ABSTRACT
BACKGROUND: Identifying prognosticators/predictors of COVID-19 severity is the principal focus for early prediction and effective management of the disease in a time-bound and cost-effective manner. We aimed to evaluate COVID-19 severity-dependent alteration in inflammatory and coagulopathy biomarkers. METHODS: A hospital-dependent retrospective observational study (total: n = 377; male, n = 213; and female, n = 164 participants) was undertaken. COVID-19 exposure was assessed by performing real-time PCR on nasopharyngeal (NP) swabs. Descriptive and inferential statistics were applied for both continuous and categorical variables using Rstudio-version-4.0.2. Pearson correlation and regression were executed with a cut-off of p < 0.05 for evaluating significance. Data representation by R-packages and ggplot2. RESULTS: A significant variation in the mean ± SD (highly-sever (HS)/moderately severe (MS)) of CRP (HS/MS: 102.4 ± 22.9/21.3 ± 6.9, p-value < 0.001), D-dimer (HS/MS: 661.1 ± 80.6/348.7 ± 42.9, p-value < 0.001), and ferritin (HS/MS: 875.8 ± 126.8/593.4 ± 67.3, p-value < 0.001) were observed. Thrombocytopenia, high PT, and PTT exhibited an association with the HS individuals (p < 0.001). CRP was correlated with neutrophil (r = 0.77), ferritin (r = 0.74), and WBC (r = 0.8). D-dimer correlated with platelets (r = -0.82), PT (r = 0.22), and PTT (r = 0.37). The adjusted odds ratios (Ad-OR) of CRP, ferritin, D-dimer, platelet, PT, and PTT for HS compared to MS were 1.30 (95% CI -1.137, 1.50; p < 0.001), 1.048 (95% CI -1.03, 1.066; p < 0.001), 1.3 (95% CI -1.24, 1.49, p > 0.05), -0.813 (95% CI -0.734, 0.899, p < 0.001), 1.347 (95% CI -1.15, 1.57, p < 0.001), and 1.234 (95% CI -1.16, 1.314, p < 0.001), respectively. CONCLUSION: SARS-CoV-2 caused alterations in vital laboratory parameters and raised ferritin, CRP, and D-dimer presented an association with disease severity at a significant level.
ABSTRACT
H. pylori (ubiquitous) and anemia together represent one of the growing health concerns globally. Gastroduodenal sequelae of H. pylori infection are distinguished; however, for the H. pylori infection and its implication in the development of anemia, iron has a significant health impact. We aimed to evaluate H. pylori infection-associated anemia by employing a logistic regression analysis model. A retrospective (case-control) study design-based assessment of the H. pylori associated-anemia. The study area was geo-referenced by QGIS/QuickMapServies. Descriptive and inferential statistical analyses were accomplished using the R-base-R-studio (v-4.0.2)-tidyverse. A p-value < 0.05 was the statistical significance cut-off value. A ggplot2 package was used for data representation and visualization. Mean ± SD age, Hb, MCV, ferritin, and RBC for overall study participants were measured to be 44.0 ± 13.58, 13.84 ± 2.49, 83.02 ± 8.31, 59.42 ± 68.37, and 5.14 ± 0.75, respectively. Decreased levels of Hb (infected vs. uninfected: 13.26 ± 2.92 vs. 14.42 ± 1.75, p < 0.001) ferritin (infected vs. uninfected: 48.11 ± 63.75 vs. 71.17 ± 71.14, p < 0.001), and MCV (infected vs. uninfected: 81.29 ± 9.13 vs. and 84.82 ± 6.93, p < 0.05) were measured to be associated with H. pylori infection when compared with H. pylori uninfected control group. Moreover, the magnitude (prevalence) of anemia (infected vs. uninfected: 78% vs. 21%, p < 0.001), iron deficiency anemia (IDA) (infected vs. uninfected: 63.3% vs. 36.6%, p < 0.001), and microcytic anemia (infected vs. uninfected: 71.6% vs. 46.1%, p < 0.001) were significantly different among the H. pylori-infected participants. The higher likelihood of developing anemia (AOR; 4.98, 95% CI; 3.089-8.308, p < 0.001), IDA (AOR; 3.061, 95% CI; 2.135-4.416, p < 0.001), and microcytic anemia (AOR; 3.289, 95% CI; 2.213-4.949, p < 0.001) by 398%, 206.1%, and 229%, respectively, was associated with H. pylori-infected. We recommend the regular monitoring of hematological parameters and eradication of H. pylori infection to minimize the extra-gastric health consequences of H. pylori infection.
