Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with abnormal liver function tests. We hypothesized that early altered liver biochemistries at admission might have different clinical relevance than subsequent changes during hospitalization. A single-center retrospective study was conducted on 540 consecutive hospitalized patients, PCR-diagnosed with SARS-CoV-2. Liver test abnormalities were defined as the elevation of either gamma-glutamyltransferase (GGT), alanine aminotransferase (ALT), or aspartate aminotransferase (AST), above the upper limit of normality set by our laboratory. Linear mixed models (LMM) evaluated longitudinal associations, incorporating all available follow-up laboratory chemistries. By the end of the follow-up period, 502 patients (94.5%) were discharged (109 (20.5%) died). A total of 319 (64.3%) had at least one abnormal liver test result at admission. More prevalent were elevated AST (40.9%) and GGT (47.3%). Abnormalities were not associated with survival but with respiratory complications at admission. Conversely, LMM models adjusted for age and sex showed that longitudinal increases during hospitalization in ferritin, GGT, and alkaline phosphatase (ALP), as well as a decreased albumin levels, were associated with reduced survival. This dual pattern of liver damage might reconcile previous conflicting reports. GGT and ALP trajectories could be useful to determine who might need more surveillance and intensive care.

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Background: The usual inverse correlation between thyrotropin (TSH) and thyroid hormone disappears in syndromes of central resistance to thyroid hormone, where both are high. TSH and thyroid hormone are also simultaneously high when there is an elevation of the set point of the thyroid regulation axis. This can be estimated with indices, such as the Parametric Thyroid Feedback Quantile-based Index (PTFQI), which was designed for the general population. The PTFQI is positively associated with diabetes prevalence, but association with other pathologies has not been yet explored. The aim of this project was to explore the potential relationship of the PTFQI with metabolic and cardiovascular disease in a sample of ambulatory adult patients from Spain. Methods: A cross-sectional study was carried out among the patients who underwent thyroid hormones measurement (6434 measurements from September to November 2018 in a central laboratory in Spain). We retrospectively reviewed clinical records of a subgroup of adults aged >18 years with normal TSH and free thyroxine (fT4) belonging to groups that represent extreme PTFQI ( n = 661). Individuals with known conditions interfering the thyroid axis were excluded (remaining n = 296). Logistic and linear regression models adjusted for age and sex were used to calculate odds ratio (OR) of diseases and differences of clinical parameters, and 95% confidence intervals [CI]. Results: Across levels with higher PTFQI, there was an increase in the prevalence of type 2 diabetes (High vs. Low PTFQI OR: 2.88 [CI: 1.14–7.86], p -Trend = 0.02), ischemic heart disease (16.4% vs. 0%, unadjusted Haldane–Anscombe corrected OR: 23.90 [CI: 1.36–21.48], adjusted p -Trend = 0.04), atrial fibrillation (OR: 8.13 [CI: 1.33–158.20], p -Trend = 0.05), and hypertension (OR: 3.19 [CI: 1.14–9.94], p -Trend = 0.05). While the prevalence of type 2 diabetes was similarly associated with TSH and fT4, ischemic heart disease, atrial fibrillation, and hypertension were more strongly associated with the differences in fT4 values. Conclusions: Type 2 diabetes, ischemic heart disease, atrial fibrillation, and hypertension may be associated with a higher central regulation set point for thyroid hormone. These findings should be confirmed in other populations.