Thyrotoxic Hypokalemic Paralysis and 131-I Therapy


Question

I have a 28 yo white male with thyrotoxicosis and periodic hypokalemic paralysis. He is 5 days post RAI and seems to be having an exacerbation of the thyrotoxicosis and paralysis. I started him on Tapazole 30, have him well beta blocked and on 20 meq KCl daily. Is there anything else I can do that won't partially negate the 131I? I think he's probably had enough effect that it will work but would prefer to be as sure as possible to get the thyrotoxicosis behind him. DrRoudebush@aol.com

Response

All the things you can do will to some extent reduce the effectiveness of the 131-I, but probably are necessary. Obviously the KCl and beta blocker are primary. Methimazole will block further production of thyroid hormone, but PTU would be a better choice since it blocks T4 -> T3 conversion. However a drug such as Oragrafin - .5gm qd - or amiodarone- would be more effective given over the short term to reduce T3 generation. KI is theoretically of minor value . It would normally block thyroid hormone release, but may have little effect in the presence of a gland undergoing radiation damage.

Usually once you start treatment with KCl, beta blockers and antithyroid meds the paralysis disappears, never to return. Best regards, L De Groot,MD 20 Apr 2004

Thyroid Cyst, and Mild Hyperthyroidism, in Pregnancy


Question

I am an endocrinologist in Salisbury, NC. I saw a 37yo WF in her first trimester with a distant history of solitary thyroid cyst. The pt was clinically euthyroid. On exam she had a readily palpable 3+ cm R sided thyroid nodule. Her tsh was <0.003 and FT4 was 1.00 (upper limit of nl 1.54).Old records requested. Could only retrieve FNA x 2 done in ~1994 and the second done 1995. The first was read as benign and the second was without sig cellularity but without any suspicious findings. Apparently an US had been done but not available. No old labs either.

My assessment: subclinical thyrotoxicosis , solitary thyroid cyst, recurrence probable , pregnancy.

My question: Now pt is in her second trimester with stable thyroid indices. I have not recommended thionamides given her clinically euthyroid status and her mild biochemical levels. However, I wonder whether I should re-biopsy the cyst now. I have not thus far biopsied because of the fact of her earlier benign report and because of my concern for the cyst/nodule now being autonomous and that biopsy would lead to misleading results. I cannot do an I123 scan on her now. Do you think this management plan is reasonable? I have advised her to strongly consider surgical excision in an elective fashion in the postpartum setting. Thanks- Carey Robar

Response

- The situation is surely complicated. It is unlikely that the TSH suppression is due just to the normal high hCG of early pregnancy. It is also surprising that it could be due to a thyroid cyst. So one wonders about a functional thyroid lesion (probably adenoma) associated with the prior cyst, or Graves disease, since she does not have hyperemesis syndrome.

I would recheck TSH, freeT4 and T3 to be certain of the degree of hyperthyroidism. I would also do an US, and anti-TPO and anti-TG antibodies, as well as TSAb.

Although one can argue the merits, I would trend to treat the hyperthyroidism with anti-thyroid drugs, even if mild. If the US shows one lesion with a cystic and solid component, it would be of interest to biopsy the solid area. Fortunately the chance of malignancy would be small. If the an t ibodies are positive, it would suggest that the cyst/adenoma is incidental, and that the patient has mild Graves' Disease. Let us know what further develops. L De Groot,MD 15 Apr 2004

Thyrotoxicosis, Ventricular Fibrillation, Hypokalemia


Question

I wonder what you think of the following patient I am in charge for:

Caucasian male, 30years old, police man. He has never been ill before.

After strenuous exercise (squash for some hours) the night before he is losing consciousness the next day in the morning in the office. The emergency doctor diagnoses ventricular fibrillation of the heart and defibrillates twice. A treatment with amiodarone i.v. is started. When coming to our emergency unit after intubation he had another two episodes of ventricular fibrillation and blood analysis reveals a potassium of 2,6mmol/l. In order to exclude pulmonary embolism a spiral computer-tomography with iodine containing contrast medium is performed. This CT was negative. Drug screening was also negative. There was no paretic episode as far as one could judge under sedation and artificial ventilation. After extubation (with normal potassium levels obviously) he had a normal neurological status.

