Overview, Uses, Side Effects, Precautions, Interactions, Dosing and Reviews

Andersen, H. O., Hjelt, K., Waever, E., and Overgaard, K. The age-related incidence of meconium ileus equivalent in a cystic fibrosis population: the impact of high-energy intake. J Pediatr Gastroenterol.Nutr 1990;11(3):356-360. View abstract.

Ansaldi-Balocco, N., Santini, B., and Sarchi, C. Efficacy of pancreatic enzyme supplementation in children with cystic fibrosis: comparison of two preparations by random crossover study and a retrospective study of the same patients at two different ages. J Pediatr Gastroenterol.Nutr 1988;7 Suppl 1:S40-S45. View abstract.

Aparisi, L., Rodrigo, J. M., Serra, M. A., Del Olmo, J., Bisquert, M., and Raga, F. [Efficacy of a new microencapsulated pancreatin versus a conventional preparation, in the treatment of steatorrhea of pancreatic origin]. Rev.Esp.Enferm.Apar.Dig. 1989;76(1):25-30. View abstract.

Beverley, D. W., Kelleher, J., Macdonald, A. , Littlewood, J. M., Robinson, T., and Walters, M. P. Comparison of four pancreatic extracts in cystic fibrosis. Arch Dis.Child 1987;62(6):564-568. View abstract.

Bragelmann, R., Armbrecht, U., Rosemeyer, D., Schneider, B., Zilly, W., and Stockbrugger, R. W. The effect of pancreatic enzyme supplementation in patients with steatorrhoea after total gastrectomy. Eur.J Gastroenterol.Hepatol. 1999;11(3):231-237. View abstract.

Braggion, C. and Mastella, G. [Clinical trial of several preparation types of the pancreatic extract Pancrex V in the treatment of cystic fibrosis]. Minerva Pediatr 11-30-1985;37(21-22):891-896. View abstract.

Brown, A., Hughes, M., Tenner, S., and Banks, P. A. Does pancreatic enzyme supplementation reduce pain in patients with chronic pancreatitis: a meta-analysis. Am J Gastroenterol. 1997;92(11):2032-2035. View abstract.

Bruno, M. J., Haverkort, E. B., Tijssen, G. P., Tytgat, G. N., and van Leeuwen, D. J. Placebo controlled trial of enteric coated pancreatin microsphere treatment in patients with unresectable cancer of the pancreatic head region. Gut 1998;42(1):92-96. View abstract.

Buckle, R. M. Maintenance therapy of pancreatic steatorrhoea with concentrated pancreatic extract. Br.J Clin.Pract. 1965;19(12):683-686. View abstract.

Carroccio, A., Pardo, F., Montalto, G., Japichino, L., Iacono, G., Collura, M., and Notarbartolo, A. Effectiveness of enteric-coated preparations on nutritional parameters in cystic fibrosis. A long-term study. Digestion 1988;41(4):201-206. View abstract.

Chazalette, J. P. A Double-Blind Placebo-Controlled Trial of a Pancreatic Enzyme Formulation (Panzytrat 25 000) in the Treatment of Impaired Lipid Digestion in Patients with Cystic Fibrosis. Drug Investigation 1993;5(5):274.

Delchier, J. C., Vidon, N., Saint-Marc Girardin, M. F., Soule, J. C., Moulin, C., Huchet, B., and Zylberberg, P. Fate of orally ingested enzymes in pancreatic insufficiency: comparison of two pancreatic enzyme preparations. Aliment.Pharmacol Ther. 1991;5(4):365-378. View abstract.

DiMagno, E. P., Malagelada, J. R., Go, V. L., and Moertel, C. G. Fate of orally ingested enzymes in pancreatic insufficiency. Comparison of two dosage schedules. N.Engl.J Med 6-9-1977;296(23):1318-1322. View abstract.

Duhamel, J. F., Vidailhet, M., Le Luyer, B., Douchain, F., Jehanne, M., Clavel, R., and Guillot, M. [Multicenter comparative study of a new formulation of pancreatin in gastro-resistant microgranules for the treatment of exocrine pancreatic insufficiency in children with mucoviscidosis]. Ann.Pediatr.(Paris) 1988;35(1):69-74. View abstract.

Elliott, R. B., Escobar, L. C., Lees, H. R., Akroyd, R. M., and Reilly, H. C. A comparison of two pancreatin microsphere preparations in cystic fibrosis. N.Z.Med.J. 3-25-1992;105(930):107-108. View abstract.

Ewald, N., Bretzel, R. G., Fantus, I. G., Hollenhorst, M., Kloer, H. U., and Hardt, P. D. Pancreatin therapy in patients with insulin-treated diabetes mellitus and exocrine pancreatic insufficiency according to low fecal elastase 1 concentrations. Results of a prospective multi-centre trial. Diabetes Metab Res Rev. 2007;23(5):386-391. View abstract.

Farkas, G., Leindler, L., and Mihalovits, G. [Dose-dependent effect of pancreatin replacement upon the pancreatic function in the period after pancreatic surgery]. Magy.Seb. 2001;54(6):347-350. View abstract.

Farkas, G., Takacs, T., Baradnay, G., and Szasz, Z. [Effect of pancreatin replacement on pancreatic function in the postoperative period after pancreatic surgery]. Orv.Hetil. 12-5-1999;140(49):2751-2754. View abstract.

FitzSimmons, S. C., Burkhart, G. A., Borowitz, D., Grand, R. J., Hammerstrom, T., Durie, P. R., Lloyd-Still, J. D., and Lowenfels, A. B. High-dose pancreatic-enzyme supplements and fibrosing colonopathy in children with cystic fibrosis. N.Engl.J Med 5-1-1997;336(18):1283-1289. View abstract.

Gan, K. H., Heijerman, H. G., Geus, W. P., Bakker, W., and Lamers, C. B. Comparison of a high lipase pancreatic enzyme extract with a regular pancreatin preparation in adult cystic fibrosis patients. Aliment.Pharmacol.Ther. 1994;8(6):603-607. View abstract.

Glasbrenner, B., Malfertheiner, P., Kerner, W., Scherbaum, W. A., and Ditschuneit, H. [Effect of pancreatin on diabetes mellitus in chronic pancreatitis]. Z.Gastroenterol. 1990;28(6):275-279. View abstract.

Guarner, L., Rodriguez, R., Guarner, F., and Malagelada, J. R. Fate of oral enzymes in pancreatic insufficiency. Gut 1993;34(5):708-712. View abstract.

Halgreen, H., Pedersen, N. T., and Worning, H. Symptomatic effect of pancreatic enzyme therapy in patients with chronic pancreatitis. Scand J Gastroenterol. 1986;21(1):104-108. View abstract.

Halm, U., Loser, C., Lohr, M., Katschinski, M., and Mossner, J. A double-blind, randomized, multicentre, crossover study to prove equivalence of pancreatin minimicrospheres versus microspheres in exocrine pancreatic insufficiency. Aliment.Pharmacol.Ther. 1999;13(7):951-957. View abstract.

Herrerias, J. M., Gomez, Parra M., Garcia Montes, J. M., Petit, M. A., and Valladolid Leon, J. M. [A comparative cross-over study of pellet pancreatin and tablet pancreatin in chronic pancreatitis]. Rev.Esp.Enferm.Apar.Dig. 1989;76(6 Pt 2):651-653. View abstract.

Isaksson, G. and Ihse, I. Pain reduction by an oral pancreatic enzyme preparation in chronic pancreatitis. Dig.Dis.Sci 1983;28(2):97-102. View abstract.

Jones, R., Franklin, K., Spicer, R., and Berry, J. Colonic strictures in children with cystic fibrosis on low-strength pancreatic enzymes. Lancet 8-19-1995;346(8973):499. View abstract.

Lancellotti, L., Cabrini, G., Zanolla, L., and Mastella, G. High- versus low-lipase acid-resistant enzyme preparations in cystic fibrosis: a crossover randomized clinical trial. J Pediatr.Gastroenterol.Nutr. 1996;22(1):73-78. View abstract.

Lankisch, P. G., Lembcke, B., Goke, B., and Creutzfeldt, W. Therapy of pancreatogenic steatorrhoea: does acid protection of pancreatic enzymes offer any advantage? Z.Gastroenterol. 1986;24(12):753-757. View abstract.

Larvin, M., McMahon, M. J., and Thomas, W. E. G. Creon (enteric coated pancreatin microspheres) for the treatment of pain in chronic pancreatitis: A double blind randomised placebo-controlled crossover study (abstract). Gastroenterology 1991;1000:A283.

Lauque, S., Nourhashemi, F., Baudouin, M., Ghisolfi-Marque, A., Beziat, F., Moreau, J., Dyard, F., Vellas, B., and Albarede, J. L. Assessment of the effectiveness of drug therapies on nutritional status in the elderly: “concerning a randomised, double-blind clinical study of the activity of pancreatic extracts and a placebo during the renutrition of elderly subjects suffering from protein caloric undernutrition”. J Nutr.Health Aging 1998;2(1):18-20. View abstract.

Layer, P. and Groger, G. Fate of pancreatic enzymes in the human intestinal lumen in health and pancreatic insufficiency. Digestion 1993;54 Suppl 2:10-14. View abstract.

Layer, P. and Keller, J. Pancreatic enzymes: secretion and luminal nutrient digestion in health and disease. J Clin Gastroenterol. 1999;28(1):3-10. View abstract.

Littlewood, J. M., Kelleher, J., Walters, M. P., and Johnson, A. W. In vivo and in vitro studies of microsphere pancreatic supplements. J Pediatr.Gastroenterol.Nutr. 1988;7 Suppl 1:S22-S29. View abstract.

Mac Sweeney, E. J., Oades, P. J., Buchdahl, R., Rosenthal, M., and Bush, A. Relation of thickening of colon wall to pancreatic-enzyme treatment in cystic fibrosis. Lancet 3-25-1995;345(8952):752-756. View abstract.

Malesci, A., Gaia, E., Fioretta, A., Bocchia, P., Ciravegna, G., Cantor, P., and Vantini, I. No effect of long-term treatment with pancreatic extract on recurrent abdominal pain in patients with chronic pancreatitis. Scand.J Gastroenterol. 1995;30(4):392-398. View abstract.

McHugh, K., Thomson, A., and Tam, P. Case report: colonic stricture and fibrosis associated with high-strength pancreatic enzymes in a child with cystic fibrosis. Br.J Radiol. 1994;67(801):900-901. View abstract.

Milla, C. E., Wielinski, C. L., and Warwick, W. J. High-strength pancreatic enzymes. Lancet 3-5-1994;343(8897):599. View abstract.

