Suicide after colorectal cancer-a national population-based study.

AIM: A cancer diagnosis is often associated with physical as well as emotional distress. Previous studies indicate a higher risk for suicide in patients diagnosed with cancer. The aim of this study was to investigate the prevalence of death by suicide in a national cohort of patients with newly diagnosed colorectal cancer compared with a matched control group to determine if patients with colorectal cancer had an increased incidence of death by suicide. METHOD: This national Swedish cohort was retrieved from the register-based research database CRCBaSe, which includes all patients diagnosed with colorectal cancer between 1997-2006 (rectal) and 2008-2016 (colon) and six controls for each patient matched by age, sex, and county. Cause specific mortality due to suicide was modelled using Cox proportional hazards model and adjusted for known risk factors. RESULTS: The main analysis included patients operated for colorectal cancer, 55 578 patients compared with 307 888 controls. The first year after diagnosis the hazard ratio (HR) for suicide among patients operated for colorectal cancer was 1.86 (CI: 1.18-2.95) compared to controls. Suicide was more common among men than women (HR 2.08; 1.26-3.42 vs. 1.09; 0.32-3.75). A subgroup analysis of the 9198 patients who did not undergo surgery after diagnoses found a seven-fold increase of suicide (HR 7.03; 3.10-15.91). CONCLUSION: Suicide after surgery for colorectal cancer was almost twice as high as in the control group, mainly driven by excess mortality among men. Although the cases were few in the subgroup of nonoperated patients, the considerably higher risk of suicide indicates that more resources might be needed in this group. Evaluation of risk factors for suicide among patients with colorectal cancer should be performed for early identification of individuals at risk.

Sonographic postpartum anal sphincter defects and the association with pelvic floor pain and dyspareunia.

INTRODUCTION: Pelvic floor pain and dyspareunia are both important entities of postpartum pelvic pain, often concomitant and associated with perineal tears during vaginal delivery. The association between postpartum sonographic anal sphincter defects, pelvic floor pain, and dyspareunia has not been fully established. We aimed to determine the prevalence of postpartum anal sphincter defects using three-dimensional endoanal ultrasonography (3D-EAUS) and evaluate their association with symptoms of pelvic floor pain and dyspareunia. MATERIAL AND METHODS: This prospective cohort study followed 239 primiparas from birth to 12 months post delivery. Anal sphincters were assessed with 3D-EAUS 3 months postpartum, and self-reported pelvic floor function data were obtained using a web-based questionnaire distributed 1 year after delivery. Descriptive statistics were compared between the patients with and without sonographic defects, and the association between sonographic sphincter defects and outcomes were analyzed using logistic regression. RESULTS: At 3 months postpartum, 48/239 (20%) patients had anal sphincter defects on 3D-EAUS, of which 43 (18%) were not clinically diagnosed with obstetric anal sphincter injury at the time of delivery. Patients with sonographic defects had higher fetal weight than those without defects, and a perineum <2 cm before the suture was a risk factor for defects (odds ratio [OR], 6.9). Patients with sonographic defects had a higher frequency of dyspareunia (OR, 2.4), and pelvic floor pain (OR, 2.3) than those without defects. CONCLUSIONS: Our results suggest an association between postpartum sonographic anal sphincter defects, pelvic floor pain, and dyspareunia. A perineal height <2 cm, measured by bidigital palpation immediately postdelivery, was a risk factor for sonographic anal sphincter defect. We suggest offering pelvic floor sonography around 3 months postpartum to high- risk women to optimize diagnosis and treatment of perineal tears and include perineum <2 cm prior to primary repair as a proposed indication for postpartum follow-up sonography.

Use of endoanal ultrasound in detecting obstetric anal sphincter injury immediately after birth.

