Vahide Baysal Akkaya

The role of helper and regulatory T cells in the pathogenesis of vitiligo

BACKGROUND Alterations in cellular immunity, including CD4(+) T and CD8(+) T lymphocytes, have been proposed in the pathogenesis of vitiligo. There is also a proposed role for cytokines in the depigmentation observed in vitiligo. However, previous reports on the role of cytokines in the pathogenesis of vitiligo have been few in number. OBJECTIVE The purpose of this investigation was to assess the role of the major cytokines produced by T-helper 1 and 2 cells as well as T-helper 17 and regulatory T cells in the pathogenesis of vitiligo. METHODS Forty patients with vitiligo and 40 age- and sex-matched healthy control subjects were enrolled in the study. Serum interleukin (IL)-4, IL-6, IL-10, IL-17, interferon-gamma, tumor necrosis factor-beta, and transforming growth factor-beta levels were detected by enzyme-linked immunosorbent assay in both groups. The correlations of serum cytokine levels with age of onset, sex, duration of disease, type and activity of vitiligo, percentage of involved body area, Koebner positivity, family history, and the presence of associated autoimmune diseases were assessed. RESULTS Serum transforming growth factor-beta levels were significantly decreased in the vitiligo group compared with the control group (P = .004). No difference was detected between the patient and control groups in mean levels of serum IL-6, IL-10, and tumor necrosis factor-beta. In the patients with vitiligo, serum IL-17 levels were positively correlated with the extent of body area involvement (rho = 0.329, P = .038). LIMITATIONS Tissue cytokines compared with those in the peripheral blood were not measured. CONCLUSION Although multiple factors have been implicated in the pathogenesis of vitiligo, reduced serum transforming growth factor-beta levels, as observed in patients in the current investigation, may contribute to enhanced cellular immunity. This may facilitate the occurrence of vitiligo by leading to diminished maturation of regulatory T cells, followed by impaired inhibition of inflammation.

Brachioradial pruritus successfully treated with gabapentin

Brachioradial pruritus (BRP) is a mysterious entity characterized by localized pruritus of the dorsolateral aspect of the arm. The precise etiology of BRP remains unknown, but sun exposure and/or cervical spine lesions seem to be triggering or at least aggravating factors. Many treatment alternatives including non‐steroidal anti‐inflammatory drugs, topical capsaicin, topical corticosteroids, photoprotection, carbamazepine and acupuncture have been used with different success rates. Recently, gabapentin, an antiepileptic agent, has been reported to be an effective therapeutic agent in BRP. Herein, we report a 64‐year‐old man with BRP who showed good response to gabapentin therapy.

A case of multiple, eruptive pyogenic granuloma developed on a region of the burned skin: can erythromycin be a treatment option?

Pyogenic granuloma (PG) is a common, acquired, benign angiomatous proliferation of the skin and mucous membranes that develops spontaneously or traumatically. PG usually occurs in children and young adults and predominantly located on neck, hands, and extremities. There are numerous theories about the pathogenesis of PG, but the etiology is not clear. Although the occurance of PG after trauma to the skin is very common, multiple lesions of PG secondary to burn are rare in the literature. In this report, we present a case of multiple, eruptive PG that developed on the burned skin of a 17-month-old boy. After oral erythromycin treatment for 8 weeks, the lesions clearly improved.

Immunohistochemical galectin-3 expression in non-melanoma skin cancers

Galectin-3 is a ss-galactoside-binding lectin. It participates in a variety of normal and pathologic processes, including cancer progression. In this study, we evaluated the pattern of expression of galectin-3 in cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), and its correlation with the grade of differentiation in SCC and tumor size. Galectin-3 expression was evaluated by immunohistochemistry in 31 SCCs, 30 BCCs, and 29 non-tumoral skin samples. Galectin-3 expression was higher in normal epidermis than in non-melanoma skin cancers, except for cytoplasmic immunoreactivity in SCC. Cytoplasmic galectin-3 immunoreactivity was significantly higher than nuclear immunoreactivity in non-melanoma skin cancers. Cytoplasmic galectin-3 immunoreactivity was significantly higher in SCC than in both circumscribed and infiltrative BCCs, but no difference was detected between these two types of BCC. Cytoplasmic galectin-3 immunoreactivity predominated within SCCs (p=0.000), and a positive correlation was detected between tumor size and cytoplasmic immunoreactivity (r=0.385, p=0.043). There was no correlation between galectin-3 staining and tumor differentiation and lymph node metastasis. Decreased nuclear galectin-3 expression and cytoplasmic immunoreactivity in tumors are important factors in the progression from the normal to the cancerous state in non-melanoma skin cancers. We speculate that cytoplasmic galectin-3 expression may be one of the factors that contribute to tumor aggressiveness in SCC.

