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Mast Cells and Fibrosis on Testicular Biopsies in Male Infertility

Testicular dysfunction correlates with increased testicular mast cells. Mast cells can activate fibroblasts and promote collagen synthesis. The aim of the study was to examine testicular mast cells containing tryptase, and the relationship between mast cells and different fibrosis stages of interstitium and peritubular region of testes. Testicular biopsies obtained from 33 infertile men were assigned to 2 groups: normal spermatogenesis ( n = 10) and defective spermatogenesis ( n = 23). Total, interstitial, and peritubular mast cells were examined immunohistochemically using antihuman tryptase. The fibrosis stage was evaluated using vimentin and alpha-smooth muscle actin. The ratio of tubules with sclerosis to total tubules was also calculated. In all cases, mast cells were mainly localized in the interstitium. The number of total mast cells was significantly higher in defective spermatogenesis than in normal spermatogenesis ( p =. 048). In both groups, interstitial mast cells were higher than peritubular mast cells. However, the increase in peritubular region was much higher than the increase in interstitium. Total, peritubular, and interstitialmast cell counts were not different from each other, according to the changing fibrosis stages. Total and interstitial mast cells were significantly higher in the cases with sclerosing seminiferous tubules than in the cases with no sclerosis ( p =. 04 and p =. 024, respectively). The mast cells and the mast cell product tryptase could be involved in the etiology of defective spermatogenesis, especially whenever the last stage (tubular hyalinization and sclerosis) takes place.

The changes in expression of ICAM-3, Ki-67, PCNA, and CD31 in psoriatic lesions before and after methotrexate treatment

Although the effectiveness of methotrexate (MTX) in the treatment of psoriasis is very well established, the mechanism of action is poorly understood. It was suggested that the therapeutic effect of MTX in psoriasis might be mediated by inhibition of adhesion molecule expression. The aim of our study was to investigate the different effects of MTX treatment on cell proliferation, inflammatory infiltrate, adhesion molecules, and angiogenesis in psoriasis, and to clarify the mechanism by which MTX exerts its therapeutic effects. Clinical response, the morpho–phenotypic changes, epidermal thickness, and mitosis count were analyzed and the expression of CD31 and ICAM-3, proliferative markers such as Ki-67, PCNA, were evaluated by immunohistochemical techniques in lesional psoriatic epidermis, before and after the treatment with MTX in ten patients. In posttreatment biopsies a decrease in the degree of epidermal hyperplasia and a significant reduction in the severity of the inflammatory infiltrate (P<0.05) were observed. In addition, CD31 and ICAM-3 expression was significantly decreased on dermal cellular infiltrate, (respectively; P<0.05, P<0.01). Ki67 and PCNA expression were suppressed concurrently in about 90% of cases (P<0.01). We suggest that MTX may have an inhibitory effect on an initial integral component of the pathways that lead to psoriasis. Immunopharmacologic intervention in adhesion event has the potential to improve psoriasis. Inhibition of revascularization may be another mechanism of action of MTX.

Neutrophilic dermatosis of the hands (localized Sweet's syndrome) in association with chronic hepatitis C and sarcoidosis

Summary We report a case of recurrent localized Sweets syndrome (SS) with pulmonary sarcoidosis and hepatitis C virus infection. Hepatitis C may be the triggering factor for both Sweets syndrome and sarcoidosis through stimulation of T helper 1 immune responses involved in the pathogenesis of both diseases.

Effects of levosimendan on myocardial ischaemia-reperfusion injury

Background and objective: Levosimendan has a cardioprotective action by inducing coronary vasodilatation and preconditioning by opening KATP channels. The aim of this study was to determine whether levosimendan enhances myocardial damage during hypothermic ischaemia and reperfusion in isolated rat hearts. Methods: Twenty‐one male Wistar rats were divided into three groups. After surgical preparation, coronary circulation was started by retrograde aortic perfusion using Krebs‐Henseleit buffer solution and lasted 15 min. After perfusion Group 1 (control; n = 7) received no further treatment. In Group 2 (non‐treated; n = 7), hearts were arrested with cold cardioplegic solution after perfusion and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. In Group 3 (levosimendan treated; n = 7), levosimendan was added to the buffer solution during perfusion and the hearts were arrested with cold cardioplegic solution and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. At the end of the reperfusion period, the hearts were prepared for biochemical assays and for histological analysis. Results: Tissue malondialdehyde levels were significantly lower in the levosimendan‐treated group than in the non‐treated group (P = 0.019). The tissue Na+‐K+ ATPase activity was significantly decreased in the non‐treated group than in the levosimendan‐treated group (P = 0.027). Tissue myeloperoxidase (MPO) enzyme activity was significantly higher in the non‐treated group than in the levosimendan‐treated group (P = 0.004). Electron microscopic examination of the hearts showed cardiomyocytic degeneration at the myofibril, mitochondria and sarcoplasmic reticulum in both non‐treated and levosimendan‐treated groups. The severity of these findings was more extensive in the non‐treated group. Conclusions: Treatment with levosimendan provided better cardioprotection with cold cardioplegic arrest followed by global hypothermic ischaemia in isolated rat hearts.

