Oya Nermin Sivrikoz

Diagnostic value of susceptibility-weighted imaging of abdominal wall endometriomas during the cyclic menstrual changes: a preliminary study.

OBJECTIVE The purpose of this study is to investigate the value of susceptibility-weighted imaging (SWI) for the evaluation of cyclic morphological and hemorrhagic changes in abdominal wall endometriomas (AWE). MATERIALS AND METHODS Fourteen patients with a total of 17 lesions who were admitted with complaints of abdominal wall mass and cyclic pain were evaluated by MRI. Patients were scanned during the first three days of the menstrual cycle and during the mid-cycle phase (day 13-15). In addition to conventional images SWI was performed. The signal changes within the lesions on SWI were compared and graded on both studies. RESULTS There was no significant difference in the size of the lesions in the early days of the menstruation compared to the mid-menstrual period. The SWI taken on mid-cycle phase showed that the center was hyperintense and the peripheral zone was hypointense in all lesions. A signal void related to increased blood and the shrinkage of complete disappearance of hyperintensity in the venter of the lesion was seen 15 (88%) of the 17 cases on the SWI series performed during the menstrual phase scan. CONCLUSION SWI is a sensitive technique and has the capability to show hemorrhage and deposition of hemosiderin within the lesions. For patients suspected with AWE, valuable diagnostic findings may be obtained if the MRI examination including SWI is performed during the early and mid phase menstrual cycle.

Sirenomelia: a review of embryogenic theories and discussion of the differences from caudal regression syndrome

Abstract Objective: To discuss the pathological features of sirenomelia in the light of our 10 cases and review the current theories. Methods: We identified 10 patients with sirenomelia from our hospital database. All clinical details and the autopsy features of 10 cases were noted. Results: Of the 10 children with sirenomelia seven had bilateral renal agenesis, three had bladder agenesis and one had a renal hypoplasia. Single umbilical artery was found in 60% of children with sirenomelia. External genitalia was ambiguous in seven of 10 patients. Conclusions: Even though the etiology of caudal regression syndrome (CRS) and sirenomelia remains unknown we tend to believe that sirenomelia and CRS might be different entities.

The Role of Parafibromin, Galectin-3, HBME-1, and Ki-67 in the Differential Diagnosis of Parathyroid Tumors

OBJECTIVES Parathyroid carcinoma (PC) is a rare parathyroid tumor compared to parathyroid adenoma (PA) and atypical parathyroid adenoma (APA). Recent studies have suggested parafibromin has a role in the differential diagnosis of parathyroid tumors. We sought to determine the role of parafibromin as well as galectin-3, Ki-67, and HBME-1 as diagnostic markers in the differential diagnosis of parathyroid tumors. METHODS A total of 92 cases diagnosed with PA, APA, or PC at Sifa University and Private Ege Pathology Laboratory between 2006-2012 were included in the study. Parafibromin (microarray), galectin-3, Ki-67, and HBME-1 were evaluated using immunohistochemistry in all parathyroid tumors. RESULTS Eighty-four cases were diagnosed with PA, six with APA, and two with PC. The study group consisted of 82 females and 10 males. Their mean age was 50.9 years, and the mean tumor diameter was 1.97 cm. Parafibromin was negative in the two PC cases but positive in all APA and PA cases. Positivity was observed with galectin-3 in 17 adenoma cases, three atypical adenomas, and two carcinoma cases. Positivity with HBME-1 was found in 26 PA cases and one PC case. Parafibromin and galectin-3 expression was significant between the three tumor groups but not for HBME-1 expression. Parafibromin expression increased in PA whereas galectin-3 expression decreased. A statistical significance was found between the three tumor groups according to the Ki-67 score (p=0.010). Additionally, the Ki-67 proliferation index was under 1% in PAs. CONCLUSION The number of PCs in our series was small so our data mostly reflects the immunohistochemical characteristics of PAs. Parafibromin expression, galectin-3 negativity, and a Ki-67 proliferation index under 1% were estimated as beneficial in the differential diagnosis of difficult parathyroid tumors.

Comparison between resveratrol and cabergoline in preventing ovarian hyperstimulation syndrome in a rat model.

