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1.
Dig Dis Sci ; 2021 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-33590405

RESUMO

BACKGROUND AND AIMS: Conventional adenomas (CAs) and serrated polyps (SPs) are precursors to colorectal cancer (CRC). Understanding metachronous cancer risk is poor due to lack of accurate large-volume datasets. We outline the use of natural language processing (NLP) in forming the Partners Colonoscopy Cohort, an integrated longitudinal cohort of patients undergoing colonoscopies. METHODS: We identified endoscopy quality data from endoscopy reports for colonoscopies performed from 2007 to 2018 in a large integrated healthcare system, Mass General Brigham). Through modification of an established NLP pipeline, we extracted histopathological data (polyp location, histology and dysplasia) from corresponding pathology reports. Pathology and endoscopy data were merged by polyp location using a four-stage algorithm. NLP and merging procedures were validated by manual review of 500 pathology reports. RESULTS: 305,656 colonoscopies in 213,924 patients were identified. After merging, 76,137 patients had matched polyp data for 334,750 polyps. CAs and SPs were present in 86,707 (28.5%) and 55,373 (18.2%) colonoscopies. Among patients with polyps at index screening colonoscopy, 14,931 (33.4%) had follow-up colonoscopy (median 46.4, interquartile range 33.8-62.4 months); 91 (0.2%) and 1127 (2.5%) patients developed metachronous CRC and high-risk polyps (polyps ≥ 10 mm or CAs having high-grade dysplasia/villous/tublovillous histology or SPs with dysplasia). Genetic data were available for 23,787 (31.7%) patients with polyps from the Partners Biobank. The validation study showed a positive predictive value of 100% for polyp histology and locations. CONCLUSION: We created the Partners Colonoscopy Cohort providing essential infrastructure for future studies to better understand the natural history of CRC and improve screening and post-polypectomy strategies.

2.
BMC Med ; 18(1): 370, 2020 Dec 02.
Artigo em Inglês | MEDLINE | ID: mdl-33261611

RESUMO

BACKGROUND: Observational studies have shown that milk consumption is inversely associated with colorectal, bladder, and breast cancer risk, but positively associated with prostate cancer. However, whether the associations reflect causality remains debatable. We investigated the potential causal associations of milk consumption with the risk of colorectal, bladder, breast, and prostate cancer using a genetic variant near the LCT gene as proxy for milk consumption. METHODS: We obtained genetic association estimates for cancer from the UK Biobank (n = 367,643 women and men), FinnGen consortium (n = 135,638 women and men), Breast Cancer Association Consortium (n = 228,951 women), and Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome consortium (n = 140,254 men). Milk consumption was proxied by a genetic variant (rs4988235 or rs182549) upstream of the gene encoding lactase, which catalyzes the breakdown of lactose. RESULTS: Genetically proxied milk consumption was associated with a reduced risk of colorectal cancer. The odds ratio (OR) for each additional milk intake increasing allele was 0.95 (95% confidence interval [CI] 0.91-0.99; P = 0.009). There was no overall association of genetically predicted milk consumption with bladder (OR 0.99; 95% CI 0.94-1.05; P = 0.836), breast (OR 1.01; 95% CI 1.00-1.02; P = 0.113), and prostate cancer (OR 1.01; 95% CI 0.99-1.02; P = 0.389), but a positive association with prostate cancer was observed in the FinnGen consortium (OR 1.07; 95% CI 1.01-1.13; P = 0.026). CONCLUSIONS: Our findings strengthen the evidence for a protective role of milk consumption on colorectal cancer risk. There was no or limited evidence that milk consumption affects the risk of bladder, breast, and prostate cancer.

