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2014 | 10 | 1 |
Article title

The effect of glycemic control on CEA, CA 19-9, amylase and lipase levels

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EN
Abstracts
EN
Background: Diabetes mellitus is closely related to
pancreas cancer. In this study we aimed to investigate
the effect of hyperglycemia on tumor and inflammation
markers, as well as pancreatic exocrine functions.Methods: A total of 98 consecutive diabetic patients
with poor glycemic control, and 50 healthy controls were
included in the study. We measured hsCRP, erythrocyte
sedimentation rate (ESR), CA19-9, CEA, amylase and lipase
in addition to routine biochemistry tests, before and after
euglycemia was achieved.Results: Fasting blood glucose, HbA1c, CA19-9,CEA,
hsCRP, ESR, triglycerides, AST, ALT, GGT, ALP, total
cholesterol and LDL-C levels decreased significantly with
the regulation of glycemic control. Amylase and lipase
levels increased with the regulation of glycemic control.
After glycemic control, CA19-9 and CEA levels were still
higher, whereas amylase and lipase levels were still lower
in the diabetic group compared with the control group.
Basal HbA1c showed significant correlation with CA19-9,
CEA, amylaseand lipase.Conclusions: We propose to repeat observations of tumor
markers after hyperglycemia is resolved, in order to avoid
unnecessary invasive tests. Our data also suggest that
pancreatic exocrine function was improved with lowering
blood glucose in a short period of time.
Keywords
Publisher
Journal
Year
Volume
10
Issue
1
Physical description
Dates
online
17 - 9 - 2014
accepted
29 - 7 - 2014
received
30 - 3 - 2014
References
  • [1] Giovannucci E., Harlan D.M., Archer M.C., et al., Diabetesand cancer: a consensus report, Diabetes Care., 2010, 33,1674-1685.[WoS]
  • [2] Noy A., Bilezikian J.P., Clinical review 63: Diabetes andpancreatic cancer: clues to the early diagnosis of pancreaticmalignancy, J Clin Endocrinol Metab., 1994, 79, 1223-1231.
  • [3] Locker G.Y, Hamilton S., Harris J., et al., ASCO 2006 update ofrecommendations for the use of tumor markers in gastrointestinalcancer, J Clin Oncol, 2006, 24, 5313-5327.[Crossref]
  • [4] Pines E., Slama J.L., Holeman A., et al., Unusually high level ofCA 19-9 in chronic pancreatitis, Gastroenterol Clin Biol, 1995,19, 641-642.
  • [5] Mukae H., Hirota M., Kohno S., et al., Elevation of tumorassociatedcarbohydrate antigens in patients with diffusepanbronchiolitis, Am Rev Respir Dis, 1993, 148, 744-751.
  • [6] Inayama Y., Uesato M., Takase K., et al., Immunohistochemicalstudy of CA 19-9 and SPan-1 in cases of hydronephrosis, UrolInt, 1996, 57, 93-98.
  • [7] Uygur-Bayramicli O., Dabak R., Orbay E., et al., Type 2 diabetesmellitus and CA 19-9 levels, World J Gastroenterol, 2007, 13,5357-5359.[Crossref][WoS]
  • [8] Benhamou P.Y., Vuillez J.P., Halimi S., et al., Influence ofmetabolic disturbances of diabetes mellitus on serum CA 19-9tumor marker, Diabete Metab, 1991, 17, 39-43.
  • [9] Banfi G., Ardemagni A., Bravi S., et al., Are diabetic metaboliccompensation and CA19.9 really correlated? Int J Biol Markers,1996, 11, 207-210.
  • [10] Gul K., Nas S., Ozdemir D., et al., CA 19-9 level in patientswith type 2 diabetes mellitus and its relation to the metaboliccontrol and microvascular complications, Am J Med Sci, 2011,341, 28-32.[WoS]
  • [11] Dandona P., Freedman D.B., Foo Y., et al.,. Exocrine pancreaticfunction in diabetes mellitus. J Clin Pathol, 1984, 37, 302-306.