Traumatic lingual ulcer in a child: Riga–Fede disease

Riga–Fede disease RFD is an extremely rare, benign inflammatory disorder characterized by reactive, traumatic ulceration of the oral mucosa especially located on the tongue. It is most commonly associated with natal or neonatal teeth in newborns. Mucosal lesions are often caused by repetitive traumatic damage due to backward and forward motions of the tongue over the lower incisors. Failure to diagnose and treat these lesions properly may result in inadequate food intake, growth retardation and permanent lingual deformity. We report a 15‐month‐old healthy infant with tongue ulcer diagnosed as RFD based on history and clinical features.

Isotretinoin treatment induces oxidative toxicity in blood of patients with acne vulgaris: a clinical pilot study

Acne vulgaris is the one of the most common skin diseases. Although isotretinoin (13‐cis‐retinoic acid) is an effective and well‐tolerated medication, it has a wide range of side effects. Because the effects of isotretinoin on oxidant and antioxidant systems have not yet been clarified, we investigated plasma and erythrocyte antioxidant vitamins, lipid peroxidation (LP), reduced glutathione (GSH) and glutathione peroxidase (GSH‐Px) values in patients with acne vulgaris before and after isotretinoin treatment. The study was performed on the blood plasma and erythrocytes of 31 acne vulgaris patients. Blood samples were taken from the patients before treatment and after isotretinoin (oral and 0·5–0·7 mg·kg–1) treatment for 2 months. Plasma amtioxidant vitamins, erythrocyte malondialdehyde, GSH and GSH‐Px levels were measured. Plasma vitamin E (p < 0·001), lipid peroxidation (LP) and serum high‐density lipoprotein cholesterol (p < 0·001) values were significantly lower in the treatment group than in the pre‐treatment group, although erythrocyte LP (p < 0·001), GSH (p < 0·01) and GSH‐Px (p < 0·001), aspartate aminotransferase (p < 0·05), alanine aminotransferase (p < 0·05), density lipoprotein cholesterol (p < 0·001) and total cholesterol (p < 0·01) levels were significantly higher in the treatment group than in the pre‐treatment group. Vitamins A, C and β‐carotene concentrations did not change significantly between the two groups. In conclusion, the results of the current study indicate that isotretinoin treatment induces oxidative stress and liver damage by decreasing plasma vitamin E and increasing erythrocytes GSH‐Px, GSH and liver enzyme values. Copyright

Evaluation of serum sCD40L and homocysteine levels with subclinical atherosclerosis indicators in patients with psoriasis: a pilot study

Psoriasis is a chronic inflammatory process associated with an increased risk of cardiovascular risk factors. sCD40L has been suggested to have a possible role in the pathogenesis, of psoriasis and is known to be associated with inflammation, atherogenesis and cardiovascular events. This study investigated cardiovascular risk factors (sCD40L and homocysteine) as well as subclinical atherosclerosis indicators in psoriatic patients and control subjects. The study included 56 consecutive patients with chronic plaque‐type psoriasis and 53 age and gender matched healthy controls admitted to a university hospital. Serum sCD40L and homocysteine levels were measured by ELISA. Carotid artery intima‐media thickness and brachial artery flow mediated dilatation (FMD) measurements were determined ultrasonographically. Subjects who had a history of cardiovascular diseases and cardiovascular risk factors and receiving any systemic treatment were excluded from the study. Plasma sCD40L levels were significantly higher in psoriasis patients compared with healthy controls (1.33 ± 0.72 vs. 0.98 ± 0.70 ng/ml P = 0.012), whereas plasma homocysteine levels did not differ significantly between the two groups. FMD was significantly reduced in the psoriasis group compared to the controls (3.83 ± 5.03 vs. 8.45 ± 7.27% P = 0.0001). Multiple linear regression analyses indicated a significant association between psoriasis, sCD40L, and FMD. Psoriatic patients had higher sCD40L levels than healthy controls, which may lead to an increase in cardiovascular diseases. sCD40L may be a more reliable and early predictive marker of cardiovascular events in psoriatic patients. New treatment options that will be developed over sCD40L will benefit in prevention of psoriasis and its cardiovascular comorbidities.