Mischler, E. H., Parrell, S., Farrell, P. M., and Odell, G. B. Comparison of effectiveness of pancreatic enzyme preparations in cystic fibrosis. Am J Dis.Child 1982;136(12):1060-1063. View abstract.

Miyoshi, H. and Kanzaki, T. Drug eruption (erythema multiforme type) due to a digestive enzyme drug. J Dermatol. 1998;25(1):28-31. View abstract.

Mossner, J. Is there a place for pancreatic enzymes in the treatment of pain in chronic pancreatitis? Digestion 1993;54 Suppl 2:35-39. View abstract.

Mossner, J., Secknus, R., Meyer, J., Niederau, C., and Adler, G. Treatment of pain with pancreatic extracts in chronic pancreatitis: results of a prospective placebo-controlled multicenter trial. Digestion 1992;53(1-2):54-66. View abstract.

Nakamura, T., Takebe, K., Kudoh, K., Ishii, M., Imamura, K., Kikuchi, H., Kasai, F., Tandoh, Y., Yamada, N. , Arai, Y., and . Effects of pancreatic digestive enzymes, sodium bicarbonate, and a proton pump inhibitor on steatorrhoea caused by pancreatic diseases. J Int Med Res 1995;23(1):37-47. View abstract.

Neoptolemos, J. P., Ghaneh, P., Andren-Sandberg, A., Bramhall, S., Patankar, R., Kleibeuker, J. H., and Johnson, C. D. Treatment of pancreatic exocrine insufficiency after pancreatic resection. Results of a randomized, double-blind, placebo-controlled, crossover study of high vs standard dose pancreatin. Int.J.Pancreatol. 1999;25(3):171-180. View abstract.

Nouisa-Arvanitakis, S., Stapleton, F. B., Linshaw, M. A., and Kennedy, J. Therapeutic approach to pancreatic extract-induced hyperuricosuria in cystic fibrosis. J Pediatr 1977;90(2):302-305. View abstract.

O’Keefe, S. J. and Adam, J. Assessment of adequacy of pancreatic enzyme replacement with the multiple-phase carbon-14-triolein test. S.Afr.Med J 11-17-1984;66(20):763-765. View abstract.

O’Keefe, S. J., Cariem, A. K., and Levy, M. The exacerbation of pancreatic endocrine dysfunction by potent pancreatic exocrine supplements in patients with chronic pancreatitis. J Clin Gastroenterol. 2001;32(4):319-323. View abstract.

Oades, P. J., Bush, A., Ong, P. S., and Brereton, R. J. High-strength pancreatic enzyme supplements and large-bowel stricture in cystic fibrosis. Lancet 1-8-1994;343(8889):109. View abstract.

Ong, P. S., Oades, P. J., Bush, A., and Brereton, R. J. Colonic stricture in a boy with cystic fibrosis. Postgrad.Med J 1995;71(835):309-312. View abstract.

Patchell, C. J., Desai, M., Weller, P. H., Macdonald, A., Smyth, R. L., Bush, A., Gilbody, J. S., and Duff, S. A. Creon 10,000 Minimicrospheres vs. Creon 8,000 microspheres–an open randomised crossover preference study. J Cyst.Fibros. 2002;1(4):287-291. View abstract.

Petersen, W., Heilmann, C., and Garne, S. Pancreatic enzyme supplementation as acid-resistant microspheres versus enteric-coated granules in cystic fibrosis. A double placebo-controlled cross-over study. Acta Paediatr.Scand 1987;76(1):66-69. View abstract.

Ramo, O. J., Puolakkainen, P. A., Seppala, K., and Schroder, T. M. Self-administration of enzyme substitution in the treatment of exocrine pancreatic insufficiency. Scand.J Gastroenterol. 1989;24(6):688-692. View abstract.

Robinson, P. J., Olinsky, A., Smith, A. L., and Chitravanshi, S. B. High compared with standard dose lipase pancreatic supplement. Arch Dis.Child 1989;64(1):143-145. View abstract.

Sack, J., Blau, H., Goldfarb, D., Ben-Zaray, S., and Katznelson, D. Hyperuricosuria in cystic fibrosis patients treated with pancreatic enzyme supplements. A study of 16 patients in Israel. Isr.J Med Sci. 1980;16(6):417-419. View abstract.

Salen, G. and Prakash, A. Evaluation of enteric-coated microspheres for enzyme replacement therapy in adults with pancreatic insufficiency. Curr Ther Res 1979;25:650-656.

Santini, B. and Ivaldi, A. P. [Pancreatic extract therapy in exocrine pancreatic insufficiency]. Minerva Gastroenterol.Dietol. 1993;39(3):133-137. View abstract.

Shin, S. Y., Hur, G. Y., Ye, Y. M., and Park, H. S. A case of occupational rhinitis caused by porcine pancreatic extract developing into occupational asthma. J Korean Med Sci. 2008;23(2):347-349. View abstract.

Silber, W. Pankreoflat in benign diseases of the oesophagus: a blind therapeutic trial. S.Afr.Med J 7-7-1973;47(26):1137-1138. View abstract.

Slaff, J., Jacobson, D., Tillman, C. R., Curington, C., and Toskes, P. Protease-specific suppression of pancreatic exocrine secretion. Gastroenterology 1984;87(1):44-52. View abstract.

Stapleton, F. B., Kennedy, J., Nousia-Arvanitakis, S., and Linshaw, M. A. Hyperuricosuria due to high-dose pancreatic extract therapy in cystic fibrosis. N.Engl.J Med 7-29-1976;295(5):246-248. View abstract.

Stead, R. J., Skypala, I., and Hodson, M. E. Treatment of steatorrhoea in cystic fibrosis: a comparison of enteric-coated microspheres of pancreatin versus non-enteric-coated pancreatin and adjuvant cimetidine. Aliment.Pharmacol.Ther. 1988;2(6):471-482. View abstract.

Stead, R. J., Skypala, I., Hodson, M. E., and Batten, J. C. Enteric coated microspheres of pancreatin in the treatment of cystic fibrosis: comparison with a standard enteric coated preparation. Thorax 1987;42(7):533-537. View abstract.

Stern, M., Plettner, C., and Gruttner, R. [Pancreatic enzyme replacement in mucoviscidosis (CF): clinical evaluation of a gastric acid-resistant pancreatin preparation in encapsulated microtablet form]. Klin.Padiatr. 1988;200(1):36-39. View abstract.

Taylor, C. J. and Steiner, G. M. Fibrosing colonopathy in a child on low-dose pancreatin. Lancet 10-21-1995;346(8982):1106-1107. View abstract.

Van Hoozen, C. M., Peeke, P. G., Taubeneck, M., Frey, C. F., and Halsted, C. H. Efficacy of enzyme supplementation after surgery for chronic pancreatitis. Pancreas 1997;14(2):174-180. View abstract.

Williams, J., Macdonald, A., Weller, P. H., Fields, J., and Pandov, H. Two enteric coated microspheres in cystic fibrosis. Arch Dis.Child 1990;65(6):594-597. View abstract.

Zentler-Munro, P. L., Assoufi, B. A., Balasubramanian, K., Cornell, S., Benoliel, D., Northfield, T. C., and Hodson, M. E. Therapeutic potential and clinical efficacy of acid-resistant fungal lipase in the treatment of pancreatic steatorrhoea due to cystic fibrosis. Pancreas 1992;7(3):311-319. View abstract.

Zentler-Munro, P. L., Fine, D. R., Batten, J. C., and Northfield, T. C. Effect of cimetidine on enzyme inactivation, bile acid precipitation, and lipid solubilisation in pancreatic steatorrhoea due to cystic fibrosis. Gut 1985;26(9):892-901. View abstract.

Bergner A, Bergner RK. Pulmonary hypersensitivity associated with pancreatin powder exposure. Pediatrics 1975;55:814-7. View abstract.

Brady MS, Garson JL, Krug SK, et al. An enteric-coated high-buffered pancrelipase reduces steatorrhea in patients with cystic fibrosis: a prospective, randomized study. J Am Diet Assoc. 2006;106(8):1181-6. View abstract.

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Carroccio A, Guarino A, Zuin G, et al. Efficacy of oral pancreatic enzyme therapy for the treatment of fat malabsorption in HIV-infected patients. Aliment Pharmacol Ther. 2001;15(10):1619-25. View abstract.

Catarci M, Berlanda M, Grassi GB, Masedu F, Guadagni S. Pancreatic enzyme supplementation after gastrectomy for gastric cancer: a randomized controlled trial. Gastric Cancer. 2018;21(3):542-551. View abstract.

Gardner TB, Munson JC, Morden NE. The FDA and Prescription Pancreatic Enzyme Product Cost. Am J Gastroenterol. 2014;109(5):624-5. View abstract.

Graff GR, Maguiness K, McNamara J, et al. Efficacy and tolerability of a new formulation of pancrelipase delayed-release capsules in children aged 7 to 11 years with exocrine pancreatic insufficiency and cystic fibrosis: a multicenter, randomized, double-blind, placebo-controlled, two-period crossover, superiority study. Clin Ther. 2010;32(1):89-103. View abstract.

Guidance for Industry Exocrine Pancreatic Insufficiency Drug Products – Submitting NDAs. Available at: https://www.fda.gov/ucm/groups/fdagov-public/@fdagov-drugs-gen/documents/document/ucm071651.pdf. Accessed March 29, 2019.

Kahl S, Schütte K, Glasbrenner B, et al. The effect of oral pancreatic enzyme supplementation on the course and outcome of acute pancreatitis: a randomized, double-blind parallel-group study. JOP. 2014;15(2):165-74. View abstract.

Kim H, Yoon YS, Han Y, et al. Effects of Pancreatic Enzyme Replacement Therapy on Body Weight and Nutritional Assessments After Pancreatoduodenectomy in a Randomized Trial. Clin Gastroenterol Hepatol. 2019 Sep 12. pii: S1542-3565(19)30990-5. View abstract.

Lee SK, Kim MS, Lee UH. Acute generalized exanthematous pustulosis induced by a digestive enzyme drug, Festal(®). Clin Exp Dermatol. 2018;43(3):321-323. View abstract.

Munck A, Duhamel JF, Lamireau T, et al. Pancreatic enzyme replacement therapy for young cystic fibrosis patients. J Cyst Fibros. 2009;8(1):14-8. View abstract.

