Sanyal Debmalya, Raychaudhuri Moutusi
Department of Endocrinology, KPC Medical College, Kolkata, West Bengal, India.
Department of Pediatric Endocrinology, Institute of Child Health, Kolkata, West Bengal, India.
Indian J Endocrinol Metab. 2016 Jul-Aug;20(4):554-7. doi: 10.4103/2230-8210.183454.
According to common perception, hypothyroidism is held responsible for obesity. However, linking them causally is controversial. Overt hypothyroidism is associated with modest weight gain, but there is a lack of clarity regarding subclinical hypothyroidism. Novel view indicates that changes in thyroid-stimulating hormone (TSH) could well be secondary to obesity. The increasing prevalence of obesity further confounds definition of normal TSH range in population studies. Thyroid autoantibody status may help in establishing the diagnosis of subclinical hypothyroidism in obesity. High leptin levels may play a role in the hyperthyrotropinemia of obesity and also increase susceptibility to thyroid autoimmunity and subsequent hypothyroidism. There is at most a modest effect of L-T4 treatment in overt hypothyroidism in inducing weight loss; benefit in subclinical hypothyroidism is not established with no data supporting thyroid hormone use in euthyroid obese patients.
根据普遍认知,甲状腺功能减退被认为是肥胖的原因。然而,将两者建立因果关系存在争议。显性甲状腺功能减退与适度体重增加有关,但亚临床甲状腺功能减退的情况尚不清楚。新观点表明,促甲状腺激素(TSH)的变化很可能是肥胖的继发结果。肥胖患病率的上升进一步混淆了人群研究中正常TSH范围的定义。甲状腺自身抗体状态可能有助于肥胖患者亚临床甲状腺功能减退的诊断。高瘦素水平可能在肥胖患者的促甲状腺激素血症中起作用,还会增加甲状腺自身免疫及随后甲状腺功能减退的易感性。左甲状腺素(L-T4)治疗对显性甲状腺功能减退患者的体重减轻至多只有适度效果;亚临床甲状腺功能减退患者是否获益尚无定论,且没有数据支持在甲状腺功能正常的肥胖患者中使用甲状腺激素。