3.
Clin Nutr ; 2020 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-33199044

RESUMO

BACKGROUND & AIMS: Arachidonic acid (AA) is metabolized by cyclooxygenases and lipoxygenases to pro-inflammatory eicosanoids, which according to experimental research modulate tumor cell proliferation, differentiation, and apoptosis. We employed the Mendelian randomization design to test the hypothesis that higher plasma phospholipid AA concentrations are associated with increased risk of 10 site-specific cancers. METHODS: Two genetic variants associated with plasma phospholipid concentrations of AA (rs174547 in FADS1 [P = 3.0 × 10-971] and rs16966952 in PDXDC1 [P = 2.4 × 10-10]) in the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium were used as genetic instruments. The associations of those variants with cancer were taken from the UK Biobank (n = 367,643), FinnGen consortium (n = 135,638), International Lung Cancer Consortium (n = 27,209), Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome consortium (n = 140,254), Breast Cancer Association Consortium (n = 228,951), Ovarian Cancer Association Consortium (n = 66,450), and BioBank Japan (n = 212,453). RESULTS: Higher genetically predicted plasma phospholipid AA concentrations were associated with increased risk of colorectal and lung cancer. Results were consistent across data sources and variants. The combined odds ratios per standard deviation increase of AA concentrations were 1.08 (95% CI 1.05-1.11; P = 6.3 × 10-8) for colorectal cancer and 1.07 (95%CI 1.05-1.10; P = 3.5 × 10-7) for lung cancer. Genetically predicted AA concentrations had a suggestive positive association with esophageal cancer (odds ratio 1.09; 95% CI 1.02-1.17; P = 0.016) but were not associated with cancers of the stomach, pancreas, bladder, prostate, breast, uterus, or ovary. CONCLUSION: These results indicate that AA may be implicated in the development of colorectal and lung cancer and possibly esophageal cancer. Treatments with plasma AA-lowering properties should be evaluated for clinical benefit.

5.
Elife ; 92020 10 13.
Artigo em Inglês | MEDLINE | ID: mdl-33046214

RESUMO

Laboratory studies have suggested oncogenic roles of lipids, as well as anticarcinogenic effects of statins. Here we assess the potential effect of statin therapy on cancer risk using evidence from human genetics. We obtained associations of lipid-related genetic variants with the risk of overall and 22 site-specific cancers for 367,703 individuals in the UK Biobank. In total, 75,037 individuals had a cancer event. Variants in the HMGCR gene region, which represent proxies for statin treatment, were associated with overall cancer risk (odds ratio [OR] per one standard deviation decrease in low-density lipoprotein [LDL] cholesterol 0.76, 95% confidence interval [CI] 0.65-0.88, p=0.0003) but variants in gene regions representing alternative lipid-lowering treatment targets (PCSK9, LDLR, NPC1L1, APOC3, LPL) were not. Genetically predicted LDL-cholesterol was not associated with overall cancer risk (OR per standard deviation increase 1.01, 95% CI 0.98-1.05, p=0.50). Our results predict that statins reduce cancer risk but other lipid-lowering treatments do not. This suggests that statins reduce cancer risk through a cholesterol independent pathway.

6.
Int J Cancer ; 2020 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-32895918

RESUMO

Studies of sleep duration in relation to the risk of site-specific cancers other than breast cancer are scarce. Furthermore, the available results are inconclusive and the causality remains unclear. We aimed to investigate the potential causal associations of sleep duration with overall and site-specific cancers using the Mendelian randomization (MR) design. Single-nucleotide polymorphisms associated with the sleep traits identified from a genome-wide association study were used as instrumental variables to estimate the association with overall cancer and 22 site-specific cancers among 367 586 UK Biobank participants. A replication analysis was performed using data from the FinnGen consortium (up to 121 579 individuals). There was suggestive evidence that genetic liability to short-sleep duration was associated with higher odds of cancers of the stomach (odds ratio [OR], 2.22; 95% confidence interval [CI], 1.15-4.30; P = .018), pancreas (OR, 2.18; 95% CI, 1.32-3.62; P = .002) and colorectum (OR, 1.48; 95% CI, 1.12-1.95; P = .006), but with lower odds of multiple myeloma (OR, 0.47; 95% CI, 0.22-0.99; P = .047). Suggestive evidence of association of genetic liability to long-sleep duration with lower odds of pancreatic cancer (OR, 0.44; 95% CI, 0.25-0.79; P = .005) and kidney cancer (OR, 0.44; 95% CI, 0.21-0.90; P = .025) was observed. However, none of these associations passed the multiple comparison threshold and two-sample MR analysis using FinnGen data did not confirm these findings. In conclusion, this MR study does not provide strong evidence to support causal associations of sleep duration with risk of overall and site-specific cancers. Further MR studies are required.

