RESUMEN
A too-high gestational weight gain, in combination with steadily increasing obesity rates among women of reproductive age, represents an enormous obstetrical problem, as obesity and high gestational weight gain are associated with enhanced fetal growth, low vital parameters, and increased cesarean section rates. This medical record-based study investigates the association patterns between too-low as well as too-high gestational weight gain, according to the 2009 Institute of Medicine (IOM) guidelines, and fetal growth, as well as birth mode and pregnancy outcome. The data of 11,755 singleton births that had taken place between 2010 and 2020 at the Public Clinic Donaustadt in Vienna, Austria, were analyzed. Birth weight, birth length, head circumference, APGAR scores, and pH values of the arterial umbilical cord blood described fetal growth as well as the vital parameters after birth. Gestational weight gain was classified as too low, recommended, or too high according to the different weight status categories of the IOM guidelines. Birth weight, birth length, and head circumference of the newborn were significantly increased (p < 0.001) among underweight, normal-weight, and overweight women who gained more weight than recommended. Among obese women, only birthweight was significantly (p < 0.001) higher among women who gained more weight than recommended. Furthermore, a too-high gestational weight gain was significantly associated with an increased risk of macrosomia and emergency cesarean sections among underweight, normal-weight, and overweight women, but not among obese ones. Obese and morbidly obese women experiencing excessive gestational weight gain showed no significantly increased risk of macrosomia or emergency cesarean section. However, among obese mothers, a too-low gestational weight gain reduced the risk of emergency cesarean sections significantly (p = 0.010). Consequently, the IOM recommendations for gestational weight gain fit only partly for pregnant women in Austria. In the case of obese and morbidly obese women, new guidelines for optimal pregnancy weight gain should be considered.
Asunto(s)
Ganancia de Peso Gestacional , Obesidad Mórbida , Complicaciones del Embarazo , Recién Nacido , Estados Unidos/epidemiología , Embarazo , Femenino , Humanos , Peso al Nacer , Macrosomía Fetal , Sobrepeso/complicaciones , National Academies of Science, Engineering, and Medicine, U.S., Health and Medicine Division , Cesárea/efectos adversos , Delgadez , Resultado del Embarazo/epidemiología , Aumento de Peso , Desarrollo Fetal , Complicaciones del Embarazo/epidemiología , Índice de Masa Corporal , Factores de RiesgoRESUMEN
Hypothetically, K-ras mutations can be used as a marker of disseminated tumor cells (DTCs) in patients with K-ras mutated primary carcinoma. This study focused on the development of a useful assay for detecting low numbers of DTCs in potential target tissues of metastatic K-ras codon 12 mutated colorectal cancer. Tumor, liver, lymph node and bone marrow tissues from 46 colorectal carcinoma patients were examined for K-ras codon 12 mutations with a new double enriched nested (DEN)-PCR and the incidence of mutations was compared to those obtained from three established assays. DEN-PCR followed by sequencing found one mutated cell within 107 K-ras codon 12 wild-type cells and was more sensitive than other methods (1:106-1:102). Colon carcinomas (26/46) and adenomas (1/3) harbored mutations in K-ras codon 12. Sixteen of these 27 mutated tumors were found with all assays, two with three methods and one with the two most sensitive assays. In 8 cases, only DEN-PCR identified the K-ras mutation, and thus prevailed over the other methods used (p<0.002). Eight of 26 patients with K-ras mutated colorectal carcinoma also harbored K-ras mutated DTCs in liver and lymph nodes, respectively, and 4 in bone marrow. For liver and lymph node samples, DTC-mutations were identical to those in the primary carcinoma but those in bone marrow differed from the respective mutation in the primary carcinoma. In conclusion, DEN-PCR is a highly sensitive method for detecting K-ras mutations as marker of early and late tumor cell dissemination in tissues potentially harboring colorectal carcinoma metastases.
Asunto(s)
Neoplasias Colorrectales/patología , Genes ras/genética , Metástasis de la Neoplasia/diagnóstico , Reacción en Cadena de la Polimerasa , Anciano , Anciano de 80 o más Años , Biomarcadores de Tumor/metabolismo , Línea Celular Tumoral , Femenino , Humanos , Masculino , Persona de Mediana Edad , Mutación , Estadificación de NeoplasiasRESUMEN
The aim of this study was to compare the ratio of K-ras codon 12 and 13 mutations in various tissues of colorectal cancer patients. Multiple samples of inconspicuous mucosa and a sample of carcinoma tissue were taken from 36 colorectal cancer patients (group I) and these results were compared with those from polyp and carcinoma tissues of another 48 colorectal cancer patients (group II). A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to detect the respective point mutations. The results of this assay were complemented by sequencing the K-ras mutations. In mucosa tissue, the ratio of codon 12 and 13 mutations was nearly equal (0.9:1) whereas the respective ratio in tumour tissue showed a strong preponderance of K-ras codon 12 mutations (14:1, p=0.004). In polyp tissue of patients from group II, the ratio was 2.7:1 and that in carcinomas was 19:1 (p=0.053). The prevalence of both types of mutation was 14.6% in all mucosa samples, corresponding to 30.6% of group I patients. The K-ras mutation rate in carcinoma tissue of the same patients was 38.9%. Similarly, 33.4% of all polyp and 41.7% of all carcinoma samples from group II harboured K-ras codon 12 and/or 13 mutations. Sequencing confirmed 59 of 60 K-ras codon 12 mutations, but due to the detection limit for sequencing (1:10(4)) only 10 of 20 K-ras codon 13 mutations were confirmed. It is concluded that after balanced induction K-ras codon 12 mutations increase in frequency relative to K-ras codon 13 mutations during tumour progression.