Rejected

Anomalous left coronary artery arising from the pulmonary artery (ALCAPA) syndrome is a very rare congenital heart disease with an incidence of one in 300,000 and a high rate of mortality early in life if left untreated. Adult-type ALCAPA presents when significant collaterals develop from the right coronary artery (RCA) to the left coronary artery (LCA). Even with the collaterals, chronic sub-endocardial ischemia occurs in most cases, and patients die from sudden cardiac death. Here we present a case of a 38-year-old female who lived an active and healthy life and presented with chest pain and palpitations. Initial electrocardiography (EKG) showed atrial fibrillation with rapid ventricular response. Although initial cardiac enzymes were negative and there were no ischemic EKG changes, troponins became elevated over the course of the hospital stay and the patient underwent a left heart catheterization. Results revealed a dilated RCA extending to the left ventricle and an anomalous left main originating from the pulmonary artery with complete occlusion. The patient received medical management for acute coronary syndrome, including heparin infusion for 48 hours, aspirin, metoprolol, and atorvastatin. She was referred to a tertiary care facility for surgical correction of anomaly of the coronary arteries. The next day, the patient arrived in the emergency department with an acute onset of speech difficulty and left-sided weakness. A brain CT without contrast showed hematoma in the right frontal lobe. The patient underwent surgical evacuation of the hematoma with marked improvement of her weakness. The patient recovered after a successful surgical repair involving translocation of the left main coronary artery to the aorta. It has been reported that ALCAPA should be considered in a young adult with dilated cardiomyopathy and mitral regurgitation (MR). Other common presentations include acute myocardial infarction, angina, and dyspnea on exertion. Sudden cardiac death is not uncommon; however, it tends to decrease with age of diagnosis. Interestingly, our patient was known to have MR with regular follow-up at the cardiology clinic for years. Echocardiogram never showed any abnormalities other than MR. She never received further workup to address the reason of MR, although she has no underlying chronic conditions that can explain it. In relatively young patients with a healthy lifestyle presenting with chest pain, a broader look at etiologies should be considered. We would like to emphasize the importance of looking up for possible coronary artery disease, especially in young individuals.

The Ultrasound-guided erector spinae plane block (US-ESPB), used as an anesthesiological block for opioid-sparing approach and for postoperative analgesia, could represent an involuntary cause of hemodynamic instability. This hemodynamic instability is accentuated by a greater diffusion of local anesthetic in the epidural space.

Progranulin (PGRN) is a secreted growth factor that helps to regulate neuronal survival by blocking tumor necrosis factor-alpha (TNFα) receptors. The antioxidant alpha-lipoic acid (ALA) is used in diabetic neuropathy to improve nerve conduction and relieve neuropathic pain, but its effects on PGRN levels have not yet been elucidated.

Patients with myelofibrosis (MF) experience an array of symptoms that impair health-related quality of life (HRQoL). Fedratinib, an oral, selective Janus-kinase 2 (JAK2) inhibitor, was investigated in the randomized, placebo-controlled, phase III JAKARTA study in adult patients with intermediate- or high-risk JAK-inhibitor-naïve MF. The effect of fedratinib 400 mg/d on patient-reported MF symptoms and HRQoL in JAKARTA was assessed. Participants completed the modified Myelofibrosis Symptom Assessment Form (MFSAF v2.0), which evaluates 6 key MF symptoms (night sweats, early satiety, pruritus, pain under ribs on the left side, abdominal discomfort, bone/muscle pain). The modified MFSAF v2.0 was completed during the first 6 treatment cycles and at end of cycle 6 (EOC6). Symptom response was a ≥50% improvement from baseline in total symptom score (TSS). Overall HRQoL was assessed by EQ-5D-3L health utility index (HUI) score. The MFSAF-evaluable population comprised 91/96 patients randomized to fedratinib 400 mg and 85/96 patients randomized to placebo. Mean baseline TSS was 17.6 and 14.7 for fedratinib and placebo, respectively, and mean EQ-5D-3L HUI was 0.70 and 0.72. Fedratinib elicited statistically significant and clinically meaningful improvements in TSS from baseline versus placebo at all postbaseline visits. Symptom response rates at EOC6 were 40.4% with fedratinib and 8.6% with placebo (OR 7.0 [95% CI, 2.9-16.9];  < 0.001), and a significantly higher proportion of fedratinib-treated patients achieved clinically meaningful improvement from baseline on the EQ-5D-3L HUI at EOC6 (23.2% versus 6.5%;  = 0.002). Fedratinib provided clinically meaningful improvements in MF symptoms and overall HRQoL versus placebo in patients with JAK-inhibitor-naïve MF.

