Ileum and colon perforation following peritoneal dialysis-related peritonitis and high-dose calcium polystyrene sulfonate

A rare but severe complication, intestinal necrosis, has been reported after sodium polystyrene sulfonate (SPS; Kayexalate) and sorbitol intake. Some case reports described bowel perforation following calcium polystyrene sulfonate (CPS; Kalimate) administration. We report a case of ileum and colon perforation following peritoneal dialysis-related peritonitis and high-dose Kalimate in a 59-year-old female patient. The patient had a history of hypertension, diabetes mellitus, and end-stage renal disease (ESRD). During hospitalization for peritoneal dialysis-related peritonitis, she developed hyperkalemia, and Kalimate was administered orally. However, severe abdominal distension and pain occurred just one day after Kalimate intake. An urgent surgery disclosed several perforations in the ileum and sigmoid colon. Pathology of the resected gut showed transmural necrosis and perforation with basophilic angulated crystals. The patient finally expired during hospitalization due to refractory septic shock

Lack of a Y-Chromosomal Complement in the Majority of Gestational Trophoblastic Neoplasms

Gestational trophoblastic neoplasms (GTNs) are a rare group of neoplastic diseases composed of choriocarcinomas, placental site trophoblastic tumors (PSTTs) and epithelioid trophoblastic tumors (ETTs). Since these tumors are derivatives of fetal trophoblastic tissue, approximately 50% of GTN cases are expected to originate from a male conceptus and carry a Y-chromosomal complement according to a balanced sex ratio. To investigate this hypothesis, we carried out a comprehensive analysis by genotyping a relatively large sample size of 51 GTN cases using three independent sex chromosome genetic markers; Amelogenin, Protein Kinase and Zinc Finger have X and Y homologues that are distinguishable by their PCR product size. We found that all cases contained the X-chromosomal complement while only five (10%) of 51 tumors harbored the Y-chromosomal complement. Specifically, Y-chromosomal signals were detected in one (5%) of 19 choriocarcinomas, one (7%) of 15 PSTTs and three (18%) of 17 ETTs. The histopathological features of those with a Y-chromosome were similar to those without. Our results demonstrate the presence of a Y-chromosomal complement in GTNs, albeit a low 10% of cases. This shortfall of Y-chromosomal complements in GTNs may reinforce the notion that the majority of GTNs are derived from previous molar gestations

Clinicopathological Significance of Loss of ARID1A Immunoreactivity in Ovarian Clear Cell Carcinoma

Recent genome-wide analysis has demonstrated that somatic mutations in ARID1A (BAF250) are the most common molecular genetic changes in ovarian clear cell carcinoma (OCCC). ARID1A mutations, which occur in approximately half of OCCC cases, lead to deletion of the encoded protein and inactivation of the putative tumor suppressor. In this study, we determined the significance of loss of ARID1A immunoreactivity with respect to several clinicopathological features in a total of 149 OCCCs. First, we demonstrated that ARID1A immunohistochemistry showed concordance with the mutational status in 91% of cases with 100% sensitivity and 66% specificity. Specifically, among 12 OCCC cases for which ARIDA mutational status was known, ARIDIA immunoreactivity was undetectable in all 9 cases harboring ARID1A mutations and was undetectable in one of 3 cases with wild-type ARID1A. With respect to the entire cohort, ARID1A immunoreactivity was undetectable in 88 (59%) of 149 OCCCs. There was no significant difference between ARID1A negative and positive cases in terms of histopathologic features, age, clinical stage, or overall survival. In conclusion, this study provides further evidence that mutations in ARID1A resulted in loss of ARID1A protein expression in OCCC, although no significant differences between ARID1A positive and negative cases were observed with respect to any clinicopathological features examined

Expression of Mutant Nuclear Beta-Catenin Correlates with Non-Invasive Hepatocellular Carcinoma, Absence of Portal Vein Spread, and Good Prognosis

