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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This series of three articles reviews the designs of studies which can be used to identify risk factors of a disease, here: diabetes or complications of diabetes. In the present issue of Diabete & Metabolisme, the first article of the series, we give the definition of a risk factor, along with measures of its force--relative risk and odds ratio, followed by the epidemiological definitions of the diseases: diabetes, coronary heart disease and hypertension. Risk factors are further discussed and we complete the discussion by some observations on the bias which can arise from a study or from its analysis, which can lead the researcher to the wrong conclusion. The three types of epidemiological studies which are used to determine whether factors are associated with a disease: observational or cross-sectional studies, cohort studies and case-cohort studies will be described in the second of the series in the next issue of the journal. Examples will be provided of each of these study types; their advantages and disadvantages will be discussed. In a third issue, the final paper will provide some examples of the study types and the identification of risk factors. The first examples involve diabetes and pancreatic cancer, the second birth weight and non-insulin dependent diabetes. Having found an association between a risk factor and diabetes, then we will discuss whether it can be considered to be a risk factor and if so and whether it is likely to be a cause of the disease.
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PMID:Risk factors and their identification. First Part: What is a risk factor? 778 49

Streptozotocin diabetes prevents induction of pancreatic tumors in several animal models, suggesting a pivotal role for islet cell products in the pathogenesis of pancreatic cancer. To test the hypothesis that altered gastrointestinal peptide levels in streptozotocin diabetes influence tumor growth, human pancreatic cancer cells (MIA PaCa-2) were implanted subcutaneously into streptozotocin diabetic nude mice. After 3 weeks, tumors in the control group weighed 43 mg and tumors in the diabetic group weighed 12 mg (P < 0.001). Plasma insulin and IGF-1 levels were significantly decreased in the streptozotocin-treated animals compared to those of control (insulin: 23 microU/ml vs 31 microU/ml, P < 0.001; IGF-1: 254 ng/ml vs 324 ng/ml, P < 0.001). In contrast, somatostatin and glucagon were significantly elevated in the streptozotocin diabetic group relative to control levels (somatostatin: 179 pg/ml vs 54 pg/ml, P < 0.001; glucagon: 290 pg/ml vs 134 pg/ml, P < 0.001). Competitive binding studies revealed specific cell surface receptors for insulin (Kd = 15.5 nM), IGF-1 (Kd = 30.0 nM), and somatostatin (Kd = 2.5 nM) on the MIA PaCa-2 cells. Receptors for glucagon were absent. In an in vitro cell proliferation assay, cell division was promoted by insulin (P < 0.01, max + 11%) and IGF-1 (P < 0.01, max + 10%). Somatostatin inhibited cell division (P < 0.01, max - 18%). No effect was seen with glucagon. The growth of pancreatic cancer, particularly in diabetes, may be influenced by gut peptides in a receptor-dependent fashion.
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PMID:GI hormonal changes in diabetes influence pancreatic cancer growth. 779 56

The relationship between diabetes mellitus and cancer risk was investigated using data from an integrated series of case-control studies conducted in Northern Italy between 1983 and 1992. Cases were 9,991 patients with incident, histologically confirmed neoplasms below age 75, including 181 cancers of the oral cavity and pharynx, 316 of the oesophagus, 723 of the stomach, 828 of the colon, 498 of the rectum, 320 of the liver, 58 of the gall bladder, 362 of the pancreas, 242 of the larynx, 3,415 of the breast, 726 of the endometrium, 971 of the ovary, 125 of the prostate, 431 of the bladder, 187 of the kidney, 208 of the thyroid, 80 Hodgkin's lymphomas, 200 non-Hodgkin's lymphomas and 120 multiple myelomas. Controls were 7,834 subjects in hospital for acute, non-neoplastic, non-metabolic, non-hormone-related disorders. A history of diabetes was reported by 5.1% of male and 5.4% of female controls. Significantly elevated relative risks (RRs) among subjects with diabetes were observed for cancers of the liver [RR = 2.8, 95% confidence interval (CI) 2.0-3.9], pancreas (RR = 2.1, 95% CI 1.5-2.9) and endometrium (RR 3.4, 95% CI 2.7-4.3). After allowance for obesity and education as well as age and sex, the RRs were 3.0 for liver, 2.3 for pancreas, and 2.8 for endometrium. Diabetic subjects had no elevated risk for any of the other cancer sites considered. For liver and endometrial cancer the RRs remained elevated up to 10 years after diagnosis of diabetes (RR 2.6 and 2.0 respectively), while the RR for pancreatic cancer declined from 3.2 in the first 5 years after diagnosis of diabetes to 2.3 from 5 to 9 years and to 1.3 (95% CI 0.7-2.3) 10 or more years since diagnosis. This suggests that the relationship between diabetes mellitus and liver and endometrial cancer is probably real, while that with pancreatic cancer is compatible with diabetes being an early symptom of the disease, or at least of preneoplastic lesions.
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PMID:A case-control study of diabetes mellitus and cancer risk. 794 3

