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Clinical Neuroscience

JUNE 02, 2009

[Pain sensitivity changes in schizophrenic patients and animal models - Part II.]

TUBOLY Gábor, HORVÁTH Györgyi

[Diminished pain sensitivity in schizophrenic patients has been reported for more than 50 years, however little is known about the substrate and the basic mechanisms underlying altered pain sensitivity in this disease, therefore, relevant animal models are of decisive importance in the study of psychiatric diseases. The authors report a review consisting of two parts focusing on pain sensitivity changes in patients and in different animal models which proved the eligibility as schizophrenia models and pain sensitivities have also been determined. The second part of this article analyzed the results regarding knock out mice as schizophrenia models. These data proved that several genes have significant role in the pathomechanism of schizophrenia; therefore deficiency in one gene does not produce animals showing all signs of this disease. As regards the pain sensitivity changes, only a few data are available with controversial results. Data originated from complex chronic animal models indicate that they might be more adequate methods for studying the mechanisms of schizophrenia including the pain-sensitivity changes.]

Hungarian Immunology

FEBRUARY 20, 2005

[Experimental arthritis model]

SZÁNTÓ Sándor, GONDA Andrea, MIKECZ Katalin, GLANT Tibor, SZEKANECZ Zoltán

[Animal models of experimental arthritis can be used to understand pathophysiology of the arthritic processes in patients and provide opportunity to develop new therapeutic approaches. The animal models can be divided into different categories based on the pathomechanism of the model and on the features that resemble human inflammatory joint diseases. This review provides an overview of the most widely used types of experimental arthritis models emphasizing their advantages and limitations in the basic arthritis research.]

Hypertension and nephrology

FEBRUARY 28, 2011

[The importance of epithelial-mesenchymal transition in kidney fibrosis]

NAGY SZAKÁL Dorottya, SZEBENI Beáta, SZIKSZ Erna, HIMER Leonóra, REUSZ György, VÁSÁRHELYI Barna, TULASSAY Tivadar, VANNAY Ádám

[Epithelial-mesenchymal transition (EMT) plays a central role in physiological and pathological processes of embryogenesis, carcinogenesis and tissue fibrosis. During EMT epithelial cells may transform to myofibroblasts, which are the effector cells of fibrosis. In our summary the process of EMT and its medical importance will be reviewed in relation to renal fibrosis. Regardless of the initiating cause the final common mechanism of organ fibrosis is similar in the different chronic renal diseases. It always involves major inflammatory responses, however the molecular mechanisms involved are still elusive. The EMT now takes centre stage as the point of convergence between inflammation and the progression of degenerative fibrotic diseases. Understanding the pathomechanism of EMT and the significance of signalling pathways involved in this process may lead to a new therapeutic approach in the treatment of chronic renal diseases.]

Hungarian Immunology

MARCH 20, 2002

[Patomechanism of hereditary angioneurotic oedema and provoking factors of oedematous attacks]

FARKAS Henriette

[The author describes the genetic background of hereditary angioneurotic edema, an autosomal dominant disorder. The pathomechanism of edemaformation and the significance of major mediator substances are explained along with clinical manifestations and their management. A special emphasis is placed on prophylaxis, the mainstay of which is the elimination of precipitating factors. The latter include mechanical trauma, diagnostic and therapeutic interventions performed in the cephalic-cervical region, mental stress, and sex hormones. The effect of endocrine therapies, ACE inhibitors, and infections - Helicobacter pylori in particular - on the natural course of the disease is also discussed.]

Lege Artis Medicinae

JULY 20, 2006

[WEGENER’S GRANULOMATOSIS PRESENTING AS MASTOIDITIS: A DIAGNOSTIC CHALLENGE]

