Hyperglucagonemia â€“ a Potent Threat which can Worsen the Diabetes Mellitus
Background: Diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic coma (HHNK) are two serious acute complications of diabetes mellitus. DKA consists of the biochemical triad of hyperglycemia, ketonemia and acidemia. In DKA and HHNK dehydration and sodium depletion is seen. Lack of insulin causes hyperglycemia and also inhibits entry of potassium into the cells leading to hyperkalemia. Moreover Hyperglucagonemia also contributes to hyperglycemia and can worsen the diabetic state.
Study Design: This study was retrospective, analytical case control study. Non - probability convenient sampling technique was used.
Materials and Methods: We reviewed the hospital admissions and patients coming to OPD with type1 & 2 diabetes mellitus as well as diabetic complications like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic non-ketotic coma (HHNK). We compared the groups for plasma glucose, plasma osmolality, plasma glucagon, serum electrolytes and arterial blood gases (ABGs) with control group.
Results: Twelve persons were considered as control being non-diabetic with normal oral glucose tolerance. Mean plasma glucose level & mean plasma osmolality level in the patients of uncontrolled type 2 diabetes mellitus, uncontrolled type I diabetes mellitus, DKA and HHNK was significantly higher (p < 0.001) as compared with control subjects. Mean plasma glucagon level in the patients of uncontrolled type I diabetes mellitus and DKA was found significantly higher (p < 0.001) as compared with control subjects. Serum potassium level was significantly higher in patients of uncontrolled type 2 diabetes mellitus, uncontrolled type 1 diabetes mellitus, HHNK (p <0.001) and DKA (p <0.01) as compared with control subjects. Arterial pH was significantly lower in patients of DKA (p < 0.001), uncontrolled type 1 diabetes mellitus (p < 0.05) and HHNK (p < 0.01). Arterial PCO2 was significantly lower in patients of DKA (p < 0.05). Plasma bicarbonate levels were found significantly lower in patients of DKA (p < 0.001) and HHNK (p < 0.01).
Discussion: The present study showed that in type 1 DM hyperglucagonemia was more marked leading to excessive ketone bodies production and resulting in DKA. The ketoacids formed during DKA are strong acids that fully dissociate at physiological pH. So ketonuria lead to excretion of positively charged cations (Na+, K+, NH4+). Moreover, the hydrogen ions were titrated by plasma bicarbonate ions, resulting in metabolic acidosis and retention of anions lead to increase in the plasma anion gap in DKA. The degree of hyperosmolality and hyperglycemia was more marked in patients with HHNK as compared with DKA. The osmotic effects of glycosuria resulted in impairment reabsorption of NaC1 and H2O and ultimately hyponatremia. Whereas Serum potassium level was found to be significantly higher in uncontrolled type I diabetes mellitus, uncontrolled type 2 diabetes mellitus, DKA and HHNK. These observations were according to the results of previous studies.
Conclusions: Hyperglucagonemia causes marked hyperglycemia under conditions of relative insulin deficiency and can worsen the diabetic state like development of DKA when insulin deficiency becomes absolute as in type 1 diabetes mellitus.
Key words: Diabetes mellitus (DM), diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic non-ketotic coma (HHNK), arterial blood gases (ABGs), plasma osmolality.
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