvessel density (p=0.000). Stromal expression of leptin in SCC was associated with large tumour size (p=0.04), advanced stage (p=0.01) and tumours arising in sites other than head and neck (p=0.01). CONCLUSION: Leptin could have a more important role in pathogenesis of cutaneous SCC rather than BCC that may reflect the trivial role of obesity in induction of BCC. The expression of leptin by tumour and stromal cells of SCC could co-operate in its progression by promoting angiogenesis with subsequently acquiring large tumour size and then advanced stage.

Diagnostic and prognostic role of galectin 3 expression in cutaneous melanoma.

Many of the histopathologic criteria used to diagnose melanoma overlap with atypical but otherwise benign naevi such as dysplastic or Spitz naevi. Galectin-3 is a member of the galectin gene family and is expressed at elevated levels in a variety of neoplastic cell types. The aim of the present study was to investigate the diagnostic value of galectin-3 expression compared with homatropine methyle bromide-45(HMB-45) (one of the established and widely used immunohistochemical melanocytic markers) together with assessment of its prognostic value in melanoma lesions. This study was carried out on 21 cases of melanoma and 20 benign pigmented naevi. Galectin-3 was expressed in all the examined benign and malignant melanocytic lesions. The nucleocytoplasmic pattern of galectin-3 appeared in malignant cases only with 42.86% sensitivity, 100% specificity, and 70.73% accuracy. This pattern tended to be associated with thick melanoma (P = 0.08) and reduced survival (P = 0.22). The intensity of galectin-3 assessed by H-score was significantly of higher values in malignant lesions compared with benign lesions (P < 0.0001). The best cut-off value for discrimination between benign and malignant melanocytic lesions was 295 with 95% sensitivity, 70% specificity, and 83% accuracy. The diagnostic power of galectin-3 in distinguishing between benign and malignant melanocytic lesions relies on the pattern and the intensity of its expression. The nucleocytoplasmic pattern of galectin-3 expression carries greater probability of a malignant phenotype and a poor prognostic impact on patients' outcome.

Helicobacter pylori infection in patients with chronic urticaria: correlation with pathologic findings in gastric biopsies.

BACKGROUND: Chronic urticaria is a persistent urticaria lasting longer than 6 weeks, affecting 20% of the general population. Various infectious agents have been reported as causes of urticaria, including Helicobacter pylori, which is a common worldwide bacterial infection. Its role in inducing allergic conditions, such as chronic urticaria, has been suggested in some reports and ignored in others. AIMS: To assess the prevalence of H. pylori infection in patients with chronic urticaria and to explore the possible etiopathogenetic link between them. METHODS: Thirty-five patients suffering from chronic urticaria and 10 normal control individuals were subjected to upper endoscopic gastric biopsies to assess and semiquantify H. pylori infection and to address other pathologic abnormalities, using routine hematoxylin and eosin staining and Giemsa staining. RESULTS: Forty percent of control subjects and 57% of patients were positive for H. pylori infection, but the difference did not reach statistically significant levels (P = 0.47). The severity of urticarial symptoms was greater in the H. pylori-positive than in the H. pylori-negative group (P = 0.019). Heavy bacterial colonization (P = 0.008) and intense gastric inflammation (P < 0.0001) were associated significantly with severe clinical manifestations. Eighty percent of the H. pylori-positive urticaria group experienced complete remission after receiving eradication therapy for H. pylori. CONCLUSIONS: Helicobacter pylori may have a role in the exacerbation of urticarial symptoms, even though it is not involved directly in its etiology, and its eradication may lead to symptom improvement in a considerable number of infected urticaria patients. The severity of symptoms is dependent on the density of bacterial infection and the intensity of inflammatory infiltrate in the gastric biopsy.