NAGY Pál, Z.SZABÓ László, DOMJÁN Gyula, GADÓ Klára, BALOGH Károly

[INTRODUCTION - Wegener's granulomatosis has an uncertain pathomechanism, but is probably autoimmune in origin. In typical cases the mucosa of the nose, paranasal sinuses and of the lower respiratory tract, as well as the lungs and the kidneys are affected. Patients present with sinusitis, recurrent pneumonia or renal disease associated with microhaematuria, pyuria or azotaemia. Fever, polyarthralgia or polyarthritis may also occur. The underlying pathologic changes are necrotizing vasculitis, granulomas and parenchymal necrosis. The diagnosis is based on a combination of the clinical picture, microscopic findings and immunofluorescent demonstration of cANCA. CASE REPORT - A 27-year-old woman presented with symptoms of unilateral mastoiditis. In the following 7 months she underwent 7 operations in 4 hospitals for a locally progressive, destructive process of uncertain etiology showing a septic course. The clinical picture was not specific, the cANCA test was not definitive, and the histologic findings were initially interpreted as nonspecific inflammation. Repeated biopsies, multiple reviews of the microscopic specimens, consultations, differential diagnostic considerations, and, finally, the success of the treatment with corticosteroids and cyclophosphamide led to the diagnosis of Wegener’s granulomatosis. Currently the patient has been in remission for 32 months. CONCLUSION - The definitive diagnosis of Wegener’s granulomatosis, particularly of its localized or limited form, may be problematic despite well-defined diagnostic criteria. Setting up the correct diagnosis may take months or years. In case of unusual respiratory or otological symptoms, and in view of ineffective medical or surgical treatment, Wegener’s granulomatosis has to be considered. An atypical clinical picture, inconclusive histologic, radiologic and laboratory findings warrant the need for close collaboration of various specialists. This is particularly important since state-of-the-art therapy of Wegener’s granulomatosis promises a favourable prognosis.]

Clinical Neuroscience

JULY 10, 2005

[Frontotemporal dementia - Part II Differential diagnosis, genetics, molecular pathomechanism and pathology]

GALARIOTIS Vasilis, BÓDI Nikoletta, JANKA Zoltán, KÁLMÁN János

[This is a comprehensive paper in three parts covering history, prevalence, clinical forms, differential diagnosis, genetics, molecular pathomechanism, pathology, clinical diagnosis and treatment of frontotemporal dementia (FTD). The second part focuses on the differential diagnosis, genetics, molecular pathomechanism and pathology. The clinical diagnosis of frontotemporal dementia is based on the presence of a prominent disturbance of the executive function and of frontal lobe syndrome or a progressive aphasic syndrome without severe global cognitive impairment. Of other dementias, it is primarily Alzheimer’s disease that it should be differentiated from, but other psychiatric disorders must also be ruled out. The disease has familial and sporadic forms. Recent identification of mutations in the gene encoding the microtubule-associated tau protein in the inherited frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has demonstrated that various tau dysfunctions can lead to neurodegeneration. Tau gene mutations have varied effects on the biology and function of the protein. This heterogeneous pathomechanism explains the wide range of clinical and neuropathological features observed in the FTDP-17. Tau and ubiquitin antibodies can be detected by sensitive immunohistochemical methods. The diagnosis of FTD should be based on neuropathological examination, and this is also the only method by which it can be definitely differentiated from other types of dementias.]

Clinical Neuroscience

JULY 20, 2010

[Clinical, radiological and genetic aspects of leukodystrophies]

LÁSZLÓ A, ELPELEG ON, HORVÁTH K, JAKOBS C, KÓBOR J, GAL A, BARSI P, KELEMEN A, SARACZ J, SVÉKUS A, TEGZES A, VÖRÖS E

[The authors summarize the pathomechanism of the myelination process, the clinical, radiological and the genetical aspects of the leukodystrophies, as in 18q deletion syndrome, adrenoleukodysrtophy, metachromatic leukodystrophy, Pelizaeus-Merzbacher leukodystrophy, Alexander disease and olivo-ponto-cerebellar atrophy (OPCA).]

Lege Artis Medicinae

FEBRUARY 21, 2006

[THE WORLDWIDE EPIDEMIC OF TYPE 2 DIABETES - CAUSES AND CONSEQUENCES]

JERMENDY György

[The prevalence of type 2 diabetes mellitus has recently dramatically increased worldwide. While many factors contribute to the startling data, including changes in the diagnostic criteria of glucose intolerance, increase of life expectancy, manifestation of diabetes at younger ages, and increased detection of unrecognized diabetes due to more efficient screening, the genuine, steep rise in the incidence of diabetes is explained by the increasing prevalence of obesity. Among the late complications of both diabetes and obesity, cardiovascular diseases are particularly important. Insulin resistance due to visceral obesity plays a central role in the pathomechanism of type 2 diabetes. In the prevention of both type 2 diabetes and obesity, non-pharmacological intervention such as life style changes should be considered first. Supplementary pharmacological treatment should target all cardiovascular risk factors.]

Lege Artis Medicinae

JANUARY 20, 2010

[Special problems of hypertension in women]

KAPOCSI Judit, DEÁK György

[Menopause and pregnancy are especially vulnerable periods of women’s life regarding hypertension. The “Guidelines for the Management of Arterial Hypertension”, issued by the European Society of Hypertension and the European Society of Cardiology, dedicates a separate chapter to hypertension in women. The renewed guidelines of the Hungarian Society of Hypertension also pays a special attention to hypertension detected during pregnancy. In this article, the euthors review the topics of hypertension detected during menopause and pregnancy, discussing pathomechanism and therapy.]