7.
EBioMedicine ; 59: 102956, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32805626

RESUMO

BACKGROUND: Tumour necrosis factor (TNF) inhibitors are used in the treatment of certain autoimmune diseases but given the role of TNF in tumour biology and atherosclerosis, such therapies may influence the risk of cancer and cardiovascular disease. We conducted a Mendelian randomization study to explore whether TNF levels are causally related to cardiovascular disease and cancer. METHODS: Single-nucleotide polymorphisms associated with TNF levels at genome-wide significance were identified from a genome-wide association study of 30 912 European-ancestry individuals. Three TNF-associated single-nucleotide polymorphisms associated with higher risk of autoimmune diseases were used as instrumental variables. Summary-level data for 14 cardiovascular diseases, overall cancer and 14 site-specific cancers were obtained from UK Biobank and consortia. FINDINGS: Genetically-predicted TNF levels were positively associated with coronary artery disease (odds ratio (OR) 2.25; 95% confidence interval (CI) 1.50, 3.37) and ischaemic stroke (OR 2.27; 95% CI 1.50, 3.43), and inversely associated with overall cancer (OR 0.54; 95% CI 0.42, 0.69), breast cancer (OR 0.51; 95% CI 0.39, 0.67), and colorectal cancer (OR 0.20; 95% CI 0.09, 0.45). There were suggestive associations of TNF with venous thromboembolism (OR 2.18; 95% CI 1.32, 3.59), endometrial cancer (OR 0.25; 95% CI 0.07, 0.94), and lung cancer (OR 0.45; 95% CI 0.21, 0.94). INTERPRETATION: This study found evidence of causal associations of increased TNF levels with higher risk of common cardiovascular diseases and lower risk of overall and certain cancers.

8.
Cancer Med ; 9(18): 6836-6842, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32717139

RESUMO

Insulin-like growth factor-1 (IGF-1) is involved in several processes relevant to carcinogenesis. We used 416 single-nucleotide polymorphisms robustly associated with serum IGF-1 levels to assess the potential causal associations between this hormone and site-specific cancers through Mendelian randomization. Summary-level genetic association estimates for prostate, breast, ovarian, and lung cancer were obtained from large-scale consortia including individuals of European-descent. Furthermore, we estimated genetic associations with 14 site-specific cancers in European-descent individuals in UK Biobank. Supplementary analyses were conducted for six site-specific cancers using summary-level data from the BioBank Japan Project. Genetically predicted serum IGF-1 levels were associated with colorectal cancer. The odds ratio (OR) per standard deviation increase of IGF-1 levels was 1.11 (95% confidence interval [CI] 1.01-1.22; P = .03) in UK Biobank and 1.22 (95% CI 1.09-1.36; P = 3.9 × 10-4 ) in the BioBank Japan Project. For prostate cancer, the corresponding OR was 1.10 (95% CI 1.01-1.21; P = .04) in UK Biobank, 1.03 (95% CI 0.97-1.09; P = .41) in the prostate cancer consortium, and 1.08 (95% CI 0.95-1.22; P = .24) in the BioBank Japan Project. For breast cancer, the corresponding OR was 0.99 (95% CI 0.92-1.07; P = .85) in UK Biobank and 1.08 (95% CI 1.02-1.13; P = 4.4 × 10-3 ) in the Breast Cancer Association Consortium. There was no statistically significant association between genetically predicted IGF-1 levels and 14 other cancers. This study found some support for a causal association between elevated serum IGF-1 levels and increased risk of colorectal cancer. There was inconclusive or no evidence of a causal association of IGF-1 levels with prostate, breast, and other cancers.

