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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-one abdominal fascial wound dehiscences occurred in 2,761 patients undergoing major abdominal surgery during a 5-year period (1%). Twenty-two specific local and systemic risk factors were analyzed and compared with the risk factors of a control group of 38 patients undergoing similar procedures without dehiscence. Through multivariate analysis, each factor was assessed as an independent statistical variable. Significant factors (p less than 0.05) were found to include age over 65, wound infection, pulmonary disease, hemodynamic instability, and ostomies in the incision. Additional systemic risk factors that were found to be significant included hypoproteinemia, systemic infection, obesity, uremia, hyperalimentation, malignancy, ascites, steroid use, and hypertension. Risk factors not found to be important independent variables included sex, type of incision, type of closure, foreign body in the wound, anemia, jaundice, and diabetes. When dehiscence and control groups were combined, 30% of patients with at least five significant risk factors developed dehiscence, and all the patients with more than eight risk factors developed a wound dehiscence. There was an overall mortality of 29%, which was directly related to the number of significant risk factors. The co-existence of 9 risk factors portended death in one third of the patients, and all the patients with more than 10 risk factors died.
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PMID:Factors influencing wound dehiscence. 832 36

The relationship between body mass index (BMI) at different ages and subsequent endometrial-cancer risk was investigated in a multicentre case-control study conducted between 1988 and 1991 in Vaud, Switzerland, and Northern Italy on 272 histologically confirmed incident cases of endometrial cancer and 571 controls admitted to hospital for acute, non-neoplastic conditions, unrelated to known or potential risk factors for endometrial cancer. The risk of endometrial cancer increased with increasing BMI in the 3rd decade of age (20 to 29 years), in the 5th decade (40 to 49 years) and in the 7th decade (60 to 69 years), although the risk estimates tended to be substantially higher at older ages: compared with women whose BMI (kg m-2) was less than 20, the relative risks (RR) were 1.8 for BMI greater than or equal to 25 at age 20 to 29, 2.7 for BMI greater than or equal to 30 at age 40 to 49 and 3.8 at age 60 to 69. All the trends in risk were significant, except that for BMI at age 25 after allowance for current BMI. When data were examined in separate strata of current BMI, among women of normal body mass at diagnosis no significant effect of past overweight was observed. In contrast, among subjects over-weight at diagnosis, there were significant direct relationships with BMI at ages 20 to 29 and 40 to 49. To reduce endometrial cancer risk, it is therefore important to avoid obesity in later middle and older age, and the benefit can be even greater for women who were overweight at younger age.
Int J Cancer 1992 Feb 20
PMID:Body mass at different ages and subsequent endometrial cancer risk. 153 22

The influence of dietary lipids on immune function has come under serious study only within the past two decades. It is clear from whole-animal studies that obesity and consumption of diets high in fat, particularly unsaturated fat, depress immunocompetence and enhance risk for serious infectious disease and cancer. In vitro systems, cell cultures and the tools of molecular biology are moving nutrition and immunology closer together with promise of significant benefits.
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PMID:Dietary lipids and immune function. 154 20

A workshop on the high risk group and the preventive oncology of renal cell carcinoma was held in Kyoto on September 7, 1990. The following subjects were presented: 1. Cohort study of renal cell carcinoma (Dr. Hirayama). 2. Pathoepidemiological study on the background of occurrence of renal cell carcinoma (Dr. Aoki). 3. Case-control study on renal cell carcinoma (Dr. Watanabe). 4. Geographic distribution of renal cell carcinoma in Japan (Dr. Minowa). 5. Pathological findings of small renal cell carcinoma (Prof. Yatani). 6. Pathoepidemiological study on occurrence of renal cell carcinoma (Dr. Tsuchihashi). 7. Clinical evaluation of small renal cell carcinoma (Dr. Masuda). 8. Clinical (biological) characteristics of renal cell carcinoma (Dr. Satomi). 9. Mass screening program for renal cell carcinoma on private urological clinic (Dr. Mishina). 10. Early stage detection of renal cell carcinoma (Dr. Ohe). 11. A review on the literature of epidemiology for renal cell carcinoma (Dr. Nakagawa). Possible risk factors reported for renal cell carcinoma were as follows: 1) Work in petroleum-related and dry-cleaning industries were positive risk. A predominant lifetime occupation as a professional was negative risk. 2) Milk or coffee consumption and use of artificial sweeteners were positive. Drinking of alcohol was negative. 3) Obesity was positive. 4) Personal history of cancer was positive. 5) Cigarette smoking was positive. 6) Exposure to radiation or hydrocarbon was positive. 7) Use of estrogen, diuretic and pain relievers was positive. 8) History of myocardial infarction, hypertension and diabetes mellitus was positive.
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PMID:[A workshop on the high risk group and the preventive oncology of renal cell carcinoma]. 156 64

