Hyperglycemia is due to a hormonal and inflammatory response to stress, causing increased hepatic glucose production and insulin resistance with a consequent worsening of beta cell function, leading to hydroelectrolytic disorders, neutrophil and endothelium dysfunction, increased oxidative stress and systemic inflammation.¹ Type 2 Diabetes Mellitus is a disease caused by reduced secretion or impaired insulin action, and is generally related to factors that increase insulin resistance, such as sedentary lifestyle, a diet rich in carbohydrates and fats and overweight. It increases the risk of cardiovascular events, end-stage renal disease, amaurosis, peripheral neuropathies and lower limb ulcerations, being one of the main causes of premature deaths.^two

Glucocorticoids are natural hormones produced by the human body, belonging to a group of steroids secreted in the adrenal cortex, known as cortisol, which act on specific receptors of the hypothalamus and pituitary gland. In stressful situations, adrenal secretion is activated, causing an increase in blood cortisol levels, which triggers homeostatic adjustment including the release of carbohydrates and glucose, effects on hemodynamics and fluid balance and anti-inflammatory effects. The release of excess glucocorticoids in chronic stress leads to stimulation of glucose-6-phosphatase, promoting greater release of glucose from pancreatic cells into the bloodstream, favoring hyperglycemia and the resistance of tissues to the action of insulin.^two

Corticosteroids can be synthesized and used effectively in anti-inflammatory and immunosuppressive therapy, indicated for different diseases of inflammatory or allergic origin: respiratory, dermatological, endocrine, neoplastic, osteomuscular, transplants and autoimmune diseases. However, side effects, resulting from its metabolic action, are associated with the continuous use of these drugs, such as hypertension, dyslipidemia, osteoporosis and hyperglycemia that can lead to the development of diabetes mellitus in predisposed individuals.³ The occurrence of hyperglycemia is due to an increase in hepatic gluconeogenesis and peripheral antagonism to the action of insulin, which cause reduced glucose uptake in muscle and fat tissue. Hyperglycemia can then induce the onset of diabetes, being related to the dose and duration of treatment, being, in most cases, reversible with the stop of the administration of glucocorticoids. However, individuals with a genetic predisposition may remain diabetic.⁴

Constant monitoring must exist for these patients in order to obtain an early diagnosis and adequate treatment. The researchers reinforce that corticosteroids are drugs that have a high potential for morbidity and mortality if used inappropriately, being very important the attitude of professionals in the use of these drugs for the shortest possible time, in offering a less harmful alternative therapy, in association with other medications that decrease the required dose or alternate day regimens, in order to reduce side effects.⁵

Biotécnica has in its product line kits for determining parameters related to diabetes and its monitoring: Glucose, HbA1c and Frutosamine.

Baby Ferreira
Sac@biotecnicaltda.com.br
35 3214-4646

BIBLIOGRAPHIC REFERENCES:

1. Brazilian Diabetes Society. Blood glucose control in hospitalized patients. SBD Official Positioning No. 03/2015, 2015.
2. PEREIRA, AFA et al. Relationship between the hormone cortisol and the metabolic syndrome. XVII SEPA - Student Seminar on Academic Production, UNIFACS, v.17 (2018).
3. SALVIANO, CMT et al. Corticosteroid-induced hyperglycemia: an integrative review. Academic Vision, Curitiba, v.21 n.1, Jan. - Mar./2020 - ISSN 1518-8361.
4. PEREIRA, ALC et al. Systemic use of corticosteroids: literature review. Med Cutan Iber Lat Am 2007; 35 (1): 35-50.
5. FAIÇAL, S et al. Systemic effects and withdrawal syndrome in chronic corticosteroid users. Rev Ass Med Brasil 1998; 44 (1): 69-74.