Nagai M, Sho M, Satoi S, et al. Effects of pancrelipase on nonalcoholic fatty liver disease after
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Ramesh H, Reddy N, Bhatia S, et al. A 51-week, open-label clinical trial in India to assess the efficacy and safety of pancreatin 40000 enteric-coated minimicrospheres in patients with pancreatic
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Safdi M, Bekal PK, Martin S, Saeed ZA, Burton F, Toskes PP. The effects of oral pancreatic enzymes (Creon 10 capsule) on steatorrhea: a multicenter, placebo-controlled, parallel group trial in subjects with chronic pancreatitis. Pancreas. 2006;33(2):156-62. View abstract.

Saito T, Nakai Y, Isayama H, et al. A multicenter open-label randomized controlled trial of pancreatic enzyme replacement therapy in unresectable pancreatic cancer. Pancreas. 2018;47:800-806. View abstract.

Santini B, Antonelli M, Battistini A, et al. Comparison of two enteric coated microsphere preparations in the treatment of pancreatic exocrine insufficiency caused by cystic fibrosis. Dig Liver Dis. 2000;32(5):406-11. View abstract.

Satoi S, Sho M, Yanagimoto H, et al. Do pancrelipase delayed-release capsules have a protective role against non-alcoholic fatty liver disease after pancreatoduodenectomy in patients with pancreatic cancer? A randomized controlled trial. J Hepatobiliary Pancreat Sci. 2016;23(3):167-73. View abstract.

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Smyth RL, van Velzen D, Smyth AR, et al. Strictures of ascending colon in cystic fibrosis and high-strength pancreatic enzymes. Lancet 1994;343:85-6. View abstract.

Stern RC, Eisenberg JD, Wagener JS, et al. A comparison of the efficacy and tolerance of pancrelipase and placebo in the treatment of steatorrhea in cystic fibrosis patients with clinical exocrine pancreatic insufficiency. Am J Gastroenterol. 2000;95(8):1932-8. View abstract.

Taylor CJ, Thieroff-Ekerdt R, Shiff S, Magnus L, Fleming R, Gommoll C. Comparison of two pancreatic enzyme products for exocrine insufficiency in patients with cystic fibrosis. J Cyst Fibros. 2016;15(5):675-80. View abstract.

Thorat V, Reddy N, Bhatia S, et al. Randomised clinical trial: the efficacy and safety of pancreatin
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Friday Fix: ABCs of Vitamins

Common vitamin and mineral deficiencies in people with cancer include vitamins A, C and E, beta-carotene, selenium, folate, magnesium, iron and zinc. These deficiencies may be caused by reduced food intake, increased nutrient needs and/or increased nutrient losses.

We asked Maria Petzel, senior clinical dietitian for the Pancreas Surgery Program at MD Anderson Cancer Center in Houston and an emeritus member of the Scientific and Medical Advisory Board for the Pancreatic Cancer Action Network, what pancreatic cancer patients should know about vitamins.

Here are seven things to know:

• In general, vitamin and mineral supplements are not recommended for pancreatic cancer patients unless they are known to have a deficiency.
• If you’re undergoing chemotherapy and/or radiation, and are known to have a deficiency, it’s important to talk about vitamin and mineral supplements with your treating physician, because they could affect treatment.
• Fat-soluble vitamins are A, D, E and K. For this reason, fat malabsorption – the inability to absorb nutrients – may contribute to deficiencies in these vitamins, as well as calcium, iron and zinc.
• Pancreatic enzymes may help improve fat malabsorption and nutrient digestion; speak with your healthcare team about this option.
• Patients who have had the Whipple surgery can be deficient in B-12 and iron. Patients who are experiencing diarrhea can be deficient in iron and zinc.
• Bone health is very important for patients who have had the Whipple surgery, so they need to get adequate vitamin D and calcium. Vitamin D is lacking in a typical diet these days, plus, our sun exposure is limited, so discuss vitamin D supplements with your physician. Unlike vitamin D, calcium can’t be measured through a blood test, so be vigilant about getting enough calcium in your diet and then monitor through bone density screenings.
• Healthy foods and/or nutritional supplement drinks can help replace vitamins and minerals. Here’s a recipe with bok choy and salmon, both good sources of calcium.

For more information about diet and nutrition for pancreatic cancer patients, including a free booklet and resources to find a dietitian, contact PanCAN Patient Services.

Pancreatitis Diet | Columbia Surgery

Overview | Causes | Genetics | Symptoms | Diagnosis | Treatment | Auto Islet Transplants | Diet | Prognosis | FAQ

Nutrition is a vitally important part of treatment for patients with pancreatitis. The primary goals of nutritional management for chronic pancreatitis are:

• Prevent malnutrition and nutritional deficiencies
• Maintain normal blood sugar levels (avoid both hypoglycemia and hyperglycemia)
• Prevent or optimally manage diabetes, kidney problems, and other conditions associated with chronic pancreatitis
• Avoid causing an acute episode of pancreatitis

To best achieve those goals, it is important for pancreatitis patients to eat high protein, nutrient-dense diets that include fruits, vegetables, whole grains, low fat dairy, and other lean protein sources. Abstinence from alcohol and greasy or fried foods is important in helping to prevent malnutrition and pain. 

Nutritional assessments and dietary modifications are made on an individual basis because each patient’s condition is unique and requires an individualized plan.   Our Pancreatitis Program offers nutritional and gastrointestinal support for those with pancreatitis.

Vitamins & Minerals 

Patients with chronic pancreatitis are at high risk for malnutrition due to malabsorption and depletion of nutrients as well as due to increased metabolic activity. Malnutrition can be further affected by ongoing alcohol abuse and pain after eating. Vitamin deficiency from malabsorption can cause osteoporosis, digestive problems, abdominal pain, and other symptoms.

Therefore, patients with chronic pancreatitis must be tested regularly for nutritional deficiencies. Vitamin therapies should be based on these annual blood tests. In general, multivitamins, calcium, iron, folate, vitamin E, vitamin A, vitamin D, and vitamin B12 may be supplemented, depending on the results of blood work.

If you have malnutrition, you may benefit from working with our Registered Dietitian who can guide you towards a personalized diet plan.

Risk of diabetes in chronic pancreatitis

Chronic pancreatitis also causes the pancreas to gradually lose its ability to function properly, and endocrine function will eventually be lost. This puts patients at risk for type 1 diabetes. Patients should therefore avoid refined sugars and simple carbohydrates. 

Enzyme Supplementation

If pancreatic enzymes are prescribed, it is important to take them regularly in order to prevent flare-ups.

The healthy pancreas is stimulated to release pancreatic enzymes when  undigested food reaches the small intestine. These enzymes join with bile and begin breaking down food in the small intestine.

Since your pancreas is not working optimally, you may not be getting the pancreatic enzymes you need to digest your food properly. Taking enzymes can help to digest your food, thus improving any signs or symptoms of steatorrhea (excess fat in the stool, or fat malabsorption). In turn this will improve your ability to eat better, lowering your risk for malnutrition.

Alcohol

If pancreatitis was caused by alcohol use, you should abstain from alcohol. If other causes of acute pancreatitis have been addressed and resolved (such as via gallbladder removal) and the pancreas returned to normal, you should be able to lead a normal life, but alcohol should still be taken only in moderation (maximum of 1 serving/day). In chronic pancreatitis, there is ongoing inflammation and malabsorption — patients gradually lose digestive function and eventually lose insulin function — so regular use of alcohol is unwise.

Smoking

People with pancreatitis should avoid smoking, as it increases the risk for pancreatic cancer.

Next Steps

If you or someone you care for is dealing with a pancreatitis, the Pancreas Center is here for you. The Pancreatitis Program works with nutritionists to provide helpful diet suggestions that help manage the impact of the disease. 

Call us at (212) 305-4795 or use our online form to get in touch today.

To keep learning about pancreatitis:

Overview | Causes | Genetics | Symptoms | Diagnosis | Treatment | Auto Islet Transplants | Diet | Prognosis | FAQ

Related Services

Related Topics

Association between vitamin C intake and the risk of pancreatic cancer: a meta-analysis of observational studies

Vitamin B6, vitamin B12 and methionine and risk of pancreatic cancer: a meta-analysis | Nutrition Journal

Role of Vitamin D in the Prevention of Pancreatic Cancer

Pancreatic cancer is a malignancy of poor prognosis which is mostly diagnosed at advanced stages. Current treatment modalities are very limited creating great interest for novel preventive and therapeutic options. Vitamin D seems to have a protective effect against pancreatic cancer by participating in numerous proapoptotic, antiangiogenic, anti-inflammatory, prodifferentiating, and immunomodulating mechanisms. 25-hydroxyvitamin D [25(OH)D] serum concentrations are currently the best indicator of vitamin D status. There are three main sources of vitamin D: sun exposure, diet,and dietary supplements. Sun exposure has been associated with lower incidence of pancreatic cancer in ecological studies. Increased vitamin D levels seem to protect against pancreatic cancer, but caution is needed as excessive dietary intake may have opposite results. Future studies will verify the role of vitamin D in the prevention and therapy of pancreatic cancer and will lead to guidelines on adequate sun exposure and vitamin D dietary intake.

1. Introduction

1.1. Epidemiology

Pancreatic cancer exhibits some of the lowest overall survival rates in oncology, and its incidence has been underestimated for years. Approximately 6% of all cancer-related deaths are associated with pancreatic cancer and around 32,000 Americans are diagnosed and die from this disease annually [1]. It is the fourth leading cause of cancer mortality in both men and women. One-year and 5-year survival rates are estimated at 24% and 4.3%, respectively [2]. One of the main reasons for this dismal prognosis is the lack of an effective screening method as pancreatic cancer is difficult to diagnose in its early disease stages. At time of diagnosis, 52% of patients have distant metastases and in 26% of cases, the disease has spread locoregionally [2].

Pancreatic cancer has a higher prevalence among men and African-Americans. Results from several epidemiologic studies have suggested that several environmental factors may be associated with developing pancreatic cancer, but tobacco smoking was the only established risk factor [3]. It was shown that a larger waist circumference and waist-to-hip ratio were associated with a statistically significant increased risk of developing pancreatic cancer, although greater body mass index and lack of total physical activity were not identified as risk factors [3]. According to Patel et al., obesity and central adiposity are correlated to increased pancreatic cancer risk [4]. Diabetes mellitus was associated with greater pancreatic cancer incidence [5, 6], although there is limited data supporting the theory that sugars or sweets are pathogenetically implicated [7]. Finally, high red and processed meat intake was linked to elevated risk but this is probably secondary to carcinogenic substances used during meat processing.

1.2. Current Treatment Modalities

The only existing pancreatic cancer treatment which offers the potential of cure is surgical resection. Nevertheless, as stated above, most patients are diagnosed at advanced stage and are not likely candidates for surgical therapy [2].

