Thyroid hormones are characterized by a wide and multifarious influence on human metabolism. The thyroid gland (actuated by TSH) produces hormones, mainly T4 and small amounts of T3. Tissue deiodinases convert T4 into T3, which together with thyroxine-binding globulin, transthyretin, albumin, or apolipoprotein B100 provides proper bioavailability of those hormones [1,2]. The T4 into T3 conversion is not 100% efficient. There are three types of tissue deiodinases; biologically active T3 is one of three possible products of their activity, produced by D1 (deiodinase 1) and D2 (deiodinase 2); the others are biologically inactive: reverse T3 (rT3) and T2, produced by D3 (deiodinase 3), the main TSH/T4 inactivating enzyme [3]. Disturbance of their mutual balance results in a change of the T3 to T4 proportion, which, together with a lack of pituary–thyroid axis engaging (normal TSH), defines the euthyroid sick syndrome (ESS). In the ESS, the thyroid gland shows no signs of dysfunction, nonetheless, the levels of thyroid hormones are abnormal or close to the limits of the normal range. Practically, ESS is the opposite of the subclinical thyroid disorders group, where only TSH, but not T3 or T4 level is abnormal. [4]. It was described to occur in patients with a number of acute and chronic diseases, such as heart diseases, acute stroke, and cancer, among the patients of intensive care and geriatric units. Many studies investigated the probable link between thyroid disorders history and cancer, suggesting an interconnection between them [5,6,7,8,9,10]. Diverse mechanisms may constitute a basis for ESS development, regardless of them, it is usually considered to be associated with poor prognosis. Expression of tissue deiodinases seems to gain more impact on our understanding of cancer biology; we know that chronic inflammation, myocardial infarction, tissue repair, critical illness, and neoplasia: basal cell carcinoma, colon cancer—may cause D3 reactivation, reducing—at first intracellular—T3 level [3,11]. An extreme example may be “consumptive hypothyroidism”, where not only T3 but also TH level is affected by the massive activity of D3 in tumor tissue, usually occurring in infantile hemangioma patients [12]. Also intracellular regulation of TH concentration—on a microscale not involving systemic regulators—is a process important for cancerogenesis [13]. Interestingly, it was reported that levothyroxine users’ risk of developing pancreatic cancer (PDAC) is about 25% higher than in the general population [14]. Nevertheless, so far little is known about thyroid hormone tissue conversion in PDAC patients. To investigate it, we assumed two aims of this study: first, to describe thyroid hormones levels in the study population according to selected clinical features, putting a special emphasis on sick euthyroid syndrome frequency, and second, to check if thyroid hormones concentrations or their conversion ratio have a prognostic impact on overall survival (OS).