Search

The aim of this study was to investigate the nutritional risk status and use of nutritional support among cancer patients enrolled in palliative home care services. Differences in the use of nutritional support in relation to nutritional, social and clinical factors, as well as survival were also investigated.Structured telephone interviews were conducted with cancer patients enrolled in all 21 palliative home care services in the Stockholm region. An interview guide was designed to investigate topics related to the patient's nutritional situation.Interviews with 621 patients were analysed. Sixty-eight percent of the patients were scored as at nutritional risk according on a modified version of NRS-2002. Nutritional support was used by 55% of the patients, with oral nutritional supplements most common and 14% using artificial nutrition. Use of nutritional support was related to low BMI and severe weight loss and was more common in patients with shorter survival times.These findings demonstrate that nutritional support is used to treat already malnourished patients with shorter survival time, rather than to prevent malnutrition. A more structured approach to nutritional issues for patients in palliative phases, which considers life expectancy and psycho-social aspects of nutritional issues, could help identify potential candidates for nutritional support.

We examined the associations of body mass index (BMI), waist circumference, a history of diabetes, and cigarette smoking with risk of pancreatic cancer among 37,147 women and 45,906 men followed up during 560,666 person-years in the Swedish Mammography Cohort and the Cohort of Swedish Men; 136 incident cases of pancreatic cancer were diagnosed. The multivariate rate ratio (RR) of pancreatic cancer for obese women and men (BMI > or =30 kg/m(2)) was 1.81 (95% CI: 1.04-3.15) compared to those with a BMI of 20-25 kg/m(2). For a difference of 20 cm (about two standard deviations) in waist circumference, the multivariate RRs were 1.32 (95% CI: 0.73-2.37) among women and 1.74 (95% CI: 1.00-3.01) among men. Pancreatic cancer risk was associated with history of diabetes (multivariate RR: 1.88; 95% CI: 1.09-3.26) and cigarette smoking (multivariate RR for current compared with never smokers: 3.06; 95% CI: 1.99-4.72). Current smokers of > or =40 pack-years had a five-fold elevated risk compared with never smokers. Risk among past smokers approached the RR for never smokers within 5-10 years following smoking cessation. Findings from this prospective study support positive relationships of overall obesity, abdominal adiposity, diabetes and smoking with risk of pancreatic cancer.

Glutamine is the principal energy source for enterocytes, but it is not known whether parenteral or enteral supplementation is most ben- eficial to gut integrity. The aim of this study was to evaluate the effects of glutamine in uni- or bidirectional supply on the viability of intestinal mucosa of starved rats during incu- bation in Ussing chambers. Seg- ments of jejunum from rats starved for 48 h were randomly mounted in Ussing chambers with three nutrient solutions: Krebs buffer without glu- tamine; 6 mM glutamine added to the mucosal side; 6 mM glutamine added to the mucosal side and 0.6 mM glutamine to the serosal side. ATP content of the mucosa, electrophysiology, and 51 Cr-ethyl- enediaminetetraacetate (EDTA) per- meability were studied during 180 min of incubation. The addition of glutamine to both sides of the stripped mucosa improved ATP lev- els compared to the Krebs solution (P

The cosecretion of insulin and islet amyloid polypeptide (IAPP) is altered when isolated rat pancreatic islets are incubated in culture media conditioned by human pancreatic cancer cells.Pancreatic cancer is usually associated with impaired glucose tolerance. This study investigates the tumor-derived influence on beta-cell secretion of pancreatic islets.Four conditioned media were prepared from two human pancreatic cancer cell lines (Panc-1 and HPAF), a hamster pancreatic cancer cell line (PC-1), and a fibroblast cell line (Ag1523). Isolated rat pancreatic islets were incubated first in the conditioned media or nonconditioned control medium for 24 h, then in the same kind of media containing 100 microM carbamylcholine for 90 min. Insulin and IAPP secretion were measured by radioimmunoassay.Islets in media conditioned by Panc-1 and HPAF cells demonstrated dissociation of insulin and IAPP secretion. During 24-h incubation, the dissociation was expressed as selectively decreased insulin secretion. With addition of 100 microM carbamylcholine, the dissociation was expressed as normal secretion of insulin and hypersecretion of IAPP. As a result, the IAPP/insulin molar ratios were increased in both groups during both time periods. The islets in PC-1 and Ag1523 media did not show any significant changes in insulin and IAPP secretion.

Sir, We thank the authors of this letter for their interest in our manuscript “Diffusion-weighted magnetic resonance imaging of pancreas tumours” [1] and for their valuable and interesting comments. The aim of our study was not to evaluate whether diffusion-weighted (DW)MR imaging of the pancreas can differentiate between pancreas cancer and mass-forming pancreatitis. As a part of the “Discussion” section in our manuscript, we considered it valuable to comment on the false positive findings of the comprehensive MR examination in two patients with mass-forming pancreatitis where DWI was correct in characterizing these lesions as non-malignant. Furthermore we stressed, in the “Discussion” section, that the issue of whether DW MRI can help in distinguishing between these two entities needs to be examined in studies with larger patient groups. The role of DW MRI in differentiation of pancreas cancer and massforming pancreatitis is currently a “hot topic” and there are many reports in the literature with variable results. For example, there are studies showing that ADC values of mass-forming pancreatitis are higher [2, 3] or lower [4, 5] than ADC values of pancreas cancer. Additionally, one study shows that ADC values of mass-forming pancreatitis are indistinguishable from ADC values of the remaining gland [6]. The variability of the ADC values of mass-forming pancreatitis compared with those of pancreas cancer in the aforementioned reports may be explained by the nature of inflammation in the cases of mass-forming pancreatitis, which may happen in the form of either acute relapsing pancreatitis in the setting of chronic pancreatitis that may show increased ADC values or predominant fibrosis that will reveal lower ADC values [6]. Regarding the use of the selected b value of 500 mm/s, we do agree that the T2 shine-through effect might be present, as is not the case in DW images when higher b values (800 or 1,000 mm/s) are selected. But this effect is eliminated in the corresponding ADC map [7, 8], whose use combined with the DW images with b values of 0 and 500 mm/s was a part of the evaluation in the present study. In that way, we did not encounter difficulties with the T2 shine-through effect in benign lesions in DW images with a b value of 500 mm/s. We would like to thank the authors of this letter once again for their interesting comments and express even our belief that the possible role of DW MR imaging in differentiating between pancreas cancer and massforming pancreatitis has to be thoroughly examined. This reply refers to Letter to the Editor available at http://dx.doi.org/10.1007/ s00330-010-1729-3

