An Answer I Didn't Want - PVFS - Final Diagnosis?

[anonymous45]

It's been quite a while since I've been active here, and my health has been up and down. But for the sake of the community, I figured I should share what I've learned.

My hypothyroidism appears to be both primary and secondary, TPO-Ab borderline but definitely positive, yet fluctuating function not explained by thyroid cell death - thus likely pituitary related also. It is important to remember that this was triggered by a major viral infection, which was very likely EBV (Epstein-Barr Virus).

Pituitary dysfunction is backed up by the fact that I also have fluctuating morning cortisol levels, with 2 values weeks apart being 235nmol/L and 552nmol/L (range 180 - 620). Further to this, I have consistently elevated prolactin (mild - thus not prolactinoma), and very low DHEA-S levels. Combined with symptoms of fatigue, unrefreshing sleep, poor appetite, and poor immunity it could be a wide range of issues; most of which have been ruled out.

The 2 leading theories at present are primary hypothalamus or pituitary damage caused by viral inflammation, and post-viral fatigue syndrome [PVFS] (related to ME/CFS). The latter is the diagnosis I recieved from an endocrinologist, and does fit the immunological profile of my symptoms.

Ongoing hypothyroidism is ruled out at this stage, since both fT3 and fT4 have been properly optimised with a combination of T3 (12.5mcg) and T4 (75mcg). Iron, Vitamin D, Folate, and B12 have all been checked and are optimal (I now take 75mcg/3000IU vitamin D every other day). Coeliac and other sensitivities are negative.

As much as I hate to admit it, the theory of PVFS does fit my blood work and symptoms. It does not fail to explain any of my abnormal test results, including normal Sed rate and normal CRP.

Therefore I must pursue this line of enquiry as if it is correct, and use the results of that as a final differential diagnosis.

Current Investigational Interventions:

-DHEA 50mg per day - to replace blood-confirmed deficiency, with a goal to raise DHEA-S above 10µmol/L (currently 4.7 µmol/L; normal range 7.56 - 17.28 µmol/L).

-200mg Coenzyme Q10 + 20mg sublingual NADH (as seen in CFS studies to mitigate increased oxidative stress).

-Omega-3 Fatty acids to complement diet (540mg EPA, 360mg DHA).

-As required use of low-dose hydrocortisone first thing, when morning fatigue is severe (5-10mg depending on severity - no adrenal suppression from this dose). This will make up for the deficit occasionally caused by low CRH/ACTH production and poor sensitivity.

-On/Off cycling of Inosine Pranobex (a.k.a. Immunovir/Neosine Forte) 1000mg x 3 per day. This has been shown to restore impaired NK cell function and reverse immunological changes that occur as a result of severe EBV infection.

Further to this, I intend to privately test ADH/Vasopressin levels, since my body water content is high, but blood volume is low (despite adequate sodium). This would explain the idiopathic episodes of hypotension. I would also like to test if I am still seropositive for EBV, HHV-6, or CMV - since if this is the case, symptoms could resolve far quicker with proper antiviral therapy. However antibody titers are expensive, and this is unlikely to occur until I have saved for these tests.

The good news is that the progression suggests I will eventually fully recover anyway, since overall symptoms have become gradually less severe over the last 2 years; despite flare-ups. If the positive TPOab was a red-herring, and my hypothyroidism is neurally mediated, then that too may one day make a full recovery (though unlikely). It could take 10 years for all damaged rogue B-cells to die off, but if this is the correct diagnosis, then I am comfortable mitigating symptoms as they gradually resolve.

Perhaps this is my final diagnosis. Perhaps there is an end in sight.

[greygoose]

My hypothyroidism appears to be both primary and secondary, TPO-Ab borderline but definitely positive, yet fluctuating function not explained by thyroid cell death - thus likely pituitary related also.

How do they know that thyroid cell-death is not the cause of fluctuating results? Secondary hypo doesn't usually have fluctuations. It's low TSH and low thyroid hormones.

Ongoing hypothyroidism is ruled out at this stage, since both fT3 and fT4 have been properly optimised with a combination of T3 (12.5mcg) and T4 (75mcg).

That's a very low dose. What were your last thyroid hormone results, just out of curiosity?

[anonymous45 in reply to greygoose]

Fluctuations from secondary hypothyroidism are more consistent with autoimmune dysfunction due to inflammatory processes than direct damage to the pituitary, making the second theory more likely.

The reason for assuming it's not primary, is that my TSH fluctuates entirely out of sync with fT4 concentrations. For primary, the correct detection by the hypothalamus would reduce TSH on increased fT4 (and fT3) release from cell death. Whereas in this pattern, it seems more like the TSH is not responding appropriately to serum fT4/fT3 concentrations.

My last few blood tests are as follows: (RANGES: TSH 0.2 - 4.0 mIU/L; fT4 12-22 pmol/L; fT3 3.1 - 6.80 pmol/L)

TSH - 1.55; fT4 17.1; fT3 5.3

+~3 months

TSH - 2.05; fT4 19.7; fT3 5.29

+ ~8-10 weeks

TSH - 1.75; fT4 23.1; fT3 5.4

+~2 months

TSH 0.9; fT4 21.1; fT3 5.6

I don't have the latest set of results in front of me yet (being posted). But I believe my fT4 has stabilised around 19-21, and fT3 is hopefully consistently stable around 5.6 - 5.9. Adding the T3, despite the small dose, made a much bigger difference than switching Thyroxine from 50mcg to 75mcg.

It is worth noting, that I occasionally experience a metabolic slowing associated with coldness, tiredness, and poorer psychomotor function. In this instance, I will take an additional 12.5mcg T3 which usually speeds things up within a few hours of the second dose.

My TSH has only ever peaked around 3.5, despite fT4 being as low as 13.9. My GP agrees that TSH is not an appropriate way to monitor function due to the abnormal relationship to thyroid hormones, and lack of appropriate increase when my fT4 was rather low.

[Aurealis]

Ongoing hypothyroidism is ruled out at this stage, since both fT3 and fT4 have been properly optimised with a combination of T3 (12.5mcg) and T4

Are you sure you mean ‘optimal’, not just ‘in range’? Do you know for certain that your ME/CFS symptoms don’t disappear if you slightly increase your T3 dose.

A complex explanation is seldom more accurate than a simpler one to explain the same situation.

[anonymous45 in reply to Aurealis]

See my reply above regarding optimal. I had aimed to keep my TSH around 1.0; however it doesn't seem to be useful regarding monitoring of actual serum concentrations of thyroid hormone. My goal now is to maintain an fT4 of around 19-21, and fT3 between 5.6 and 6.0.

And ah, indeed I have applied Occam's razor to this situation. Going beyond 0.5-1 tablet (12.5mcg - 25mcg) of T3 per day only results in increased sweating, tremor, but no improvement in day-to-day fatigue symptoms or cognitive functions. However, psychomotor function responds well to additional T3, and I often use poor temperature tolerance and reduced ability to sweat as markers of when I require an additional dose of T3.

Unfortunately, based on symptomology and various blood panels, the simplest explanation that fits all the data is currently PVFS/ME/CFS. If you have any other suggestions, please do share. I am very happy to persue other avenues, I only care about getting the final DDX right, and treating/managing as well as possible from there.

[Aurealis in reply to anonymous45]

Sorry but I can’t see a reply about optimal. It’s about symptoms not test results.

[anonymous45 in reply to Aurealis]

Apologies, my reply to grey goose includes that information.

[Aurealis in reply to anonymous45]

You don’t sound optimal to me, but if you think you are then you must be, well done, congratulations. Job done.