Evaluation of activatory and inhibitory natural killer cell receptors in non-segmental vitiligo: a flow cytometric study

Background  Recent observations established the role of altered cellular immunity and autoimmune hypothesis in the pathogenesis of vitiligo. There have been several reports discussing T‐cell and natural killer (NK) cell populations, but NK cell receptors were not evaluated in vitiligo.

Persistent hoarseness in a patient with pachyonychia congenita: an early sign of laryngeal involvement

A 13-month-old boy, born of a nonconsanguineous marriage, presented with extensor hyperkeratotic papules and subungual hyperkeratosis with yellow–brown discoloration of the nail plate affecting all 20 nails, developing within the first few months of life. Whitish plaques were also observed on the oral mucosa. His mother reported progressive hoarseness, especially on crying. Treatment for onychomycosis and oral candidiasis for 2 months yielded no improvement. Multiple courses of antimicrobials for presumed upper respiratory tract infection did not improve the hoarseness. There were no other known medical problems, and his growth and development were within the normal range. Natal teeth, hair abnormalities, and abnormal dentition were not found. The family history regarding other ectodermal disorders was noncontributory. On physical examination, there was subungual hyperkeratosis and yellow–brown discoloration of all the nails (Fig. 1), symmetric follicular hyperkeratotic papules on the extensor surface of the knees and elbows, and palmar blisters. Intraoral examination showed irregularly shaped whitish plaques on the dorsal tongue, palate, buccal mucosa, and both sides of the labial commissure, together with angular cheilitis (Fig. 2). Sweating was normal. A complete ophthalmologic examination (including pupil dilation) showed normal results. Potassium hydroxide (KOH) examination and fungal culture of scrapings of the nail and from the whitish mucosal plaques yielded negative findings. Laryngeal examination under general anesthesia using an endoscopic video information system revealed a slightly elevated, white, hyperkeratotic plaque of 3–4 mm in diameter that extended from the posterior commissure to the anterior interarytenoid mucosa, and two small whitish clear papules, measuring 1–2 mm in diameter, on the upper part of the left vocal cord (Fig. 3). There was no history of any problems with respiratoryobstruction. The boy was otherwisegenerally healthy with unremarkable findings on systematic examination. The results of laboratory investigation, including 1346 Figure 1 Clinical appearance of hypertrophic nail dystrophy and discoloration of the toenails

A case of cutaneous leishmaniasis presenting as facial cellulitis

Figure 1. (a) Clinical appearance of erythematous lesion resembling cellulitis on the left cheek. (b) Complete healing of the facial lesion after the therapy. Dear Editor, The clinical spectrum of cutaneous leishmaniasis (CL) is very broad. It can represent a diagnostic challenge for physicians when the disease occurs in a nonendemic area where experience is limited. Given the wide variability of clinical findings, it is one of the ‘‘great imitators’’, making it necessary to consider accurate clinical, epidemiological, laboratory and histopathological criteria to make the diagnosis. This report seeks to highlight an unusual case of CL involving the face and mimicking facial cellulitis in an immunocompetent patient living in a non-endemic area. A 66-year-old woman presented to our dermatology department with redness and swelling of the left side of her face, which were reported to have started 6 months prior. The lesion started as a red papule and a few weeks later an asymptomatic swelling appeared at that site and gradually extended. Subjective symptoms, including pruritus, fever and pain, were not reported. The patient was immunocompetent and lived in a non-endemic area. She denied facial trauma, insect bites or traveling to an endemic area for CL. Her personal and family histories were not contributory, either. Due to the suspected diagnosis of facial cellulitis, she had been treated with a variety of antimicrobial agents, such as oral amoxicillinclavulanate, cefuroxime axetil for 7 days, and i.v. broad-spectrum antibiotic for 14 days. However, this treatment had not improved her condition. Dermatological examination revealed a slightly scaly, erythematous, edematous, infiltrated plaque 6 cm · 4 cm in diameter on her left cheek (Fig. 1a). No regional lymph nodes were found. Her general physical and systemic examinations were normal. Results of complete blood counts, erythrocyte sedimentation rate, C-reactive protein, blood biochemis-