Pancreatic cancer has been extensively researched in recent years, but overall survival after diagnosis is almost unchanged since the time of Whipple. In the meantime, we have tried to determine the factors influencing surgical risk, resectability and survival. Between 1968 and 1992, 516 patients with pancreatic cancer were monitored; 160 patients with cancer of the body-tail were excluded. Eighty-five of the remaining 356 patients with pancreatic head cancer were resected, while the remainder underwent only palliative procedures. Surgical outcome, in terms of operative mortality or complications, was correctly predicted preoperatively in > 80% of patients. The preoperative evaluation of the resectability of pancreatic cancer has been investigated with different, mainly invasive, procedures. CT scan, associated with angiography and laparoscopy is reported to give better results, with a resectability rate up to 78%. 67% of our patients who were diagnosed as resectable according to CT-scan features and serum CA 19-9 < 200 U/ml, were actually resected; furthermore 40% had a potentially curative resection. Most of our 'curative' resections (80%) were within this group of patients. Multivariate analysis showed only 4 factors influencing long-term survival: TNM stage, diabetes, age > 70 years, tumour grading.
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PMID:[Prediction of resectability and of surgical risk in pancreatic carcinoma; conditioning factors of survival after resective intervention]. 795 82

The period 1981-1993, 124 patients underwent resection for pancreatic cancer; they represented 30.8% of all patients observed in that period. Surgical procedures were a pancreatoduodenectomy (PD) in 100 cases, a total pancreatectomy (TP) in 3 cases and a distal pancreatectomy in 21 cases. PD was performed by the injection of Neoprene into the residual pancreatic stump, rather than of pancreatojejunal anastomosis; in 37 cases a pylorus-preserving PD was performed. Adjuvant treatments were given in addition to resection in 75 patients: 47 underwent intraoperative radiation therapy, following a PD in 41 cases, a TP in 1 case and a distal pancreatectomy in 5 cases. Overall operative mortality was 2.4%, overall morbidity 26.6%. In the 103 patients undergoing PD or TP mortality was 2.9% and morbidity 29.1%. Postoperative diabetes occurred in 12.8% of patients undergoing PD with Neoprene injection. Overall median survival was 16 months. Survival was significantly related to UICC staging distribution, to the radical nature of the operation or to adjuvant treatments. No relationship was found between survival and the type of resection (PD versus distal pancreatectomy) or the pylorus preservation. Pancreatic resection, whenever technically possible, represents the treatment of choice of localised pancreatic cancer, in association with adjuvant treatments.
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PMID:[Personal experience in surgical resection of pancreatic carcinoma]. 795 85

We described three septicemia cases in which blood cultures yielded gram-positive cocci identified as Leuconostoc spp. and Pediococcus spp. Patients were three male adults aged 63 to 71 years with severe underlying diseases, pancreatic cancer, esophageal cancer and diabetes mellitus with chronic renal failure. They had fever and chills at the onsets of septicemia with acute obstructive suppurative cholangitis, acute pneumonia, and infection complicated with invasion sites of esophageal cancer contagious to bronchus and subcutaneous tissue. Blood cultures yielded catalase and oxidase negative highly vancomycin-resistant (MIC: 1024 micrograms/ml <) gram-positive cocci showing alpha or gamma hemolysis on blood agar plates. Two cases were polymicrobial infections. In one case with esophageal cancer, clinical symptoms persisted after the start of antimicrobial chemotherapy and the patient died 10 days later associated with complications of esophageal cancer. Leuconostoc lactis, Leuconostoc mesenteroides subsp. dextranicum, and Pediococcus acidilactici wee identified by physiological reactions. These strains were also highly resistant to teicoplanin and fosfomycin, and tolerant to all rested beta-lactams such as benzylpenicillin. This is the first report in Japan to our knowledge on the identification of Leuconostoc spp. and Pediococcus spp. isolated from human infectious diseases.
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PMID:[Microbiological and clinical studies of vancomycin resistant Leuconostoc spp. and Pediococcus spp. isolated from septicemia patients]. 796 99