Despite continuing research, limited progress has been made in the treatment of advanced pancreatic cancer. For over a decade, gemcitabine was the acceptable standard treatment, but its use as monotherapy in advanced and metastatic stages of pancreatic cancer has been in question as only small benefit has been shown. Multiple gemcitabine-based therapeutical regimens have been studied (i.e. gemcitabine combined with molecular targeting agents, farnesyltransferase inhibitors, and metalloproteinase inhibitors) [2]. The combination of gemcitabine plus erlotinib is the only one that seems to prolong survival [8].

Therefore, treatment for patients with advanced pancreatic cancer is primarily palliative. Initial monotherapy with 5-fluorouracil (5-FU) has been widely administered, but it did not demonstrate any benefit for overall quality of life or survival. Response rates were less than 10% [9]. Clinical trials with chemoradiation and multiple chemotherapeutic regimens (doxorubicin or doxorubicin/mitomycin, cisplatin) alongside 5-FU failed to prolong overall survival, although response rates were better with some of the regimens. Increased toxicity was another reason that these regimens were not explored further [10–12].

1.3. Genetic Basis for Pancreatic Cancer

The genetic basis of pancreatic cancer has been extensively studied. Mutation or silencing of p53, p1, and DPC4/s mad4 genes is associated with pancreatic cancer, but K-ras mutations (in codons 12, 13, and 16) are the most frequently noticed mutations [13]. K-ras mutations have also been found to poor prognostic factors for patients who have undergone surgery and adjuvant chemoradiation. It should also be noted that in a preclinical study Fleming et al showed that certain deleting K-ras mutations may result in altering cancerous behavior of pancreatic tumor cells [14].

2. Vitamin D Is a Protective Factor

Due to the fact that pancreatic cancer carries one of highest mortality rates and is very resistant to treatment, there are efforts to find protective factors. Vitamin D seems to prevent not only pancreatic cancer, but also colon, ovary, and breast cancer [15–18]. According to a most recent epidemiological analysis by Garland et al, raising serum levels of vitamin D would prevent 58000 new cases of breast cancer and 49000 of new cases of colorectal cancer each year [19].

2.1. Sources of Vitamin D

There are three main vitamin D sources for humans: sunlight exposure (ultraviolet B radiation: UVB), diet, and dietary supplements [20, 21]. Sunlight irradation is the most important, and early-life exposure has already been associated with decreased cancer risk in several malignancies, such as prostate cancer [22–24]. Brief body exposure directly to direct sunlight during summer is all that is required to make enough cholecalciferol (vitamin D₃) for the daily vitamin D requirements. During sun exposure, UVB radiation (wavelength of 290 to 315 nm) pierces through the skin and converts 7-dehydrocholesterol (provitamin D3) in the skin to previtamin D3. Since previtamin D3 is very unstable, it is rapidly transformed to its more stable form of vitamin D3, which is then absorbed across the subcutaneous capillary bed to enter general circulation [20, 25]. Mohr et al. (2010) confirmed earlier findings that the incidence of pancreatic cancer was higher in countries with lower UVB irraidiance [26]. There is an ever growing number of ecological studies regarding cancer incidence that corroborate the inverse correlation of pancreatic cancer to solar UVB exposure in Western and in Asian countries [27–34]. Ecological studies are very helpful when examining such a topic, as much of the risk for cancer occurs with early-life effects in the first 20 years of life, starting with conception [35]. A recent study used Hill’s criteria of causality to assess the value of UVB and vitamin D in reducing cancer risk and concluded that results for several cancers satisfy these criteria [36, 37]. Vitamin D intoxication secondary to prolonged sun exposure is not observed, as excess previtamin D3 and vitamin D3 readily absorb sunlight and are converted into inactive photoproducts [38]. Thus, vitamin D intoxication through sunlight has never been reported in life guards, who experience excessive sun exposure [38]. There are public health concerns since excess ultraviolet radiation exposure is implicated in skin cancer, development of cataract, premature photoageing and skin hypersensitivity when certain drugs are concomitantly used, even with a short amount of time of sun exposure [39]. It is worth noting that vitamin D produced which during the sunny months (spring, summer and fall) is stored in the body fat but it is not known whether it can be actually used in winter months, unless, maybe, in case of significant adipose tissue loss [40]. Unfortunately, vitamin D production through sunlight exposure is often not sufficient for people with dark skin, urban areas as well as for those largely confined indoors [39, 41, 42]. Furthermore, latitude plays an important role because in temperate zones (23.5°–66.5°), people are unable to synthesize vitamin D for 1 month of the year due to insufficient UVB and those nearer to the poles (>66.5°) do not get enough UVB radiation for most of the year [43, 44].

In absence of required sunlight exposure, vitamin D can be obtained from dietary sources or supplements [39]. Only few foods are known to naturally contain considerable amounts of vitamin D: oily fish such as sardines, salmon, and mackerel and fish oils such as cod liver oil [40, 45]. Certain foods, such as milk, orange juice, bread, and cereal, are fortified with vitamin D [46–48]. There are two forms of supplemental vitamin D, D2, and D3 [45]. Ergosterol is produced in plants and yeast, whereas 7-dehydrocholesterol, which is its immediate precursor in the cholesterol biosynthetic pathway, is produced in animals [40, 45]. UVB sunlight radiation converts ergosterol and 7-dehydrocholesterol, into vitamin D2 (ergocalciferol) and D3 (cholecalciferol), respectively [40, 45]. Although some believe D3 is more potent than D2 [49], this has not been confirmed by the literature [50].

2.2. Metabolism of Vitamin D

Vitamin D (both D₂ and D3 forms) is converted to 25-hydroxycholecalciferol [25(OH)D-also known as calcidiol] in the liver. This form is then further hydroxylated to 1,25-dihydroxycholecalciferol [1,25(OH)₂D-also known as calcitriol] in the kidneys [20, 21]. 25-hydroxycholecalciferol is used to measure the vitamin D levels, although 1,25-dihydroxycholecalciferol is the active form [20, 21]. Therefore, hereon in this review, the term vitamin D will refer to 25-hydroxycholecalciferol, unless otherwise stated. High-affinity receptors in the nucleus help the active compound regulate gene transcription in many cells [21]. They are found not only in target organs (gut, bone, kidney, and parathyroid) [51], but also in many other tissues, such as brain, breast, colon, heart, pancreas, prostate, skin, and the immune system [52]. The rate-limiting step of the vitamin D conversion pathway is interesting: the vitamin D 1-α-hydroxylase enzyme converts 25(OH)D to 1,25(OH)₂D and was initially thought to exist only in kidneys which regulate the systemic levels of vitamin D. It has been recently found that this enzyme is expressed in many other organs as well, such as the pancreas. This locally produced calcitriol does not enter systemic circulation and therefore does not affect calcium metabolism. It remains in the region and offers protection to the cells that produce it and cells nearby [52].

2.3. Protective Action of Vitamin D and Probable Molecular Mechanisms

The importance of vitamin D in cancer prevention was originally derived from epidemiological data that associated season of diagnosis and sun exposure with cancer incidence and mortality [53–62]. From these observational studies, it was obvious that sun exposure was inversely correlated to cancer incidence and mortality. Protective features of solar radiation exposure have been attributed to elevated serum levels of 25(OH)D.

This hypothesis was later supported by dietary [58, 63] and mechanistic studies [64–66]. It has been shown that vitamin D not only has a protective but also a therapeutic effect on many malignancies [67–72]. These actions of vitamin D are mediated by a number of proapoptotic, antiangiogenic, anti-inflammatory, prodifferentiating, and immunomodulating mechanisms [16, 73, 74]. Despite theoretical concerns, evidence-based studies have shown that vitamin D has no adverse effect on chemotherapy or radiation therapy [75]. More over, there seems to be synergy with chemotherapy and radiotherapy. The role of vitamin D as an anticancer agent is just starting to be explored; however, initial results are promising [76–78]. A recent phase II study showed that high-dose calcitriol with docetaxel may increase time to progression in patients with incurable pancreatic cancer when compared to docetaxel monotherapy [79]. Paricalcitol is a less calcemic vitamin D analogue which has been found to be in vitro and in vivo effective in inhibiting tumor growth in vitro and in vivo, via upregulation of p21 and p27 tumor suppressor genes. It constitutes an attractive novel therapy for pancreatic cancer [74].

The active form of vitamin D, 1,25(OH)₂D, or calcitriol is as a steroid hormone involved in molecular mechanisms that prevent cellular malignant transformation. Some of the vital cellular actions of vitamin D are involved in intracellular signaling pathways [66], cell cycle and cellular growth [80, 81], differentiation [82, 83], adhesion [84], and apoptosis [85, 86]. Calcitriol mediates all these actions by binding to a nuclear receptor known as vitamin D receptor (VDR), which is expressed in many cell types [87]. It enters the cellular cytoplasm and binds to nuclear VDR. This complex migrates to the nucleus, binds to vitamin D-responsive elements (VDREs), and activates promoters of responsive target genes. Based on the type of complex formed, calcitriol regulates initiation or suppression of gene expression [84]. A brief account of the effects of vitamin D on cell division, differentiation, adhesion, and apoptosis is summarized below.(1)Cellular division and differentiation.(i)Vitamin D regulates the levels of p21 and p27, which in turn control the cell cycle [88].(ii)Cyclin D activates cyclin-dependant kinases (CDKs) in order to increase transcription of genes controlling the transition from G₁ to S phase. Calcitriol binds to cyclin D and inhibits this transition [88].(iii)The accuracy of DNA replication and DNA repair is controlled by cell cycle surveillance mechanisms. Tumor suppressor gene p53 is activated in case of DNA damage and increases p21 levels; therefore, CDKs are inhibited and cell cycle arrest is induced. Vitamin D is involved in this process as it regulates p21 and p53 levels [89, 90].(iv)Calcitriol increases expression of BRCA-1 and -2 tumor suppressor genes contributing in the DNA repair mechanism [91]. (2)Cell adhesion: when a cancer cell loses its adhesion features, it acquires metastatic potential. Calcitriol increases E-cadherin and changes the location of β-catenin, reducing intracellular mRNA concentration of c-myc [69].(3)Cell death (apoptosis): caspases mediate apoptosis and are activated by p53, which is increased in DNA damage. Calcitriol upregulates genes involved in apoptosis by regulating p53 levels [92, 93].

