The predictors of long-COVID in the cohort of Turkish Thoracic Society-TURCOVID multicenter registry: One year follow-up results

Objective: To evaluate long-term effects of COVID-19, and to determine the risk factors in long-COVID in a cohort of the Turkish Thoracic Society (TTS)-TURCOVID multicenter registry. Methods: Thirteen centers participated with 831 patients; 504 patients were enrolled after exclusions. The study was designed in three-steps: (1) Phone questionnaire; (2) retrospective evaluation of the medical records; (3) face-to-face visit. Results: In the first step, 93.5% of the patients were hospitalized; 61.7% had a history of pneumonia at the time of diagnosis. A total of 27.1% reported clinical symptoms at the end of the first year. Dyspnea (17.00%), fatigue (6.30%), and weakness (5.00%) were the most prevalent long-term symptoms. The incidence of long-term symptoms was increased by 2.91 fold (95% CI 1.04-8.13, P=0.041) in the presence of chronic obstructive pulmonary disease and by 1.84 fold (95% CI 1.10-3.10, P=0.021) in the presence of pneumonia at initial diagnosis, 3.92 fold (95% Cl 2.29-6.72, P=0.001) of dyspnea and 1.69 fold (95% Cl 1.02-2.80, P=0.040) fatigue persists in the early-post-treatment period and 2.88 fold (95% Cl 1.52-5.46, P=0.001) in the presence of emergency service admission in the post COVID period. In step 2, retrospective analysis of 231 patients revealed that 1.4% of the chest X-rays had not significantly improved at the end of the first year, while computed tomography (CT) scan detected fibrosis in 3.4%. In step 3, 138 (27.4%) patients admitted to face-to-face visit at the end of first year; at least one symptom persisted in 49.27% patients. The most common symptoms were dyspnea (27.60%), psychiatric symptoms (18.10%), and fatigue (17.40%). Thorax CT revealed fibrosis in 2.4% patients. Conclusions: COVID-19 symptoms can last for extended lengths of time, and severity of the disease as well as the presence of comorbidities might contribute to increased risk. Long-term clinical issues should be regularly evaluated after COVID-19.

Soluble CD40 ligand, plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor-1-antigen in normotensive type 2 diabetic subjects without diabetic complications. Effects of metformin and rosiglitazone

To evaluate subclinical inflammation and fibrinolysis in low-risk type 2 diabetic subjects and to assess the efficacy of metformin and rosiglitazone in this group Sixty-one normotensive, normoalbuminuric type 2 diabetic subjects without diabetes-related complications were included in a 4-week standardization period with glimepiride. After the standardization period, 21 subjects were excluded and the remaining 40 were randomly divided into two groups matched for age, gender, body mass index and disease duration. The first group [n = 20] received metformin [1,700 mg/day], the second group [n = 20] rosiglitazone [4 mg/day] for 12 weeks. Patients with low-density lipoprotein-cholesterol higher than 130 mg/dl at the beginning of the randomization period were treated with simvastatin [maximum dose 20 mg/day]. Twenty-three healthy controls were also recruited. Cytokine measurements were performed with ELISA kits Baseline plasma plasminogen activator inhibitor-1 [PAI-1] level of type 2 diabetic subjects was significantly elevated [p = 0.038], but baseline levels of soluble CD40 ligand [sCD40L] and thrombin-activatable fibrinolysis inhibitor-1 [TAFI] antigen did not differ from healthy controls. Twelve weeks of metformin or rosiglitazone therapy did not cause significant changes in sCD40L, PAI-1 and TAFI antigen levels. In simvastatin-treated subjects [n = 9] significant reductions of PAI-1 were achieved [p = 0.028], while sCD40L and TAFI-Ag did not differ from baseline values. Our results showed that nonobese diabetic patients at low cardiovascular risk had similar levels of subclinical markers of inflammation and fibrinolysis as matched healthy controls. Neither metformin nor rosiglitazone caused marked changes in sCD40L, PAI-1 and TAFI antigen levels. A subset of patients who received simvastatin showed a modest decrease in PAI-1 level and could contribute to beneficial vasculoprotective effect of the drug in type 2 diabetics

Plasma thiobarbituric acid-reactive substance levels in subclinical hypothyroidism

The purpose of this study was to determine thiobarbituric acid-reactive substance [TBARS] levels in subclinical hypothyroidism and to examine the effect of levothyroxine replacement on TBARS levels. A cohort of 28 female patients with subclinical hypothyroidism and 24 healthy controls were enrolled in this study. The levels of plasma TBARS, serum lipids, and high-sensitive C-reactive protein [CRP] in patients with subclinical hypothyroidism at baseline and after achieving euthyroid state by levothyroxine were assessed. TBARS levels of the patients were similar to those of the control group in the subclinical hypothyroid state and after restoration of euthyroidism by levothyroxine replacement. TBARS levels decreased after levothyroxine treatment, but did not reach statistical significance. There was no significant correlation between TBARS, lipid and CRP levels. Serum CRP levels were higher in subclinical hypothyroidism [4.28 +/- 0.9 mg/l] than in the control group [1.95 +/- 0.34 mg/l] and the difference was statistically significant [p = 0.03]. After achieving euthyroid state, CRP levels decreased significantly in patients with subclinical hypothyroidism from 4.28 +/- 0.9 to 2.32 +/- 0.6 mg/l [p = 0.006]. Our findings suggest that there is no significant alteration of plasma TBARS levels neither in subclinical hypothyroid state nor after achieving euthyroid state. Serum CRP level is higher in patients with subclinical hypothyroidism than in the control group. Normalization of thyroid state seems to effectively reduce serum CRP levels in subclinical hypothyroidism without any correlation with TBARS activity