Abstract Objective: The aim of this study is to investigate the effects of resveratrol in a rat model of ovarian hyperstimulation syndrome (OHSS) and compare with cabergoline. Design: Randomized controlled, animal study. Animal(s): Female Wistar rats. Material and methods: A rat OHSS model was used to investigate the effects of resveratrol compare with cabergoline administration for preventing OHSS. Body weight, ovary weight, diameter, vascular permeability (VP), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2) expression (immunohistochemistry), and serum estradiol (E2) levels were then compared. Results: The ovarian VEGF concentration was significantly increased in the OHSS Groups (Groups 3–5) compared with the control groups (1 and 2). But vascular permeability, VEGF, and COX-2 expressions were reduced in animals treated with the resveratrol group compared with the cabergoline group (group 5) and the severe OHSS (group 3) group. Blood E2 levels were decreased in group treated with the resveratrol group compared with the cabergoline group (group 5) and severe the OHSS (group 3) group. Conclusion(s): Our results in a rat model suggest that resveratrol has a beneficial effect on OHSS by reducing the increases in ovarian daimeter, VP, and VEGF expression associated with OHSS. These effects may be mediated by the COX-2 inhibitory capacity of resveratrol.

Synchronous Primary Endometrial Carcinoma and Metastatic Malignant Melanoma in an Ovarian Cystic Teratoma.

Abstract Malignant transformation of a benign cystic teratoma of the ovary is only rarely seen. A review of the English literature revealed no reports of a malignant melanoma developing from concurrent primary endometrial carcinoma and ovarian cystic teratoma. We report herein a 54-year-old nulliparous woman who underwent total abdominal hysterectomy and bilateral salpingo-oophorectomy for a pelvic mass and was diagnosed by histopathological examination to have a malignant melanoma developing from concurrent primary endometrial carcinoma and ovarian cystic teratoma. No foci of primary malignant melanoma except for the ovary were found upon clinical examination. The patient received postoperative interferon alpha 2B and radiotherapy. She was still asymptomatic at 12 months of follow-up Öz Overin benign kistik teratomunun malign transformasyonu oldukca nadirdir. İngiliz literaturunun gozden gecirilmesinde eş zamanlı primer endometrial karsinom ve overde kistik teratomda gelişen malign melanom olgusuna rastlanmamıştır. Burada 54 yaşında doğum yapmamış, total abdominal histerektomi ve bilateral salpingo ooferektomi sonrasında primer endometrial karsinom ve ovaryan kistik teratomda gelişen malign melanom tanısı alan bir olgu sunuyoruz. Klinik muayenede over dışında melanom saptanmadı. Hasta operasyon sonrası interferon-alpha (IFN-α) 2B ve radyoterapi tedavisi aldı. Tedavi sonrası 12 ay boyunca izlenen hasta asemptomatiktir.

The Influence of Chemokine CXCR4 and Cyclooxygenase-2 in the Recurrence of Pterygium

ABSTRACT Purpose: To investigate the role of CXCR4 and cyclooxygenase-2 in pterygium recurrence. Methods: A total of 18 primary and 9 recurrent pterygium samples were analyzed. Immunohistochemical staining using primary antibodies against cyclooxygenase-2 and CXCR4 was performed. The cyclooxygenase-2 and CXCR4 expressing cells were calculated separately on the epithelium and stroma. In addition, a correlation between the area of pterygium and CXCR4 and cyclooxygenase-2 levels was investigated. Results: In the primary pterygium group, cyclooxygenase-2 staining was more intense in the epithelium and more dominant in the stroma of the recurrence samples. The CXCR4 expression was more intense in the stroma of both groups. The highest CXCR4 expression was observed in the recurrent pterygium group. There was a strong correlation between the area of pterygium and CXCR4 and cyclooxygenase-2 of stroma. Conclusions: CXCR4 and cyclooxygenase-2 may play an important role in the recurrence of pterygium.

Chemokine CXCR-4 and cyclooxygenase-2 in the pathogenesis of pterygium

Background/aim: This study aimed to investigate the expression of chemokine receptor 4 (CXCR-4) and cyclooxygenase-2 (COX-2) in the epithelium and stroma of pterygium tissue in comparison with healthy conjunctiva. Materials and methods: The expression of CXCR4 and COX-2 was investigated by immunohistochemistry in the epithelium and stroma of the pterygium tissue of 29 eyes and compared with healthy conjunctival tissues. The correlation between CXCR4 and COX-2 expression as well as the correlation of these markers with the area of pterygium were evaluated statistically. Results: COX-2 staining scores were 1.75 ± 0.63 in the epithelium and 1.20 ± 0.62 in the stroma of the pterygium tissue. Mean CXCR-4 staining in the epithelium was 0.069 ± 0.37, whereas it was 5.0 ± 2.84 cells in the stroma. There was almost no staining of COX-2 and CXCR4 in the control samples. There was a strong positive correlation between the expression of CXCR-4 and COX-2 in the stroma of the pterygium. Conclusion: CXCR-4 and COX-2 may play important roles in the pathogenesis of pterygium.

