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Hypertension and nephrology

SEPTEMBER 30, 2020

[Routes of transmission of SARS-CoV-2 virus infection]


[The modes of transmission of SARS-CoV-2 virus have been analyzed in detail recently. It can be stated that the deposition of micro-sized virus particles on different surfaces and in the air is the main reason for the strength and spread of the epidemic all over the world. Spread of virus is present in practically every event of our lives and daily activities. The usual movements of human-human contact, the specific habits of our own lives (face smoothing, eye rubbing etc.) increase the spread. The greatest threat is posed by infected but asymptomatic individuals as carriers of the virus, and the main concern is the speed of transmission dynamics. We have strong evidence that 1.5-2 meter distance, mask wearing, and eye protection are crucial in reducing the rate of virus transmission. It can be assumed that, like normal influenza virus infections, the appearance of the coronavirus shows a seasonal appearance.]

Lege Artis Medicinae

OCTOBER 20, 2016

[Crystal deposition in the background of a thyroid nodule]

BÉLY Miklós, PÉTER Ilona, SZŐKE János, GÁTI Tamás, KOLTAI Pál

[The authors present the findings of thyroid surgery in a patient treated for rheumatoid arthritis. An operation was performed due to the rapidly enlarged thyroid. In addition to the complex developmental anomaly, different crystals were found in the surgical material, which had called attention to the possibly affected mineral metabolism. Actually/Currently, the patient is not suffering from a clinically detectable metabolic disease or arthropathia induced by any crystal. The definitive crystal deposition in tissues, however, calls the physicians attention that the patient in addition to the treatment of the underlying disease should be examined in direction of a possibly developing metabolic disease, and, if necessary, an effective therapy should be used in a very early phase. ]

Clinical Neuroscience

JULY 30, 2016

[Transthyretin familial amyloid polyneuropathy - three Hungarian cases with rare mutations (His88Arg and Phe33Leu)]

CSILLIK Anita, POZSONYI Zoltán, SOÓS Krisztina, BALOGH István, BODÓ Imre, ARÁNYI Zsuzsanna

[Introduction - Transthyretin familial amyloid polyneuropathy is a rare autosomal dominant progressive systemic disesase of adults caused by endoneural amyloid deposition due to point mutations of the transthyretin gene. It is the most severe form among hereditary polyneuropathies, being fatal within 10 years if left untreated. The disease is underdiagnosed, the late onset forms (above the age of 50) being probably more widespread than previously thought. Early diagnosis is essential as the early introduction of causal therapy (tafamidis) slows progression and prolongs survival. Patients - We report here three non-related Hungarian cases of transthyretin familial amyloid polyneuropathy with non- Val30Met mutations (His88Arg in two cases, Phe33Leu in one case). They were all characterized by late-onset, progressive, length-dependent, axonal, sensorimotor polyneuropathy and the simultaneous presentation of severe restrictive cardiomyopathy. In all three cases, clinical and electrophysiological signs of myopathy were also present, suggesting the involvement of skeletal muscles as well. In two cases, high resolution ultrasound of the peripheral nerves was also performed, which showed segmental structural alterations (change or loss of fascicular structure) and some increase of echogenicity of the interfascicular epineurium, without substantial enlargement of the nerves. Conclusion - In Hungary, mainly the rare, non-Val30Met mutation forms of transthyretin familial amyloid polyneuropathy are encountered, as in our cases. As opposed to the Val30Met forms, these mutations are characterized by late onset and simultaneous presentation of severe cardiomyopathy. Our report highlights the importance of considering transthyretin familial amyloid polyneuropathy in the differential diagnosis of late-onset, progressive, axonal polyneuropathies of unknown etiology, particularly if associated with cardiac disease.]