We were then informed that the patient was taking regularly caffeine-containing stuff in order to optimise his sport performance and also to lose weight. (178cm, 77kg at admission). Free T4, free T3 and TSH were measured and revealed thyrotoxicosis. Indeed when he came to our ward (a week after admission to our emergency unit) he presented with a small diffuse goiter. Thyroid uptake was 13% in spite of the recent high iodine load. TSH.Receptor antibodies were positive (anti human TSH receptor Ab 10,2 IU/ml, normal: below 1; or 30.3 with the anti-pork old assay, normal: below 10 ).

Electrophysiological investigation of the heart was normal in spite of a constant somewhat unclear notching of the QRS complex in the 12 lead ECG. Brugada?s syndrome was excluded by ajmaline testing. Coronary angiography showed normal coronary arteries.

A 24 hour ECG before discharge 3 weeks later showed no arrhythmia at all.

The hypothetical diagnosis of hypokalemic Graves' disease inducing ventricular fibrillation was made. The role of caffeine abuse was unclear. Therefore the patient was successfully advised to stop it. The offered automatic internal defibrillator was postponed until the thyroid situation is clear again.

This week (= 5 months later) he presented euthyroid under methimazol treatment (indeed he takes no other medication) without any complaints. He is playing squash again. Interestingly, his TSH receptor antibodies (antihuman) fell to 6,1 IU/ml.

Several questions arise:

  1. Do you agree that ventricular fibrillation can be seen as consequence of Graves' disease, induced hypokalemia? Or is it just a bad coincidence The caffeine?
  2. Would you implant the automatic defibrillator or also give him a chance without - at least until the thyroid situation is clear?
  3. How would you treat his Graves? disease ? ? We intend to have him totally thyroidectomized.
  4. What does the fall in TSH-receptor antibodies mean ?

With best regards, Michael Weissel, MD Medical University Clinic III

A-1090 Vienna, Austria

Response

You need about three experts in this case, but I will give it a shot. The presentation sounds like hypokalemic paralysis associated with thyrotoxicosis (through a still unknown mechanism). But I wonder if he had been using glucocorticoids or diuretics because of his body building. I think the caffeine may well play some though minor role, but could exacerbate a situation with low K+. The drop in TSAb, on one study, is very suggestive of a remission starting, but considering the usual assays, I guess one would need three or more points before making a line. I agree that in this young man with a dangerous cardiac complication, that thyroid removal by surgery - done by a good surgeon- is a very reasonable option and would provide protection in the future. I would not implant a defibrillator at this point. While we are not a journal for publication, I will put this in our "Ask an expert" column, and invite other comments on the case. L De Groot,MD

“Subclinical Hypothyroidism” with Normal Free T4 And TSH


Question

Dear Sir, I am a GP in a rural area with little population migration.In the last 15 months, I have seen 10 patients with more than 5 symptoms each, suggestive of hypothyroidism. 9 were females, one 14 y, eight 39-58 years old, one 69 year old male patient. All had TSH 2-3 (0.15-3.5), FT4 8-13 (8-28). I started 2 women on thyroxin. They responded-"Dr you have given me my life back". This on Thyroxin 50 mcg/75 mcg, with TSH dropping by 0.5, FT4 increasing by 4 or 5. What are the dangers of doing this without further (i.e.antibody) tests. What would be your response to criticism, using Thyroxin as a "lifestyle drug"? Dr Martin Schede, MD, Diss HC, Diss IP22 4WG, 01379-642021, UK, Martin.Schede@nhs.net

Response

Naturally it is difficult for me to support using T4 as a "life-style " drug, in the absence of any objective evidence of hypothyroidism. We all know the powerful placebo effect of the physician administering any medication. Often in time such responses wear off. I guess the real adverse effect might be to allow one to overlook the problem causing the symptoms. Excess T4 can certainly damage the heart and bones when maintained over several years. even with mild hyperthyroidism. However a dose of T4 that does not lower TSH below normal should be harmless in terms of thyroxin action on the body. I should note that this use of T4 is probably widespread, but often, unfortunately, in doses that do produce subclinical hyperthyroidism.

L De Groot,MD