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Cardiovascular disease causes significant personal, financial, and societal burden and is a major cause of mortality and morbidity globally. Dyslipidemia has proven to be a major factor that contributes to its increased incidence; thus, since a long time, low-density lipoprotein cholesterol-lowering therapies have been employed to reduce coronary artery disease-associated mortality. The first-line therapy for hyperlipidemia and dyslipidemia is statins. Evidence showed that statins decrease the level of LDL-C resulting in a lower risk of CVD (20-25% for every decrease of 1 mmol/L). However, due to statin intolerance in some patients and despite using maximal doses, they have not been successful in lowering cardiovascular-associated mortality. Moreover, bococizumab was recently suspended due to its higher immunogenicity with time, resulting in less efficacy with long-term use. Alternatives to statins are PCSK9 inhibitors which are administered subcutaneously every two or four weeks. They are injectables with considerable lipid-lowering properties. This narrative review discusses their genetics, safety, tolerability, and cost-effectiveness. It also quantifies their benefit in certain subgroups by analyzing the findings from recent randomized clinical trials. Current data from phase 2 and 3 trials (ORION, ODYSSEY, and FOURIER) suggest a favorable profile for evolocumab, alirocumab, and inclisiran with minimal tolerable side effects and superior efficacy in statin-intolerant patients. Their cost-effectiveness has not yet been established clearly, but future outcomes seem promising.
ABSTRACT
Vitamin D deficiency and periodontitis are commonly prevalent among Saudi adults. However, the association between periodontitis and vitamin D status has not been well documented. This study aims to examine the association between periodontitis and vitamin D status among adults in the Albaha region of Saudi Arabia. A case-control study of 123 Saudi adults was conducted; 60 had severe or moderate periodontitis, and 63 were periodontally healthy. Data was collected by an online self-reported sociodemographic questionnaire. All participants then underwent a full periodontal examination. Blood samples were also provided to assess participants' vitamin D statuses through serum levels of 25-hydroxyvitamin D (25(OH)D). A total of 60 cases and 63 controls matched for BMI (30.2 ± 4.86 kg/m2), age (40.01 ± 7.73 years), and sex (46.3% and 53.7% male and female, respectively) participated in the study. Mean levels of 25(OH)D were significantly lower in periodontitis participants than in controls (25.03 ± 8.55 ng/ml, 29.19 ± 12.82 ng/ml, p = 0.037, respectively). Lower odds of periodontitis were detected per unit of 25(OH)D level (OR 0.964, 95% CI; 0.931-0.999, p = 0.043). In conclusion, periodontitis is significantly associated with deficient and insufficient levels of vitamin D among Saudi adults in the Albaha region. Future longitudinal research with a larger sample size may be suggested to confirm these results.
