Malignant Bowel Obstruction in Relapsed Ovarian Cancer With Peritoneal Carcinomatosis: An Occlusive State.

OBJECTIVE: The aim of this study was to describe the clinical and oncological outcomes of women with malignant bowel obstruction (MBO) for relapsed ovarian cancer and peritoneal carcinomatosis. METHODS: A retrospective cohort study was performed in all consecutive patients admitted at Instituto Valenciano de Oncología, Valencia, Spain, between July 2013 and July 2016 with MBO for relapsed ovarian cancer and peritoneal carcinomatosis. All patients underwent the same protocol of conservative management. Surgical treatment was indicated only in selected cases. RESULTS: There were a total of 22 patients presenting 59 episodes of MBO; 17 (77.2%) of those patients presented more than 1 episode of MBO. All patients had serous epithelial ovarian cancer; 18 (81.8%) were high grade, and 4 (18.2%) low-grade tumors. The median (range) number of episodes per patient was 3 (range, 1-7) with a mean length of hospitalization of 13 (SD, 13.6) days. The median time interval between episodes of MBO (54 episodes in 17 patients) was 17 days (range, 1-727 days). Twenty of 22 patients died with a median overall survival time from the first episode of MBO of 95 days (95% confidence interval, 49-124 days). CONCLUSIONS: Patients with MBO due to relapsed epithelial ovarian cancer in the peritoneal carcinomatosis setting have a short life expectancy, presenting a median of 3 episodes of MBO until death, with a short time interval between episodes. These findings show that bowel obstruction can represent a constant status over time until death.

Treatment of Inoperable Vulvar Cancer: Where We Come From and Where Are We Going.

Vulvar cancer is a rare disease affecting elderly women that is commonly treated with surgery, radiation, and chemotherapy. When tumors compromise the urethra and the anus, or when it is in the groin lymph nodes, radiotherapy, chemotherapy, or both are necessary after surgery.The treatment of locally advanced vulvar cancer has suffered significant changes though the recent decades. So far, the best sequence of treatment is not known: surgery, chemotherapy, or radiotherapy. The radical surgeries usually need a long recovery term both in the region of the vulva and in the area of the groin lymph nodes. When it is performed, convalescence can delay other treatments, such as radiotherapy and chemotherapy. On the other hand, the use of radiotherapy and chemotherapy as a first step treatment can result in a complete elimination of the disease in at least 30% of the cases or substantial reduction of its size, allowing less extensive surgery. Therefore, the historical evolution of locally advanced vulvar cancer is reviewed.

¿Hiperplasia endometrial atípica o adenocarcinoma de endometrio? Un reto / Atypical endometrial hyperplasia or endometrial adenocarcinoma? A challenge

Objetivo: Conocer la prevalencia de adenocarcinoma de endometrio en pacientes con diagnóstico de hiperplasia endometrial atípica tras biopsia endometrial. Pacientes y métodos: Veinte pacientes con diagnóstico de hiperplasia endometrial atípica tras biopsia endometrial histeroscópica en consulta y/o tras resección endometrial histeroscópica en quirófano. Resultados: Se realizó una histerectomía a 15 pacientes y se encontraron 8 casos de adenocarcinoma de endometrio. Dos pacientes fueron reintervenidas mediante laparoscopia para realizar una linfadenectomía

Objective: To determine the prevalence of endometrial adenocarcinoma in patients with a diagnosis of atypical endometrial hyperplasia after endometrial biopsy. Patients and methods: Twenty patients with a diagnosis of atypical endometrial hyperplasia after endometrial biopsy by means of office hysteroscopy and/or after endometrial resection by means of operative hysteroscopy. Results: Hysterectomy was performed in 15 patients and eight cases of endometrial adenocarcinoma were found. Reintervention was required in two patients, who underwent laparoscopic lymphadenectomy

H63D homozygotes with hyperferritinaemia: Is this genotype, the primary cause of iron overload?