Risk factors for pancreatic cancer were examined in a cohort study of 13,979 residents of a retirement community. After 9 years of follow-up, 65 incident cases of pancreatic cancer were identified. An increased risk of pancreatic cancer was associated with a history of diabetes and cholecystectomy. Higher intake of vegetables, fruits, dietary beta-carotene, and vitamin C were each associated with a reduced risk of pancreatic cancer, although none of these associations was statistically significant. Risk of pancreatic cancer decreased with increasing tea consumption but was unrelated to coffee consumption. No strong or consistent association was seen between either smoking or alcohol consumption and risk of pancreatic cancer, but a consistent and significant increase in risk followed cholecystectomy.
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PMID:A prospective study of pancreatic cancer in the elderly. 776 51

The relationship between family history of selected neoplasms in first-degree relatives and the risk of pancreatic, liver, and gallbladder cancer was investigated using data from a case-control study conducted in northern Italy on 320 histologically confirmed incident cases of liver cancer, 58 of gallbladder cancer, 362 of pancreatic cancer, and 1408 controls admitted to the hospital for acute, nonneoplastic, nondigestive tract disorders. Significant associations were observed between family history of hepatocellular carcinoma and primary liver cancer [relative risk (RR) = 2.4; 95% confidence interval (CI), 1.3 to 4.4], between family history of pancreatic cancer and pancreatic cancer (RR = 3.0; 95% CI, 1.4 to 6.6), and between family history of gallbladder cancer and gallbladder cancer (RR = 13.9; 95% CI, 1.2 to 163.9). The elevated risk of liver cancer associated with family history was not materially modified by adjustment for tobacco, alcohol, and personal history of cirrhosis and hepatitis (RR = 2.9; 95% CI, 1.5 to 5.3). Similarly, the risk for pancreatic cancer did not appreciably change after allowance for tobacco, alcohol, dietary factors, and medical history of diabetes and pancreatitis (RR = 2.8; 95% CI, 1.3 to 6.3). This pattern of risk would support the existence of a genetic component in the familial aggregation of liver and pancreatic cancer. In terms of population attributable risk, approximately 3% of the newly diagnosed liver and pancreatic cancers would be related to this familial component.
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PMID:Family history and the risk of liver, gallbladder, and pancreatic cancer. 801 68

To assess the risk of pancreatic cancer in subjects with tropical calcifying pancreatitis (TCP), we have followed 185 patients with TCP from the Diabetes Research Center in Madras, India for an average of 4.5 years. The diagnosis of TCP was based upon long-standing epigastric pain, laboratory tests, presence of pancreatic calculi, endoscopic retrograde cholangiopancreatography (ERCP) findings, and ultrasonography. During the follow-up period, 24 patients died from all causes, with 6 deaths (25%) from cancer of the pancreas. Three pancreatic cancers were biopsy positive. Average age at onset of pancreatic cancer was 45.6 +/- 7.3 years--considerably younger than for Western populations. When compared with the background pancreatic cancer rate, subjects with TCP appear to have a significantly increased risk of pancreatic cancer: relative risk = 100, 95% CI = 37-218. Even under the most stringent assumptions (restricting the analysis to biopsy-proven cases, assuming that the true background rate of pancreatic cancer in Madras resembles high-risk Western populations, assuming that tropical pancreatitis begins at birth) the risk is still elevated: relative risk = 5, 95% CI = 1.03-3-14.6. The exact mechanism linking various forms of pancreatitis to pancreatic cancer remains to be elucidated.
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PMID:Risk of pancreatic carcinoma in tropical calcifying pancreatitis: an epidemiologic study. 810 73

While the association between pancreatic cancer and diabetes is well recognized, little is known about glucose tolerance and insulin secretion in patients with this tumour. Thirty patients with pancreatic cancer not complicated by diabetes, 10 with nonpancreatic cancer, and 10 healthy subjects were studied for glucose tolerance and insulin secretion in response to an oral glucose load. Twenty of the 30 patients with pancreatic cancer (70%) had impaired glucose tolerance compared with none of the patients in the other two groups. In most of these 20 patients' insulin responses were higher than those of patients with non-pancreatic cancer or healthy subjects. The results indicate that about two-thirds of patients with pancreatic cancer have abnormal glucose tolerance; this intolerance is associated with elevated insulin secretion, suggesting that it may be due to a peripheral resistance to insulin.
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PMID:Glucose tolerance and insulin secretion in pancreatic cancer. 812 96


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