Vitamin D is implicated in other molecular pathways as well. It is known to decrease vascular growth factor (VEGF), which is essential in tumor angiogenesis [45]. VDR growth control has been recently found to vary considerably between different malignancies suggesting tissue-specificity of the above vitamin D dependent pathways [94]. Finally, vitamin-D-binding-protein (DBP) is considered to be deglycosylated in cancer patients causing inability to activate macrophages. More specifically, Gc protein-derived macrophage activating factor (GcMAF) is a naturally derived form of human DBP with a single terminal O-linked GalNac sugar residue and plasma levels of O-linked trisaccharide glycosylated DBP have been found associated with GcMAF precursor activity. Studies in cancer patients have shown that α-N-acetylgalactosaminidase (nagalase) activity is inversely correlated to this precursor activity, and this could explain why cancer patients are relatively unable to activate macrophages. However, reports on this subject have been conflicting [95].

Recent studies have demonstrated the role of vitamin D in pancreatic cancer. It reduces the risk for pancreatic cancer by regulating cell cycle and differentiation [96]. Vitamin D 1-α-hydroxylase enzyme levels were found elevated in malignant pancreatic cells, suggesting that vitamin D is a protective factor [96]. EB1089, an calcitriol analogue with low calcemic activity, is a potent inhibitor of parathyroid hormone-related peptide (PTHRP) production in vitro and has shown protective features concerning proliferation and differentiation of pancreatic cancer cells [97] and xenografted malignant cells [98].

2.4. Role of Dietary Vitamin D

Although several environmental factors have been studied, only smoking has been found to be strongly associated with pancreatic cancer. Serum levels of vitamin D have been extensively studied in several malignancies. Prediagnostic levels were not always associated with incidence [99] but numerous studies have shown that higher serum levels at diagnosis are correlated with increased survival [100–104]. The literature concerning the role of diet in the development of pancreatic cancer is minimal. One study that examined dietary vitamin D intake and pancreatic cancer was not able to show an association [105]. However, this could be attributed to the fact that the median reported dietary intake of vitamin D in this study was about half of the U.S. defined required daily intake of vitamin D. Skinner et al. suggested a role of dietary vitamin D in pancreatic cancer oncogenesis and prevention. They monitored dietary vitamin D intake and pancreatic cancer incidence over a period of 16 years. They used a standardized 131-item semiquantitative food-frequency questionnaire to monitor vitamin D intake. The final analysis of their prospective cohort study showed that participants that consumed ≥600 IU/d of dietary vitamin D had 41% lower risk for pancreatic cancer when compared to those consuming <150 IU/d [63]. The results of the American Institute for Cancer Research Report [106] as well as those of the most recent systematic review of the Tufts Practice Center sponsored by the Institute of Medicine and the World Health Organization [107] have been valuable regarding vitamin D-calcium interactions and Dietary Reference Intake (DRI) recommended values are concerned. Nonhypercalcemic analogues of the active form of cholecalciferol may offer chemoprevention against gastrointestinal cancer by tightly regulating cell differentiation.

One of the major limitations in the analyses of these studies is the lack of an accurate nutrient database in order to assess vitamin D levels in dietary, supplemental and pharmaceutical sources. A widely accepted reference is the United States Department of Agriculture (USDA) National Nutrient Database, which is currently being revised. The new version should be compared to the current one in order to assess, whether the association which found between vitamin D and pancreatic cancer actually exists.

2.5. Adequate Levels and Sources of Vitamin D

There is a continuous debate concerning the adequate level of vitamin D in the human body. Even though there is no established consensus, 25(OH)D levels lower than 20 ng per liter (50 nmol per liter) are usually defined as vitamin D deficiency [108, 109]. 25(OH)D levels ranging from 21–29 ng (52–72 nmol per liter) are considered as relatively insufficient and levels greater than 30 ng (75 nmol per liter) can be accepted sufficient [110, 111]. Finally, experts consider levels exceeding 150 ng per liter (374 nmol per liter) as vitamin D intoxication [45]. Unfortunately, all these reference levels are based on myoskeletal studies and the required levels for nonskeletal functions might be different. In malignancies, vitamin D levels are high both systemically as well as locally therefore, the optimum level is expected to be higher. Garland et al. assume that this level will be at least as high as 40 to 50 ng/mL (100–125 nmol/L), and some experts consider these levels as adequate to prevent malignancies [16, 73]. However, opinions vary as cohorts have contradictory results on this subject [112, 113]. A most recent study reported that greatly increased vitamin D concentrations were associated with a statistically significant 2-fold increase in overall pancreatic cancer risk therefore, recommendations on increasing vitamin D intake should be thoroughly considered [114].

Regarding the distribution of pancreatic cancer risk, there have been two studies suggesting a U-shaped serum 25(OH)D level dose-disease relation [115, 116]. These findings have not been reproduced by other studies but the differences may be attributed to differences in the vitamin D pancreatic risk association between men and women [63], smokers and nonsmokers [117], and high and low residential UVB exposure [115]. A critical approach by Grant et al. (2009) [117] supports that data on U-shaped distribution are too limited to be used as basis for public health policies. The review of the International Agency for Research on Cancer also noted the need to further assess the potential for U-shaped association between vitamin D status and risk of pancreatic cancer [116].

In order to achieve serum levels of 50 ng/ml, oral supplementation of 4000 IU/day vitamin D is recommended or a supplementation of 2000 IU/day plus 12 minutes of daily sun exposure of 50% of the body surface area [16]. These doses are very unlikely to cause intoxication; however, it is advisable to monitor vitamin D levels every 3 months. Finally, optimum and adequate levels of vitamin D need to be defined for each disease category and recommendations are still under debate. Even though the daily dietary requirements vary with age and sun exposure, the currently accepted vitamin D daily dietary intake is 200–600 IU/day [16].

2.6. Assessment of Vitamin D Levels

Serum 25(OH)D is used to estimate vitamin D body levels. However, as most tissues express vitamin D 1-α-hydroxylase (CYP27B1), the active form of vitamin D, 1,25(OH) vitamin D, may be increased locally. Therefore, based on the systemic levels of 25(OH)D, we are likely to underestimate the local active form concentration, which is the most important factor for tumor suppression [16]. Depending on sun exposure, 25(OH)D levels also tend to fluctuate around the year. Daily levels do not fluctuate significantly within the same season, but they are known to vary greatly between seasons. Consequently, it should be noted that serum levels reflect dietary intake as well as sun exposure and they do not represent long-term exposure, which is of interest in epidemiological studies. Serum vitamin D levels are also thought to be influenced by genotype (VDR polymorphisms, CYP27A1, CYP27B1, CYP24A1 variant alleles) as the latter affects vitamin D transport and metabolism [73, 118–120]. The best method of estimating vitamin D serum levels is yet to be defined.

3. Conclusion

Recent literature has provided plenty of information concerning the preventive and therapeutic role of vitamin D in many malignancies, including pancreatic cancer. Daily doses needed to achieve protective levels have not been determined yet, and it is possible that levels vary between cancer types and stages. Increase vitamin D levels seem to protect against pancreatic cancer but caution is needed as greatly increased dietary intake may have opposite results. No accurate nutrient database has been established yet; therefore, interpretation of data should be done with caution. Better assessment of sun exposure in the future as well as better food compositional data may help clarify whether the association between vitamin D and pancreatic cancer actually exists. Ongoing clinical trials will assist in verifying the role of vitamin D in the prevention and therapy of pancreatic cancer and in clarifying the molecular pathways implicated. Future studies will lead to guidelines concerning adequate sun exposure and vitamin D dietary intake.

Conflict of Interests

The authors declare no conflict of interest.

Declaration of Helsinki

Conformed.

Pancreatic Insufficiency | MUSC Health

What is pancreatic insufficiency?

Pancreatic Insufficiency (EPI) is a condition which occurs when the pancreas does not make enough of a specific enzyme the body uses to digest food in the small intestine.

The pancreas is a glandular organ. That means the pancreas secretes juices that maintain the proper function of the body. The pancreas produces both enzymes and hormones.

Enzymes and Hormones

Enzymes are catalysts that perform specific chemical functions in the body, such as breaking down foods, or synthesizing DNA. Enzymes control chemical reactions. The pancreas also secretes digestive enzymes which are released into the small intestine and play an important role in breaking down food products for absorption.

Hormones are signaling chemicals that tell the body how to respond to a specific stimulus. The adrenal gland releases a hormone when you are shocked or frightened. The islet cells of the pancreas secrete the hormones insulin and glucagon into the bloodstream. Insulin causes the body’s cells to take up glucose from the blood; glucagon causes the liver to release glucose into the blood.

Symptoms of pancreatic insufficiency

Symptoms may include:

• abdominal pain and tenderness
• loss of appetite
• feelings of fullness
• weight loss and diarrhea

Pancreatic insufficiency may also cause bone pain and muscle cramps.

What causes pancreatic insufficiency?

When the pancreas becomes damaged, pancreatic enzymes are not produced, and malabsorption results. Malabsorption is the result of food that is not properly converted into usable energy by the digestive system.

The pancreas may become damaged by:

• recurring inflammation of the pancreas
• previous pancreatic surgery
• it is rarely caused by cancer

Additionally, there are genetic factors that may cause damage to the pancreas:

• cystic fibrosis, a disease damages glandular organs by creating mucus that impairs their function
• Shwachman-Diamond Syndrome, a rare autosomal recessive disorder

Risk factors of pancreatic insufficiency

Chronic pancreatitis is a serious risk factor resulting from too many instances of pancreatic inflammation. It has many causes, but chronic alcohol abuse is the most common one in western countries. Chronic pancreatitis and subsequent insufficiency can also run in families (hereditary pancreatitis and cystic fibrosis).

Severe malabsorption may cause deficiencies in vitamins and minerals.

Clinical features of pancreatic insufficiency

Patients with chronic pancreatitis may not have any symptoms. However, with ongoing destruction of the gland and loss of its function, symptoms of malabsorption may develop. Chronic pancreatitis can also manifest with abdominal pain, and diabetes.

Diagnosis of pancreatic insufficiency

Pancreatic insufficiency is suspected in a patient who develops diabetes, upper abdominal pain and features of malabsorption. Bowel movements classically are bulky, loose and foul smelling; because of their oily nature, they may float in the toilet bowl, and are difficult to flush.

Simple investigations used to diagnose chronic pancreatitis include:

• an abdominal X-ray (which can show calcifications in the pancreas)
• stools collected and analyzed for high fat content
• CT scan
• MRI scan
• endoscopic ultrasound

Occasionally, the pancreas becomes so chronically inflamed that a scarred mass may develop which can be difficult to distinguish from pancreatic cancer.

Treatment of pancreatic insufficiency

When chronic pancreatitis is discovered, attempts are made to remove causative factors.

