Thyroiditis steroid treatment

This would occur most likely through each cell shrinking in size in response to the energy deficit (and/or in extreme situations from some cells dying via either apoptosis or necrosis, depending on location). [4] This may occur as a result of there not being enough ATP to maintain cellular functions: notably failure of the Na/K ATPase, resulting in a loss of the gradient to drive the Na/Ca antiporter which normally keeps Ca +
2 out of cells so that it does not build to toxic levels that will rupture cell lysosomes leading to apoptosis. An additional feature of a low energy state is failure to maintain axonal transport via Dynein/Kinesin ATPases, which in many diseases results in neuronal injury to both the brain and/or periphery. [5]

During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.

Studies indicate that slight thyroid deficiency/imbalance (sub clinical) during the perinatal period can result in delayed neuropsychological development in neonate and child or permanent neuropsychiatric damage in the developing fetus or autism or mental retardation. Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result in significantly reduced IQs and causes psychomotor deficits. Women with the highest levels of thyroid-stimulating hormone (TSH) and lowest free levels of thyroxin 17 weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age 8. Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, affecting millions of children. Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. Collectively, reports show that 30-60% of women positive for TPO antibodies in pregnancy develop postpartum thyroiditis, the researchers point out, calling it “a strong association.” Without treatment, many of the women with thyroiditis on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About % of pregnant women develop thyroiditis after birth. Studies have also established a connection between maternal thyroid disease and babies born with heart defects.

Thyroiditis steroid treatment

thyroiditis steroid treatment


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