Increased levels of lactate dehydrogenase and hypertension are associated with severe illness of COVID-19.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is amid an ongoing pandemic. It has been shown that patients with cardiovascular comorbidities are at higher risk of severe illness of COVID-19. AIM: To find out the relationship between cardiovascular comorbidities and severe illness of COVID-19. METHODS: The clinical data of 140 COVID-19 patients treated from January 22, 2020 to March 3, 2020 at our hospital were retrospectively collected. The clinical characteristics were compared between patients with mild illness and those with severe illness. RESULTS: There were 75 male patients and 65 female patients (53.6% vs 46.4%). The mean age was 45.4 ± 14.6 years (range, 2-85 years). Most of the patients had mild illness (n = 114, 81.4%) and 26 patients had severe illness (18.6%). The most common symptom was fever (n = 110, 78.6%), followed by cough (n = 82, 58.6%) and expectoration (n = 51, 36.4%). Eight patients were asymptomatic but were positive for severe acute respiratory syndrome coronavirus 2 RNA. Patients with severe illness were significantly more likely to be hypertensive than those with mild illness [(10/26, 38.4%) vs (22/114, 19.3%), P = 0.036]. The levels of lactate dehydrogenase were significantly higher in the severe illness group than in the mild illness group (299.35 ± 68.82 vs 202.94 ± 63.87, P < 0.001). No patient died in either the severe illness or the mild illness group. CONCLUSION: Hypertension and elevated levels of lactate dehydrogenase may be associated with severe illness of COVID-19.

Correlation Analysis Between Serum Uric Acid, Prealbumin Level, Lactate Dehydrogenase, and Severity of COVID-19.

Objective: To analyze the correlation between serum uric acid, prealbumin levels, lactate dehydrogenase (LDH), and the severity of COVID-19. Methods: The data from 135 patients with COVID-19 was collected, and the patients were divided into a non-severe group (110 cases) and a severe group (25 cases), according to the severity of illness. Sixty cases with normal physical examinations over the same period and 17 cases diagnosed with other viral pneumonia in the past five years were selected as the control group to analyze the correlation between the detection index and the severity of COVID-19. Results: Serum albumin and prealbumin in the severe group were significantly lower than those in the non-severe group (p < 0.01); serum uric acid in the severe group was lower than that in the non-severe group (p < 0.05). LDH and C-reaction protein (CRP) in the severe group were higher than those in non-severe group (p < 0.01); the levels of albumin, prealbumin, serum uric acid, and LDH in the severe group were significantly different from those in healthy control group (p < 0.01) and the levels of prealbumin, serum uric acid, LDH, and CRP in the severe group were significantly different from those in the other viral pneumonia group (p < 0.01). Serum albumin and prealbumin were positively correlated with the oxygenation index (p < 0.001), while LDH was negatively correlated with oxygenation index (p < 0.001). Conclusion: Serum albumin, prealbumin, the oxygenation index, and LDH are risk factors of COVID-19.

MicroRNA-192 suppresses cell proliferation and induces apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes by downregulating caveolin 1.

Fibroblast-like synoviocytes (FLSs) play an important role in the pathogenesis of rheumatoid arthritis (RA). This study was conducted to explore the role of microRNA (miR)-192 in the regulation of the biology of RA-FLSs. The expression of miR-192 in RA and healthy synovial tissues was measured. The effects of overexpression of miR-192 on RA-FLS proliferation and apoptosis were investigated. Luciferase reporter assay and Western blot analysis were performed to identify direct target genes of miR-192. RA synovial tissues had significantly lower levels of miR-192 than healthy controls (P = 0.004). Moreover, miR-192 levels were 2.9-fold lower in RA-FLSs relative to normal human FLSs (P < 0.05). Ectopic expression of miR-192 significantly inhibited the proliferation and caused a cell cycle arrest at the G0/G1 phase in RA-FLSs. Moreover, miR-192 overexpression triggered apoptosis, which was accompanied by an increase in caspase-3 activity and Bax/Bcl-2 ratio. Caveolin 1 (CAV1) was identified to be a direct target of miR-192. Overexpression of miR-192 led to a reduction of endogenous CAV1 in RA-FLSs. Silencing of CAV1 significantly decreased cell proliferation and promoted apoptosis in RA-FLSs. Rescue experiments with a miR-192-resistant variant of CAV1 showed that enforced expression of CAV1 restored cell proliferation and attenuated apoptosis in miR-192-overexpressing RA-FLSs. In conclusion, miR-192 is downregulated in RA synovial tissues and restoration of its expression elicits growth-suppressive effects on RA-FLSs by targeting CAV1. The miR-192/CAV1 pathway may represent a novel target for prevention and treatment of RA.