Multiple pilar sheath acanthomas on the scrotal region

Turkderm-Turk Arch Dermatol Venereolgy 2017;51:18-20

Sweet's syndrome exhibiting the Koebner phenomenon at the site of dermatofibroma

Sweet′s syndrome (SS), also known as acute febrile neutrophilic dermatosis, is characterized by fever, neutrophilia, and inflammatory skin lesions. SS can be associated with several conditions, such as infections, malignancy, autoimmune disease, vaccination, pregnancy, and drug exposure. We present a woman with SS; skin lesions developed at the site of dermatofibroma and scratched area. To the best of our knowledge, this is the first case of SS developed at the site of dermatofibroma.

Basaloid follicular hamartoma on the upper eyelid

Basaloid follicular hamartoma (BFH) is a benign rare neoplasm of the hair follicles whose clinical and histological appearance is very similar to basal cell carcinoma. Although these hamartomas are considered to be benign lesions, malignant differentiations have been reported. It may be generalized or localized, familial or sporadic, and BFH can be accompanied by systemic diseases. Although there are many clinical forms of BFH, they all have the same histopathological features. Basaloid follicular hamartoma is a folliculocentric tumor limited to the superficial dermis. Involvement of the deep reticular dermis or soft tissue is not seen in BFH [1]. We present a 52-year-old man with a solitary, hyperpigmented, asymptomatic, slow growing skin tumor on his left upper eyelid. A 52-year-old man presented with a slowly developing asymptomatic left upper eyelid lesion (over 4 years). Dermatological examination showed a solitary, smooth surfaced, hyperpigmented nodule measuring 1 cm in diameter (Figure 1), and there were no other similar skin lesions or significant internal diseases exhibited. He had no family history of similar lesions. The lesion was locally excised, and the specimen was grossly measured to be 1.2 × 0.7 × 0.2 cm. Figure 1 A solitary, smooth surfaced, hyperpigmented 1 cm nodule is located on the left upper eyelid of a 52-year-old man Low-power light microscopy revealed a well-circumscribed and completely removed lesion in the dermis, without connections to the epidermis (Figure 2). Microscopically, the tumor revealed strands and cords of small basaloid cells emanating from the infundibular portion of the hair follicle. The tumor stroma was scant and mildly fibrocellular. There was no nuclear pleomorphism, mitotic activity, apoptotic cells, or cleft formation between the tumor and the stroma (Figure 3), and upon immunohistochemical examination, Bcl-2 stained only in the outermost basal cells (Figure 4). Cd34 was positively stained in the peritumoral stroma and blood vessels (Figure 5), and CD10 was stained in the peritumoral stroma as well as the matrical cells (Figure 6). Figure 2 Low-power light microscopy revealed a well-circumscribed and completely removed lesion in the dermis, without connections to the epidermis (hematoxylin-eosin, original magnification at 40×) Figure 3 A biopsy specimen with basaloid follicular hamartoma shows strands and cords of small, basaloid cells emanating from the infundibular portion of the hair follicle. The tumor stroma was scant and mildly fibrocellular. There was no nuclear pleomorphism, ... Figure 4 Bcl-2 stains only the outermost basal cells in BFH (Bcl-2, 100×) Figure 5 CD34 is positive in the peritumoral stroma and blood vessels (CD34 100×) Figure 6 CD10 stains the peritumoral stroma of BFH, as well as the matrical cells (CD10 100×) Basaloid follicular hamartoma was first described in 1969 by Brown et al. as “generalized hair follicle hamartoma” with associated alopecia, aminoaciduria, and myasthenia gravis [2]. The term “basaloid follicular hamartoma” was first used for a patient who had a localized and solitary type of the lesion, without associated abnormalities, by Mehregan and Baker in 1985 [3]. Morohashi et al. described BFH as an abortive growth of secondary hair germs with a limited differentiation toward the upper follicular portion of the hair shaft [4]. Basaloid follicular hamartoma may manifest with different clinical presentations, such as a solitary lesion, or as multiple lesions with a generalized or localized distribution. Basaloid follicular hamartoma may present as individual or linearly distributed, small, skin-colored to brown papules or plaques, or as multiple lesions in a generalized distribution on the face, scalp, and occasionally, the trunk. Basaloid follicular hamartoma may be a familial, congenital, or acquired condition. Several forms of generalized BFH have been described: (1) sporadic form, multiple BFH without systemic disease; (2) generalized acquired form, female patients with generalized BFHs associated with alopecia and autoimmune diseases, such as myasthenia gravis or systemic lupus erythematosus, in which the lesions are found mainly on the face and periorificial areas; (3) generalized familial form, an autosomal dominant disease that may or may