A Review on Joint Carotid Intima-Media Thickness and Plaque Area Measurement in Ultrasound for Cardiovascular/Stroke Risk Monitoring: Artificial Intelligence Framework

Journal of Digital Imaging - Cardiovascular diseases (CVDs) are the top ten leading causes of death worldwide. Atherosclerosis disease in the arteries is the main cause of the CVD, leading to...     

Salmonella infection-associated acute rhabdomyolysis. Some pathogenic considerations

Rhabdomyolysis is a syndrome characterized by extended myolysis, elevation of serum aminotransferases and creatine kinase, and myoglobinuria. It is a rare but well-established complication of a spectrum of infectious diseases. Salmonella infections have been connected with this syndrome as well. We present here the case of a 58-year-old female affected by Charcot-Marie-Tooth (CMT) disease, a type of hereditary neuropathy, who presented with acute renal failure and rhabdomyolysis syndrome in the course of Salmonella infantis gastroenteritis. We formed some considerations on the pathogenesis of rhabdomyolysis in this specific setting based on certain experimental works on the Salmonella pathogenic cycle. We concluded that the calcium-dependent mechanism coupled with a predisposing factor might be of major significance in the development of this complication.     

A fatal <Emphasis Type="Italic">Mycobacterium chelonae</Emphasis> infection in an immunosuppressed patient with systemic lupus erythematosus and concomitant Fahr’s syndrome

We present a case of systemic Mycobacterium chelonae infection in an immunosuppressed patient with systemic lupus erythematosus (SLE), idiopathic hypoparathyroidism, and hypothyroidism. The patient was treated for 3 months for skin infection with clarithromycin monotherapy. Since her condition deteriorated, the antibiotic therapy was switched to intravenously administered clindamycin, cloxacillin, and meropenem. Due to further deterioration and isolation of M. chelonae from the blood culture, antimicrobial therapy was changed to azithromycin and amikacin. Drug-test sensitivity was performed, and the isolate was susceptible to clarithromycin only. The patient’s deteriorating status prevented orally administered medication with clarithromycin (parenteral formulation is not registered in Croatia). The same antibiotic regime was continued until the isolation of Pseudomonas aeruginosa and Candida albicans. In addition, extensive calcifications in her brain were found on a computed tomography (CT) scan, which suggested Fahr’s syndrome. Despite all measures and supportive care, the patient developed multiorgan failure and eventually died. There has been an increase in the number of infections by rapidly growing mycobacteria, but only a few cases of severe systemic infection with M. chelonae have been described. If the infection is diagnosed early and a patient is treated with appropriate drugs, dissemination can be avoided despite immunosuppression. For serious skin, bone, and soft-tissue disease, a minimum of 4 months of a combined drug therapy is necessary. This is the first report of M. chelonae infection in Croatia and the first-described M. chelonae infection in a patient with concomitant Fahr’s syndrome.     

Blockade of KATP Channels Reduces Endothelial Hyperpolarization and Leukocyte Recruitment upon Reperfusion After Hypoxia

Ischemia/reperfusion injury in renal transplantation leads to slow or initial nonfunction, and predisposes to acute and chronic rejection. In fact, severe ischemia reperfusion injury can significantly reduce graft survival, even with modern immunosuppressive agents. One of the mechanisms by which ischemia/reperfusion causes injury is activation of endothelial cells resulting in inflammation. Although several therapies can be used to prevent leukocyte recruitment to ischemic vessels (e.g. antiadhesion molecule antibodies), there have been no clinical treatments reported that can prevent initial immediate neutrophil recruitment upon reperfusion. Using intravital microscopy, we describe abrogation of immediate neutrophil recruitment to ischemic microvessels by the K_ATP antagonist glibenclamide (Glyburide™). Further, we show that glibenclamide can reduce leukocyte recruitment in vitro under physiologic flow conditions. ATP-regulated potassium channels (K_ATP) are important in the control of cell membrane polarization. Here we describe profound hyperpolarization of endothelial cells during hypoxia, and the reduction of this hyperpolarization using glibenclamide. These findings suggest that control of endothelial membrane potential during ischemia may be an important therapeutic tool in avoiding ischemia/reperfusion injury, and therefore, enhancing transplant long-term function.