beta -catenin has functions both in the cadherin-mediated cell adhesion system and in the signalling pathway that mediates dorsal axis patterning in the embryo; it has been shown to be aberrantly expressed or mutated in diverse types of human tumour, but the biological significance of this remains to be clarified. To elucidate the clinical implications of aberrant beta -catenin expression and the potential differences between mutant and wild-type beta - catenin protein expression in hepatocellular carcinoma (HCC) , the protein expression was analysed by immunohistochemical staining, supplemented by the analysis of gene mutation. Among 372 unifocal primary HCCs, beta -catenin was detected in the tumour cell membrane alone in 272 tumours (group A) and also in the nuclei in 100 (group B), In group A, 148 tumours had decreased beta - catenin expression, but the reduction did not correlate with invasion or prognosis. When compared with group A, however, group B had significantly lower frequencies of hepatitis B surface antigen carrier (p= 0.015), and alpha -fetoprotein elevation (p = 0.0003), but more often had non-invasive HCC (p -catenin expression strongly correlated with mutation of the gene (p -catenin correlated positively with non-invasive (stage 1) tumour and inversely with portal vein tumour thrombi (stage 3 HCC), and had significantly better 5-year survival,p < 0. 001 and p < 0.0003, respectively, These results suggest that beta - catenin mutation plays an important role in the tumourigenesis of a subset of HCC of good prognosis, and that mutant and mild-type nuclear beta - catenin proteins are not functionally equivalent. Copyright (C) 2000 John WileySons, Ltd

Expression of Rsf-1, a Chromatin-Remodeling Gene, in Ovarian and Breast Carcinoma

Rsf-1 protein is a member of a chromatin-remodeling complex that plays an important role in regulating gene expression and cell proliferation. Our previous study showed that Rsf-1 was an amplified gene that participated in the development of ovarian serous carcinoma. To further elucidate the role of Rsf-1 in ovarian cancer, we studied Rsf-1 immunoreactivity in 294 ovarian tumors of various histologic types. Because the Rsf-1 amplicon overlaps an amplified region reported in breast cancer, we included 782 neoplastic and normal breast tissues for comparison. Immunohistochemistry was performed on tissue microarrays using a 4-tiered scoring system. Overexpression of Rsf-1 was defined as a nuclear immunointensity of 3+ to 4+ because of a strong correlation between 3+ and 4+ immunointensity and Rsf-1 gene amplification, based on our previous fluorescence in situ hybridization analysis. Rsf-1 overexpression was observed in 25% of high- grade ovarian serous carcinomas and in only rare cases (<7%) of low-grade ovarian serous, ovarian endometrioid, and invasive breast carcinomas but not in any ovarian serous borderline tumors, ovarian clear cell carcinomas , ovarian mucinous carcinomas, intraductal carcinomas of the breast, and normal ovaries and breast tissues. Thus, overexpression of Rsf-1 was significantly associated with high-grade ovarian serous carcinoma (P < .05 ), as compared with other types of ovarian tumors and breast carcinomas. Our results provide evidence that Rsf-1 expression is primarily confined to high-grade serous carcinoma, the most aggressive ovarian cancer. Because Rsf-1 overexpression occurs in only a small number of breast carcinomas, it is unlikely that Rsf-1 is a critical gene in the development of breast carcinoma. using a 4-tiered scoring system. Overexpression of Rsf-1 was defined as a nuclear immunointensity of 3+ to 4+

Cystic and Adenofibromatous Clear Cell Carcinomas of the Ovary Distinctive Tumors That Differ in Their Pathogenesis and Behavior: A Clinicopothologic Analysis of 122 Cases

Ovarian clear cell carcinomas (CCC) typically present Its large adnexal, stage I tumors and are generally considered highly malignant. They are frequently associated with endometriosis and. less often with clear cell adenofibromas. We hypothesized that CCCs are a heterogeneous group of tumors, some arising from a cyst and others from an adenofibroma. To test this hypothesis, 122 cases of CCC were retrieved from the surgical pathology files of National Taiwan University Hospital (74) The Johns Hopkins Hospital ( 23). and Serei Mikatahara General Hospital (23) (1985 to 2006). Cases were divided into 3 subgroups: (1) cystic. (2) adenofibromatous, and (3) indeterminate. Various features were analyzed including: age, race, laterality, tumor size, architectural pattern ( papillary, tubulo-cystic, solid, mixed patterns). grade, mitotic index, association with endometriosis including atypical endometriosis/ intraepithelial carcinoma, stage and Survival. Nearly 70% of all the patients were diagnosed as stage I. The 2-year and 5-year Survival (all stages) was 78% and 68%, respectively. Striking, clinicopathologic differences were observed between cystic and adenofibromatous CCCs. Cystic CCC was more frequently diagnosed as stage I compared with adenofibromatous CCC (75% vs. 44%). Conversely, adenofibromatous CCCs were diagnosed more often in advanced stages (stages II-IV) compared with cystic CCCs (56% vs. 18% ). Both the cystic adenofibromatous CCC Corms were associated and with endometriosis and atypical endometriosis / intraepithelial Carcinoma. but the frequency was much higher in the cystic group. Specifically, endometriosis was found in 91%, of cystic CCCs and atypical endometriosis/ intraepithelial carcinoma in 62% of these cases, whereas endometriosis was found in 44% of adenofibromatous CCCs and atypical endometriosis/intraepithelial carcinoma in 11% of cases. A predominantly papillary pattern was seen in 47% of cystic CCCs, whereas none of the adenofibromatous carcinomas displayed a predominantly papillary pattern. A more favorable outcome was observed for cystic CCCs compared with adenofibromatous CCCs (all stages) which was accounted for by the high proportion of stage I tumors. The 2-year and 5- year survival For the cystic CCCs was 82% and 77% and for the adenofibromatous CCCs (all stages), 62% and 37% respectively. In summary, Subdividing ovarian CCCs into cystic and adenofibromatous CCC reveals differences in a number of clinicopathologic features including their association with endometriosis, histologic patterns, stage distribution, and clinical behavior. Because there were a relatively small number of adenofibromatous CCCs in this series, additional cases Must he studied to confirm these findings

