Intraarticular lesions in calcifying tendinitis: incidence and association with the acromion index

Introduction  

Intraarticular pathologies are a common finding during arthroscopy for rotator cuff lesions. Both rotator cuff tears as well as cartilage lesions have been described as correlating with the acromion index.     

Hyalinizing cholecystitis and associated carcinomas: clinicopathologic analysis of a distinctive variant of cholecystitis with porcelain-like features and accompanying diagnostically challenging carcinomas

We describe a clinicopathologically distinct subtype of cholecystitis, the extensively calcific version of which has been presented in the clinical literature as "porcelain gallbladder (PG)." This cholecystitis, which we propose to refer to as hyalinizing cholecystitis (HC), is characterized by dense, paucicellular hyaline fibrosis transforming the gallbladder (GB) wall into a relatively thin and uniform band. The process diffusely effaces most of the normal structures of GB, and some cases show calcifications. To determine the clinicopathologic associations of HC, we systematically analyzed 4231 cholecystectomies (606 of which had carcinoma) histopathologically, in addition to a targeted search in our databases. Ninety-six cases of HC were identified (1.6% of cholecystectomies). Patients with HC were a decade older than ordinary cholecystitis patients (56 vs. 47; P<0.001), suggesting that HC may be a long-term complication of chronic injury in some patients. Calcifications of variable amounts and degrees were identified in two thirds of the cases. In addition, 10 cases showed diffuse marked calcifications and were considered separately as "complete porcelain" GB. Thirty-eight HC cases had carcinoma with a calculated frequency of 15% and an odds ratio of cancer risk of 4.6. Only 42% of the invasive cases were associated with calcifications; none of the 10 diffusely calcific cases had carcinoma. HC-related carcinomas were challenging diagnostically. They did not form distinct masses or any significant thickening (mean thickness, 2.6 vs. 4.0 mm in ordinary adenocarcinomas; P<0.002). Microscopically, they had widely scattered and bland-appearing glands embedded in the thin band of hyaline stroma of HC, commonly showing a disappearing lining, leaving behind the granular, necrotic intraluminal debris (regression) with or without calcifications, which could be the only sign of cancer in some sections. The morphologic features that allowed the recognition of these glands as malignant included their longitudinal axis parallel to the surface, their irregular contours, clear cytoplasm with distinct borders, nuclear irregularities, and washed-off chromatin. Surface epithelium, if preserved (and it was not in most cases), typically showed carcinoma in situ of either denuding or micropapillary types. HC-associated carcinomas, with a median survival of 7 months, appeared to have a clinical course at least as aggressive as that of regular carcinomas (median survival 12 months; P=0.02). In conclusion, HC is a distinct clinicopathologic entity, which is often associated with carcinoma, and the carcinomas arising from this group are often very subtle and prone to misdiagnosis microscopically. As HC is typically devoid of epithelium, any glandular elements on the wall of HC should be regarded as a suspect for carcinoma. This study also confirms recent findings in the radiology literature-it is not the complete (diffusely calcific) PG that is associated with cancer. Instead, a distinct, histopathologically defined form of cholecystitis, HC with minimal or no calcifications (incomplete PG), is associated with invasive carcinoma. Thus, imaging protocols ought to focus on the correlates of HC rather than fixating on calcifications. Further studies into the pathogenesis of this process and its mechanisms of progression to carcinoma are warranted.     

Is hyperandrogenemia protective for fibrocystic breast disease in PCOS?

The aim of this study is to evaluate the fibrocystic breast disease rates and its association with different clinical, endocrine and metabolic parameters between main polycystic ovary syndrome (PCOS) phenotypes. One hundred thirty two consecutive women were included in the study. Body mass index, serum follicle-stimulating hormone, luteinizing hormone (LH), progesterone, estradiol, testosterone, dehydroepiandrosterone sulphate, fasting glucose, low density lipoprotein (LDL-C), total cholesterol, high density lipoprotein, insulin, insulin sensitivity and fibrocystic breast disease rates were compared among different phenotypes of PCOS. Group 1: Polycystic ovaries (PCO)-anovulation (n = 32), Group 2: Hyperandrogenemia (HA)-anovulation (n = 28), Group 3: HA-PCO (n = 29), Group 4: HA-PCO-anovulation (n = 43). There were statistically significant differences between the different phenotype groups in terms of waist-hip ratio (p = 0.006), serum LDL-C (p = 0.008), LH (p = 0.002), estradiol (p = 0.022), fasting glucose (p = 0.001), progesterone (p = 0.007), free testosterone levels (p < 0.001) and Ferriman-Gallwey (FG) scores (p < 0.001). Different phenotype groups had significantly different fibrocystic breast disease rates. (p = 0.016). Higher free testosterone >3 pg/dl was protective for fibrocystic disease (RR = 0.316, 95:% CI 0.109-0.912, p = 0.033). Higher FG scores were more protective for fibrocystic disease (RR = 0.005, 95:% CI 0.001-0.042, p < 0.001). Group 3 ovulatory PCOS patients with PCO and hyperandrogenemia phenotype had lower risk to develop fibrocystic disease, while higher rates were observed in group 1 anovulatory-normoandrogenemic PCOS patients. Hyperandrogenemia is protective for fibrocystic diseases in PCOS.