Prognosis

Introduction

Morbidity related to Hashimoto's thyroiditis (HT) typically results from failure to reach the diagnosis of hypothyroidism or to institute L-thyroxine (L-T4) replacement therapy in adequate doses on part of the treating physician, or from failure on the part of the patient to take the replacement medication (i.e. non-compliance of the patient).

With early diagnosis, timely institution of L-T4 replacement therapy, informed patient follow-up care, and attention to other attendant complications, the prognosis in HT is excellent, with patients leading a normal life. Untreated myxedema coma has a poor prognosis and a high mortality rate. Even with early detection and appropriate treatment, mortality ranges from 30% to 60% (Werner, 2000; Arlot, 1991).

The study by Ono et al reported that, as revealed through multivariable logistic regression, a higher in-hospital mortality rate in myxedema coma was associated with older age and catecholamine use (with or without steroids) (Ono et al., 2017).

Transient periods of thyrotoxicosis sometimes occur, and rarely the illness may progress to full hyperthyroid Graves' disease with active orbito-pathy (exophthalmos, inflamed eyes).

The increased prevalence of lipid disorders in association with untreated hypothyroidism has the potential to increase morbidity from coronary artery disease in patients with untreated or undertreated HT. A study by Sato et al suggested that in patients with heart failure, those with subclinical hypothyroidism have a worse prognosis, finding a significant increase in the rates of cardiac events and all-cause mortality in heart failure patients in the study with subclinical hypothyroidism compared with those who were euthyroid (Sato et al., 2018).

The relationship between papillary thyroid carcinoma (PTC) and HT has been controversial. Some investigations reported that the risk for PTCs is increased in patients with HT (Anand, Singh, Kushwaha, Hussain, & Sonkar, 2014). However, other studies have not observed a positive correlation (Jankovic, Le, & Hershman, 2013). The frequency of the association between PTC and HT ranges from 9% to 58% in a series of studies (Fugazzola, Colombo, Perrino, & Muzza, 2011). Whether HT represents a host immune response to PTC or just a chance occurrence remains unclear. Recently, studies have also focused on the influence of HT on the prognosis of PTC patients associated with HT. Several authors reported that the presence of HT in PTC is associated with smaller tumor size, less tumor invasion, a lower frequency of lymph node metastasis, less advanced TNM stage, and better prognosis (Kim, 2009; Kurukahvecioglu, 2007; Repplinger, 2008; Kiml 2011). In contrast, other studies reported that PTCs that coexist with HT are more likely to be bilateral and multifocal, resulting in a higher frequency of lymph node metastases (Consorti, 2010; Kebebew, 2001; Kim, 2010). Meta-analyses have indicated that HT is present in 26% of multifocal patients compared with 21% of unifocal patients (Lee, Kim, Choi, & Kim, 2003). Zhu et al. (2016) studied 763 PTC patients with and without HT. They reported that PTC patients with HT tended to exhibit multifocality (46.6% versus 21.6%, P < 0.001) and greater capsular invasion (43.3% versus 29.2%, P < 0.001) as compared to PTC patients without HT.