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The aim of this study was to assess the clinical effectiveness of Hydroxychloroquine-based regimens versus standard treatment in patients with the coronavirus disease admitted in 2019 to a hospital in Saudi Arabia. A comparative observational study, using routine hospital data, was carried out in a large tertiary care hospital in Al Baha, Saudi Arabia, providing care to patients with COVID-19 between April 2019 and August 2019. Patients were categorized into two groups: the Hydroxychloroquine (HCQ) group, treated with HCQ in a dose of 400 mg twice daily on the first day, followed by 200 mg twice daily; the non HCQ group, treated with other antiviral or antibacterial treatments according to protocols recommended by the Ministry of Health (MOH) at the time. The primary outcomes were the length of hospital stay, need for admission to the intensive care unit (ICU), time in ICU, and need for mechanical ventilation. Overall survival was also assessed. 568 patients who received HCQ (treatment group) were compared with 207 patients who did not receive HCQ (control group). HCQ did not improve mortality in the treated group (7.7% vs. 7.2%). There were no significant differences in terms of duration of hospitalization, need for and time in ICU, and need for mechanical ventilation among the groups. Our study provides further evidence that HCQ treatment does not reduce mortality rates, length of hospital stay, admission and time in ICU, and need for mechanical ventilation in patients hospitalized with COVID-19.
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BACKGROUND: CTCF encodes 11-zinc finger protein which is implicated in multiple tumors including the carcinoma of the breast. The Present study investigates the association of CTCF mutations and their expression in breast cancer cases. METHODS: A total of 155 breast cancer and an equal number of adjacent normal tissue samples from 155 breast cancer patients were examined for CTCF mutation(s) by PCR-SSCP and automated DNA sequencing. Immunohistochemistry (IHC) method was used to analyze CTCF expression. Molecular findings were statistically analyzed with various clinicopathological features to identify associations of clinical relevance. RESULTS: Of the total, 16.1% (25/155) cases exhibited mutation in the CTCF gene. Missense mutations Gln > His (G > T) in exon 1 and silent mutations Ser > Ser (C > T) in exon 4 of CTCF gene were analyzed. A significant association was observed between CTCF mutations and some clinicopathological parameters namely menopausal status (p = 0.02) tumor stage (p = 0.03) nodal status (p = 0.03) and ER expression (p = 0.04). Protein expression analysis showed 42.58% samples having low or no expression (+), 38.0% with moderate (++) expression and 19.35% having high (+++) expression for CTCF. A significant association was found between CTCF protein expression and clinicopathological parameters include histological grade (p = 0.04), tumor stage (p = 0.04), nodal status (p = 0.03) and ER status (p = 0.04). CONCLUSIONS: The data suggest that CTCF mutations leading to its inactivation significantly contribute to the progression of breast cancer.
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BACKGROUND: Members of the HMGN protein family modulate chromatin structure and influence epigenetic modifications. HMGN1 and HMGN2 are highly expressed during early development and in the neural stem/progenitor cells of the developing and adult brain. Here, we investigate whether HMGN proteins contribute to the chromatin plasticity and epigenetic regulation that is essential for maintaining pluripotency in stem cells. RESULTS: We show that loss of Hmgn1 or Hmgn2 in pluripotent embryonal carcinoma cells leads to increased levels of spontaneous neuronal differentiation. This is accompanied by the loss of pluripotency markers Nanog and Ssea1, and increased expression of the pro-neural transcription factors Neurog1 and Ascl1. Neural stem cells derived from these Hmgn-knockout lines also show increased spontaneous neuronal differentiation and Neurog1 expression. The loss of HMGN2 leads to a global reduction in H3K9 acetylation, and disrupts the profile of H3K4me3, H3K9ac, H3K27ac and H3K122ac at the Nanog and Oct4 loci. At endodermal/mesodermal genes, Hmgn2-knockout cells show a switch from a bivalent to a repressive chromatin configuration. However, at neuronal lineage genes whose expression is increased, no epigenetic changes are observed and their bivalent states are retained following the loss of HMGN2. CONCLUSIONS: We conclude that HMGN1 and HMGN2 maintain the identity of pluripotent embryonal carcinoma cells by optimising the pluripotency transcription factor network and protecting the cells from precocious differentiation. Our evidence suggests that HMGN2 regulates active and bivalent genes by promoting an epigenetic landscape of active histone modifications at promoters and enhancers.