9.
PLoS Med ; 17(7): e1003178, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32701947

RESUMO

BACKGROUND: Smoking is a well-established cause of lung cancer and there is strong evidence that smoking also increases the risk of several other cancers. Alcohol consumption has been inconsistently associated with cancer risk in observational studies. This mendelian randomisation (MR) study sought to investigate associations in support of a causal relationship between smoking and alcohol consumption and 19 site-specific cancers. METHODS AND FINDINGS: We used summary-level data for genetic variants associated with smoking initiation (ever smoked regularly) and alcohol consumption, and the corresponding associations with lung, breast, ovarian, and prostate cancer from genome-wide association studies consortia, including participants of European ancestry. We additionally estimated genetic associations with 19 site-specific cancers among 367,643 individuals of European descent in UK Biobank who were 37 to 73 years of age when recruited from 2006 to 2010. Associations were considered statistically significant at a Bonferroni corrected p-value below 0.0013. Genetic predisposition to smoking initiation was associated with statistically significant higher odds of lung cancer in the International Lung Cancer Consortium (odds ratio [OR] 1.80; 95% confidence interval [CI] 1.59-2.03; p = 2.26 × 10-21) and UK Biobank (OR 2.26; 95% CI 1.92-2.65; p = 1.17 × 10-22). Additionally, genetic predisposition to smoking was associated with statistically significant higher odds of cancer of the oesophagus (OR 1.83; 95% CI 1.34-2.49; p = 1.31 × 10-4), cervix (OR 1.55; 95% CI 1.27-1.88; p = 1.24 × 10-5), and bladder (OR 1.40; 95% CI 1.92-2.65; p = 9.40 × 10-5) and with statistically nonsignificant higher odds of head and neck (OR 1.40; 95% CI 1.13-1.74; p = 0.002) and stomach cancer (OR 1.46; 95% CI 1.05-2.03; p = 0.024). In contrast, there was an inverse association between genetic predisposition to smoking and prostate cancer in the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome consortium (OR 0.90; 95% CI 0.83-0.98; p = 0.011) and in UK Biobank (OR 0.90; 95% CI 0.80-1.02; p = 0.104), but the associations did not reach statistical significance. We found no statistically significant association between genetically predicted alcohol consumption and overall cancer (n = 75,037 cases; OR 0.95; 95% CI 0.84-1.07; p = 0.376). Genetically predicted alcohol consumption was statistically significantly associated with lung cancer in the International Lung Cancer Consortium (OR 1.94; 95% CI 1.41-2.68; p = 4.68 × 10-5) but not in UK Biobank (OR 1.12; 95% CI 0.65-1.93; p = 0.686). There was no statistically significant association between alcohol consumption and any other site-specific cancer. The main limitation of this study is that precision was low in some analyses, particularly for analyses of alcohol consumption and site-specific cancers. CONCLUSIONS: Our findings support the well-established relationship between smoking and lung cancer and suggest that smoking may also be a risk factor for cancer of the head and neck, oesophagus, stomach, cervix, and bladder. We found no evidence supporting a relationship between alcohol consumption and overall or site-specific cancer risk.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Análise da Randomização Mendeliana/métodos , Neoplasias/etiologia , Fumar/genética , Bancos de Espécimes Biológicos , Grupo com Ancestrais do Continente Europeu/genética , Feminino , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Humanos , Masculino , Neoplasias/genética , Polimorfismo de Nucleotídeo Único , Reino Unido
10.
Diabetes ; 69(7): 1588-1596, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32349989

RESUMO

We conducted a two-sample Mendelian randomization study to investigate the causal associations of type 2 diabetes mellitus (T2DM) with risk of overall cancer and 22 site-specific cancers. Summary-level data for cancer were extracted from the Breast Cancer Association Consortium and UK Biobank. Genetic predisposition to T2DM was associated with higher odds of pancreatic, kidney, uterine, and cervical cancer and lower odds of esophageal cancer and melanoma but not associated with 16 other site-specific cancers or overall cancer. The odds ratios (ORs) were 1.13 (95% CI 1.04, 1.22), 1.08 (1.00, 1.17), 1.08 (1.01, 1.15), 1.07 (1.01, 1.15), 0.89 (0.81, 0.98), and 0.93 (0.89, 0.97) for pancreatic, kidney, uterine, cervical, and esophageal cancer and melanoma, respectively. The association between T2DM and pancreatic cancer was also observed in a meta-analysis of this and a previous Mendelian randomization study (OR 1.08; 95% CI 1.02, 1.14; P = 0.009). There was limited evidence supporting causal associations between fasting glucose and cancer. Genetically predicted fasting insulin levels were positively associated with cancers of the uterus, kidney, pancreas, and lung. The current study found causal detrimental effects of T2DM on several cancers. We suggest reinforcing the cancer screening in T2DM patients to enable the early detection of cancer.

