Duygu Düşmez

Coexistence of osteopoikilosis and discoid lupus erythematosus: a case report.

Abstract: Osteopoikilosis is an uncommon, benign sclerosing bone dysplasia characterised by typical roentgenographic findings and usually seen in patients with dermatological problems. We report a case of osteopoikilosis and discoid lupus erythematosus presenting with skin and mucosal involvement, an association that has never previously been reported. We also discuss the differential diagnosis and the clinical pathologies accompanying osteopoikilosis in the literature.

Bcl-2, iNOS, p53 and PCNA expression in normal, disordered proliferative, hyperplastic and malignant endometrium

We attempted to determine Bcl‐2, inducible nitric oxide synthase (iNOS), p53 and proliferating cell nuclear antigen (PCNA) expression, and the relationships between them, in endometrioid adenocarcinomas and precursor lesions. Expression of Bcl‐2, iNOS, p53 and PCNA were investigated immunohistochemically in 91 samples from benign (proliferative (pEM), secretory (sEM), disordered proliferative (dEM), inactive/atrophic (aEM), hyperplastic endometrium) and malignant endometrial tissue. Staining scores for Bcl‐2 in the dEM, endometrial hyperplasia (EMH) and endometrioid cancer (ECA) groups were higher than in the pEM group (P = 0.004; P = 0.036 and P = 0.020, respectively). A significant difference in proliferating cell nuclear antigen staining was found between simple and complex EMH samples (P = 0.000). An inverse relationship was found between iNOS and p53 in the hyperplasia group (r = −0.533, P = 0.019). While a significant difference was found in p53 staining in ECA between the pEM, dEM and EMH groups, no such difference was found in iNOS staining. In addition, there was no direct relationship between iNOS and p53 in the ECA group. It was concluded that the interaction between iNOS, p53 and Bcl‐2 in proliferative processes in the development of type 1 endometrioid adenocarcinomas is different from that in tumors originating in other organs.

The early erosive vesicular stage of lipoid proteinosis: clinical and histopathological features

SIR, A 40-year-old man reported the slow progressive appearance, during the previous 6 years, of pruritic erythematous lesions on the trunk, buttock, abdomen, axilla, genital area and forearm (Fig. 1a). Lesions consisted of follicular papules, comedones, milia and cysts. Lesional areas were alopecic (Fig. 1b), and diffuse alopecia was also present on the scalp and beard area, along with comedones and cysts. The patient reported severe skin dryness, especially in the involved areas. No impairment of salivary or lacrimary function was noted. Serological and haematological tests were all normal or negative. Because of the diffuse presence of cysts and comedones, a diagnosis of chloracne had been made in another institution; the clinical diagnosis was confirmed histologically by the presence of infundibular cysts and a granulomatous foreign body reaction to keratin scales. A further biopsy was performed: the most striking histological feature was a lymphocytic infiltrate involving eccrine glands and coils along with a characteristic epithelial hyperplasia (Figs 1c,d). This picture fits perfectly with that reported in the literature as being characteristic of syringolymphoid hyperplasia, also known as syringotropic mycosis fungoides or syringotropic cutaneous T-cell lymphoma (CTCL). The hair follicles were involved by the lymphocytic infiltrate in a manner similar to that of the eccrine glands. Follicles were surrounded by a dense lymphocytic infiltrate, with extensive exocytosis. Occasional Pautrier microabscesses were evident in the follicular sheath. This pattern is that of pilotropic mycosis fungoides, a form of folliculotropic CTCL. Many follicles were entirely trans-

Immunohistological analysis of mast cell numbers in the intratumoral and peritumoral regions of prostate carcinoma compared to benign prostatic hyperplasia.

Recently, some studies reported the presence of mast cells in various malignancies and their role in tumor growth. The aim of the study was to determine the utility of mast cell numbers in evaluating benign and malignant prostate lesions, and to ascertain whether there are variations in the numbers of mast cells with the Gleason grade. The relationship between mast cell numbers and patient age was also investigated. Retrospectively, 104 prostate specimens were examined for the presence of mast cells. The study group consisted of 57 benign prostatic hyperplasias and 47 prostate carcinomas. The paraffin sections were stained with anti-human mast cell tryptase immunohistologically. The numbers of positively staining cells in five high-power fields were counted, and their mean was calculated. There was no relationship found between mast cell numbers and age statistically. The mean mast cell numbers of the intratumoral region were significantly different from those of the peritumoral region (p = 0.0001). While the difference between benign hyperplasia and the intratumoral region was found to be significant (p = 0.0001), no difference between hyperplasia and the peritumoral region was noted (p = 0.762). There was no statistical difference between Gleason score groups (p = 0.452), and there was no interaction between score groups and intraperitumoral regions (p = 0.355).