Lege Artis Medicinae

DECEMBER 15, 2015

[The positive additive effect of rosuvastatin on platelet aggregation parameters in patients with cerebrovascular disease]

FEHÉR Gergely

[Statin therapy is the cornerstone of anti-atherosclerotic treatment, and it considered obligatory in the secondary prevention of atherosclerotic diseases. Rosuvastatin is well-known and efficacious lipid-lowering agent and seems to have benefitial antiplatelet efficacy and anti-inflammatory profile. The aim of our study was to determined the antiplatelet effect of 20 mg rosuvastatin (Xeter®, Richter Gedeon Nyrt.) in clopidogrel treated cerebrovascular patients. 20 patients with documented ischaemic cerebrovascular events and on 75 mg clopidogrel daily treatment were included in our study. 20 mg generic rosuvastatin significantly decreased total cholesterol (5.67 vs. 3.99 mmol/l, p<0.05), low-density lipoprotein (3.11 vs. 1.92 mmol/l, p<0.05) and trigliceride levels (1.75 vs. 1.29 mmol/l, p<0.05), and there was a non-significant high-density lipoprotein increasing (1.28 vs. 1.36 mmol/l, p=0.09) and high-sensitive C-reactive protein level decreasing tendency (3.35 vs. 2.99 mg/l, p=0.07). Rosu­vastatin treatment significantly decreased ADP 5 µM (46.15 vs. 31.35%) and collagen 2 mg/ml (68.62 vs. 52.22%) induced platelet aggregation (p<0.05). 20 mg rosuvastatin has a robust antilipaemic profile with benefitial additive effect on agonist induced platelet aggregation.]

Lege Artis Medicinae

NOVEMBER 03, 2015

[Current questions on Pneumococcus infections: cardiovascular complications, cardiotoxicity and new opportunities for prevention among elderly people]


[The respiratory tract infections, first of all severe pneumonia are associated with severe cardiovascular adverse events the significance of which that had not been recognised so far. Among the adverse events, the development of acute coronaria syndromes, heart failure, arrhythimias are the most important ones leading to significatly higher mortality even after several years. In the development of acute coronaria syndrome , the proinflammatory activites play the cenral role leading to the instability of coronaria plaques and plaque rupture associated with formation of platelet thrombi. The constriction of coronariae, peripherial vasodilatation and hypoxia also contribute to the deleterius complications. The role of pneumococci in this process seems to be especially significant since this pathogen exhibit a unique direct cardiotoxic effect, namely directly invades the myocardium and produce cardiotoxic substances. As a consequence, impairement of cardiomyocite function and contractility and formation of microscopic lesions in which later collagen deposition and long-term cardiac scarring can be detected. These pathological processes are developed despite of antibiotic treatment, consequently, vaccination against pneumococcal infection seems to be the only method for efficacious prevention of the myocardium damage and cardiovascular adverse events. According to the results of the CAPITA study, the conjugate polisaccharide vaccine decrease the number of pneumococcal pneumonia and invasive pneumococcal infections by 45 and 75% resp. in the elderly population. The recognition of the direct and indirect role of pneumococci in the development of early and late cardiovascluar adverse events gives a new aspect of the beneficial effect of efficacious vaccination.]

Hypertension and nephrology

SEPTEMBER 20, 2014

[Signaling pathways in renal fibrosis]


[Myofibroblasts are the main effector cells of tissue fibrosis in chronic kidney disease. These cells are the main source of collagen rich extracellular matrix in the fibrous tissue. Recent hypotheses suggest that pericytes are the major progenitors of myofibroblasts. Platelet derived growth factor, transforming growth factor β and Wingless/Int signaling pathways play important role in pericyte activation. There are experimental evidences that blocking this pathways inhibits tissue fibrosis, therefore they might be targets for the development of antifibrotic drugs in the future.]


MAY 30, 2014

[Determining sclerostin level in healthy men]