11.
Int J Cancer ; 147(7): 1895-1903, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32215913

RESUMO

Whether thyroid dysfunction plays a causal role in the development of cancer remains inconclusive. We conducted a two-sample Mendelian randomization study to investigate the associations between genetic predisposition to thyroid dysfunction and 22 site-specific cancers. Single-nucleotide polymorphisms associated with four traits of thyroid function were selected from a genome-wide association meta-analysis with up to 72,167 European-descent individuals. Summary-level data for breast cancer and 21 other cancers were extracted from the Breast Cancer Association Consortium (122,977 breast cancer cases and 105,974 controls) and UK Biobank (367,643 individuals). For breast cancer, a meta-analysis was performed using data from both sources. Genetically predicted thyroid dysfunction was associated with breast cancer, with similar patterns of associations in the Breast Cancer Association Consortium and UK Biobank. The combined odds ratios of breast cancer were 0.94 (0.91-0.98; p = 0.007) per genetically predicted one standard deviation increase in TSH levels, 0.96 (0.91-1.00; p = 0.053) for genetic predisposition to hypothyroidism, 1.04 (1.01-1.07; p = 0.005) for genetic predisposition to hyperthyroidism and 1.07 (1.02-1.12; p = 0.003) per genetically predicted one standard deviation increase in free thyroxine levels. Genetically predicted TSH levels and hypothyroidism were inversely with thyroid cancer; the odds ratios were 0.47 (0.30-0.73; p = 0.001) and 0.70 (0.51-0.98; p = 0.038), respectively. Our study provides evidence of a causal association between thyroid dysfunction and breast cancer (mainly ER-positive tumors) risk. The role of TSH and hypothyroidism for thyroid cancer and the associations between thyroid dysfunction and other cancers need further exploration.

12.
Nutrients ; 12(2)2020 Feb 19.
Artigo em Inglês | MEDLINE | ID: mdl-32092884

RESUMO

We conducted a two-sample Mendelian randomization study to explore the associations of iron status with overall cancer and 22 site-specific cancers. Single-nucleotide polymorphisms for iron status were obtained from a genome-wide association study of 48,972 European-descent individuals. Summary-level data for breast and other cancers were obtained from the Breast Cancer Association Consortium and UK Biobank. Genetically predicted iron status was positively associated with liver cancer and inversely associated with brain cancer but not associated with overall cancer or the other 20 studied cancer sites at p < 0.05. The odds ratios of liver cancer were 2.45 (95% CI, 0.81, 7.45; p = 0.11), 2.11 (1.16, 3.83; p = 0.02), 10.89 (2.44, 48.59; p = 0.002) and 0.30 (0.17, 0.53; p = 2 × 10-5) for one standard deviation increment of serum iron, transferrin saturation, ferritin and transferrin levels, respectively. For brain cancer, the corresponding odds ratios were 0.69 (0.48, 1.00; p = 0.05), 0.75 (0.59, 0.97; p = 0.03), 0.41 (0.20, 0.88; p = 0.02) and 1.49 (1.04, 2.14; p = 0.03). Genetically high iron status was positively associated with liver cancer and inversely associated with brain cancer.