Alterations of glucose metabolism occur frequently in association with pancreatic cancer. Whether diabetes predisposes or is a consequence of pancreatic cancer has not been settled. We have found that induced diabetes prevents development of pancreatic cancer in the hamster model and that genetically diabetic Chinese hamsters resist pancreatic cancer induction, whereas the nondiabetic strain does not. Also, preliminary clinical data indicates that diabetes is associated with pancreatic cancer and that the two conditions develop simultaneously. We have found diabetes or impaired glucose tolerance in 76% of the pancreatic cancer patients at the time of cancer diagnosis. The diabetic condition improved after 75% pancreatectomy. Although the preliminary observations suggest that diabetes accompanies the disorder of pancreatic cancer, additional data are needed before any conclusion can be drawn.

About 80% of pancreatic cancer patients have glucose intolerance or frank diabetes. This observation has led to the following two hypotheses: i. pancreatic cancer causes the associated diabetes and ii. the conditions associated with diabetes promote the development of pancreatic cancer. Evidence supporting both hypotheses has been accumulated in previous studies. This article reviews these studies, especially those that have been conducted recently.

Our studies have shown that almost all preneoplastic and neoplastic tumors induced in hamsters contain endocrine cells. Because the induced pancreatic cancer resembles the human disease in many respects, it was of interest to find out whether human pancreatic cancer also produce endocrine cells. To examine the participation of the endocrine cells in the exocrine pancreatic cancer, we first examined 32 human pancreatic cancers with the antibodies against insulin, glucagon, somatostatin, PP, VIP, gastrin, and calcitonin or by argyrophilic reaction (1). Thirty (79%) cancers showed ei therfew or many ceils immunoreactive with all but anti-gastrin-, -VIP, and -calcitoniu. Many cells showed an argyrophilic reaction. In 17 cases, the number of stained cells was excessive and the morphology of tumors was consistent with mixed ductal-islet tumor. Argyrophilic ceils and cells immunoreactive with antiinsulin and -glucagon were the predominant in such cases. However, becat~se the biopsy material we used was small and only a few sections from each tumor were examined, it was not possible to determine whether several types of immunoreactive cells reside at the same location, or whether some cells produce more than one peptide. In subsequent studies, we examined larger sections of surgical material from 9 pancreatic cancer patients by serial sections and by using a multilabeled immunohistochemical technique developed at our institute. With this method, we visualized 4 peptides in the same islet. In this study, we also included antibodies against other pancreatic hormones, including pancreastatin, chromogranin A, serotonin, and neuron-specific enolase (NSE). We found that all 9 cancers contained cells immunoreactive with all of the antibodies used, except for pancreastatin, which was missing in 3 cases ,and for PP, which was not detectable in two cases, Here again, insulin was the predominant cell type, followed by glucagon and somatostatin ceils. Many of these hor-mones were found within the same glands. Colocalization of some hormones, such as insulin and serotonin and NSE and glucagon, was indicated. Similar to the situation in hamsters, most endocrine cells were localized on the base of the glands, but many were also within the epithelium and some seem to reach the lumen by a slender neck. In several cases, accumulation of endocrine cells was found in the papillary projections of the malignant epithelium. Because endocrine cells are found at different levels of the malignant epithelium and within the lumen, it seemed that the endocrine ceils migrated within the epithelium, were shed into the lumen like the tumor cells and were replaced by new endocrine cells at the base of the malignant glands. Although many of these endocrine cells resembled the corresponding endocrine cells in the normal islets, some of these endocrine cells were atypical. Some had granules on the supranuclear cell portion. A few endocrine cells were found in the invasive portion of the cancers, including those that had invaded the periuneural space. There were also atypical cells with cytoplasmic vacnolization and irregular granular distribution, possibly as a reflection of the altered synthesis, storage, or release of the granules. On the other hand, differences in the staining intensity could indicate their endocrine activity. Consequently, it appears that in both humans and hamsters, endocrine cells participate in the development of exocrine pancreatic cancer, and these endocrine cells seem to be malignant and have endocrine activity. Nevertheless, participation of endocrine cells in the exocrine pancreatic cancer is conceptually and practically important, particularly in view of epidemiological studies, which link pancreatic cancer with diabetes. In fact, it has been established that more than 80% of pancreatic cancer patients develop frank diabetes or altered glucose tolerance. Our immunohistochemical and experimental studies, as well as clinical studies by Permert and associates (2-4), have led us to believe that endocrine cell proliferation in exocrine pancreatic cancer may cause alteration in hormonal homeostasis leading to glucose metabolic abnormalities. However, studies are required to substantiate this view.