In many of the older case studies, elevated TPO antibodies in the blood have been used as one important factor in diagnosing HE.
However, I have read many other case studies indicating that there are so many healthy people with elevated TPO antibodies (up to 20% of the pop.) that this may not be the best way of diagnosing HE.
I even have a friend who was experiencing chronic pain for 2.5 years and personality changes. All neurological tests were negative. His blood was checked and he had elevated TPO antibodies. He was diagnosed with HE and was shortly after admitted to the hospital for high dose IV steroid therapy (we were in the hospital getting the IV steroids at the same time). His pain and personality changes did not respond to steroids at all. He was discharged on 60 mg prednisone per day. After 1 week there was still no positive response. He was experiencing the typical (and crappy) side effects to the steroids.
My question to his diagnosis is does he really have HE? Is he being treated for an autoimmune response that he isn’t really having? And subsequently is he being subjected to some pretty bad side effects for nothing? Maybe he is one of those people with elevated TPO antibodies in his blood and they are not hurting him (or at least not causing his pain). Since the steroid treatment, he has begun treatment for fibromyalgia (he hasn’t been diagnosed with fibromyalgia yet). I’m interested to see how he does and what diagnosis ends up sticking.
In a case study from 2007, Hashimoto’s encephalopathy presenting with progressive cerebellar ataxia, it indicates the serum autoantibodies against the amino (NH2) terminal region of α enolase (NAE) as a useful diagnostic marker of Hashimoto’s encephalopathy. The patient in the study had the anti-NAE antibodies as well as the antithyroid antibodies in her blood. Unfortunately, the full text was not available for free, so I do not know how her treatment worked out. However, the anti-NAE antibody indicator may be a better indicator of HE than the anti-TPO antibodies.
The article states, “The detection of antithyroid antibodies in patient sera is helpful but not sufficient for the diagnosis of Hashimoto’s encephalopathy because of the high prevalence of antibodies in the normal population.”
In a 2008 case study, Case report of a patient with Hashimoto’s encephalopathy associated with Basedow’s disease mimicking Creutzfeldt-Jakob disease, the patient had increased titer of anti-TPO antibody, anti-Tg antibody, and anti-NH2 terminal of alpha-enolase (NAE) antibody. Again, here’s this mention of the anti-NAE antibody that I haven’t seen mentioned in too many of the older case studies. In this case, the high dose IV steroid therapy alleviated her symptoms.
A very interesting 2009 case study in Japan had more data on the Anti-NAE antibodies, Anti-NAE autoantibodies and clinical spectrum in Hashimoto’s encephalopathy. The article states, “Recently, we discovered serum autoantibodies against the NH2-terminal of a-enolase (NAE) as a specific diagnostic marker for HE. We analyzed these serum anti-NAE autoantibodies and the clinical features in 84 cases of HE. The 84 patients consisted of 26 men and 58 women, from many institutions throughout Japan and other countries. A total of 37 patients carried anti-NAE antibodies (44%).”
More interestingly, the article states “The patients with anti-NAE antibodies tended to exhibit acute encephalopathy.” Perhaps the level of these anti-NAE antibodies can indicate how acute the symptoms are. If that proves to be even somewhat true, we could more easily monitor our health by periodically checking our anti-NAE antibody levels. We could be more proactive in monitoring for relapses. However, there are currently conflicting studies indicating whether or not the level of antibodies correlates to the severity of the symptoms. In some cases they do, in some cases they don’t. This is something I am particularly interested in studying.
Thyroidmanager.org states, “Recently, autoantibodies against the amino (NH2)-terminal of α-enolase (referred to as NAE) were reported to be highly specific in sera from a limited number of HE patients (68-83% with HE; 11%, 2 of 17 with HT without any neuropsychiatric features; none of controls [50 individuals] including those with other neurological or immunological conditions involving encephalopathy [25 individuals])”
A 2006 case study, Steroid-Responsive Encephalopathy Associated with Autoimmune Thyroiditis, states “The putative role of thyroid autoimmunity in the pathogenesis of Hashimoto encephalopathy is complicated by the fact that serum TPO levels are elevated in approximately 10% of healthy adults, and the prevalence of individuals with elevated TPO levels increases with increasing age.”
The study had used elevated anti-TPO antibodies as one of the criteria for the study. Another criteria for the study was responsiveness to steroids. The data indicated that many of the patients who did not respond to steroids (those that were taken out of the initial study) ended up being diagnosed with other disorders (they did not have HE).
The study states, “We hypothesize that patients with an encephalopathy associated with thyroid antibodies who do not markedly improve with corticosteroids represent those with a nonautoimmune or noninflammatory disorder, and our 4 patients who underwent autopsy and who did not respond to high-dose corticosteroids support this contention. We suspect that most of the other nonresponders in Table 5, and most others who do not respond to corticosteroids,have an underlying neurodegenerative or prion disorder.”
My ending thoughts on this post:
Considering the high incidence of elevated anti-TPO antibodies in the healthy population, the anti-NAE antibodies should be checked as an indicator of HE. The anti-NAE antibodies also appear to indicate acute encephalopathy. Anti-NAE antibodies should also be checked when a patient is exhibiting HE like symptoms.
When TPO antibodies are used as a major criteria for diagnosing HE, it is possible another neurodegenerative disorder may be going undiagnosed. However, considering how treatable HE is, it might still be useful to try steroids as an initial therapy. If there is no positive response to the steroids, another diagnosis should be considered before continuing to subject the patient to the side effects of the steroids.