Journal of internal medicine
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Estimation of kidney function is often part of daily clinical practice, mostly done by using the endogenous glomerular filtration rate (GFR)-markers creatinine or cystatin C. A recommendation to use both markers in parallel in 2010 has resulted in new knowledge concerning the pathophysiology of kidney disorders by the identification of a new set of kidney disorders, selective glomerular hypofiltration syndromes. These syndromes, connected to strong increases in mortality and morbidity, are characterized by a selective reduction in the glomerular filtration of 5-30 kDa molecules, such as cystatin C, compared to the filtration of small molecules <1 kDa dominating the glomerular filtrate, for example water, urea and creatinine. ⋯ The syndromes are characterized by proteomic changes promoting the development of atherosclerosis, indicating antibodies and specific receptor-blocking substances as possible new treatment modalities. Presently, the KDIGO guidelines for diagnosing kidney disorders do not recommend cystatin C as a general marker of kidney function and will therefore not allow the identification of a considerable number of patients with selective glomerular hypofiltration syndromes. Furthermore, as cystatin C is uninfluenced by muscle mass, diet or variations in tubular secretion and cystatin C-based GFR-estimation equations do not require controversial race or sex terms, it is obvious that cystatin C should be a part of future KDIGO guidelines.
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Meta Analysis
Efficacy and safety of thrombolytic therapy for portal venous system thrombosis: A systematic review and meta-analysis.
The role of thrombolytic therapy in patients with portal venous system thrombosis (PVST) remains ambiguous. This study aimed to systematically collect available evidence and evaluate the efficacy and safety of thrombolysis for PVST. ⋯ Early initiation of thrombolysis should be effective for the treatment of PVST. But its benefits for PVST secondary to acute pancreatitis are weakened.
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Atherosclerotic cardiovascular disease is the leading cause of death globally. Despite its important risk of premature atherosclerosis and cardiovascular disease, familial hypercholesterolemia (FH) is still largely underdiagnosed worldwide. ⋯ In the last two decades, major progress has been made in clinical and genetic diagnostic tools and the therapeutic arsenal against FH. Improving prevention, diagnosis, and treatment and making them more accessible to all patients will help reduce the lifelong burden of the disease.
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Experimental trials in organisms ranging from yeast to humans have shown that various forms of reducing food intake (caloric restriction) appear to increase both overall and healthy lifespan, delaying the onset of disease and slowing the progression of biomarkers of aging. The gut microbiota is considered one of the key environmental factors strongly contributing to the regulation of host health. Perturbations in the composition and activity of the gut microbiome are thought to be involved in the emergence of multiple diseases. ⋯ There is substantial evidence for the efficacy of fasting in improving insulin signaling and blood glucose control, and in reducing inflammation, conditions for which, additionally, the gut microbiota has been identified as a site of both risk and protective factors. Accordingly, human gut microbiota, both in symbiont and pathobiont roles, have been proposed to impact and mediate some health benefits of fasting and could potentially affect many of these diseases. While results from small-N studies diverge, fasting consistently enriches widely recognized anti-inflammatory gut commensals such as Faecalibacterium and other short-chain fatty acid producers, which likely mediates some of its health effects through immune system and barrier function impact.
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Since the beginning of the SARS-CoV-2 pandemic in 2020, researchers worldwide have made efforts to understand the mechanisms behind the varying range of COVID-19 disease severity. Since the respiratory tract is the site of infection, and immune cells differ depending on their anatomical location, studying blood is not sufficient to understand the full immunopathogenesis in patients with COVID-19. It is becoming increasingly clear that monocytes, dendritic cells (DCs), and monocytic myeloid-derived suppressor cells (M-MDSCs) are involved in the immunopathology of COVID-19 and may play important roles in determining disease severity. ⋯ In contrast, airways of patients with severe COVID-19 display hyperinflammation with elevated levels of inflammatory monocytes and monocyte-derived macrophages, and reduced levels of tissue-resident alveolar macrophages. These monocyte-derived cells contribute to excess inflammation by producing cytokines and chemokines. Here, we review the current knowledge on the role of monocytes, DCs, and M-MDSCs in COVID-19 and how alterations and the anatomical distribution of these cell populations may relate to disease severity.