Rheumatology ChannelThe probability of developing diabetes mellitus (SDM) is greatly increased in patients on long-term hormone therapy.What are the characteristics of SDM and how to treat it?
Speaker: Zhu Kaisi Collation: Xing Rui Source: China Rheumatology Public Forum What is steroidal diabetes mellitus?
A disorder of glucose metabolism caused by exogenous administration of glucocorticoids that meets the diagnostic criteria for diabetes is called steroidal diabetes mellitus (SDM) without a previous history of diabetes.
SDM falls under the category of secondary in the typology of diabetes. Compared with type 2 diabetes, steroidal diabetes has its own clinical and therapeutic characteristics.
Epidemiological features: steroid diabetes occurs in about 10-40% of cases with glucocorticoid application, and the average time to the onset of clinically induced diabetes is 6 weeks, but it can also occur at any time of treatment.
Mechanisms of glucocorticoids elevating blood glucose (1) Glucocorticoids stimulate hepatic gluconeogenesis including increasing the activity of key enzymes for hepatic gluconeogenesis, promoting muscle protein breakdown to release amino acids and lipolysis to release free fatty acids, thus increasing the substrate for hepatic gluconeogenesis.
(2) Inhibition of glucose uptake and utilization by peripheral tissues. Experimental studies have found that high concentrations of glucocorticoids not only inhibit the binding of insulin to its receptors, but also impair the action of the post-insulin receptor glucose transport system in peripheral tissues.
(3) Increase hepatic gluconeogen synthesis This effect of glucocorticoids is achieved by increasing the activity of hepatic gluconeogen synthase.
(4) “Permissive” and “synergistic” effects on glucagon, epinephrine and growth hormone glucagon (5) Reduces renal tubular reabsorption of glucose.
Pathophysiological characteristics of SDM (1) Steroidal diabetes mellitus has a compensatory insufficiency of insulin secretion. If the pancreatic B-cell reserve function is insufficient and the response to hyperglycemia is sluggish, the extra insulin secreted is not enough to counteract the effect of glucose metabolism by various glucose-raising hormones in the body, which leads to steroid diabetes during glucocorticoid therapy.
(2) The pathological changes of steroidal diabetes mellitus are close to insulin non-dependent diabetes mellitus in both weight and morphology, but to a lesser extent, and these can partially explain the difference in clinical symptoms between the two SDM occurrence related factors (1) Dose and duration of treatment are closely related to diabetes mellitus occurrence. The higher the dose of glucocorticoids and the longer the duration of application, the more serious the damage to glucose metabolism, which is significantly and positively correlated with the dose.
(2) Patients with kidney disease are prone to steroid diabetes, which may be related to the fact that they tend to be highly edematous in kidney disease, affecting the binding of insulin to receptors on muscle and fat cells.
(3) Age, family history of diabetes, obesity, and other predisposing factors for type 2 diabetes, also have a significant effect on the development of steroid diabetes. Therefore, the elderly, positive family history of diabetes and obesity should be considered as high-risk groups.
Clinical characteristics of SDM The process of glucocorticoid-induced diabetes is similar to the development of type 2 diabetes, i.e. insulin resistance – impaired B-cell function – reduced glucose tolerance – diabetes mellitus. However, there are some differences: (1) the disease develops faster and most of them do not have the typical “three more and one less” symptoms; (2) the sugar excretion threshold of the kidney is lowered and the blood glucose is not proportional to the urine sugar value; (3) it is reversible and the hyperglycemia of many patients can be gradually relieved after stopping the drug, but some of them do not recover, suggesting that the disease is irreversible.
Blood glucose characteristics of steroid diabetes: (1) postprandial blood glucose is elevated, especially in the afternoon to bedtime blood glucose is difficult to control. (2) Fasting blood sugar is mostly normal or slightly elevated. (3) Hypoglycemia is likely to occur in the early morning and morning.
7 treatment strategies of SDM The treatment principles of steroidal diabetes are the same as those of type 2 diabetes, including diet, exercise therapy and selection of reasonable hypoglycemic drugs, but with its own characteristics (1) For normal fasting blood glucose, when the participant’s blood glucose is <10mmol/L, reasonable diet and moderate exercise, close monitoring of blood glucose changes, and observation for at least 2 weeks before considering drug therapy.
(2) When the effect of simple diet control and exercise treatment is not good, and the postprandial blood sugar is >10mmol/L, oral hypoglycemic drug treatment should be considered, and how to choose the drug should be decided according to the characteristics of the patient’s blood sugar, age, weight, liver and kidney function and other conditions. The recommended application of pioglitazone/pioglitazone + metformin can prevent and delay early steroidal diabetes.
(3) Specially proposed are thiazolidinediones, glucocorticoid-induced insulin resistance with the opposite mechanism of action of thiazolidinediones for insulin resistance, which can be used to treat steroidal diabetes mellitus. For example, troglitazone improves the secretory function of pancreatic islet cells since reducing insulin resistance, and pioglitazone can reverse dexamethasone-induced insulin resistance and restore normal glucose metabolism.
(4) Insulin therapy choose short-acting insulin, the dose before lunch and dinner exceeds the amount before breakfast, if the blood sugar is still high from afternoon to bedtime, change the short-acting insulin before breakfast to medium-acting insulin.
(5) Glucocorticoids should be taken with meals, and the dose should be reduced in time as the primary disease improves; insulin should be reduced or stopped in time when glucocorticoids are reduced.
(6) Monitor blood glucose, and monitor blood glucose at multiple points: fasting blood glucose, postprandial blood glucose and bedtime blood glucose.
(7) Blood glucose control target: fasting blood glucose <6.1mmol/L, 2h postprandial <10mmol/L, bedtime <7.8mmol/L. The blood glucose control target of the elderly, patients with slow response to hypoglycemia and patients with short course of treatment can be relaxed appropriately.
Due to the patient’s severe skin disease “aspergillosis”, the long-term application of large amounts of hormones has led to “steroidal diabetes”, “osteoporosis”, “hypertension” and other side effects. hypertension” and other side effects.