Authors P. Rajeshwari , P.R. Prasad , M. Nagaprasanth3*, Salma Mahaboob R4 1 2 1 Associate Professor in Biochemistry at Fathima Institute of Medial Sciences, Kadapa, Andhra Pradesh, India 2 Professor in Biochemistry at Apollo Institute of Medical Science and Research, Chittoor, Andhra Pradesh, India 3 Assistant Professor in Urology at Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, Telangana, India 4 Assistant Professor in Biochemistry at Fathima Institute of Medial Sciences, Kadapa, Andhra Pradesh, India *Corresponding Author M. Nagaprasanth Assistant Professor in Urology at Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, Telangana, India Email: [email protected]
Introduction Insulin is usually required for treatment i.e
Diabetes mellitus complications a group of patients are insulin dependent. Due to the above metabolic disorders presenting with features this diabetes is also called as brittle hyperglycemia resulting from insulin deficiency diabetes. or decreased glucose utilization and increased It is sometimes divided into two types glucose production. The metabolic abnormalities Type IA: It is due to an autoimmune reaction and of diabetes mellitus causes secondary immunological markers such as antibodies to beta pathophysiological changes in multiple organ islet cell glutamate decarboxylase and insulin system resulting in increased morbidity and itself are present. mortality. Type IB: Immunological markers of autoimmunity are not seen in this type. It is Types of Diabetes Mellitus therefore considered an idiopathic disease. Type I DM It is due to pancreatic beta cell destruction leading Type II DM to insulin deficiency. It is more common in It is characterized by variable degree of insulin children, adolescents and young adults usually resistance impaired insulin secretion and increased below 30 years. These subjects are genetically glucose production. It is preceded by a period of susceptible and are prone to develop ketosis. abnormal glucose homeostasis classified as
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JMSCR Vol||06||Issue||11||Page 741-744||November 2018 impaired fasting glucose or impaired glucose 4) Central Obesity tolerance. Typically it develops with increasing 5) Accelerated cardiovasscular disease. age but again age is no bar and can occur in obese This is probably due to post receptor signaling children and adolescents also. defect in target tissues e.g skeletal muscle. The early terminology of insulin dependent and non insulin dependent diabetes mellitus is not Complications of Diabetes Mellitus used now because type II patients also ultimately Hyperglycemia has wide spread effects on require insulin. different organs and vascular system leading to various complications. MODY: Maturity Onset Diabetes of Young Acute complications This type is characterized by early onset of 1. Diabetic ketoacidosis hyperglycaemia impaired insulin secretions and 2. Hyperglycemic hyperosmolar state autosomal dominant inheritance. Several types of Chronic complications MODY are known depending upon the genetic Micro vascular defects in beta cell functions. They are all 1) Retinopathy and macular odema leading to characterized by insulin resistance and present blindness like type II DM. 2) Neuropathy– Sensory, motor and Gestational Diabetes autonomic Insulin resistance seen in late pregnancy may lead 3) Nephropathy – leading to end stage renal to IGT and frank diabetes called gestational disease. diabetes mellitus. Most subjects revert to normal Macro vascular glucose tolerance after delivery but have increased 1) Coronary artery disease and MI risk of developing DM in future. 2) Cerebrovascular disease stroke etc Diagnosis of Diabetes Mellitus 3) Peripheral vascular disease. According to WHO guidelines any one of the Others following is sufficient to diagnose DM. 1) Cataract and glaucoma 1) Fasting blood glucose levels > 126 mg% 2) Infections – foot ulcer, osteomyelitis etc 2) PPBS levels >200 mg% 3) Skin infections – Candida and other fungal 3) Random blood glucose levels > 200 mg% infections with symptomes of diabetes mellitus. Normal Blood Glucose Levels Diabetic Ketoacidosis FBS: 100 MG % It is the most dreaded acute complication resulting PPBS [2hrs] : 140 mg% after 75gm glucose load from uncontrolled diabetes mellitus leading to Impaired glucose Tolerance serve hyperglycemia. It is characterized by FBS : 101 – 126 mg % dehydreation, hyponatremia, hyperkalemia, PPBS [2hrs]: 140 - 200 mg% after 75gm glucose acidosis and increased anion gap. common clinical load features are nausea, vomiting, pain abdomen, tachycardia, letharginess and CNS depression Insulin Resistance Syndrome with hyperventilatin. Patients breath often has a Also known as metabolic syndrome or the fruity odour of acetone. Ketone body test is syndrome X, it is characterized by strongly positive in urine. 1) Insulin resistance [increased blood glucose Assessment of Glycemic control levels inspite of decreased insulin level] It is done by monitoring blood glucose and 2) Hypertension glucosylated haemoglobin. Blood glucose levels 3) Dyslipidemia indicate the recent glycemic status while HbA1c
