Abstract
Long-term exposure to dampness microbiota induces multi-organ morbidity. One of the symptoms related to this disorder is non-thyroidal illness syndrome (NTIS). A retrospective study was carried out in nine patients with a history of mold exposure, experiencing chronic fatigue, cognitive disorder, and different kinds of hypothyroid symptoms despite provision of levothyroxine (3,5,3′,5′-tetraiodothyronine, LT4) monotherapy. Exposure to volatile organic compounds present in water-damaged buildings including metabolic products of toxigenic fungi and mold-derived inflammatory agents can lead to a deficiency or imbalance of many hormones, such as active T3 hormone. Since the 1970s, the synthetic prohormone, levothyroxine (LT4), has been the most commonly prescribed thyroid hormone in replacement monotherapy. It has been presumed that the peripheral conversion of T4 (3,5,3′,5′-tetraiodothyronine) into T3 (3,5,3′-triiodothyronine) is sufficient to satisfy the overall tissue requirements. However, evidence is presented that this not the case for all patients, especially those exposed to indoor air molds. This retrospective study describes the successful treatment of nine patients in whom NTIS was treated with T3-based thyroid hormone. The treatment was based on careful interview, clinical monitoring, and laboratory analysis of serum free T3 (FT3), reverse T3 (rT3) and thyroid-stimulating hormone, free T4, cortisol, and dehydroepiandrosterone (DHEA) values. The ratio of FT3/rT3 was calculated. In addition, some patients received adrenal support with hydrocortisone and DHEA. All patients received nutritional supplementation and dietary instructions. During the therapy, all nine patients reported improvements in all of the symptom groups. Those who had residual symptoms during T3-based therapy remained exposed to indoor air molds in their work places. Four patients were unable to work and had been on disability leave for a long time during LT4 monotherapy. However, during the T3-based and supportive therapy, all patients returned to work in so-called “healthy” buildings. The importance of avoiding mycotoxin exposure via the diet is underlined as DIO2 genetic polymorphism and dysfunction of DIO2 play an important role in the development of symptoms that can be treated successfully with T3 therapy.
Highlights
Seven patients had been already diagnosed by hypothyreosis with clear or borderline levels of thyroidstimulating hormone (TSH) and free T4 (FT4); two patients had normal TSH and FT4 concentrations before initiating LT4 monotherapy
Two patients had been diagnosed with newly onset asthma during the time when they were exposed to indoor air molds
While on LT4 monotherapy, six patients presented with very severe/ severe imbalance in the free T3 (FT3) and reverse T3 (rT3) levels with FT3/rT3 ratios ranging from 0.75 to 1.3
Summary
Long-term exposure to molds in water-damaged buildings (WDB) has been associated with numerous health problems including allergic airway symptoms [1,2,3], fungal sinusitis [1, 2, 4], abnormalities in T and B cells [5,6,7], infection sensitivity [6, 8], asthma [9,10,11], respiratory infections [3, 11, 12], central and peripheral neuropathy and polyendocrinopathy [8], neurologic symptoms [1, 4, 13], neuropsychological cognitive dysfunction (CD) [14,15,16], neuropsychiatric symptoms [3, 14, 17], and chronic fatigue (CF) [6, 14, 18]. DIO enzymes affect the thyroid hormone regulation by controlling thyroid hormone homeostasis at the cellular level, such as in the case of symptoms in mold exposure or in other situations in which there is a lack of active T3 hormone in the peripheral tissues or brain [45]. A deficiency of active cellular T3 hormone has been described as a non-thyroidal illness syndrome (NTIS) [46]. The patients with this disease presents with normal function of thyroid or with required exogenous T4 with normal thyroidstimulating hormone (TSH), free T4 (FT4), and free T3 (FT3) values in the blood, but still with symptoms of hypothyroidism. The major part of T3 is generated locally from T4 by DIO2 in most tissues of the body and in the brain, especially at the hypothalamus–pituitary level [47]
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