The effect of testosterone treatment on prostate histology and apoptosis in men with late-onset hypogonadism.

Abstract Objectives: To investigate the effect of testosterone replacement therapy (TRT) on prostate histology and apoptosis in men with late-onset hypogonadism (LOH). Methods: The study included 25 men, having LOH with prostate-specific antigen (PSA) level of 4 ng/ml or less. All patients underwent transrectal ultrasound guided prostate biopsy at baseline, and received testosterone undecanoate treatment for 1 year. Prostate biopsy was repeated at the end of 1 year of testosterone therapy. In addition to clinical and biochemical parameters, prostate histology and apoptotic index (AI) were compared before and after the TRT. Results: The mean serum total testosterone significantly increased from 178.04 ± 51.92 to 496.28 ± 103.73 ng/dl (p = 0.001). No significant differences were observed in serum total and free PSA level, prostate volume and maximal urinary flow rate. There were also no significant differences in AI, stroma/epithelial cells ratio, Ki-67 positive cells and atrophy score of prostate tissue before and after the TRT. Conclusions: This study demonstrated that TRT did not affect serum PSA level, prostate volume and maximal urinary flow rate. This study also suggests that TRT does not cause the risk for prostate cancer development, because of no significant differences in prostate histology after TRT.

The eclipse naevus and cockade naevus: are they two of a kind?

of excessive fat deposits, and weight loss might also be beneficial. While the genes for congenital generalized lipodystrophy and familial partial lipodystrophy have recently been idendified, the pathogenesis of acquired partial lipodystrophy remains unknown. However, it has been associated with autoimmune diseases, in particular renal disease. Up to one-third develop mesangiocapillary (membranoproliferative) glomerulonephritis, typically years after the onset of the lipodystrophy. Complement anomalies have been implicated in its pathogenesis. Patients commonly have low complement C3 levels and circulating C3 nephritic factor, and in vitro studies have shown C3 nephritic factor to cause lysis of adipose tissue. Other reported associations include systemic lupus erythematosus, dermatomyositis, hypothyroidism and pernicious anaemia, coeliac disease and dermatitis herpetiformis, rheumatoid arthritis, temporal arteritis, leucocytoclastic vasculitis, Raynaud’s phenomenon and cutaneous vasculits, and POEMS syndrome. In most cases the partial lipodystrophy preceded the associated disorder by years. C3 nephritic factor was not detected in the majority of these cases, suggesting another factor responsible for the changes seen in patients with partial lipodystrophy.

Mycobacterium tuberculosis infection within parotid gland Warthin tumor.

Tuberculosis of the parotid gland is extremely unusual. Tuberculosis comprises 2.5% to 10% of parotid gland lesions. Two clinical forms of parotid gland tuberculosis infection exist. One is a diffuse parenchymatous disease (either primary or secondary to nodal disease), resembling common infection. The second is a chronic, slow-growing, painless, and firm parotid mass mimicking a neoplasm. Most of these patients were diagnosed after parotid gland surgery and histopathologic evaluation. Warthin tumor is a well-known benign neoplasm of the salivary glands. It is the second most common tumor of the parotid gland. Mycobacterium tuberculosis within Warthin tumor is also unusual. Five cases with parotid gland tuberculosis within Warthin tumor were reported in the literature. In this report, we present a new patient with parotid gland tuberculosis within the Warthin tumor. This type parotid gland pathology is an extremely rare entity, and to the best of our knowledge, this is the second documented case using polymerase chain reaction. We also discussed the possible mechanisms of development of infection within Warthin tumor.