13.
J Affect Disord ; 263: 722-727, 2020 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-31780135

RESUMO

INTRODUCTION: Severe Mental Illness (SMI) encompasses schizophrenia, schizoaffective disorder, and bipolar affective disorder. SMI is associated with increased physical morbidity and mortality. Acute pancreatitis is the leading cause of gastroenterological hospitalisation. This study investigates the relationship between SMI and acute pancreatitis and determines the risk factors for development of pancreatitis. MATERIAL AND METHODS: The first study phase was a retrospective cohort analysis. Acute admissions for pancreatitis were determined for people with an SMI diagnosis between January 2007 and March 2016 from a secondary care mental health register. Standardised admission ratio (SAR) for acute pancreatitis was determined for SMI patients. The second phase was a case-control study to compare exposures between SMI subjects admitted for acute pancreatitis ("cases") and the age-, gender-, and diagnosis-matched SMI subjects without admission for acute pancreatitis ("controls"), with a ratio of 1:4. Univariate and multivariate conditional logistic regression estimated the effect of exposures including diagnosis of alcohol use disorder (AUD). RESULTS: A total of 22,337 SMI subjects were identified during the observation period. The SAR for acute pancreatitis was significant (2•33 (95% Ci: 1•97, 2•74; n = 148)). In the nested case-control study, SMI patients with co-morbid AUD elevated the risk of acute pancreatitis dramatically with an adjusted odds ratio 16•10 (5•92, 43•79). LIMITATIONS: Diagnosis of co-morbid AUD may be under represented in population CONCLUSIONS: SMI is associated with a significantly elevated risk of acute pancreatitis. Co-morbid AUD is a risk factor in development of pancreatitis in this group.

14.
J Clin Neurol ; 14(3): 426-427, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29971985
15.
BMJ Case Rep ; 20172017 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-28775081

RESUMO

A 64-year-old man with a complex medical history and previous cervical arthritis with discectomy presents with a 2-day history of neck and lower back pain and shortness of breath, associated with left-sided muscle weakness. He has a fever with severe sepsis causing acute renal failure. MRI spine shows evidence of left cervical facet joint septic arthritis at C6-T1. He required 6 weeks of intravenous antibiotics and intensive support with ventilation and haemofiltration. After completion of antibiotics, he made a full recovery and regained neurological function before discharge.


Assuntos
Artrite Infecciosa/complicações , Vértebras Cervicais/microbiologia , Cervicalgia/microbiologia , Articulação Zigapofisária/microbiologia , Antibacterianos/uso terapêutico , Artrite Infecciosa/tratamento farmacológico , Artrite Infecciosa/microbiologia , Febre/microbiologia , Humanos , Dor Lombar/microbiologia , Masculino , Pessoa de Meia-Idade , Debilidade Muscular/microbiologia
16.
BMJ Case Rep ; 20162016 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-27908913

RESUMO

A previously well woman aged 63 years presents to the emergency department with vomiting, palpitations and 3 presyncopal episodes. She had no previous medical or cardiac history, with the patient stating that she tried a herbal remedy of boiled comfrey leaves for insomnia 18 hours before arrival to the department. Her ECG showed multiple abnormalities, including bradycardia, second-degree atrioventricular node block, Mobitz Type 2, a shortened QT interval, downsloping ST depression and presence of U waves. After viewing the images of comfrey and foxglove, it highlighted the possibility of mistaken ingestion of Digitalis, containing the organic forms of cardiac glycosides, such as digoxin and digitoxin. Raised serum digoxin levels confirmed this. The patient was haemodynamically stable, and given digoxin-binding antibodies. After 5 days of cardiac monitoring, her ECG returned to normal rhythm, and she was discharged home.


Assuntos
Acidentes , Anticorpos Heterófilos/uso terapêutico , Bloqueio Atrioventricular/induzido quimicamente , Confrei , Digitalis/envenenamento , Digoxina/envenenamento , Intoxicação por Plantas/diagnóstico , Distúrbios do Início e da Manutenção do Sono/tratamento farmacológico , Anticorpos Heterófilos/imunologia , Bradicardia/etiologia , Digitalis/imunologia , Digoxina/imunologia , Eletrocardiografia , Feminino , Humanos , Pessoa de Meia-Idade , Folhas de Planta/envenenamento , Intoxicação por Plantas/complicações , Intoxicação por Plantas/tratamento farmacológico , Plantas Medicinais , Resultado do Tratamento , Vômito/etiologia
17.
Eur J Obstet Gynecol Reprod Biol ; 185: 74-7, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25528733