[The aim of this study is to evaluate the relationship of serum sclerostin levels with age, cystatin C, bone mineral density (BMD) and biochemical markers of bone turnover in healthy Hungarian men over 50 years of age. We determined serum levels of sclerostin and examined its relationship with age, cystatin C, osteocalcin, C-terminal telopeptides of type-I collagen, procollagen type 1 amino-terminal propeptide, 25- hydroxyvitamin D, parathyroid hormone, and L1-L4 (LS) and femur neck (FN) BMD data available from 194 randomly selected ambulatory men belonging to the HunMen cohort. In the study population as a whole (n=194; age (median, range): 59 (51-81) years), statistically significant correlation was found between sclerostin and age (r=0.211; p=0.003), cystatin C (r=0.246; p=0.001), FN-BMD (r=0.147; p=0.041) and LS BMD (r=0.169; p=0.019). Compared with middle-aged men (age: ≤ 59 years, n=98), elderly men (age > 59 years, n=96) had significantly higher serum sclerostin levels (67.8±15.9 pmol/l vs. 63.5±14; p=0.047). Among men with normal (T score >-1,0) FN-BMD, the elderly had significantly higher serum sclerostin levels as compared with the middle-aged (70.4±17 pmol/l vs. 63.9±11.5 pmol/l; p=0.019). Furthermore, among the elderly men cystatin C was the only significant predictor of serum sclerostin levels (standardized regression coefficient (béta) = 0,487; p<0,001). Our results show that in the studied healthy elderly cohort sclerostin levels significantly increase with age, along with the deterioration of kidney function as determined by plasma cystatin C levels. ]

Clinical Neuroscience

MARCH 30, 2013

[Inclusion body myositis - a rarely recognized disorder]


[Inclusion body myositis is the most common disabling inflammatory myopathy in the elderly. It is more frequent in men and after the age of 50 years. Inflammatory and degenerative features coexist. There is a T-cell mediated autoimmunity driven by in situ clonally expanded cytotoxic CD8-positive T-cells invading non-necrotic muscle fibres expressing MHC-I antigen. The hallmarks of degeneration are the deposition of protein aggregates and the formation of vesicles. The course of the disease is slow and the diagnosis is usually set after several years. The muscle weakness and wasting is assymetric, affecting predominantly distal muscles of the upper extremity and proximal muscles of the legs. The signs and clinical course can be characteristic, but the diagnosis is established by muscle biopsy. There is currently no evidence based effective treatment for sIBM. Prednisone, azathioprine, methotrexate, cyclosporine and IFN-β failed. Oxandrolon did not improve symptoms. Treatment with intravenous immunglobuline (IVIG) induced in some patients a transient improvement of swallowing and of muscle strenght, but the overall study results were negative. A T-cell depleting monoclonal antibody (alemtuzumab), in a small uncontrolled study slowed down disease progression for a six-month period. Repeated muscle biopsies showed the reduction of T-cells in the muscle and the suppression of some degeneration associated molecules. An effective therapeutic mean should act on both aspects of the pathomechanism, on the inflammatory and the degenerative processes as well.]

Hypertension and nephrology

DECEMBER 30, 2012

[Molecular mechanisms leading to renal fibrosis: the origin of myofibroblasts]

HIMER Leonóra, SZIKSZ Erna, KOVÁCS S. Krisztián, ÓNODY Anna, Reusz Anna, REUSZ György, FEKETE Andrea, TULASSAY Tivadar, VANNAY Ádám

[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]

Hungarian Immunology

DECEMBER 20, 2002

[Molecular and cellular basis of fibrosis: recent insights to the pathomechanism of scleroderma from animal models and fibroblast studies]

LAKOS Gabriella, SHINSUKE Takagawa, JOHN Varga

[Scleroderma is a chronic, progressive connective tissue disorder featuring inflammation, fibrosis, vascular injury, and immunologic abnormalities. Fibrosis, a hallmark of the disease, is characterized by excessive synthesis and deposition of extracellular matrix components, mainly type I collagen in affected tissue. The key target organs are the skin, lungs, kidneys, gastrointestinal tract and heart. The pathogenesis of fibrosis remains poorly understood, and effective treatments are lacking. While unifying concept to explain the pathogenesis of fibrosis has not yet emerged, multiple alterations result in the development of pathological tissue fibrosis have been recently identified. Transforming growth factor-β, a potent profibrotic cytokine plays a key role in the process. There is growing knowledge on identifying the cytokine and growth factor mediators of fibrosis, characterizing their interactions, and in delineating the cellular and molecular signaling pathways that are activated by these mediators. This review summarizes recent results obtained from fibroblast studies, animal models, and gene expression experiments. A major goal of investigations into the pathomechanism of fibrosis is identifying new therapeutic targets for scleroderma.]