Obesity is known to adversely affect breast cancer prognosis. Since obesity is associated with increased oestrogen levels, and oestrogens are growth stimulators of oestrogen receptor (ER)-positive breast carcinomas, we evaluated the relationship between the ER and progesterone receptor (PR) status of the neoplastic tissue and obesity in a series of 615 breast cancer patients. Both ER and PR concentrations were significantly and positively correlated with obesity by multiple regression analysis. Furthermore, the estimated probability of having an ER+/PR+carcinoma was significantly higher in obese patients (odds ratio 2.65, 95% confidence interval 1.56-4.48). This association between receptor-positive status and obesity was observed both in premenopausal and postmenopausal patients. Our data suggest, therefore, that obesity plays a role in determining the ER status of breast cancer and raise the possibility that ER presence in breast carcinomas occurring in obese patients is not indicative of a favourable prognosis.
Eur J Cancer 1992
PMID:Relation between steroid receptor status and body weight in breast cancer patients. 156 60

Associations of body fat and body fat distribution with breast cancer were studied in 16,355 postmenopausal women with a natural menopause, aged 49 to 68 years, participating in a breast cancer screening project (the Diagnostic Investigation of Mammary Cancer [DOM] project in Utrecht, The Netherlands). One hundred nineteen women had breast cancer detected at first screening. Fat distribution was assessed by contrasting groups of subscapular and triceps skinfold thickness. No relationship between fat distribution and breast cancer was found. After adjustment for age, women in the highest quartile of Quetelet's index (QI) (weight/height2) had an odds ratio of 1.65 (95% confidence interval [CI], 0.97 to 2.81) compared with women in the the lowest quartile (test for trend, P less than 0.05). For subscapular skinfold and triceps skinfold, the odds ratios were 2.23 (95% CI, 1.28 to 3.91) and 2.01 (95% CI, 1.21 to 3.32), respectively, comparing the highest with the lowest quartile. The authors conclude that in postmenopausal women, overall obesity is associated with increased risk of breast cancer, whereas fat distribution, as measured by contrasting groups of subscapular and triceps skinfold thicknesses, is not related to breast cancer.
Cancer 1992 Jun 01
PMID:Obesity and subcutaneous fat patterning in relation to breast cancer in postmenopausal women participating in the Diagnostic Investigation of Mammary Cancer Project. 157 95

In a population-based case-control study of kidney cancer in New South Wales, Australia, data from structured interviews with 489 cases of renal cell cancer (RCC) and 147 cases of renal pelvic cancer (CaRP) diagnosed in 1989 and 1990, and 523 controls from the electoral rolls, confirmed the link between obesity and RCC. In addition, regular consumption of 'diet' pills independently increased the risk for this cancer. A diagnosis of hypertension at least two years before interview raised the risk for RCC, and regular use of beta-blockers, a class of antihypertensive drug, independently increased the risk for RCC and CaRP (risk ratio = 1.5-1.8). No independent effect was found for use of diuretics. Additional information provided by this study includes increased risks associated with kidney injury (RCC, CaRP)--possibly attributed to recall bias--and kidney infection (CaRP), as well as a nonsignificantly raised risk linked with kidney stones (RCC, CaRP) and a significantly reduced risk for RCC in persons giving a history of lower urinary tract infection. No significant association of RCC was found with hormonal factors (age at menarche or menopause; child-bearing; regular use of oral contraceptives or estrogens; hysterectomy or oophorectomy).
Cancer Causes Control 1992 Jul
PMID:Risk factors for kidney cancer in New South Wales, Australia. II. Urologic disease, hypertension, obesity, and hormonal factors. 161 19