OBJECTIVES: Hereditary haemochromatosis is a disease that affects iron metabolism and leads to iron overload. Homozygosity for the H63D mutation is associated with increased transferrin saturation (TS) and ferritin levels. Our objective was to find out if the homozygosity of H63D mutation was the primary cause of iron overload. PATIENTS AND METHODS: We studied 45 H63D homozygotes (31 males and 14 females) with biochemical iron overload and/or clinical features of haemochromatosis. The simultaneous detection of 18 known HFE, TFR2 and FPN1 mutations and sequencing of the HAMP gene were performed to rule out the possible existence of genetic modifier factors related with iron overload. RESULTS: Values of biochemical iron overload, measured as percentage TS and serum ferritin concentration (SF), in our H63D homozygotes were significantly higher in patients than in controls: TS 55 +/- 15% vs. 35 +/- 15% and SF 764 (645-883) microg/L vs. 115 (108-123) microg/L for patients and controls, respectively. These H63D homozygotes presented extreme hyperferritinaemia and no additional mutations in HFE, TFR2, FPN1 and HAMP genes were detected. CONCLUSIONS: The lack of additional mutations in our H63D homozygotes suggests that this genotype could be the primary cause of iron overload in these patients. Despite our results, we cannot entirely discount the possibility that one or more genetic modifier factor exists, simply because we were unable to find it, although there was a precedent in the HFE gene. Genetic modifier factors have been described for C282Y mutations in the HFE gene, but at the present time they have never been reported in H63D homozygotes.

Frequency of CARD15 polymorphisms in patients with Crohn's disease from Toledo, Spain: genotype-phenotype correlation.

Crohn's disease (CD) presents a complex multifactorial etiology with genetic and environmental factors contributing to the disorder. Epidemiological studies have shown that three major CARD15 polymorphisms, R702W, G908R, and 1007fs, are associated with CD. We studied the frequencies of these three polymorphisms in patients from Toledo, Spain, and compared them with the frequencies found in studies of other populations. A total of 183 patients with CD and 172 healthy controls from Toledo, Spain, were included in this study. All of these individuals were genotyped for the three CARD15 polymorphisms R702W, G908R, and 1007fs. Frequencies were analyzed to identify any genotype-phenotype associations. The control population exhibited frequencies of CARD15 polymorphisms similar to the results of previous studies, 3.4%, 1.1%, and 2.0% for the R702W, G908R, and 1007fs polymorphisms, respectively, whereas CD patients had allele frequencies of 7.6%, 3.0%, and 4.6%, respectively. Significant associations were found between the presence of R702W and patients carrying two susceptibility variants with early age of onset and stricturing pattern.

Frequency of HFE H63D, S65C, and C282Y mutations in patients with iron overload and controls from Toledo, Spain.

Hereditary hemochromatosis (HH) is an autosomal recessive disease caused by a defective iron absorption. C282Y is the most frequent HFE gene mutation causing HH in Northern European populations and their descendants. However, two other mutations, H63D and S65C, have been described as pathogenic changes. In this study, we have tried to evaluate the frequency of these three mutations in our community. Eighty-three patients with clinical and/or biochemical features of hemochromatosis and 150 controls were screened for H63D, S65C, and C282Y mutations using a PCR-restriction fragment length polymorphism (RFLP)-based strategy. In contrast to previous studies, 7% of the patients were homozygous for C282Y mutation. The remaining patients were 20% H63D homozygous, 10% H63D/C282Y compound heterozygous, 1% H63D/S65C compound heterozygous, 22% H63D heterozygous, 2% C282Y heterozygous, 2% S65C heterozygous, and 36% of patients lacked any of the three mutations studied, despite the fact that they showed clinical/biochemical features of hemochromatosis. We observed a high frequency of the H63D mutation in both the control group and patients, whereas the main genotypes implicated in HH in our series were H63D homozygous and H63D/C282Y compound heterozygous. We propose that the H63D mutation be analyzed in HH patients from our geographic area. Moreover, further studies are needed to elucidate the role of this mutation in the development of HH and the genetic, environmental or other factors that affect the genotype-phenotype correlation between H63D and hemochromatosis.