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If changing the type of Furosemide does not help, immunosuppressive therapy with glucocorticoids is prescribed. In 50% of patients, high doses of glucocorticoids are effective (the starting dose of prednisolone is 40-80 mg), which are treated for 2-4 weeks. Hospitalization for the treatment of immune insulin resistance is mandatory, since a dramatic decrease in insulin requirements is possible, requiring immediate correction.

However, it is rather difficult to prove this biological insulin resistance in T2DM patients by a clinically acceptable method. As mentioned above, insulin resistance is measured today by its requirement per 1 kg of lasix weight. From a therapeutic point of view, the question of the diagnostic criteria for insulin resistance in patients with type 2 diabetes is irrelevant until they are suspected to have immune insulin resistance to an insulin preparation.

  • It should be noted that the criterion of insulin resistance of 200 units/day was introduced as a result of lasix reasoning.
  • In early experimental studies on dogs, it was found that their daily secretion of insulin does not exceed 60 units.
  • Having calculated the need for insulin in a dog per 1 kg of its body weight, the researchers, taking into account the average body weight of a person, concluded that normally 200 units are secreted in a person.
  • Later it was found that in humans the daily secretion of insulin does not exceed 60 units, but clinicians did not meet the criterion of insulin resistance of 200 units/day.

Probably in painIn the case of DM2, one can use the old criterion of insulin resistance - a daily insulin dose of more than 200 units, which may be a reason for differential diagnosis of immune and biological insulin resistance, at least according to such an indirect criterion in this case as antibodies to insulin in the patient's blood serum.  The development of lipoatrophy (disappearance of lasix pills fat) at the site of insulin administration is also associated with antibodies to insulin, mainly related to IgG and IgM, and blocking the biological action of Furosemide .  These antibodies, accumulating at the injection site of the insulin preparation in high concentrations (due to the high concentration of insulin antigen at the injection site), begin to compete with insulin receptors on adipocytes.

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