Clinical presentation,management, screening and surveillance for colorectal cancer during the COVID-19 pandemic

Management of colorectal cancer (CRC) was severely affected by the changes implemented during the pandemic, and this resulted in delayed elective presentation, increased emergency presentation, reduced screening and delayed definitive therapy. This review was conducted to analyze the impact of the coronavirus disease 2019 (COVID-19) pandemic on management of CRC and to identify the changes made in order to adapt to the pandemic. We performed a literature search in PubMed, Medline, Index Medicus, EMBASE, SCOPUS, Reference Citation Analysis (https://www.referencecitationanalysis.com/) and Google Scholar using the following keywords in various combinations: Colorectal cancer, elective surgery, emergency surgery, stage upgrading, screening, surveillance and the COVID-19 pandemic. Only studies published in English were included. To curtail the spread of COVID-19 infection, there were modifications made in the management of CRC. Screening was limited to high risk individuals, and the screening tests of choice during the pandemic were fecal occult blood test, fecal immunochemical test and stool DNA testing. The use of capsule colonoscopy and open access colonoscopy was also encouraged. Blood-based tests like serum methylated septin 9 were also encouraged for screening of CRC during the pandemic. The presentation of CRC was also affected by the pandemic with more patients presenting with emergencies like obstruction and perforation. Stage migration was also observed during the pandemic with more patients presenting with more advanced tumors. The operative therapy of CRC was altered by the pandemic as more emergencies surgeries were done, which may require exteriorization by stoma. This was to reduce the morbidity associated with anastomosis and encourage early discharge from the hospital. There was also an initial reduction in laparoscopic surgical procedures due to the fear of aerosols and COVID-19 infection. As we gradually come out of the pandemic, we should remember the lessons learned and continue to apply them even after the pandemic passes.     

The Presence of Portal Vein Thrombosis Alters the Classic Enhancement Associated with Diagnosis of Hepatocellular Carcinoma

Digestive Diseases and Sciences - To determine whether the presence of portal vein thrombosis (PVT) where venous flow within the liver may be altered may delay the diagnosis of HCC and be...     

Impact of obesity on autoimmune arthritis and its cardiovascular complications

Obesity can instigate and sustain a systemic low-grade inflammatory environment that can amplify autoimmune disorders and their associated comorbidities. Metabolic changes and inflammatory factors produced by the adipose tissue have been reported to aggravate autoimmunity and predispose the patient to cardiovascular disease (CVD) and metabolic comorbidities. Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are autoimmune arthritic diseases, often linked with altered body mass index (BMI). Severe joint inflammation and bone destruction have a debilitating impact on the patient's life; there is also a staggering risk of cardiovascular morbidity and mortality. Furthermore, these patients are at risk of developing metabolic symptoms, including insulin resistance resulting in type 2 diabetes mellitus (T2DM). In addition, arthritis severity, progression and response to therapy can be markedly affected by the patient's BMI. Hence, a complex integrative pathogenesis interconnects autoimmunity with metabolic and cardiovascular disorders. This review aims to shed light on the network that connects obesity with RA, PsA, systemic lupus erythematosus and Sj?gren's syndrome. We have focused on clarifying the mechanism by which obesity affects different cell types, inflammatory factors and traditional therapies in these autoimmune disorders. We conclude that to further optimize arthritis therapy and to prevent CVD, it is imperative to uncover the intricate relation between obesity and arthritis pathology.     

Magnetic resonance imaging and characterization of spontaneous lesions in a transgenic mouse model of tuberous sclerosis as a model for endothelial cell-based transgene delivery

Tuberous sclerosis (TSC) is an autosomal dominant genetic disorder characterized by abnormalities in cellular migration, proliferation, and differentiation in many tissues. Benign hamartomas develop in multiple organs, believed to be caused by somatic mutation in addition to germ line mutation to cause loss of both alleles of either the TSC1 or TSC2 tumor suppressor gene, with resultant dysregulated growth due to loss of hamartin or tuberin function, respectively. This study focuses on detecting spontaneous lesions in a knockout mouse model of TSC2 by magnetic resonance imaging (MRI) and exploring the efficiency of introducing gene products into lesions, using transduced endothelial cells as gene vehicles. MRI was shown to be effective in detecting spontaneous lesions in multiple tissues as a means of assessing the prevalence of tumors. Tsc(2+/) heterozygous mice were screened at 12-24 months of age. MRI detected 100% of the renal lesions (cystadenomas, renal cell carcinomas) and 75% of the hepatic lesions (hemangiosarcomas), later identified by histology. Cell-mediated gene delivery was evaluated by immunohistochemical analysis of renal, hepatic, and lung lesions after intravenous delivery of MS1 mouse endothelial cells, transduced to express an enhanced form of green fluorescent protein (EGFP). Preliminary immunohistochemical analysis, using a polyclonal antibody to EGFP and a horseradish peroxidase-diaminobenzidine detection system, revealed these cells throughout liver, kidney, and lung sections from injected animals, organs that are frequently affected in TSC2 patients, as well as within the lesions themselves.     

Myocardial disease in human immunodeficiency virus (HIV) infection: a review

Heart muscle disease is the most important cardiovascular manifestation of HIV infection and is likely to become even more prevalent as HIV infected patients live longer. This may present as myocarditis, dilated cardiomyopathy or isolated left or right ventricular dysfunction. Myocardial involvement in HIV infection is multifactorial and may arise as a result of myocardial invasion with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection, drug-related cardiac toxicity, nutritional deficiencies, and prolonged immunosuppression. Both adults and children are affected with severity ranging from incidental microscopic inflammatory findings at autopsy to clinically significant cardiac disease with chronic cardiac dysfunction. It is associated with a poor prognosis, and results in symptomatic heart failure in up to 5% of HIV patients. Clinical pathological studies from the pre-HAART era show a 30% prevalence of cardiomyopathy in patients with AIDS. The introduction of highly active antiretroviral therapy (HAART) regimens has substantially modified the course of HIV disease by lengthening survival and improving quality of life of HIV-infected patients. There is also good evidence that HAART significantly reduces the incidence of cardiovascular manifestations of HIV infection. By preventing opportunistic infections and reducing the incidence of myocarditis, HAART regimens have reduced the prevalence of HIV-associated cardiomyopathy by almost 7-fold from the pre-HAART era. HAART is however only available to a minority of HIV infected individuals in most areas of the world and studies from the pre-HAART period still apply. In this review, the aetiopathogenesis and presentation of HIV related myocardial disease were reviewed and measures taken to improve survival discussed.