Little is known about the relationship between psoriasis and allergic contact dermatitis (ACD).

A 58-year-old male patient, previously healthy, presented with right flank pain of few hours duration. Initial workup showed an elevated creatinine and right hydroureteronephrosis. Computed tomography imaging revealed a retroperitoneal soft tissue mass encasing the right common iliac artery which is a first reported case in its anatomical distribution. Patient was referred to interventional radiology service where a percutaneous nephrostomy tube was placed followed by double J stenting. Subsequently, treatment with steroids was started. Follow up imaging a few months later revealed progressive resolution of the inflammatory process.

A large number of coronavirus disease 2019 (COVID-19) recovered patients are suffering from related symptoms. We conducted telephone interviews with 186 COVID-19 recovered medical doctors to determine the post-COVID symptoms, duration, and associated risk factors. About 70% of participants had at least one acute post-COVID symptom, including fatigue (43.0%), sleep disturbance (13.4%), lack of concentration (11.8%), breathing difficulty (10.2%), headache (6.5%), and muscle pain (6.5%). However, about 24% of participants reported having long post-COVID symptoms. Logistic regression analysis showed that female sex (odds ratio {OR}, 2.79; 95% CI, 1.28-6.06; p-value: 0.010) and comorbid conditions (OR, 2.28; 95% CI, 1.08-4.79; p: value, 0.030) are risk factors for the long post-COVID symptoms.

Although primarily a respiratory virus, coronavirus-19 acts on the gastrointestinal tract to cause symptoms such as anorexia, nausea, vomiting and diarrhea. One possible mechanism involves the ACE2 receptor, which serves as the primary receptor for virus entry into the gastrointestinal epithelium. We describe the case of a 54-year-old-male with recent coronavirus disease 2019 (COVID-19) infection, who later presented with nausea, vomiting, diarrhea and progressively worsening diffuse abdominal pain for 1 week. He was diagnosed to have a small bowel obstruction; however, continued to have progressively worsening pain and failed conservative management. No cause for the obstruction was found in the operating room. Gastrointestinal involvement occurs in at least two-thirds of patients with coronavirus infection. Viral entry into the small bowel, triggering an inflammatory response, and virus-induced microthrombosis of the microcirculation have been postulated as a possible mechanism for paralytic ileus/small bowel obstruction.

Although total hip arthroplasty (THA) is considered to be the most successful orthopedic operation in restoring mobility and relieving pain, common Metal-on-Metal (MoM) implants developed in the past decade suffer from severe inflammatory reactions of the surrounding tissue caused by the premature corrosion and degradation of the implant. A substantial amount of research has been dedicated to the investigation of mechanically driven fretting and crevice corrosion as the primary mechanism of implant failure. However, the exact mechanism by which hip implant breakdown occurs remains unknown, as current fretting and crevice corrosion studies have failed to completely replicate the corrosion characteristics of recovered implants. Here, we show that minor electric potential oscillations on a model hip implant replicate the corrosion of failed implants without the introduction of mechanical wear. We found in a controlled lab setting that small electrical oscillations, of similar frequency and magnitude as those resulting from ambient electromagnetic waves interacting with the metal of the implant, can force electrochemical reactions within a simulated synovial fluid environment that have not been previously predicted. In lab testing we have shown the replication of titanium, phosphorous, and oxygen deposition onto the surface of ASTM astm:F75 CoCrMo metal alloy test specimens, matching the chemical composition of previously retrieved wear particles from failed patient prosthetics. Our results demonstrate that the electrical activity and ensuing electrochemical activity excites two corrosion failure modes: direct dissolution of the medically implantable alloy, leaching metal ions into the body, and surface deposition growth, forming the precursor of secondary wear particles. We anticipate our findings to be the foundation for the future development and testing of electrochemically resistant implantable material.