RESUMEN
Breast cancer is the most common malignancy affecting women worldwide, and early diagnosis of breast cancer is the key to its successful and effective treatment. Traditional imaging techniques such as mammography and ultrasound are used to detect and configure breast abnormalities; unfortunately, these modalities have low sensitivity and specificity, particularly in young patients with dense breast tissue, breast implants, or post-surgical scar/architecture distortions. Therefore, breast magnetic resonance imaging (MRI) has been superior in the characterization and detection of breast cancer, especially that with invasive features. This review article explores the importance of breast MRI in the early detection of invasive breast cancer versus traditional tools, including mammography and ultrasound, while also analyzing the use of MRI as a screening tool for high-risk women. We will also discuss the different MRI features for invasive ductal carcinoma and lobular carcinoma and the role of breast MRI in the detection of ductal carcinoma in situ with a focus on the utilization of new techniques, including MR spectroscopy and diffusion-weighted imaging.
RESUMEN
High altitude pulmonary edema (HAPE) occurs in individuals rapidly ascending at altitudes greater than 2,500 m within one week of arrival. HAPE is characterized by orthopnea, breathlessness at rest, cough, and pink frothy sputum. Several mechanisms to describe the pathophysiology of HAPE have been proposed in different kinds of literature where most of the mechanisms are reported to be activated before a drop in oxygen saturation levels. The majority of the current studies favor diffuse hypoxic pulmonary vasoconstriction (HPV) as a pathophysiological basis for HAPE. However, some of the studies described inflammation in the lungs and genetic basis as the pathophysiology of HAPE. So, there is a major disagreement regarding the exact pathophysiology of HAPE in the current literature, which raises a question as to what is the exact pathophysiology of HAPE. So, we reviewed 23 different articles which include clinical trials, review articles, randomized controlled trials (RCTs), and original research published from 2010 to 2020 to find out widely accepted pathophysiology of HAPE. In our study, we found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse HPV, and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE. Similarly, with the evaluation of the role of inflammatory mediators like C-reactive protein (CRP) and interleukin (IL-6), we found out that inflammation in the lungs seems to modulate but not cause the process of development of HAPE. Genetic basis as evidenced by increased transcription of certain gene products seems to be another promising hypoxic change leading to HAPE. However, comprehensive studies are still needed to decipher the pathophysiology of HAPE in greater detail.
RESUMEN
Stem cell therapy is emerging as a promising treatment strategy to treat patients with stroke. While there are established modes of treatment for stroke patients such as thrombolysis and endovascular intervention, most of the stroke patients frequently end up with major residual deficits or even death. The use of stem cells to treat stroke has been found to be beneficial in the animal models but strict evidence for the same in humans is still lacking. We reviewed 13 clinical trials of stem cell therapy in stroke patients conducted between 2014 and 2020 based on the search using the database PubMed, and the clinical trial registry (www.clinicaltrials.gov). We aimed to assess the safety and efficacy of stem cell treatment in stroke patients who participated in the trials. Quality assessment of the clinical trials revealed a sub-optimal score. We found mixed results regarding the efficacy of stem cells in the treatment of ischemic stroke although we could not do a quantitative analysis of the effect outcomes. Assessment for safety revealed promising results as there were only minor side effects related to cell therapy. Although stem cell therapy seems to be a promising strategy to treat stroke patients in the future, we concluded that the field needs more evidence regarding the safety and efficacy of the use of stem cells in stroke patients before we use them in the clinic.
RESUMEN
Diabetes mellitus (DM) is the most common chronic metabolic disease. Parkinson's disease (PD) is considered one of the most common neurodegenerative diseases. There are many similarities between both conditions. Both disorders are chronic diseases. Both diseases result from a decrease in a specific substance: dopamine in PD, and insulin in DM. Besides, both disorders arise due to the destruction of particular cells, dopaminergic cells in PD, and pancreatic beta-cell in DM. Recently, many epidemiological and experimental studies showed a connection between DM and PD. There are common underlying mechanisms in the pathophysiology of both diseases. These underlying mechanisms include mitochondrial dysfunction, oxidative stress, hyperglycemia, and inflammation. Insulin resistance is indeed the hallmark of DM, especially type 2 diabetes mellitus (T2DM), which plays a significant role in these pathophysiological and molecular mechanisms. Besides, many studies revealed that anti-diabetic drugs have a beneficial effect on PD. In this current literature review, we aim to explore the standard pathophysiological and molecular linkages between these two disorders as well as how DM could affect the incidence and progression of PD. We also review how anti-diabetic drugs impact PD. In the future, further experimental and expanded clinical studies are needed to fully understand the exact pathophysiological connections between the two disorders and the efficacy of insulin and other anti-diabetic drugs in the treatment of PD in diabetic patients. Fully understanding and targeting these pathophysiological and molecular links could result in de novo curative therapy for PD and DM.
RESUMEN
Spontaneous coronary artery dissection (SCAD) is a frequently missed diagnosis in patients presenting with acute coronary syndrome (ACS). Our aim was to evaluate the causes, trends, and predictors of 90-day hospital readmission in patients presenting with SCAD. The Nationwide Readmissions Database (2013 to 2014) was utilized to identify patients with primary discharge diagnosis of SCAD using the International Classification of Diseases, Ninth Revision, Clinical Modification, diagnostic code 414.12. The primary outcome was 90-day readmission. Among 11,228 patients admitted with the primary diagnosis of SCAD, 2,424 patients (21.6%) were readmitted within 90 days (68% women, 82% <65 years of age). Common causes for 90-day readmission were ACS (25%), acute heart failure (11%), acute respiratory failure (7%), and arrhythmias (5%). Multivariate predictors of 90-day readmissions were hypertension, chronic obstructive pulmonary disease, peripheral arterial disease, discharge to facility and increased length of stay (LOS) during index admission. Multivariate predictors of increased healthcare-related costs were older age, female gender, discharge to facility, and increased LOS. Over half of the readmissions (52%) occurred in first 30 days after discharge. In conclusion, we found a high rate of rehospitalization among SCAD patients, particularly within the first 30 days of index hospitalization. ACS, heart failure, and acute respiratory failure were the most common reasons for readmission. Hypertension, chronic obstructive pulmonary disease, peripheral arterial disease, and increased LOS were independent predictors of readmission. Further studies are warranted to confirm these predictors of readmission in this high-risk population.
