One of my patient is a 54 y.o., poor, medically uninsured female suffering evidently from hypothyroidism: since 2 years, she has become progressively fatter, weaker, has menorrhagia, hoarseness of her voice, decrease hearing, and feels depressed. She also complains of dry skin and water retention. Her condition has been attributed to premenopause and depression which are under no treatment because she does not tolerate HRT or antidepressants.On examination, I noticed edema of the face and extremities, bradycardia at 50-60 bpm, and a lag in relaxation of knee jerks. The cranial nerves were intact, the blood pressure was 120/80, the visual fields normal by confrontation, the fundi normal, and the untanned areas of her skin had no discoloration.To minimize her lab cost, I first ordered a TSH($28) only: it came back normal at 1.2 !Subsequent FT4 came low at 7.
Since there is no evidence of adrenal hypofunction on physical examination, can I start Levothyroxine now, and save the patient a costly serum ACTH determination ? What can I do about the possibility of a pituitary tumor in this patient who cannot afford a $2500 MRI or CT scan ? Would a simple skull x-ray or tomogram of the sella turcica sufficient ? Should I wait for the possible adenoma to shrink under T4 replacement before imaging studies ? I would appreciate your “off the book” opinion and recommendations based on your experience with central hypothyroidism taking into consideration the limited paying capacity of this patient.
Thank you very much for your work on this website. Aloha and Mahalo!
Dr. Michel Soucy,
Hawi, Hawaii 96755
This is an interesting case because the clinical examination clearly demonstrates hypothyroid signs and symptoms, but the serum TSH comes back normal! Still, serum FT4 is decreased, and the straightforward diagnosis is then central hypothyroidism. The question is if this patient can safely be started on thyroxine without knowing if central hypothyroidism is absent. For, starting thyroxine in a patient with hypocortisolism may provoke an Addison’s crisis. Although physical examination didn’t give a clue on the existence of cortisol deficiency, this by no means rules out hypoadrenalism. Dr. Soucy is reluctant to order more tests because the finances of the patient do not allow this. Certainly the ACTH assay would be a bad idea, because ACTH in central hypoadrenalism is not elevated and the ACTH assay cannot reliably discriminate between normal and subnormal values. Also a single plasma cortisol test will not answer the question because a random cortisol may be normal despite the presence of hypoadrenalism. A dynamic test (ACTH stim test, insulin tolerance test, or metyrapone test) would be indicated to diagnose central hypoadrenalism, but this might be too expensive for the patient as well, and can be dangerous if not carefully supervised. But is it really central hypothyroidism? This entity is not very prevalent. In this age group (54 years) the most likely cause is a pituitary adenoma – the mass effect reduces pituitary hormone secretion. However, in most cases of pituitary adenomas the first hormones which fail are GH and the gonadotropins; TSH and ACTH follow much later. Consequently, isolated TSH deficiency is rare, and in this particular patient should be associated with loss of gonadotropin secretion as well. But, we are informed that the patient is not amenorrheic but has menorrhagia which speaks against central hypogonadism. So, is the TSH value of 1.2 mU/l a valid one? Is the assumption that there is no interference in the TSH assay by heterophilic antobodies? Could there have been an error in the lab, or switch of samples? After all, the pre-test likelihood of primary hypothyroidism in this lady is pretty high, much higher than that of central hypothyroidism. I would therefore put my money on a repeat TSH-test, or on a TPO-antibody test. If one of these tests results in an elevated value that is clear evidence of primary thyroid failure. Of course, primary autoimmune hypothyroidism is associated with primary autoimmune adrenal failure, which if unrecognized puts the patient again at risk for developing Addison’s crisis if only treated with thyroxine. But the co-existence of these two disorders is less frequent than that of TSH- and ACTH-deficiency in adults. I think the patient needs thyroxine treatment. If money is lacking to do some supplementary tests, I would start her on thyroxine alone, under the specific instruction to call or see me directly when in the coming weeks she feels not better but worse, becomes nauseated or dizzy etc. This must be a feasible management plan: after all, Hawaii is not that big an island! ( ED-At least an 8 AM cortisol, FSH, and lateral skull x-ray could be checked despite the financial constraints, and further evaluation done depending on these results. Correct diagnosis is very important here before treatment.)
Dr. Wilmar Wiersinga