• reduce high blood fat (triglyceride) levels
• reduce alcohol use or abuse
• stimulate pancreatic duct drainage using dilation, or stents
• surgery

There are reports of the use of antioxidants (selenium, vitamin A, vitamin C, and vitamin E) to reduce ongoing inflammation.

Conclusion

In terms of maldigestion from chronic pancreatitis, enzyme supplements are usually prescribed. These supplements are in the form of pills which contain pancreatic enzymes. The pills are taken before and during each meal.

Depending on the type of supplements, an antacid may also be prescribed, as some pancreatic supplements are broken down by gastric acid.

Dietary changes are also suggested; a low fat diet (30g fat per day) will reduce the amount of steatorrhea and sometimes abdominal pain associated with chronic pancreatitis. Since fat can be so significantly malabsorbed, supplements of fat soluble vitamins (vitamin D, A, E, and K) may be prescribed.

90,000 Vitamins and trace elements involved in the regulation of pancreatic function and carbohydrate metabolism (Cr, K, Mn, Mg, Cu, Zn, Ni, vitamins A, B6)

Study to monitor the level of vitamins and trace elements that support the normal functioning of the pancreas and carbohydrate metabolism.

Synonyms Russian

Chromium, potassium, manganese, magnesium, copper, zinc, nickel, vitamin A (retinol), vitamin B6 (pyridoxal-5-phosphate).

Synonyms English

Chromium, Potassium, Manganese, Magnesia, Copper, Zinc, Nickel, Vitamin A (retinol), Vitamin B6 (pyridoxine).

Research method

High performance liquid chromatography.

What biomaterial can be used for research?

Venous blood.

How to properly prepare for the study?

• Do not eat for 8 hours before the study, you can drink clean still water.
• Do not smoke within 30 minutes prior to examination.

General information about the study

The pancreas has endocrine and exocrine functions.Endocrine function is directly related to carbohydrate metabolism in the body. Diagnostic information about the state of the pancreas and carbohydrate metabolism can be obtained from the results of a study of certain vitamins and microelements.

The role of vitamin A , or retinol , in the work of the pancreas is multicomponent and is still being studied. Thus, decreased levels of vitamin A were found in patients with type 1 diabetes mellitus and increased levels in patients with type 2 diabetes mellitus.He takes part in the work of the pancreas, carbohydrate and lipid metabolism. Vitamin B6 participates in the synthesis of proteolytic enzymes of the pancreas. Vitamin B6 also prevents endothelial dysfunction, which is characteristic of patients with diabetes mellitus, reduces insulin resistance and reduces the accumulation of lipids in the liver.

Zinc ( Zn ) participates in both the exocrine and endocrine functions of the pancreas, including the secretion of glucagon, the activation of digestive enzymes, and the secretion of insulin.Given this broad functional spectrum, dysregulation of zinc metabolism in the pancreas impairs many processes, including glycemic control, and is also associated with pancreatic cancer and chronic pancreatitis.

In diseases associated with the pancreas, especially in patients with diabetes mellitus, control the level of potassium (K) in the blood, since its level is interrelated with the level of insulin in the blood. Insulin is an important regulator of potassium homeostasis, as it prevents the body from overloading with potassium due to its intracellular buffering, thereby minimizing the effects of hyperkalemia.It is worth noting that both hypokalemia and hyperkalemia are asymptomatic, but very dangerous conditions, since they have a strong arrhythmogenic effect.

Copper ( Cu ) is an essential trace element that participates in more than 50 enzymatic processes. In diabetes mellitus, an increase in copper in the blood can be observed, but more often this is associated with inflammatory complications that these patients are susceptible to.In diagnostics, the balance of zinc and copper in patients with diabetes mellitus is also important, since these trace elements balance each other. In diabetes, zinc levels decrease, as do copper levels, which can lead to higher blood glucose levels and higher levels of insulin resistance. In addition, these micronutrients reduce the number of free radicals, reducing the risk of developing diabetic neuropathy, retinopathy and nephropathy.

Magnesium ( Mg ) is a cofactor of more than 300 enzymes involved in carbohydrate metabolism.Magnesium deficiency can stimulate increased insulin resistance in both people with and without diabetes. Magnesium deficiency is considered as a factor associated with the development and complications of type 2 diabetes mellitus.

Chromium ( Cr ) plays an important role in carbohydrate metabolism. Studies have linked chromium deficiency to hyperglycemia, increased insulin resistance, and dyslipidemia. In type 2 diabetes mellitus in combination with obesity, this deficiency can be observed in people who consume excessive amounts of rapidly absorbed carbohydrates, which increase the excretion of chromium in the urine.In addition, chromium is involved in the mechanisms of satiety and thermogenesis, and therefore in the control of food intake.

Manganese ( Mn ) is a component of the body’s antioxidant system. A sufficient amount of manganese contributes to the normal synthesis of insulin, regulates the process of glucogenesis.

According to some reports, nickel ( Ni ) in physiological concentrations is able to influence the duration of insulin action, thereby reducing the load on the pancreas.However, studies more often consider elevated nickel concentrations as a damaging factor and their role in the pathogenesis of diabetes mellitus.

What is the research used for?

• To control the balance of trace elements and the concentration of vitamins in diseases of the pancreas and diseases associated with impaired carbohydrate metabolism.
• For diagnostics of poisoning with metal compounds.

When is the study scheduled?

• For complex diagnostics in patients with newly diagnosed diseases of the pancreas and diseases associated with impaired carbohydrate metabolism.
• For preventive examinations of patients with diseases of the pancreas and diseases associated with impaired carbohydrate metabolism.
• For various pathologies to control the balance of trace elements in order to correct treatment and prevent complications in patients with pancreatic diseases and diabetes mellitus.
• For preventive examinations of patients whose activities are related to the extraction and processing, as well as contact with metal compounds.

What do the results mean?

Reference values ​​

Manganese: 0 – 2 μg / l

Magnesium: 0 – 2 μg / l

Potassium: 132.6 – 195 mg / l

Nickel: 0.6 – 7.5 μg / l

Chromium: 0.05 – 2.1 μg / l

Copper: 575 – 1725 μg / l

Zinc: 650 – 2910 μg / l

Vitamin A: 0.3 – 0.8 μg / ml

Vitamin B6: 8.7 – 27.2 ng / ml

The results are assessed by the attending physician taking into account the pathology, history, clinic and the results of other examination methods.

What can influence the result?

• Age;
• the presence of bad habits;
• comorbidities and medication.

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Products for the pancreas

The pancreas is responsible for the full existence of a person, his hormonal background, lifestyle and well-being.It is possible to regulate the health of the pancreas with the help of a correct lifestyle and a good balanced diet.

The pancreas is responsible for the full existence of a person, his hormonal background, lifestyle and well-being. If the production of enzymes and insulin is disrupted, serious diseases develop: pancreatitis and diabetes mellitus. It is possible to regulate the health of the pancreas with the help of a correct lifestyle and a good balanced diet.Not all products are equally useful for the body, there are some that will have to be abandoned forever. If the first signs of the disease appear, you should also forget about bad habits (alcohol, tobacco smoking, the use of sugary carbonated drinks, etc.).

In the difficult stage of the onset of acute symptoms of the disease, it is difficult to find an optimal diet. All meals should contain a complete nutritional composition (vitamins, minerals, polyunsaturated fatty acids). But many products that are allowed during remission become a real poison for an inflamed, irritated organ.So, during an exacerbation of pancreatic diseases, you need to eat:

• Steamed vegetables – especially useful is zucchini, which contains all the substances and vitamins necessary for a full existence.
• Baked apples – Do not eat raw.
• Porridge – especially oatmeal, buckwheat, millet and wheat – is a source of B vitamins and complex carbohydrates, thanks to which satiety comes quickly, and the feeling of hunger is eliminated for several hours.
• Freshly prepared fruit drinks and compotes.

What foods are good for the pancreas

Porridge. It is a staple product for everyone who strives to lead a healthy lifestyle and adhere to a healthy diet. They contain a large amount of vitamins and minerals that are retained after heat treatment. Buckwheat, spelled, oatmeal, rice, wheat, millet and other cereals bring great benefits to the body, saturating it for a long period.An important condition: you need to eat porridge in small portions, combining with vegetables.

Useful vegetables for the pancreas

Onions – the product contains vitamins and natural substances that can fight bacteria. People with diseases of the gastrointestinal tract and pancreas should use this product only in processed form. See also: How to save money on food. What Products Save Your Budget

Garlic – contained in the allicin composition has a bactericidal and fungicidal effect, allowing the body to remain healthy and fulfill its functional purpose.A large number of important trace elements and vitamins are able to protect from the harmful effects of the environment. Garlic should not be consumed raw during an exacerbation of pancreatitis. During such periods, you can either completely abandon its use, or steam the product, simmer it in the oven, slow cooker (without adding oil).

Zucchini is one of the healthiest foods for the pancreas. It can be boiled, steamed, baked in the oven or over a fire. The high amount of fiber in vegetables helps the body eliminate accumulated toxins that negatively affect organ health.The product does not contain coarse fibers and essential oils that irritate the walls of the gland.

Cabbage – all varieties are useful for the organ: broccoli, cauliflower, Peking cabbage, white cabbage. The product has anti-carcinogenic properties and the ability to remove toxins. Regular consumption of cabbage will help improve and facilitate the digestion of food.

Pumpkin is one of the healthiest, rich in vitamins and minerals, delicious and nutritious foods for the pancreas. The porridge comes out of it rich and healthy.And processed in the oven or steamed with other vegetables and fruits, pumpkin helps the body get rid of toxins and improve the work of the gland.

Sweet potatoes – rich in nutrients and antioxidants that are good for the pancreas. In combination with orange vegetables, they help reduce the likelihood of developing cancer and exacerbations of chronic processes.

Carrot – a vegetable that has a beneficial effect on the digestion processes and promotes the healing of wounds, erosions, and other mechanical damage to the mucous membranes.

Spinach – a leafy vegetable contains almost all B vitamins, iron and other minerals. Regular consumption of the product will help to establish digestion and improve organ function.

