Dataset Information

ICAM-1 levels in patients with covid-19 with diabetic foot ulcers: A prospective study in southeast asia.

ABSTRACT:

Background

Viral infection can compound the severity of pre-existing inflammation caused by underlying diseases. For those with a chronic, immune-related condition such as diabetic foot ulcers (DFUs), the coronavirus disease (COVID-19) serves to exacerbate the inflammatory burden. Serum levels of intracellular adhesion molecule-1 (ICAM-1), a primary mediator of cell adhesion express in the inflammatory process, are often used to indicate the gravity of all inflammatory conditions. Therefore, the purpose of this study was to investigate serum ICAM-1 levels before and after debridement in patients with DFUs who were also diagnosed as COVID-19 positive compared with those who were COVID-19 negative.

Methods

20 patients with DFUs were screened for COVID-19 and then divided into COVID-19 positive and negative groups according to the results. Before debridement, chest x-rays and blood analysis, including ICAM-1 serum levels, were performed in both groups. Only ICAM-1 serum levels were measured after debridement.

Results

Of the 20 patients included in this study, 55% were male (n = 11) and 45% were female (n = 9). The mean age was 52.9 ± 1.9 years. ICAM-1 levels in patients with DFU in the COVID-19-positive group were significantly higher than those in the COVID-19-negative group (median 317.2 vs 149.2, respectively; p < 0.001). Serum levels of ICAM-1 reduced significantly in patients with DFU in the COVID-19-positive group were significantly higher than those in the COVID-19-negative group after debridement (median 312.5 vs 130.3; p < 0.001).

Conclusion

ICAM-1 serum levels represent an additional, initial screening marker for COVID-19.

SUBMITTER: Oley MH

PROVIDER: S-EPMC7873613 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background and aimsThe Coronavirus Disease-19 (COVID-19) is posing an ongoing threat to human health. Patients of diabetic foot ulcer (DFU) are susceptible to COVID-19-induced adverse outcomes. Nevertheless, investigations into their mutual molecular mechanisms have been limited to date. In the present work, we tried to uncover the shared pathogenesis and regulatory gene targets of COVID-19 and DFU.MethodsIn this study, we chose GSE161281 as the COVID-19 data set, which contained severe acute respiratory syndrome coronavirus 2 infected human induced embryonic stem cell-derived peripheral neurons (n = 2) with uninfected controls (n = 2). The GSE134431 designated as the DFU data set, comprising full-thickness DFU (n = 13) and diabetic foot skin (n = 8) samples from diabetic patients. The differential expressed genes (DEGs) were identified from GSE161281 and GSE134431, and the common DEGs between COVID-19 and DFU were extracted. Multifactor regulatory network and co-expression network of the common DEGs were analyzed, along with candidate drug prediction.ResultsAltogether, six common DEGs (dickkopf-related protein 1 [DKK1], serine proteinase inhibitor A3 [SERPINA3], ras homolog family member D [RHOD], myelin protein zero like 3 [MPZL3], Claudin-11 [CLDN11], and epidermal growth factor receptor pathway substrate 8-like 1 [EPS8L1]) were found between COVID-19 and DFU. Functional analyses indicated that pathways of apoptotic and Wnt signaling may contribute to progression of COVID-19. Gene co-expression network implied the shared pathways of immune regulation and cytokine response participated collectively in the development of DFU and COVID-19. A multifactor regulatory network was constructed integrating the corresponding microRNAs (miRNAs) and transcription factors. Additionally, we proposed potential drug objects for the combined therapy.ConclusionOur study revealed the shared molecular mechanisms underlying COVID-19 and DFU. The identified pivotal targets and common pathways can provide new perspectives for further research and assist the development of management strategies in patients of DFU complicated with COVID-19.