Thyroid in Bariatric Surgery
Thyroid in Bariatric Surgery
This study is expected to provide novel data regarding potential structural and functional
 changes of the thyroid gland in morbidly obese adults following significant weight loss
 through bariatric surgery. These data will complement evidence from epidemiological studies
 regarding the association of obesity and alterations in thyroid function. Potentially this
 study may justify further longer-term studies regarding the effects of weight gain and/or
 weight loss on the morphology of the thyroid gland and could help to form recommendations
 regarding follow-up investigations for the thyroid in morbidly obese patients.
Alterations in thyroid function are reported in obesity. Thyroid hormones and
 thyroid-stimulating hormone (TSH) concentrations have been variously described as normal,
 elevated, or low in morbidly obese patients compared with normal weight controls. However, it
 is a common observation that a significant proportion of patients with morbid obesity display
 slightly increased serum levels of TSH, while even relatively mild elevations of serum TSH
 are associated with an increase in the occurrence of obesity. Of note, abnormalities in
 thyroid function and TSH mostly normalize after weight loss, suggesting that these
 biochemical alterations are reversible. Despite uncertainty regarding the underlying
 mechanisms, it has been suggested that neither autoimmunity nor iodine deficiency seems to
 play a critical role. Several alternative mechanisms leading to hyperthyrotropinemia have
 been hypothesized, which include impaired feedback due to decreased number of
 triiodothyronine (T3) receptors in the hypothalamus, and variations in peripheral deiodinase
 activity. Leptin, in addition to regulating body weight and satiation, has also been shown to
 mediate the production of pro-TRH in cultured fetal rat hypothalamic neurons. Partial
 regulation of TSH by leptin has been also reported in humans. In addition, peripheral thyroid
 hormone metabolism appears to be reflected by the ratio of T3 to reverse T3 (rT3)
 (T3/rT3-ratio). We have shown that the T3/rT3-ratio is significantly increased in insulin
 resistant patients compared to their insulin sensitive partners despite comparable TSH
 values. Given that obesity is strongly associated with insulin resistance, and thyroid
 hormones are known to modulate carbohydrate metabolism, e.g. by affecting cellular glucose
 uptake, possible changes in the T3/fT3 ratio following weight loss after bariatric surgery
 could be of interest.

 Data from cross-sectional studies further indicate that the thyroid structure of obese
 patients can be also affected, independent of the existence of autoimmune thyroiditis as
 indicated by the presence of auto-antibodies such as TPO. Ultrasound (US) scans are able to
 accurately characterize the echographic structure of thyroid tissue, in addition to
 estimation of thyroid volume and identification of non-palpable thyroid nodules. The typical
 normal thyroid parenchyma has a distinct high echo density due to the follicle structure,
 which contrasts well with tissue of the collar muscles. The interface between thyroid cells
 and the colloid exhibits elevated acoustic impedance, causing high-frequency acoustic waves
 to be reflected back to the US probe. However, in autoimmune thyroid diseases both
 lymphocytic infiltration and disruption of normal tissue architecture cause a reduction in
 thyroid echogenicity, whereas other tissues close by such as muscle tissue appear to remain
 unaffected. Only few previous studies reported on the morphology of the thyroid gland in
 adults with morbid obesity. Given that thyroid function has been reported to return to normal
 after weight loss, research questions are also raised about the potential reversibility of
 thyroid structural abnormalities following substantial weight loss in previously morbidly
 obese patients.
Inclusion Criteria:

 1. Obesity (BMI > 40 kg/m2)

 2. Age: 18-65

 Exclusion Criteria:

 1. Diagnosis of obesity secondary to primary endocrine or systemic disease (e.g.
 Cushing's syndrome)

 2. Evidence of clinically relevant thyroid disease

 3. Chronic systematic inflammatory disease (e.g. rheumatoid arthritis)

 4. Pregnancy

 5. Treatment with anti-inflammatory drugs (e.g. corticosteroids)

 6. Type 1 diabetes mellitus