What is important to know about pancreatic cancer

Experts: Fedor Vetshev , Professor of the Department of Faculty Surgery, Sechenov University, Doctor of Medical Sciences

Alexey Tryakin, Chief Researcher, Department of Clinical Pharmacology and Chemotherapy, N.N.N. N. Blokhina, Member of the Board of the Russian Society of Clinical Oncology (RUSSCO), Doctor of Medical Sciences

Pancreatic cancer (PC) is one of the most aggressive cancers. Life expectancy statistics for patients with this diagnosis remains one of the most lethal. Typically, cancer affects the gland itself or its ducts. And it progresses rapidly. But he does it quietly, without giving himself away. That is why a malignant tumor of the pancreas is dangerous – it is asymptomatic, almost elusive.Only a third of cases of the disease are detected at the third stage, when metastases have not yet sprouted into neighboring organs, but have already affected the blood vessels. Otherwise, the disease manifests itself when the treatment becomes almost ineffective. And no amount of money will help change the situation. The list of victims of this insidious disease includes world celebrities, owners of large capital, including Apple founder Steve Jobs, queen of the blues Aretha Franklin, and the great tenor Luciano Pavarotti.

It is compulsory to see a doctor!

Despite the fact that there are no early signs of prostate cancer and there are practically no chances of catching the disease in the initial stage, doctors advise to be attentive to your body and be alert if you suddenly lose your appetite, feel unpleasant sensations in the stomach and pancreas, or suddenly lose weight for no reason.The onset of the disease may even be associated with such banal symptoms as constipation, weakness, general malaise, and bloating. All this is a reason to go to the doctor. This usually happens, the patient comes with complaints of stomach pain or other unpleasant symptoms, while he, of course, is far from thinking that he has cancer. But the diagnostician does an MRI or CT scan and accidentally finds a node in the pancreas. When this happens, this incident is almost a happy one. More often, patients already with pronounced jaundice come to the doctor, when the tumor has spread into the bile ducts.By the way, pain and jaundice are considered the most common symptoms of pancreatic cancer. They are noted in 90% of patients. As a rule, they are accompanied by light feces, dark urine. At such a moment, they talk about a common oncological process.

Know your genome

The main risk factor for prostate cancer is genetic. “If there is a clear heredity in the family, not necessarily pancreatic cancer, but also stomach, breast, colon and small intestine cancers, it’s a reason to go to a medical genetist,” warns Alexey Tryakin.- If specialists identify a gene that causes the development of this type of cancer, they will give recommendations on what to do next. And if they do not find out, then I would still recommend to be examined at least once a year – to do an ultrasound scan, or better an MRI, in order to live in peace. ”

What does vitamin D have to do with it?

Oncologists are aware of the relationship of prostate cancer not only with genetics, but also with lifestyle. The gland, which does not tolerate either nicotine or alcohol, cruelly avenges bad habits and even excess in food, namely the excessive consumption of red meat, fried and smoked. “The risk factors for pancreatic cancer can reasonably include chronic pancreatitis, diabetes mellitus, liver cirrhosis, obesity – says our expert Fedor Vetshev . – According to the latest data, a link has been found between a long-term lack of vitamin D. A low level of insolation and vitamin deficiency, coupled with other factors, can lead to a certain condition in the body that can trigger the development of pancreatic cancer.This does not mean that if a vitamin deficiency is detected (and it is found in most people in our country), everyone will have pancreatic cancer. But this is another of the potential risk factors recognized by a number of scientists. And it must be taken into account, especially with a hereditary predisposition ” .

Treatment process

In the history of world oncology, there have not yet been cases of a complete cure for pancreatic cancer.The difficulties of treatment are associated with the biological feature of the tumor and the anatomical feature of the pancreas itself. Even if surgeons manage to operate on the tumor and remove everything radically, metastases still penetrate the liver. If the process is in the first and second stages, then treatment, as a rule, begins with a radical operation, and then postoperative chemotherapy is prescribed. If the process has spread and has already invaded large vessels passing through this area, then treatment includes chemotherapy and sometimes radiation therapy to reduce the size of the tumor and make surgery possible.In the fourth stage, when metastases have penetrated the liver or lungs, only chemotherapy is carried out in order to prolong the patient’s life as much as possible.

New in treatment

Oncological science does not stand still, and today specialists perform such manipulations that ten years ago seemed just fantastic. It is they that maximize the chance of survival of patients with pancreatic cancer. And the chances of curing prostate cancer really increase if you do the operation at the very beginning of the disease, before the metastases go further.“Currently, when it is impossible to remove a pancreatic tumor surgically, a new method of irreversible electroporation is used,” says Alexey Tryakin. – Electrodes are inserted into the tumor and thus create an electromagnetic field that kills living cells. But this method is not a panacea, because the issue is not in the local control of the tumor, but in the fact that it gives early metastases, which, in fact, kill. If we talk about chemotherapy, then until recently it was believed that it is ineffective in treating an early tumor.In recent years, evidence has emerged that drug therapy is useful to give patients after surgery in order to reduce the risk of developing metastases. Chemotherapy can now be performed before surgery. Moreover, today it is not the same chemotherapy with severe side effects. There is also a breakthrough in this direction. If the procedure is carried out correctly, then in most cases it is possible to cope with such unpleasant symptoms as nausea and vomiting, although weakness and diarrhea still remain. Of course, there are treatment regimens that are less toxic, but also less effective.And the doctor always balances between the patient’s condition and the choice of therapy methods. ”

Steve Jobs’ disease

Among the latest world news in the fight against pancreatic cancer is the development of specialists from the Salk Institute for Biological Research (USA). Scientists promise to defeat the disease even at the fourth stage. The so-called stellate cells of the pancreas in prostate cancer begin to produce proteins that create a protective membrane around the tumor.They also produce the signaling protein LIF, which stimulates tumor growth. Experiments in mice have shown that if LIF is blocked, tumor growth can be slowed down even with chemotherapy. In addition, LIF may become a more effective marker of pancreatic cancer than the one currently used (CA-19-9), it more accurately reflects both tumor growth and the response of its cells to chemotherapy.

Another scientific discovery is connected with an experiment on growing pancreatic islets “in vitro”.However, there is no talk of growing the organ itself yet. Also, doctors reject the method of transplantation. “First of all, you need to understand that pancreatic cancer is a systemic disease, not a disease of one organ, so everything will not end here with a transplant, – says Fedor Vetshev . – Even if you recall the story of Steve Jobs, then he received a liver transplant after surgery on the pancreas, because metastases reached the liver, and chemotherapy was not effective.Nevertheless, Steve Jobs fought the disease for more than eight years and was able to live longer than doctors predicted, but was unable to defeat cancer. Of course, transplantation is not a panacea, because it does not get rid of cancer. Nevertheless, in a number of cases, transplantation can probably be considered as one of the treatment options for patients with pancreatic cancer in the future ” .

Source: KIZ.RU

90,000 Pancreatic enzyme supplements for people with cystic fibrosis

Review question

We reviewed the evidence about how good pancreatic (pancreatic) enzyme supplements are for overcoming enzyme deficiencies in people with cystic fibrosis, and whether these supplements have any side effects.

Relevance

80% to 90% of people with cystic fibrosis take pancreatic enzyme supplements. In these people, the pancreas is usually unable to produce the enzymes needed to digest food, which can lead to delayed weight gain and developmental delay in children. In adults, this can lead to weight loss and malnutrition as the body does not absorb vitamins properly. In both children and adults with cystic fibrosis, malnutrition is associated with lower levels of general health, more severe lung disease, and shorter life expectancy.If the pancreas does not produce enough enzymes, then people with cystic fibrosis may also experience unpleasant symptoms such as painful, frequent, bulky, unpleasant bowel movements. Thus, pancreatic enzyme supplements are needed to help gain weight, prevent malnutrition and avoid certain vitamin deficiencies, and control intestinal symptoms. This is an updated version of the review.

Search date

The last search for evidence was conducted on 15 July 2016.

Research characteristics

The review included 13 studies involving 512 adults and children with cystic fibrosis; all of them had treatment for 4 weeks. The studies compared different preparations of pancreatic enzymes, so we were unable to combine many of the results. In addition, the design in 12 studies implied that study participants received both types of supplements for four weeks each, although the order in which they were received was randomly selected. It also made it difficult to analyze the results.Most of the studies were old; the most recent was in 2015 and the oldest in 1986.

Main results

We were able to combine data from only two small studies in which people took miniature drug capsules (microspheres) that were designed to delay drug release until it passed from the stomach into the small intestine, as well as tablets regular size, designed in the same way.The results were not clearly in favor of one treatment or the other for any of the most important outcomes (weight, height, or body mass index). However, those who took the delayed-release microcapsules had less fecal fat than those who took the delayed-release tablets (regular size), and had less abdominal pain and no need to go to the toilet. often. In another study, those people who took the delayed-release microcapsules also had less stool fat than those who took conventional drugs without the delayed-release drug.We did not find any evidence that one kind of these enteric coated microcapsules was better than another; or that enteric-coated microcapsules were better than enteric-coated mini-microcapsules (which were smaller).

We found no evidence for different doses of enzymes needed for people with different levels of pancreatic enzymes, better timing to start treatment, and different amounts of supplementation based on differences in diet (food intake) and amount of food.. Carefully designed research is needed to answer these questions.

Quality of evidence

We could not be sure that the people in the included studies were equally likely to be included in different treatment groups, as no details were published on how these decisions were made. In several studies, large numbers of participants dropped out of the studies, and the reasons for this were often not presented.In most studies, people received one treatment and then, after a while, changed it to an alternative treatment. We were able to combine the results of only two studies designed in such a way that the results may be more consistent than they really are when we analyze them. In conclusion, several studies did not fully report the results so that we can analyze them in this review. We are not sure how these factors affect our confidence in the results we found.

Detrimax 2000 instructions for use: indications, contraindications, side effects – description Detrimax 2000 Film-coated tablets (56641)

Detrimax ^® 2000 contains vitamin D ₃ (colecalciferol) – a vital fat-soluble vitamin necessary to provide activity of almost all organs and systems of the human body.

The role of vitamin D in ensuring the activity of organs and systems

Musculoskeletal system. Participates in the regulation of phosphorus-calcium metabolism: helps to absorb calcium in the intestine, maintains the necessary levels of calcium and phosphorus in the blood, activates bone metabolism. Promotes bone strength and reduces the risk of rickets and osteomalacia. Maintaining normal vitamin D levels is critical at any age, but especially in the elderly, when the risk of falls and bone fractures is increased. Vitamin D strengthens teeth by activating the production of dentin, the main constituent of dental hard tissue.Adequate levels of vitamin D in the body reduce the risk of tooth decay. Helps maintain muscle strength and neuromuscular conduction. Vitamin D deficiency is associated with muscle weakness, which, especially in the elderly, may have difficulty walking.

Endocrine system. Vitamin D is involved in the regulation of the function of almost all endocrine glands. Stimulates the synthesis of female and male sex hormones: estrogen, progesterone, testosterone.Contributes to the maintenance of the normal function of the thyroid and parathyroid glands, adrenal cortex, and insulin-secreting β-cells of the pancreas.