Case of generalized lichen amyloidosis.

A 23‐year‐old white female patient presented with a 3‐year history of a pruritic rash on the trunk, extensor surfaces of the extremities, back, abdomen, and the glutea. There was no family history of any similar dermatological disease. Dermatological examination revealed generalized rough, mildly keratotic, symmetrical dome‐shaped papules, involving dorsal and extensor surfaces of both the lower and upper extremities, abdomen, back and the glutea ( Fig. 1 ). Physical examination was normal.

Severe erythema nodosum due to Behcet's disease responsive to erythromycin

A patient with severe erythema nodosum due to Behçets disease is reported on here. Erythema nodosum lesions did not respond to classical treatments; however, they cleared after erythromycin treatment, which was prescribed for the treatment of coincidental erythrasma. Erythromycin treatment appears to be an effective treatment option in erythema nodosum. The hypothetical anti‐inflammatory effects of erythromycin, besides its antibiotic properties, are reviewed and discussed to explain such a clinical improvement.

Touch imprint cytology in biopsy of the infertile testis.

OBJECTIVE To identify different cell types in the testis by using touch imprint cytology and to compare the cytologic findings to the histopathologic diagnosis in infertile men. STUDY DESIGN This prospective study used touch imprint preparations and included 20 infertile men. The biopsy material obtained was stained with toluidine blue, May-Grünwald-Giemsa stain and Papanicolaou stain. The cytologic results for oligospermic, normospermic and azospermic men were compared to the specific histopathologic diagnosis. The proportion of spermatogenic versus Sertoli cells was calculated. The scores were compared between three groups based on the results of the histologic biopsy: normal spermatogenesis, hypospermatogenesis and incomplete spermatogenic arrest. RESULTS The mean ratio of the spermatogenic cells versus Sertoli cells was statistically significantly different in the three groups (P < .01). The mean ratio of spermatogenic cells to Sertoli cells was higher in cases with normal spermatogenesis than in cases with hypospermatogenesis and incomplete spermatogenic arrest, revealing a statistical difference (P<.01). This ratio was not statistically significantly different between the hypospermatogenesis and incomplete spermatogenic arrest groups. CONCLUSION A cytologic demonstration of germinal cells by using touch imprint preparations may be a guide for histologic diagnosis.

Sweet's syndrome in a woman with a prothrombin gene (G20210A) mutation.

A 46‐year‐old woman was admitted to our hospital with tender, erythematous plaques on her palms of 1‐year duration ( Fig. 1 ). She had a history of fever and upper respiratory tract infection. On dermatological examination, there were found to be tender erythematous papules and plaques on the palms. Physical examination was normal. Ophthalmologic examination revealed bilateral episcleritis. Laboratory tests showed the following values: white blood cell count, 15,600 cells/µL with 3% band forms, 74% segmented neutrophils, 3% monocytes, and 20% lymphocytes; red blood cell count, 4.53 × 106 cells/µL; hemoglobin, 13.2 g/dL; hematocrit value, 40.9%, and platelet count, 241 × 109 platelets/µL. The erythrocyte sedimentation rate was 52 mm/ h, and the C‐reactive protein level was 38.8 mg/dL. Cultures from blood and throat swabs for bacteria revealed no pathogenic growths. Urinanalysis, liver and kidney function tests were within normal limits. Antinuclear, anti‐DNA, and antiphospholipid antibodies were negative, and total C3 and C4 complement levels were normal. In histopathological examination, large infiltrates of neutrophils and nuclear dust were seen in a diffuse pattern within the edematous dermis. There were scattered neutrophils within the epidermis. The vascular endothelial cells were plump, but there was no fibrin in the wall of the venules ( Figs 2 and 3 ). In addition, there was a heterozygous prothrombin (G20210A) gene mutation in rapid polymerase chain reaction (PCR) analysis. She had no history of venous thrombosis or hematologic disorders. The following coagulation and thrombophilic tests were normal: activated protein C ratio (2.6; normal > 2), protein C (84%; normal: 78–106%), prothrombin time (9.8 s; normal: 7–13 s), activated partial thromboplastin time (29.6 s; normal: 22.6–35.0 s), fibrinogen (312 mg/dL; normal: 146–400 mg/dL), bleeding time (30 s, Duke method), and clotting time (5 min, Lee‐White method). Chest X‐ray, abdominal ultrasound findings and tumor marker levels were normal. Based on clinical, laboratory and histopathological findings a diagnosis of Sweets syndrome associated with prothrombin gene mutation was made. The skin lesions resolved rapidly on treatment with wet compresses of Burrows solution and oral prednisolone (1 mg/kg). The dose of prednisolone was gradually reduced, and was discontinued after 4 weeks.