RESUMO

OBJECTIVE: Gynecologists are reluctant to perform vaginal hysterectomy if the uterine size exceeds 12 weeks in the belief that complications could be higher in this group. The aim of this cohort control study was to compare demographics, surgical outcomes and safety of vaginal hysterectomy in women with non-prolapsed uteri weighing >280 g (>12 weeks size) to those with uteri weighing <280 g removed vaginally for similar indications. STUDY DESIGN: In this study, classified as Canadian Task Force II (cohort-control), the index group comprised 41 women who underwent vaginal hysterectomy for non-prolapse indications with uterine enlargement >280 g (12 weeks), while the control group consisted of 66 women with uteri <280 g. Demographic data as well as duration of surgery, blood loss, intraoperative complications and readmission rates were compared. RESULTS: Women in the two groups had statistically similar mean age, body mass index and parity (47.7 vs 44.9 yrs, 30.3 vs 32.4 kg m(-3) and 2.8 vs 2.4, respectively; p>0.05). The mean operative time was significantly longer in the index group (123.3±43.2 vs 85±32.1 min; p=1.47×10(-6)). Women with enlarged uteri had greater mean estimated blood loss (402.8±402.2 vs 160.8±123.2 ml; p<0.0001) but the mean length of stay was similar (45.4±28.7 vs 37.6±26.2 h; p>0.05). Two uteri weighing >1000 g were removed vaginally. Intra- and post-operative complications such as bladder injury, blood transfusion and pelvic sepsis were similar in both groups. CONCLUSIONS: Vaginal hysterectomy in larger non-prolapsed uteri takes longer (mean 38 min longer) and is associated with more blood loss (mean increase 242 ml) compared to normal-sized uteri but is not associated with a significant increase in complication rates.


Assuntos
Histerectomia Vaginal/estatística & dados numéricos , Útero/patologia , Adulto , Idoso , Perda Sanguínea Cirúrgica/estatística & dados numéricos , Feminino , Humanos , Pessoa de Meia-Idade , Tamanho do Órgão , Estudos Retrospectivos , Adulto Jovem
18.
Eur J Obstet Gynecol Reprod Biol ; 174: 111-4, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24412144

RESUMO

OBJECTIVE: To compare surgical outcomes in women with enlarged uteri >12 weeks' size who underwent vaginal hysterectomy compared to abdominal hysterectomy for non-prolapse indications. STUDY DESIGN: Retrospective cohort study performed between 2007 and 2012 in a North London teaching hospital. The study group comprised 39 women who had vaginal hysterectomy (VH) with uteri >12 weeks size (200g) for non-prolapse indications. The next successive total abdominal hysterectomy (TAH) following the index case for similar indications (and with similar uterine weights) served as control (n=33). The groups were compared for pre- and post-operative demographic data, and main outcome measures were estimated blood loss, operation time, length of stay and complications. RESULTS: Both VH and TAH groups had statistically similar pre-operative mean haemoglobin levels, age, body mass index, previous abdominal surgery, and American Society of Anesthesiologists (ASA) grade. Mean uterine weight (403.1±239.5 vs 460.5±236.2g) was comparable in both groups (both p>0.05). The mean duration of the procedure was similar (123.5±45.8 vs 119.8±44.9min, p=0.580) but women who had TAH lost 117ml more of blood (525.7±427.6 vs 408.2±411.8ml, p=0.039). Although overall complication rates were comparable between the groups (30.8% vs 36.4%, p=0.627), the mean post-operative stay was 55% shorter following VH (40.7±29.4 vs 90.7±46.2h, p<0.0001). CONCLUSION: In women with non-prolapsed uteri >12 weeks' size, VH is a safe and cost effective option. The vaginal route is associated with significantly lower estimated blood loss and 55% shorter post-operative stay, with no increase in complication rates.


Assuntos
Histerectomia Vaginal/métodos , Histerectomia/métodos , Doenças Uterinas/patologia , Doenças Uterinas/cirurgia , Útero/patologia , Adulto , Perda Sanguínea Cirúrgica , Estudos de Coortes , Feminino , Humanos , Tempo de Internação , Londres , Pessoa de Meia-Idade , Tamanho do Órgão , Complicações Pós-Operatórias , Estudos Retrospectivos , Resultado do Tratamento
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