Reproductive function. Vitamin D has a positive effect on reproductive function in both women and men, incl. in couples planning a pregnancy or having difficulty conceiving a child. In women with sufficient vitamin D levels, egg fertilization occurs more frequently. The absence of vitamin D deficiency can improve the results of IVF.Vitamin D is able to have a positive effect on the endometrium, inhibiting proliferative processes, improves ovarian folliculogenesis and promotes egg maturation.

Carbohydrate and fat metabolism. Vitamin D improves carbohydrate-fat metabolism, has a positive effect on glucose and insulin metabolism, and vitamin D deficiency is a risk factor for the development of insulin resistance, impaired glucose tolerance. Vitamin D can stimulate insulin secretion by β-cells of the pancreas, and also indirectly activates calcium-dependent β-cell endopeptidase, which converts proinsulin into active insulin.Vitamin D can affect tissue insulin sensitivity by stimulating the expression of insulin receptors in cells. Vitamin D can help reduce blood levels of total cholesterol, triglycerides, and low-density lipids. Due to these properties, vitamin D plays an essential role in the correction of obesity and metabolic disorders. Inhibits lipid peroxidation processes.

Cardiovascular system. Vitamin D plays an important role in maintaining the function of the cardiovascular system: it has a positive effect on the inner layer and the muscular wall of blood vessels, as well as on blood coagulation processes.It has a positive effect on the activity of the renin-angiotensin system, which is involved in the regulation of blood pressure, helping to normalize the tone of arterial vessels and preventing an increase in blood pressure.

Immune system. Contributes to the maintenance of healthy immune function by positively affecting both innate and acquired immunity. It triggers the synthesis of its own antimicrobial substances in the cells of the skin, epithelium of the respiratory and gastrointestinal tract: the proteins cathelicidin and defensin, which destroy viruses, bacteria and fungi, thereby helping to reduce the risk of developing colds.Vitamin D regulates the synthesis of substances (anti-inflammatory mediators) by immune cells that help suppress inflammatory reactions in the body, and also suppresses autoimmune reactions, preventing the development of immune-inflammatory conditions.

Nervous system. Vitamin D participates in the processes of regulation of the nervous system, positively affecting cognitive functions: memory, attention, the ability to assimilate information, performance. Vitamin D plays an important role in the brain’s defense mechanisms against damage – neuroprotection.It helps to improve mood by participating in the process of converting tryptophan (an amino acid that enters the body with food) into serotonin, a neurotransmitter that is of great importance for the psychoemotional state of a person. Vitamin D can have a positive effect on pain sensitivity by suppressing the synthesis of inflammatory mediators by immune cells.

Bronchopulmonary system. Vitamin D is essential for the maintenance of normal lung function.Participates in the maintenance of airway muscle function, regulation of immune cell activity and a healthy inflammatory response. Vitamin D helps to improve the respiratory function of the lungs and increase the body’s defenses against a wide range of infections, including tuberculosis and acute respiratory infections.

Leather. Vitamin D helps to improve metabolic processes in the skin, increase its protective properties and launch programs to restore the function of skin cells. Vitamin D is a factor protecting the skin from photoaging (in which the barrier function of the skin and collagen production decreases, the skin loses its elasticity, becomes dry and flabby, prone to the development of inflammatory changes).

Digestive system. Vitamin D affects the homeostasis of the gastrointestinal mucosa, helping to protect and maintain the integrity of the epithelial barrier and its healing ability. By influencing the function of immune cells, vitamin D helps to suppress autoimmune inflammatory processes in the intestines. Vitamin D has a positive effect on the function of the gastrointestinal tract.

Regulation of energy metabolism. Vitamin D helps to relieve fatigue and increase the tone of the body by regulating the energy potential of cells: as a result of the influence of vitamin D in the mitochondria of cells, the production of ATP (adenosine triphosphate) increases, which is its own universal source of energy for all biochemical processes in the body.

Regulation of cell growth. Vitamin D has a regulatory effect on cell growth, development and renewal.

Epidemiological studies carried out in Russia have established that a reduced concentration of vitamin D in the blood is observed in 50-92% of the adult population of working age and children, regardless of the season of the year.

The reasons for vitamin D deficiency in most of the Russian population are both its insufficient consumption with food and a low level of its synthesis in the skin due to the geographical location of the territory of the Russian Federation (low insolation).

Health disorders associated with vitamin D deficiency:

• The main manifestation of vitamin D deficiency in childhood is rickets, in adults – osteomalacia;
• Vitamin D deficiency in the elderly is primarily associated with muscle weakness, poor physical function and imbalance, and increased bone fragility.

The Food, Nutrition and Allergy Commission of the Food Committee of the European Food Safety Authority has established a link between dietary intake of vitamin D and its contribution to the normal functioning of the immune system.

Vitamin D ₃ (colecalciferol) when taken orally is almost completely absorbed (up to 80%) in the distal small intestine due to the formation of micellar compounds in the medium of the small intestine. C _max in tissues is reached after 4-5 hours, after which the concentration decreases slightly, remaining at a constant level for a long time.

* TRTS 022/2011, “Food products in terms of their labeling”;
** Does not exceed the upper permissible level of consumption, “Unified sanitary-epidemiological and hygienic requirements for goods subject to sanitary-epidemiological supervision (control)” of the EurAsEC Customs Union.

Get tested for vitamin B in the blood

Method of determination
Linked immunosorbent assay.

Study material
Blood serum

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Vitamin B12 is necessary for DNA synthesis, hematopoiesis and normal functioning of the nervous system.

Synonyms: Cobalamin; Cyanocobalamin; Antianemic vitamin.

Cobalamin; B12; Cobalamins; Cyanocobalamin; Vitamin B12.

Brief characteristics of the analyte Vitamin B12

Vitamin B12 (cobalamin) is a water-soluble vitamin that plays an important role in the functioning of the nervous system and the development of blood cells. Vitamin B12 contains cobalt and a cyano group in its structure, which form a coordination complex. In tissues, various forms of cobalamin act as coenzymes.In the human body, vitamin B12 is synthesized in very small quantities by the intestinal microflora. The main source of cyanocobalamin is animal products (nutritional yeast, milk, meat, liver, kidneys, fish, egg yolk). In human milk, vitamin B12 is contained in the form of methylcobalamin.

During digestion in the stomach, cyanocobalamin binds to the intrinsic Kastl factor – a protein produced by the parietal cells of the body and fundus of the stomach and necessary for the absorption of vitamin B12.This complex is absorbed in the small intestine, in the cells of the intestinal mucosa, vitamin B12 is released and binds to another protein – transcobalamin, which delivers cyanocobalamin to the liver and tissues.

Vitamin B12 plays an important role in metabolic processes, participates in protein, fat and carbohydrate metabolism.

The liver is the main place of vitamin B12 deposition. A large amount of cobalamin is deposited in the spleen and kidneys, slightly less in the muscles. The total supply of cobalamin in the body of an adult is about 2-5 mg.Vitamin metabolism is very slow. Vitamin B12 is excreted in the bile; in the intestine, most of it is reabsorbed.

Vitamin B12 is a cofactor for the enzyme homocysteine ​​methyltransferase, which is involved in the conversion of the amino acid homocysteine ​​to methionine. Methionine is important for the synthesis of phospholipids and the myelin sheath of neurons.

Cobalamin deficiency quickly leads to an increase in serum homocysteine ​​concentration, which has a cytotoxic effect and increases the risk of developing cardiovascular diseases.Homocysteine ​​serves as one of the best markers for determining the status of vitamin B12 in the body. However, an increase in the level of homocysteine ​​is also noted with a deficiency of folic acid, vitamin B6, in patients with renal failure, hypothyroidism, etc.

It takes a long time for the development of vitamin B12 deficiency with a reduced intake of it in the body: about 5-6 years. With its lack, the most pronounced changes are observed in rapidly dividing cells of the bone marrow, mouth, tongue and gastrointestinal tract, which leads to impaired hematopoiesis, glossitis, stomatitis and intestinal malabsorption.With a deficiency of vitamin B12, macrocytic anemia develops, hematopoietic processes are disrupted (in particular, the division and maturation of erythrocytes), the number of erythrocytes in the blood decreases, and their average volume increases, hypersegmentation of neutrophils develops, and pancytopenia occurs.

What can lead to Vitamin B12 deficiency

A number of factors can lead to impaired absorption of vitamin B12: insufficient intake of nutrients from food; decreased secretion or absence of intrinsic Castle factor, gastric resection; small intestine pathology; diseases of the pancreas, leading to an increase in the acidity of intestinal contents; long-term use of certain medicines.

Nutritional deficiency of vitamin B12 can develop in persons adhering to a vegetarian or vegan diet. Competitive consumption of vitamin B12 by microorganisms and helminths parasitizing in the small intestine can lead to the development of B12-deficiency anemia. Clinical manifestations of vitamin B12 deficiency are numerous disorders in the hematopoietic, nervous and endocrine systems, atrophy of the mucous membranes of the gastrointestinal tract, the development of funicular myelosis (damage to the spinal cord).

Cyanocobalamin deficiency often develops in the elderly and is accompanied by neurological disorders.

Infants with a genetically determined defect in the enzymes needed to convert vitamin B12 into a coenzyme, or a low level of plasma carrier protein, develop megaloblastic anemia, which manifests itself as early as the first weeks or months of life and is characterized by normal or slightly reduced levels of vitamin B12 in the blood … With anemia that develops as a result of malabsorption, the level of vitamin B12 is always low.

Since cobalamin and folic acid are involved in the same biochemical processes, a deficiency of both vitamins leads to the development of macrocytic anemia.

Therefore, it is recommended to determine their level at the same time. In true vitamin B12 deficiency, folate levels are usually normal or even elevated, but a combined deficiency is also possible. If you suspect B12-deficiency anemia, it is recommended to conduct a general clinical blood test with the determination of the absolute and relative number of reticulocytes and erythrocyte indices (MCV, MCN, MCSU), to confirm the diagnosis, as well as a biochemical blood test, including the determination of the level of total protein, albumin, ALT , AST, urea, creatinine, LDH, total bilirubin, free bilirubin, ferritin, serum iron, TIBC, transferrin, to assess the functional state of the liver, kidneys, pancreas.The main symptoms of B12-deficiency anemia are expressed by gradually increasing weakness, apathy, exercise intolerance, palpitations, dyspeptic disorders, numbness of the limbs and a gradual loss of sensitivity in the fingers.