Thyroid hormone and steroids

Cases of liver injury attributed to levothyroxine and thyroid extract have been mild-to-moderate in severity and self-limited in course, resolving within one to three months of stopping therapy.  Rechallenge with levothyroxine has been reported to result in recurrence of fever and hepatic injury, but in several instances patients have later tolerated liothyronine (T3) as a means of treating the hypothyroidism.  There have been no reports of acute liver failure, chronic hepatitis or vanishing bile duct syndrome attributed to levothyroxine therapy.  

The release of too much thyroxine in the bloodstream is known as thyrotoxicosis . This may be caused by overactivity of the thyroid gland ( hyperthyroidism ), as in Graves' disease , inflammation of the thyroid or a benign tumour. Thyrotoxicosis can be recognised by a goitre , which is a swelling of the neck due to enlargement of the thyroid gland. Other symptoms of thyrotoxicosis include intolerance to heat, weight loss, increased appetite, increased bowel movements, irregular menstrual cycle, rapid or irregular heartbeat, palpitations, tiredness, irritability, tremor, hair loss and retraction of the eyelids resulting in a ‘staring’ appearance.

The thyroid hormone/thyroxin-binding globulin (TBG) ratio and the free thyroid hormone index (FTI) were compared in 372 subjects classified according to age, sex, and biochemical and clinical findings. Age-related variations in thyroid function tests were investigated, as was the relationship between triiodothyronine uptake and TBG. Men, but not women, showed significant age-dependent changes in concentrations of thyroid hormones. FTI was as good as the thyroid hormone/TBG ratio in hyperthyroidism and was a better index of thyroid status in pregnancy, TBG deficiency, and hypothyroidism. In addition, the triiodothyronine uptake correlated extremely well with TBG (r = -, p less than ) and was very efficient in detecting decreased and significantly increased concentrations of TBG. I conclude that FTI is a better discriminator of functional status of the thyroid over a wider range of TBG values than is the thyroid hormone/TBG ratio. Further, the triiodothyronine uptake test produced diagnostic information equivalent to that of TBG estimation and thus should not be replaced in routine use.

TBG-CD is defined as undetectable TBG in serum of affected hemizygous subjects or a value lesser than % the normal mean; the current limits of detection using the most sensitive radioimmunoassay (RIA) being 5ng/dl (24). The prevalence is approximately 1:15,000 newborn males. Twenty five TBG variants having this phenotype have been characterized at the gene level. These are shown in table 1 that also contains references to the original publications. Eighteen of the 25 TBG-CDs have truncated molecules. Early termination of translation of these variants is caused in 4 by a single nucleotide substitution (TBG-CDP1, TBG-CDP2, CD5, TBG-CDB and TBG-CDT2) or by a frame shift due to one nucleotide deletion (TBG-CDY, TBG-CDN, TBG-CDNi, TBG-CD6, CD-PL, TBG-CD7, TBG-CD8, and TBG-CDJ, TBG-CDPe) or deletion of 19 nucleotides (TBG-CDH). In 5 variants mutations occurred in introns close to splice sites (TBG-CDMi, TBG-CDK, TBG-CDH, TBG-CDL and TBG-CDJa). A mutation at the acceptor splice junction caused also a frame shift producing early termination of translation in TBG-CDK (22). In contrast a nucleotide substitutions in the 5′ donor splice site of intron IV (TBG-CDL and TBG-CDJa), resulted in a complete splicing of exon 3, also producing a truncated molecule (28) and personal observation. A similar mechanism is likely responsible for CD in TBG-CDMi, though direct experimental prove was not provided (14). Single amino acid substitution was the cause of CD in five families (TBG-CDT1, TBG-CDPa, TBG-CD5, TBG-CDP3 and TBG-CDKo). In TBG-CD5 Leucine-227 with a proline was shown to cause aberrant post-translational processing (42). One TBG variant (TBG-CDNI), with two nucleotides deleted close to the carboxyl terminus, the resulting frame shift predicts an extension of the molecule by the addition of 7 nonsense residues (33). TBG-CDJ has been so far identified only in Japanese but its allele frequency in the population remains unknown (30,52) (Table. 1).

Around the world, many people start their day with a cup of coffee, a cappuccino, or an espresso. At the same time, there are many people with various thyroid conditions who rely on synthetic thyroid hormone replacement medication like levothyroxine (., Synthroid, Levoxyl, and Unithroid) to treat their hypothyroidism. And following doctor's instructions, most of those people take their thyroid pills in the morning. There is a problem, however, when coffee drinkers take their prescription thyroid medication along with their morning coffee or espresso. Find out why you should wait for that morning cup of joe.  

Thyroid hormone and steroids

thyroid hormone and steroids

TBG-CD is defined as undetectable TBG in serum of affected hemizygous subjects or a value lesser than % the normal mean; the current limits of detection using the most sensitive radioimmunoassay (RIA) being 5ng/dl (24). The prevalence is approximately 1:15,000 newborn males. Twenty five TBG variants having this phenotype have been characterized at the gene level. These are shown in table 1 that also contains references to the original publications. Eighteen of the 25 TBG-CDs have truncated molecules. Early termination of translation of these variants is caused in 4 by a single nucleotide substitution (TBG-CDP1, TBG-CDP2, CD5, TBG-CDB and TBG-CDT2) or by a frame shift due to one nucleotide deletion (TBG-CDY, TBG-CDN, TBG-CDNi, TBG-CD6, CD-PL, TBG-CD7, TBG-CD8, and TBG-CDJ, TBG-CDPe) or deletion of 19 nucleotides (TBG-CDH). In 5 variants mutations occurred in introns close to splice sites (TBG-CDMi, TBG-CDK, TBG-CDH, TBG-CDL and TBG-CDJa). A mutation at the acceptor splice junction caused also a frame shift producing early termination of translation in TBG-CDK (22). In contrast a nucleotide substitutions in the 5′ donor splice site of intron IV (TBG-CDL and TBG-CDJa), resulted in a complete splicing of exon 3, also producing a truncated molecule (28) and personal observation. A similar mechanism is likely responsible for CD in TBG-CDMi, though direct experimental prove was not provided (14). Single amino acid substitution was the cause of CD in five families (TBG-CDT1, TBG-CDPa, TBG-CD5, TBG-CDP3 and TBG-CDKo). In TBG-CD5 Leucine-227 with a proline was shown to cause aberrant post-translational processing (42). One TBG variant (TBG-CDNI), with two nucleotides deleted close to the carboxyl terminus, the resulting frame shift predicts an extension of the molecule by the addition of 7 nonsense residues (33). TBG-CDJ has been so far identified only in Japanese but its allele frequency in the population remains unknown (30,52) (Table. 1).

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