  • [12] Turgutalp K., Ozhan O., Helvaci I., et al., Serum levels of cancerbiomarkers in diabetic and non-diabetic proteinuric patients: apreliminary study, Clin Chem Lab Med, 2013, 51, 889-895.[WoS]
  • [13] Malka D., Hammel P., Sauvanet A., et al., Risk factors fordiabetes mellitus in chronic pancreatitis, Gastroenterology,2000, 119, 1324-1332.
  • [14] Levy P., Milan C., Pignon J.P., et al., Mortality factors associatedwith chronic pancreatitis. Unidimensional and multidimensionalanalysis of a medical-surgical series of 240 patients.Gastroenterology, 1989, 96, 1165-1172.
  • [15] Lowenfels A.B., Maisonneuve P., Lankisch P.G., Chronicpancreatitis and other risk factors for pancreatic cancer.Gastroenterol Clin North Am. 1999;28(3):673-685, x.[Crossref]
  • [16] Onitilo A.A., Engel J.M., Glurich I., et al.,Diabetes and cancer I:risk, survival, and implications for screening, Cancer CausesControl, 2012, 3, 967-981.[Crossref][WoS]
  • [17] Onitilo A.A., Engel J.M., Glurich I., et al., Diabetes and cancerII: role of diabetes medications and influence of shared riskfactors., Cancer Causes Control, 2012, 23, 991-1008.[WoS][Crossref]
  • [18] Bussom S., Saif M.W., Methods and rationale for the earlydetection of pancreatic cancer. Highlights from the “2010ASCO Gastrointestinal Cancers Symposium”. Orlando, FL, USA.January 22-24, 2010. JOP, 2010, 11, 128-130.
  • [19] Williams J.A., Goldfine I.D., The insulin-pancreatic acinar axis,Diabetes, 1985, 4, 980-986.[Crossref]
  • [20] Blumenthal H.T., Probstein J.G., Berns A.W., Interrelationshipof Diabetes Mellitus and Pancreatitis, Arch Surg, 1963, 87,844-850.
  • [21] Hardt P.D., Ewald N., Exocrine pancreatic insufficiency indiabetes mellitus: a complication of diabetic neuropathy ora different type of diabetes? Exp Diabetes Res., 2011, 2011,761950.[WoS]
  • [22] Hardt P.D., Brendel M.D., Kloer H.U., et al., Is pancreaticdiabetes (type 3c diabetes) underdiagnosed andmisdiagnosed? Diabetes Care., 2008, 31, S165-169.[WoS]
  • [23] Semakula C., Vandewalle C.L., Van Schravendijk C.F., et al.,Abnormal circulating pancreatic enzyme activities in more thantwenty-five percent of recent-onset insulin-dependent diabeticpatients: association of hyperlipasemia with high-titer islet cellantibodies. Belgian Diabetes Registry., Pancreas., 1996, 12,321-333.[Crossref]
  • [24] Hardt P.D., Krauss A., Bretz L., et al., Pancreatic exocrinefunction in patients with type 1 and type 2 diabetes mellitus,Acta Diabetol, 2000, 37, 105-110.
  • [25] Zini E., Osto M., Moretti S., et al., Hyperglycaemia but nothyperlipidaemia decreases serum amylase and increasesneutrophils in the exocrine pancreas of cats, Res Vet Sci, 2010,89, 20-26.[WoS]
  • [26] Patel R., Shervington A., Pariente J.A., et al., Mechanism ofexocrine pancreatic insufficiency in streptozotocin-inducedtype 1 diabetes mellitus, Ann N Y Acad Sci, 2006, 1084,71-88.
  • [27] Patel R., Atherton P., Wackerhage H., et al., Signalingproteins associated with diabetic-induced exocrinepancreatic insufficiency in rats, Ann N Y Acad Sci, 2006,1084, 490-502.
  • [28] Hayden M.R., Patel K., Habibi J., et al., Attenuation ofendocrine-exocrine pancreatic communication in type 2diabetes: pancreatic extracellular matrix ultrastructuralabnormalities, J Cardiometab Syndr, 2008, 3, 234-243.
Document Type
Publication order reference
YADDA identifier
bwmeta1.element.-psjd-doi-10_1515_med-2015-0002
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