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Graves’ disease

Posted , 4 users are following.

funmi81436
funmi81436

I was diagnosed with graves three years, I was put on  Propylthiouracil twice a day and was reduced to alternate days after 18 months.

I did a routine blood test two weeks ago. and my T4 was 77, the doctor called me and asked me to take 150mg twice a day. My last result the  liver function  was deranged and I am still on this medication. Please advice. The doctor suggested RAI or surgery 

0 likes, 4 replies

4 Replies

  • linda187
    linda187 funmi81436

    Posted

    Why were you taking Propylthiouracil instead of either Methimazole or Carbimazole?  What worked for me was having my doctor test my Total and Free Carnitine levels, my Vitamin D3 levels and my Magnesium levels.  I was deficient in everything so I added these and took them along with my Methimazole dose and was able to lower my Meds dose over time until my antibodies were no longer detected and all my levels normalized.  Perhaps if you were able to get tested for these deficiencies and added supplements, then your meds dosage could probably be lowered or even discontinued.
  • Guest
    Guest funmi81436

    Posted

    Hi funmi81, not sure if I understand it correctly, have you been taking PTU continuously or 3 years and 18 months ago your dose was reduced? 

    Your elevated T4 was found during a routine test two weeks ago. Did you have any symptoms at this time? 

    • funmi81436
      funmi81436 Guest

      Posted

      I was initially put on cabimazole which I reacted to. Then PTU for two years., after which I was then on reducing dose until two weeks ago
  • Guest
    Guest funmi81436

    Posted

    Hi funmi81436, 3 years is a long time to be continuously on antithyroid drugs and recently you have been prescribed a rather high dose of PTU again.  

    I was asking if you had any symptoms prior to your latest blood test because some patients have what is called thyroid hormone resistance. It is an inherited condition characterized by a reduced responsiveness of target tissues to thyroid hormone. As a consequence even though patients may have high thyroxine levels they have uncharacteristically mild hyperthyroid symptoms. 

    Another group of patients have a genetic mutation that activates TSH receptors even in the absence of thyroid stimulating hormone or TSI (thyroid stimulating immunoglobulins, the antibodies causing hyperthyroidism in Graves' patients). These patients have problems reaching remission even after lengthy treatment with antithyroid drugs. As far as I know, genetic testing is not widely available except maybe in research facilities. 

    There are efforts to develop alternatives to replace standard antithyroid drugs. One of these is a drug based on a monoclonal antibody called K1-70. It is an experimental drug that blocks thyroid stimulating autoantibodies binding to the thyroid. I am aware of a current clinical trial taking place near Manchester, UK.  

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