INTRODUCTION: Obstetric anal sphincter injury (OASI) complicates around 5% of deliveries in primiparas. The study objective was to assess the utility of three-dimensional endoanal ultrasonography (3D-EAUS) in the diagnosis of OASI. MATERIAL AND METHODS: The present study was designed to mirror screening settings with an unselected cohort of nulliparous women. All enrolled patients underwent clinical examination of the perineum by the caregiver, and 3D-EAUS was conducted. Post-processing of ultrasonography volume data was performed by an experienced colorectal surgeon who was blinded to all other data. The sensitivity, specificity, negative predictive value, and positive predictive value of 3D-EAUS in the diagnosis of OASI was evaluated. The trial is registered at ISCRTN: 18006769. RESULTS: A total of 680 scans were performed, of which 18.5% were judged as "non-assessable", resulting in 554 assessable recordings. Sphincter defects were observed in 12.8% of all assessable recordings on 3D-EAUS (n = 71). With clinical examination set as the reference standard, ultrasound sensitivity in the diagnosis of OASI was 30.4%, whereas its specificity was 87.9%. The negative predictive value was 96.7% and the positive predictive value was only 9.9%. Comments were left on 175 examinations, of which 74% referred to the management of the examination. CONCLUSIONS: Using 3D-EAUS in a maternity ward is demanding because staff generally have little experience in endoanal ultrasound, which contributes to difficulties in obtaining good image quality. When 3D-EAUS is performed to mirror screening settings, it adds no convincing diagnostic power to clinical examination in the diagnosis of OASI.

Anal incontinence after caesarean and vaginal delivery in Sweden: a national population-based study.

BACKGROUND: Elective caesarean delivery is increasing rapidly in many countries, and one of the reasons might be that caesarean delivery is widely believed to protect against pelvic floor disorders, including anal incontinence. Previous studies on this issue have been small and with conflicting results. The aim of present study was to compare the risk of developing anal incontinence in women who had a caesarean delivery, in those who had a vaginal delivery, and in two age-matched control groups (nulliparous women and men). METHODS: In this observational population-based study, we included all women in the Swedish Medical Birth Register who gave birth by caesarean delivery or vaginal delivery during 1973-2015 in Sweden and were diagnosed with anal incontinence according to ICD 8-10 in the Swedish National Patient Register during 2001-15. Exclusion criteria were multiple birth delivery, mixed vaginal and caesarean delivery, and four or more deliveries. We compared the diagnosis of anal incontinence between women previously delivered solely by caesarean delivery and those who solely had delivered vaginally. We also compared it with two age-matched control groups of nulliparous women and men from the Swedish Total Population Register. Finally, we analysed risk factors for anal incontinence in the caesarean delivery and vaginal delivery groups. FINDINGS: 3 755 110 individuals were included in the study. Between 1973 and 2015, 185 219 women had a caesarean delivery only and 1 400 935 delivered vaginally only. 416 (0·22 %) of the 185 219 women in the caesarean delivery group were diagnosed with anal incontinence compared with 5171 (0·37%) of 1 400 935 women in the vaginal delivery group. The odds ratio (OR) for being diagnosed with anal incontinence after vaginal delivery compared with caesarean delivery was 1·65 (95% CI 1·49-1·82; p<0·0001). When the combination vaginal delivery and caesarean delivery was compared with the nulliparous control group, the OR of being diagnosed with anal incontinence was 2·05 (1·92-2·19; p<0·0001). For the nulliparous women compared with men, the OR for anal incontinence was 1·89 (1·75-2·05; p<0·0001). The strongest risk factors for anal incontinence after vaginal delivery were high maternal age, high birthweight of the child, and instrumental delivery. The only risk factor for anal incontinence after caesarean delivery was maternal age. INTERPRETATION: The risk of developing anal incontinence increases after pregnancy and delivery. Women with known risk factors for anal incontinence should perhaps be offered a more qualified post-partum examination to enable early intervention in case of injury. Further knowledge for optimal management are needed. FUNDING: County Council of Jämtland.

Cardiovascular complications following cesarean section and vaginal delivery: a national population-based study.