To investigate an association between colon cancer and obesity during early adulthood--a potentially important period in the etiology of this disease--the authors assembled, by computer linkage, a population-based historical cohort of 52,539 men born between 1913 and 1927 residing in Hawaii (USA), for whom weight and height had been recorded in 1942-43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the identification of 737 incident cases of colorectal cancer for 1972-86. An average of 3.8 cancer-free controls were matched to each case on month and year of birth and ethnicity of the parents. A case-control analysis in each anatomic subsite of the large bowel revealed that both early and middle-age body mass increased the risk of sigmoid cancer in men in a dose-dependent fashion. The odds ratios (OR) for sigmoid cancer for the highest compared with the lowest tertiles of Quetelet index were: 2.1 (95 percent confidence interval [CI] = 1.4-3.2) and 1.7 (CI = 1.1-2.5), at ages 15-29 and in prediagnostic years, respectively. These associations were additive and independent of socioeconomic status. Men who were above the median Quetelet index in 1942 and 1972 had an OR of 2.7 (CI = 1.8-4.0), compared with those who were below the median in both periods. This study provides further evidence for an association of obesity with colon cancer in men and suggests that this association is limited to the sigmoid colon and may be related to both early and late events of colon carcinogenesis.
Cancer Causes Control 1992 Jul
PMID:Obesity in youth and middle age and risk of colorectal cancer in men. 161 22

In a case-control study involving 268 cases of endometrial cancer and an equal number of population controls, we assessed the relationship of risk to body weight and fat distribution, examining weight at various ages and current anthropometric measurements. Weight gain during later adulthood and resultant high body masses were important risk predictors, indicating that obesity is an important risk factor, even in an area where the prevalence of obesity and incidence of endometrial cancer are low. Certain fat distribution patterns were related to risk of endometrial cancer independent of general obesity. In particular, fat deposits on the trunk were associated with elevated risks, with the odds ratio for the highest versus lowest quartile of subscapular skinfolds remaining significant even after adjustment for body mass index (odds ratio = 2.9; 95% confidence interval, 1.1-7.3). Central versus peripheral obesity, as measured by the subscapular:triceps ratio, also was related to increased risk, although the association failed to remain significant after adjustment for body mass (highest to lowest quartile, odds ratio = 1.7). In contrast, upper body obesity, as assessed by the waist:thigh ratio, was unrelated to risk. These results support the need for future studies assessing the relationship of hormonal and other biological parameters of fat distribution to assist in identifying causal mechanisms for this tumor.
Cancer Res 1992 Jul 15
PMID:Relation of obesity and body fat distribution to endometrial cancer in Shanghai, China. 161 61

A case of advanced cervical carcinoma of the uterus with ectopic adrenocorticotrophic hormone (ACTH) syndrome is described. The patient was seen for general malaise 21 months after surgical treatment of the primary lesion whose histology was undifferentiated small cell carcinoma of the uterine cervix. She had extensive metastases in the liver and the abdominal wall. In addition to the typical clinical manifestations of Cushing's syndrome such as moon face, central obesity and acne vulgaris, hyperglycemia was so severe that she was in a hyperosmolar non-ketotic coma. Endocrinological examinations revealed elevated plasma ACTH and cortisol, and urinary excretion of 17-hydroxycorticosteroids and 17-ketosteroids, which were not suppressed by high-dose dexamethasone administration. Based on these clinical and laboratory findings, a diagnosis of ectopic ACTH syndrome was made. Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. These observations suggest possible involvement of the somatostatin in deteriorating glucose intolerance to develop hyperglycemic hyperosmolar non-ketotic coma as a drastic disturbance of metabolism.
Jpn J Cancer Res 1991 Jun
PMID:A case of cervical carcinoma of the uterus presenting with hyperosmolar non-ketotic coma as a manifestation of ectopic adrenocorticotropic hormone syndrome. 164 12


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