Cyclin E and P16 Immunoreactivity in Epitheloid Trophoblastic Tumor-an Aid in Differential Diagnosis

Epithelioid trophoblastic tumor (ETT) is a relatively uncommon trophoblastic tumor that can be confused with several trophoblastic and nontrophoblastic lesions, notably the placental site nodule and invasive squamous carcinoma of the cervix. In this report, we analyzed the immunoreactivity of two cell cycle-regulated proteins, cyclin E and p16, in ETTs, placental site nodules and cervical squamous carcinomas to determine whether they are useful in their differential diagnosis. Other trophoblastic lesions were also evaluated. Using an H-score based on both percentage of positively stained cells and immunointensity, we found that ETTs demonstrated a much higher cyclin E staining score than placental site nodules (P40. Only two placental site nodules had scores above the cutoff and both showed morphologic features that placed them in an intermediate position between a typical placental site nodule and an ETT, so-called "atypical PSN." p16 immunoreactivity, was not detected in any of the ETTs and placental site nodules, whereas it was strongly and diffusely positive in the vast majority of cervical squamous carcinomas examined (83/87 cases) (P<0.001). Therefore, cyclin E expression is useful in distinguishing an ETT from a placental site nodule and p 16 expression is useful in distinguishing an ETT from a cervical squamous carcinoma. The majority of other types of trophoblastic lesions showed diffuse and intense nuclear immunoreactivity for cyclin E whereas none were positive for p16. we found that ETTs demonstrated a much higher cyclin E staining score than placental site nodules (P<0.0001)

Hsd3b1 as a Novel Trophoblast-Associated Marker That Assists in the Differential Diagnosis of Trophoblastic Tumors and Tumorlike Lesions

Trophoblastic tumors and tumorlike lesions can be confused with a variety of nontrophoblastic tumors; therefore, a trophoblast-associated marker that is expressed in all types of trophoblastic lesions is useful in differential diagnosis. In this report, we assessed the potential of hydroxyl-[delta]-5-steroid dehydrogenase (HSD3B1), an enzyme that catalyzes the oxidative conversion of [delta]-5-3 [ beta]-hydroxy steroids to the [delta]-4-3-keto configuration and that is involved in steroid hormone synthesis,14 as a diagnostic trophoblastic marker. First, the gene expression profile of HSD3B1 was analyzed in silica using serial analysis of gene expression in the database deposited in the public domain and found that HSD3B1 was not expressed in 159 libraries of breast, lung, colorectal, pancreatic, ovarian carcinomas, and a wide variety of normal adult and fetal tissues. Second, an immunohistochemical analysis was performed using a commercially available anti-HSD3B1 monoclonal antibody on paraffin sections. HSD3B1 immunoreactivity was detected in intermediate trophoblast and syncytiotrophoblast in 21 early placentas, 18 complete hydatidiform moles, 67 trophoblastic tumors, including placental site trophoblastic tumors, epithelioid trophoblastic tumors, and choriocarcinomas, and 28 tumorlike lesions including placental site nodules and exaggerated placental site. HSD3B1 immunoreactivity was diffuse and intense in the majority of trophoblastic lesions with the exception of a few choriocarcinomas. In contrast, only 3 (<1 %) of 319 nontrophoblastic carcinomas from the uterus, lung, and breast reacted with the HSD3B1 antibody. Moreover, the immunoreactivity in these lesions was focal and weak. In conclusion, as compared with other trophoblastic markers, HSD3B1 is highly specific and sensitive, being expressed in all types of trophoblastic lesions but not in a variety of nontrophoblastic tumors of the uterus, lung, and breast