scott@vtx-cpd.com

Interesting!

I understand what they, are saying, but it is still quite a significant result. Normally the portal vein hypoplasia cases do not have such significant increases in bile acids.

Was the bilirubin increased?

P.s. I am not disagreeing with them! It is just an interesting discussion!

Scott x

Areti!

So lovely to hear from you. Thank you so much for your questions as always.

I have popped some ideas under your questions below:

1)how long would you withdraw from meds causing lower T4 before consider testing for hypothyroidism?

It depends a little bit on the medication and the half-life of the medication. I would normally give a good couple of weeks free of medication before testing thyroid hormone levels. If there are any equivocal results I would wait a further 2 weeks and test again!

2)if you find elevated TgAA with normal fT4 what should you do? do you start tx or retest later on?

Positive TgAA results are associated with lymphocytic thyroiditis but may be present in the circulation long before a dog becomes clinically hypothyroid. As such, TgAAs provide no information on thyroid function. TgAA positivity, uncommon in dogs with non-thyroidal illness, is suggestive of underlying pathology. A positive TgAA does, indirectly, support a diagnosis of hypothyroidism. However, if the free T4 is normal I probably not treat at that point and re-test at a later time point as you suggest.

3) I am a bit confused with lymphocytic thyroiditis. Is it not the cause of hypothyroidism? or is it a concurrent condition? as on the chart of how to interpret results says if low fT4 and positive TgAA then lymphocytic thyroiditis with hypothyroidism. Are they not the same? (hope not silly question)

Acquired primary thyroid disease accounts for the overwhelming majority of dogs with hypothyroidism. The two main causes on a cellular level are lymphocytic thyroiditis and thyroid atrophy (equally common). Lymphocytic thyroiditis is a destructive autoimmune process characterized by multifocal or diffuse infiltration of the thyroid gland by lymphocytes, macrophages and plasma cells and progressive replacement by fibrous connective tissue. By contrast, idiopathic atrophy is described as a degenerative process with minimal inflammatory change and gradual replacement of thyroid tissue by adipose and connective tissue.

Ultimately both will result in hypothyroidism.

Lymphocytic thyroiditis is slowly progressive, causing signs of hypothyroidism after about 75% of the gland has been destroyed. Its progression can be divided into four stages. The rate of progression through these stages is variable, and not all dogs develop functional hypothyroidism. Approximately 20% of TgAA-positive euthyroid dogs develop hormonal evidence of thyroid dysfunction within a year of testing, but only 5% become clinically hypothyroid. Most dogs remain TgAA positive and asymptomatic, while a small number later test negative without evidence of thyroid dysfunction. Some TgAA-positive hypothyroid dogs later become TgAA negative, supporting the concept that thyroid atrophy represents an end stage of lymphocytic thyroiditis. Theoretically, the complete destruction of all thyroid tissue leads to a reduction in immune stimulation, absence of histologic thyroiditis, and conversion to autoantibody negativity.

Yes, low free T4 and positive TgAA are part of the same process and supportive of hypothyroidism. However, patients can be hypothyroid with a low free T4 without being positive for TgAA (see about). Please let me know if this is not clear.

4)would you start oral suppl. of T3 only if on higher end of dosage and no response or would you check for concurrent diseases first?

I would definitely check for a concurrent disease first. It would be very unusual to have to use T3 supplementation.

5)How do you support the diagnosis in breeds with lower circulating t4 especially in Greyhounds?

The key thing has to be compatible clinical signs and clinicopathological tests (is the cholesterol increased). TSH, free T4 and TgAA would then all be used to support a diagnosis. The fundamental thing would only to look for this condition in dogs with compatible clinical signs.

6)is there anything we can do in patients with congenital hypothyroidism? what is the prognosis/life expectancy?

With appropriate supplementation, they can do well and actually can have a relatively normal life. It all depends on how quickly the problem is detected as if not detected early, the growth abnormalities may be left as permanent changes.

7)and last question, when we say about concurrent illness, do we mean only serious diseases or could be anything like a simple infection on a nail base for example?

It really could be anything, definitely does not have to be a severe concurrent disease.

Thanks again for your questions. If any of this is not clear, let me know.

Scott 🙂

Hey.

I think the bottom line is that there is probably not a universal gold standard.

If the PDSA are recommending, I would honestly go with that. They are very careful and considered about the information they give to clients. I would consider this good information.

Do you have a website for your business? I would love to check it out.

Scott 🙂

Thanks again for sharing Ashley.

I have popped images of the skin lesions below:

Skin Images

Let us know how the dog gets on. Great shout regarding RVC referral.

Scott x