Glucocorticosteroids asthma

Most patients with AERD can be desensitized to aspirin: following the initial adverse reaction, repeating of the dose is tolerated by more that 50% of patients, and further incremental aspirin challenges lead to a tolerance (28). Once the patient tolerates 600 mg of aspirin he is considered “desensitized” and then can take aspirin on a daily basis indefinitely without further adverse respiratory reactions. Desensitization can be also  achieved silently, for instance, without evoking initial adverse reaction providing the  challenge starts with a sub threshold dose and then the dose is slowly increased in appropriate  intervals (29). In order to maintain the tolerance a patient has to ingest aspirin on regular, usually daily basis – the tolerance state disappears after 2-5 days without aspirin with the full hypersensitivity returning after 7 days. Several protocols of desensitization have been proposed allowing for completing the procedure usually within 3 to 5 days. The standard protocol of desensitization is an extension of the oral aspirin challenge protocol and all the safety precautions recommended for the challenge should be employed.

Insufficient production of cortisol, often accompanied by an aldosterone deficiency, is called hypoadrenocorticism or Addison's disease . Most commonly, this disease is a result of infectious disease (. tuberculosis in humans) or autoimmune destruction of the adrenal cortex. As with Cushing's disease, numerous and diverse clincial signs accompany Addison's disease, including cardiovascular disease, lethargy, diarrhea, and weakness. Aldosterone deficiency can be acutely life threatening due to disorders of electrolyte balance and cardiac function.

A slightly increased number of basophilic hepatic foci were observed in chronic rat studies with budesonide, and in carcinogenicity studies there was an increased incidence of primary hepatocellular neoplasms, astrocytomas (in male rats) and mammary tumours (female rats) observed. These tumours are probably due to the specific steroid receptor action, increased metabolic burden on the liver and anabolic effects, effects which are also known from other glucocorticosteroids in rat studies and therefore represent a class effect. No similar effects have ever been observed in man for budesonide, neither in clinical trials nor from spontaneous reports.

The acute toxicity of budesonide is low and of the same order of magnitude and type as that of the reference glucocorticoids studied (beclomethasone dipropionate, flucinolone acetonide). Results from subacute and chronic toxicity studies show that the systemic effects of budesonide are less severe than or similar to those observed after administration of the other glucocorticosteroids . decreased body weight gain and atrophy of lymphoid tissues and adrenal cortex. An increased incidence of brain gliomas in male rats in a carcinogenicity study could not be verified in a repeat study, in which the incidence of gliomas did not differ between any of the groups on active treatment (budesonide, prednisolone, triamcinolone acetonide) and the control groups. Liver changes (primary hepatocellular neoplasms) found in male rats in the original carcinogenicity study were noted again in the repeat study with budesonide, as well as with the reference glucocorticosteroids. These effects are most probably related to a receptor effect and thus represent a class effect.

Glucocorticosteroids asthma

glucocorticosteroids asthma

The acute toxicity of budesonide is low and of the same order of magnitude and type as that of the reference glucocorticoids studied (beclomethasone dipropionate, flucinolone acetonide). Results from subacute and chronic toxicity studies show that the systemic effects of budesonide are less severe than or similar to those observed after administration of the other glucocorticosteroids . decreased body weight gain and atrophy of lymphoid tissues and adrenal cortex. An increased incidence of brain gliomas in male rats in a carcinogenicity study could not be verified in a repeat study, in which the incidence of gliomas did not differ between any of the groups on active treatment (budesonide, prednisolone, triamcinolone acetonide) and the control groups. Liver changes (primary hepatocellular neoplasms) found in male rats in the original carcinogenicity study were noted again in the repeat study with budesonide, as well as with the reference glucocorticosteroids. These effects are most probably related to a receptor effect and thus represent a class effect.

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