INTRODUCTION: Rates of cesarean section are rising in both developed and developing countries and while pregnancy and cesarean section are established as risk factors for thromboembolism and stroke, large population-based investigations focusing on all types of cardiovascular complication after delivery is missing. The aim was to analyze the risk of severe cardiovascular complications in the post-partum period following delivery by cesarean section. We also had a control group of vaginal deliveries and a reference group with nulliparas. MATERIALS AND METHODS: This Swedish population-based study used three national registers between 2005 and 2017 and comprised a total of 1 165 684 individuals. Unselected register data was cross-linked and cardiovascular adverse events were identified by ICD diagnosis codes. 140 128 women (209 391 deliveries) were included in the cesarean group and 614 355 women (973 429 deliveries) in the vaginal control group. The reference group comprised 411 201 age-matched nulliparous women. The primary analysis was the risk of severe cardiovascular complications within 42 days of cesarean section or vaginal delivery. The secondary analysis evaluated risk factors for cardiovascular complications. RESULTS: In the cesarean section group, 410 (0.20%) had a serious cardiovascular event within 42 days after delivery, and in the vaginal control group the number was 857 (0.09%). The risk of having an adverse cardiovascular event was significantly greater in the cesarean group (OR 2.23, CI 1.98 to 2.51) for all types of cardiovascular events. Risk factors were high BMI, preeclampsia, greater maternal age, tobacco use and acute cesarean delivery. CONCLUSIONS: The absolute numbers on severe maternal morbidity after delivery are low. However, since almost half of the world's population are affected and the frequency of elective cesarean section continues to rise, a doubling of the risk for a severe cardiovascular event within 42 days of delivery is important to consider globally.

Surgical complications after caesarean section: A population-based cohort study.

BACKGROUND: The rate of caesarean section without medical indication is rising but the risk for surgical complications has not been fully explored. METHODS: Altogether 79 052 women from the Swedish Medical Birth Register who delivered by caesarean section only from 2005 through 2016 were identified and compared with a control group of women delivering vaginally only from the same register and the same period of time. By cross-linking data with the National Patient Register the risks for bowel obstruction, incisional hernia and abdominal pain were analysed, as well as risk factors for these complications. We also analysed acute complications, uterine rupture, and placenta praevia. FINDINGS: Caesarean section is associated with an increased risk for bowel obstruction (OR 2.92; CI 2.55-3.34), surgery for bowel obstruction (OR 2.12; CI 1.70-2.65), incisional hernia (OR 2.71; CI 2.46-3.00), surgery for incisional hernia (OR 3.35; CI 2.68-4.18), and abdominal pain (OR 1.41; CI 1.38-1.44). Smoking, obesity, and more than one section delivery added significantly to the risk for these complications. INTERPRETATION: Caesarean section is considered a safe procedure, but awareness of the risk for serious complications is important when deciding on mode of delivery. In this study, more than one section, obesity and smoking significantly increased the risk for complications after caesarean section. Prevention of smoking and obesity among fertile women worldwide must continue to be a high priority.

A novel missense mutation in GALNT3 causing hyperostosis-hyperphosphataemia syndrome.

OBJECTIVE: Hyperostosis-hyperphosphataemia syndrome (HHS) is a rare hereditary disorder characterized by hyperphosphataemia, inappropriately normal or elevated 1,25-dihydroxyvitamin D(3) and localized painful cortical hyperostosis. HHS was shown to be caused by inactivating mutations in GALNT3, encoding UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyltransferase 3 (GalNAc-transferase; GALNT3). Herein, we sought to identify the genetic cause of hyperphosphataemia and tibial hyperostosis in a 19-year-old girl of Colombian origin. METHODS: Genomic DNA was extracted and sequencing analysis of the GALNT3 and fibroblast growth factor 23 (FGF23) genes performed. Serum levels of intact and C-terminal FGF23 were measured using two different ELISA methods. RESULTS: Mutational analysis identified a novel homozygous missense mutation in exon 6 of GALNT3 (1584 G>A), leading to an amino acid shift from Arg to His at residue 438 (R438H). The mutation was not found in over 200 control alleles or in any single nucleotide polymorphism databases. The R438 residue is highly conserved throughout species and in all known GalNAc-transferase family members. Modelling predicted the substitution deleterious for protein structure. Importantly, the phosphaturic factor FGF23 was differentially processed, as reflected by low intact (15 pg/ml) but high C-terminal (839 RU/ml) serum FGF23 levels. CONCLUSIONS: We report on the first missense mutation in GALNT3 giving rise to HHS, since previous GALNT3 mutations in HHS caused aberrant splicing or premature truncation of the protein. The R438H substitution likely abrogates GALNT3 activity, in turn causing enhanced FGF23 degradation and subsequent hyperostosis/hyperphosphataemia.