CD10, a transmembrane endopeptidase, has been shown to be lost as an early event in prostate cancer. We aimed at evaluating the pattern of expression of CD10 in various Gleason’s grades of prostatic adenocarcinoma in comparison with nodular hyperplasia of prostate. This retrospective study included 30 cases of nodular hyperplasia and 30 of prostatic adenocarcinoma of various Gleason’s grades. Immunohistochemical staining for CD10 was performed on all cases and positivity evaluated as percentage of cells as well as location (membranous or cytoplasmic or both). Of prostatic adenocarcinomas, grade 3 was seen in 10 foci, grade 4 in 28 and grade 5 in 22 foci. CD10 positivity in carcinoma was lower than in nodular hyperplasia, with the lowest positivity in grade 5. The pattern of expression of CD10 also changed from membranous in grade 3 to cytoplasmic in grade 5. Loss of CD10 expression appears to be associated with increasing tumour grade in carcinoma prostate and this can potentially be useful in stratification of such patients.

The occurrence of cardiovascular illness in the human immunodeficiency virus(HIV)community is increasing,with a particular focus on coronary heart disease.Patients infected with HIV have a higher risk of myocardial infarction compared to the general population in modern countries due to the development of effective antiretro-viral medications and increased life expectancy.Those not receiving highly active antiretroviral therapy(ART)may experience common cardiac consequences,including myocarditis,dilated cardiomyopathy,endocarditis,pulmonary hypertension,pericardial effusion,and cardiotoxicity associated with non-antiretroviral drugs.After the use of highly active ART,continuing immune activation and systemic inflammation seem to play a cen-tral role in this process.Recent studies suggest that protease inhibitors might negatively impact the progression of HIV-related heart failure(HF),which complicates the determination of the best therapy strategy for HIV-associated cardiomyopathy.The objective of this review is to examine the pathophysiology and correlation of various antiretroviral drugs leading to HIV-associated HF.Additionally,we explore the causes of HIV-associated atherosclerotic cardiovascular disease,including the high frequency of classic cardiovascular risk factors in HIV-infected patients,as well as HIV-related factors like the use of ART and chronic inflammation despite successful treatment of HIV infection.Numerous studies have revealed that individuals living with HIV/acquired immune deficiency syndrome frequently experience HF.In conclusion,despite advancements in HIV care,HIV-infected individuals continue to face an increased risk of HIV-associated cardiomyopathy and atherosclerosis.Further research is necessary to comprehend the underlying causes and develop effective treatments for cardiovascular disease in this population.We also discuss the currently available therapeutic options and ongoing research to mitigate the risk of cardiovascular disease and inflammation in HIV-infected individuals.

Introduction: The outbreak of coronavirus disease (COVID-19) in December 2019 called for a rapid solution, leading to repurposing of existing drugs. Due to its immunomodulatory effect and antiviral properties, hydroxychloroquine (HCQ) has been used in early 2020 for treatment of COVID-19 patients. This study was conducted to evaluate the treatment outcome of HCQ monotherapy in Malaysia. Methods: A retrospective cohort study was conducted in COVID-19 ward in Hospital Kuala Lumpur (HKL), from March to April 2020. A total of 446 COVID-19 patients were recruited, only 325 patients were finally included for analysis. Statistical analysis was done using SPSS, with a significant value set at p<0.05. Results: The mean age of the patients were 38.5 ±15.5. They were majority male, (n=210, 64.6%) Malaysian (n=239, 73.5%) and Malay ethnicity (n=204, 62.8%). Ninety-one (28%) patients received HCQ monotherapy. HCQ monotherapy was associated with worse outcome (OR: 10.29, 95% CI 1.17-90.80). There was a significant difference in mean length of stay between those with and without HCQ treatment (t323=5.868, p<0.001, 95% CI, 2.56-5.31). The average length of stay for HCQ treated group was 3.84 days longer than those without treatment. 6.6% of the patient receiving HCQ monotherapy encountered adverse drug effects. Conclusion: Similar to study reported worldwide, our study demonstrated that HCQ did not improve length of stay and the outcome of COVID-19 patients.