not be associated with hypotrichosis, hypohidrosis, and palmoplantar pitting, which appears on the face and genital region; (4) generalized congenital form, generalized BFH associated with other ectodermal defects, such as hypotrichosis and punctate keratotic pits, on the palms and soles and with cystic fibrosis [1]. The localized forms of BFH present as linear unilateral lesions or as plaques with alopecia [3–6]. The linear unilateral type of BFH is associated with lines of Blaschko and presents at birth or appears in early childhood [3, 5, 6]. Solitary BFH was first described in 1992 as a smooth plaque or a papule appearing most commonly on the face or scalp [7]. The pathogenesis of BFH has been linked to a mutation in the PTCH (patched) gene on chromosome band 9q23. However, this mutation is thought to be less severe than the PTCH gene mutation demonstrated in nevoid basal cell carcinoma syndrome (NBCS) [8–10]. The clinical differential diagnosis for BFH depends on its presentation. The most common misdiagnoses for individual lesions include basal carcinoma (BCC), intradermal melanocytic nevus, seborrheic keratosis, sebaceous hyperplasia, syringoma, angiofibroma, trichilemmoma, steatocystoma, trichoepithelioma (TE), basal cell hamartoma with follicular differentiation, and hamartoma of the sebaceous follicles. When presenting as a plaque, nevus sebaceous, lupus erythematosus, and sarcoidosis should be considered. Basaloid follicular hamartoma in a linear distribution may mimic linear epidermal nevus, lichen striatus, linear morphea, and basal cell nevus. The differential diagnosis of generalized BFH could include generalized follicular hamartoma syndrome, tuberous sclerosis, Cowden disease, multiple trichoepitheliomas, nevoid basal cell nevus syndrome, Rombo syndrome, and multiple tumors of the follicular infundibulum [11]. Basaloid follicular hamartoma is often misdiagnosed as trichoepithelioma or basal cell carcinoma, histopathologically [1]. Specifically, BFH consists of malformed and distorted hair follicles composed of cords and strands of basaloid cells. These cells are arranged in a radial, anastomosing fashion and may arise from the follicles and/or show an epidermal attachment. The tumor cells are bland, without nuclear pleomorphism, and mitotic activity is rare or absent, with little to no single cell necrosis. While the presence of peripheral palisading has been reported, this feature is typically lacking to the degree seen in BCC. The stroma is scant or absent, and when present, consists of eosinophilic compact collagen with no fibrocytes. Clefts within the fibrous stroma have been reported, and minimal clefting between the tumor and stroma has been observed, but it is not a well-accepted feature of BFH. Mucinous ground substance, if present, is usually subtle; furthermore, BCC displays a variety of histological patterns. The neoplastic cells may involve and destroy preexisting hair follicles and the interfollicular dermis, and sometimes, infiltrate the deeper dermis, subcutaneous fat, and skeletal muscle [12]. Differentiating BFH from BCC can be the most difficult aspect of the diagnosis, and additional immunohistochemical stains may help to separate BFH from BCC. Ki-67 (a proliferative marker associated with mitosis) and Bcl-2 staining are more prominent in BCC than in BFH. Bcl-2 stains only the outermost basal cells in BFH. CD 34 is an intercellular adhesion protein and cell surface glycoprotein; the ligand is CD62L (L-selectin). It is also called hematopoietic progenitor cell antigen and is a commonly used marker of hematopoietic progenitor cells and endothelial cells. CD34 also stains stromal cells and dendritic cells. In differential diagnosis it is important that the stromal cells of the BFH stain positive for CD34, but the stromal cells of BCC are negative [1, 12]. Although in BCC the stromal and tumor cells stain with CD10, in BFH, the peritumoral stroma and matrical cells stain with CD10 [13]. Histologically, TE has distinct islands of basaloid cells in a lacelike or adenoidal network and, occasionally, as solid aggregates; additionally, they exhibit a more nodular growth pattern than BFH. The tumor islands show peripheral palisading as in BCC; however, the stroma lacks the retraction artifact seen in BCC. In TE, the fibrocystic stroma is more prominent than in BFH, and it predominates over the epithelial portion. Additionally, in TE, normal follicular bulbs and papillae are seen [11]. While both BFH and TE have keratin cysts consisting of a fully keratinized center, surrounded by basophilic cells without high-grade atypia and mitoses, they are more prominent in TE. We report a case of solitary BFH that developed on the left upper eyelid of a man. Since only a few cases have been reported, presenting case reports will increase awareness of this disorder. Although BFH is a benign rare neoplasm of the hair follicles, it is important to differentiate it due to the malignancy risk and similar characteristics to other benign tumors.