Isolated lip involvement in psoriasis

A 22-year-old woman presented with a 5-year history of scaling and cracking of the lips. The lesions involved both lips completely, but the surrounding skin remained uninvolved during this period and she had no skin lesions. She complained of a burning sensation on her lips and severe discomfort during eating and speaking. She had been prescribed various medications including emollient creams and topical steroids, with no effective improvement and short remission time. Dermatological examination revealed diffuse mild erythema, adherent silvery scales and fissuring on both upper and lower lips, with minimal extension over the vermilion border (Fig. 1). The remaining oral mucosa and surrounding skin appeared normal. She had no psoriatic or any other skin lesions, and was otherwise in good general health. Routine laboratory examinations were normal. There was no personal or family history of psoriasis or any other dermatological conditions, and no history of smoking. Because of the chronic nature of the lesions and failure of multiple therapies, an incisional biopsy was taken from the lower lip. On histological examination, lamellar hyperkeratosis, parakeratosis and squamous epithelium with psoriasiform hyperplastic rete pattern, and intracorneal pustules consistent with psoriasiform dermatitis were detected. Periodic-acid–Schiff stain for fungal hyphae was negative. Based on these findings and the clinicopathological correlation, a diagnosis of isolated lip psoriasis was made. An emollient cream and a mometasone furoate 0.1% ointment once a day were prescribed and the patient followed up at 2-weeks intervals. The lesions had cleared by the end of the second week and topical steroid treatment was stopped. Two months later, the patient presented with typical psoriatic skin lesions on her palms and soles. The results of the histopathological examination of the skin biopsy taken from the right palm were consistent with psoriasis. Psoriasis rarely involves the oral mucosa and is usually associated with cutaneous lesions. Oral lesions may present on the buccal mucosa, tongue, gingiva, palate, and very rarely the lips and ⁄ or perioral area. Because neither the clinical nor the histological changes are absolutely specific for psoriasis, particularly if cutaneous lesions are absent, diagnosis is difficult. Moreover, the existence of true psoriatic lesions of the oral mucosa is disputed. However, there is some agreement that oral psoriasis, although rare, does occur and the diagnosis is best made when the clinical course of the oral lesions parallels that of skin lesions and is supported by histological examination. Some additional criteria for the diagnosis of oral psoriasis such as a positive family history and human leucocyte antigen (HLA) typing have also been considered important in supporting a diagnosis of oral psoriasis. In our case, oral biopsy showed a psoriasiform pattern. Additionally, some features such as the chronicity and clinical appearance of the lesions characterized by silvery scales also suggested a diagnosis of isolated lip psoriasis. Weighing against this diagnosis were the absence of skin lesions, lack of a family history of psoriasis and the absence of HLA typing. Thus, although some criteria for the diagnosis of mucosal psoriasis have been suggested, diagnosis of isolated lip psoriasis was made only by the histopathological and clinical findings in our case. However, 2 months after the diagnosis, appearance of skin lesions with typical clinical and histopathological features of psoriasis confirmed the initial diagnosis. Lip psoriasis can be clinically confused with chelitis, chronic eczema, actinic dermatitis, chronic candidiasis and leucoplakia. In our case, these were not supported histologically. Most cases of oral psoriasis reported in the literature have been associated with skin disease and ⁄ or intraoral Figure 1 Mild erythema, adherent silvery scales and fissuring on lips. Viewpoints in dermatology • Correspondence

Familial eruptive dermatofibromas in atopic dermatitis

Multiple eruptive dermatofibromas (MEDF) are rare and their aetiology is unknown. More than half of the patients with MEDF have underlying diseases, and more than 80% of the underlying diseases are immune mediated. Familial cases suggesting a genetic cause have also been reported. We report a case of familial eruptive dermatofibromas associated with atopic dermatitis, possibly caused by both hereditary factors and compromised immunity.

Peripheral giant cell granuloma of the mandibular condyle presenting as a preauricular mass

Preauricular mass is a common symptom for patients presenting to the otorhinolaryngologist with parotid disease. Some rare extraparotid lesions, originating from the temporomandibular joint and the mandible itself, also share the same localization and therefore are to be taken into consideration for the differential diagnosis with parotid lesions. Giant cell granuloma (GCG) was first described by Jaffe in 1953. Peripheral GCG (PGCG) is an exophytic soft tissue lesion originating from the periodontal ligament and periosteum. It is located only within the oral cavity. Central GCG (CGCG) is an uncommon benign fibro-osseous lesion generally presenting as an expansible mass with cortical bone defect. It is generally located in the mandible. The brown tumor of hyperparathyroidism and giant cell tumor must be ruled out because of the microscopic similarities of these lesions. The first case of PGCG of the mandible condyle is presented, and attention is drawn to mandibular diseases for the differential diagnosis of the preauricular mass.