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JMSCR Vol||06||Issue||11||Page 741-744||November 2018 indicates the glycemic status over the preceding 8 and risk of cardiovascular disease and – 10 weeks. overall death”. Acta Med Scand; 224: 549- The goals of glycemic controle are to maintain 555. 1. Fasting glucose levels 5. M Deepa, S Farooq, M Datta, R Deepa, V 2. 2hrs PP glucose levels– less than 180mg% Mohan: “Prevalence of metabolic 3. HbA1c – less than 7% of total HB. syndrome using WHO, ATP-III and IDF It is recommended that patients of type I diabetes definitions in Asian Indians: the Chennai should monitor blood glucose levels more Urban Rural Epidemiology Study frequently than type II DM in whome the (CURES- 34)”. Diabetes/Metabolism fluctuation are less and once daily is enough. Research and Reviews. 2006; 23 (2): 127- HbA1c should be monitored twice a year. Normal 134. individuals have glycosylated hemoglobin levels 6. Diagnosis and classification of diabetes of 6% of the total Hb. mellitus”. American diabetes association. Diabetic care. 2012; 35.(1): 64-71. Glycated Hb 7. Clinical Medicine Dr. praveen kumar and Hb molecules in which sugar residues are attached michale clark, 6th edition, 2005. to amino groups of the beta globin chain non 8. Definition, Diagnosis and Classification of enzymatically are called glycated haemoglobulins. diabetes mellitus and its complications. Adults humans have HbA1, HbA2 and HbF. HbA1 World health organization”. W.H.O has three different fractions separated by Consultation. Dept. of Non communicable chromatography i.e HbA1b and HbA1c. disease surveillance. WHO/NCD/ HbA1a1 = Fructose 1-6 bisphospate NCS/99.(2).1999;(1)-49. HbA1 a2 = Glucose 6 –phosphate 9. Klein BE, Klein R, Lee KE: “Components HbA1 b = pyruvic acid of the metabolic syndrome and risk of HbA1c = Glucose. cardiovascular disease and diabetes in Formation of glycated Hb is irreversible and its beaver dam. Diabetes Care 2002”; 25: blood concentration depends upon the life of RBC 1790 – 1794. and blood glucose levels to which it is directly 10. Role of insulin resistance in human proportional. Hence its level in the blood gives an disease”. Reaven GM: Banting lecture estimate of blood glucose over the preceding 6-8 1988.Diabetes 1988; 37: 1595 – 1607. weeks. 11. Malik S, Wong ND, Franklin SS, et al: Impact of the metabolic syndrome on References mortality from coronary heart disease, 1. Williams textbook of endocrinology (12th cardiovascular disease, and all causes in ed.). Philadelphia: Elsevier/Saunders. pp. United States adults. Circulation 2004; 1371–1435. ISBN 978-1-4377-0324-5. 110: 1245 – 1250. 2. Simple treatment to curb diabetes. , 12. Neumann NU, Frasch K: “Coherences January 20, 2014. between the metabolic syndrome, 3. Wild S, Roglic G, Green A, Sicree R, King depression, stress and physical activity”. H. Global prevalence of diabetes: Psychiatr Prax 2008; 36: 110 – 114 [in Estimates for the year 2000 and German]. projections for 2030. Diabetes Care, 2004; 13. Hall MH, Muldoon MF, Jennings JR, et al: 27 (5): 1047–53. Self- reported sleep duration is associated 4. Bengtsson C, Lapidus L, Stendahal C, with the metabolic syndrome in midlife Waldenstrom J. 2002. “Hyper uricemia adults. Sleep 2008; 31: 635 – 643.
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JMSCR Vol||06||Issue||11||Page 741-744||November 2018 14. Pryor, WA. (ed.), Free Radicals in Biology, vols. 1-5, Academic Press, New York, 1981. 15. Ames, BN., Cathcart, R., Schwiers, E. & Hochstein, P. (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 6858- 6862 16. Simon, MI. & Van Vunakis, H., Arch. Biochem. Biophys. 1964; 105, 197-206 17. Howell, RR. & Wyngaarden, JB, J. Biol. Chem., 1960; 235: 3544-3550 18. Matsushita, S., Ibuki, F. & Aoki, A., Arch. Biochem. Biophys. 1963; 102: 446-451 19. Kellogg, EW., III & Fridovich, I., J. Biol. Chem. 1971; 252: 6721-6728 20. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M, Shimomura I. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004; 114: 1752– 1761.
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