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Clinical Oncology

MAY 10, 2015

[Nutritional support in cancer anorexia-cachexia syndrome]

HARISI Revekka

[Cancer anorexia-cachexia syndrome (CACS) defi ned by ongoing loss of skeletal muscle mass, with or without loss of fat mass. In contrast to serious non tumorous cachexia it can not be reversed by conventional nutritional support. CACS affects most of cancer patients and has negative impact on physical function, anticancer treatment response, quality of life and survival. It is known that interactions between tumor and reactive host cells are responsible for tumor progression, metastasis formation and chronic infl ammation, as well. All of the processes are induced by cytokines. The CACS associated changes in carbohydrate, protein and lipid metabolism are caused by the elevated level of infl ammatory cytokines. The new anti-CACS drug development aimed at normalizing of the pathologic pathways. Up to now, megestrol-acetate (MA) administration seems to be the most effective drug in CACS treatment. MA has dual effect, stimulates the NPY activation and inhibits the synthesis and expression of infl ammatory cytokines. Its clinical effects are on line with the aboves, improves appetite, calorie intake and increases body weight. There is paradigm shift in CACS treatment, the traditional nutritional support is replaced by combination of pharmaceutical interventions, nutritional support and use of dietary supplements.]

Clinical Oncology

MAY 20, 2014

[Management of prostate cancer today]

PETRÁNYI Ágota Eszter, BODROGI István

[Although metastatic prostate cancer remains an incurable disease, the past years witnessed an extraordinary progress in the management of patients with castration resistant prostate cancer (CRPC). Development of novel agents that modulate the androgen receptor pathway, growth factor signaling pathways, immune functions and bone targeting machinery has been the focus of therapeutic strategies because of its signifi cance in the biology of prostate cancer progression. The arrival of several new agents — cabazitaxel, abiraterone acetate, enzalutamide, sipuleucel-T, denosumab and radium-223 — is changing the options and management of patients with metastatic castration resistant prostate cancer (mCRPC). Prostate cancer is a heterogeneous disease, therefore, in treatment must be considered the clinical characteristics of the disease as it manifests in an individual patient. The aim of this review is to summarize the most important new fi ndings for metastatic prostate cancers according to the different molecular pathways and to discuss their potential role on the management of this disease.]

Clinical Neuroscience

MARCH 25, 2015

[Teriflunomide: new oral immunmodulant drug in therapy of multiple sclerosis]

BENCSIK Krisztina, RÓZSA Csilla, VÉCSEI László

[Multiple sclerosis (MS) is the autoimmune, demyelinating, neurodegenerative disorder of the central nervous system (CNS). There are nine drugs available in Hungary reimbursed by the National Health Insurance Fund of Hungary (OEP) to reduce the activity of the disease, from which seven can be used as first line therapies. We have approximately 20 years of experience with the interferon b-1a/1b and glatiramer-acetate products. Though in case of approximately 30% of the patients using one of the first line drugs, the disease remains active, that we call break-through disease. The reasons for break-through disease could be the insufficient adherence and compliance, the appearance of neutralizing antibodies or the high activity of the disease. One of the oral immunomodulating drugs for MS, teriflunomide, was registered in Europe in 2013. Because of the anti-proliferative and anti-inflammatory effect of teriflunomide, it can be used for the reduction of the disease activity in the relapsing-remitting course of MS. The effect of teriflunomide was proved in one Phase II. and four Phase III. (TEMSO, TOWER, TENERE, TOPIC) studies. Teriflunomide 14 mg once daily was able to demonstrate in two consecutive placebo-controlled phase 3 clinical trials that significantly reduces the relapse rate (31.5% and 36.3%) and in both studies significantly reduces the sustained disability progression (29.8% and 31.5%) moreover delays the appearance of the clinically definitive MS in patients with clinically isolated syndrome (CIS). According to the TENERE study there were no significant differences observed between teriflunomide 14 mg and IFNb-1a s.c. in time to failure and annualized relapse rate but the treatment satisfaction domains of global satisfaction, side-effects and convenience were significantly improved with teriflunomide compared with s.c. IFNb-1a. ]

Clinical Neuroscience

JULY 30, 2014

[Natalizumab therapy, 2013]


[Multiple sclerosis (MS) is the most common chronic disease of the central nervous system in young adults. No curative therapy is known. Currently, six drugs are available that can reduce the activity of MS. The first-line drugs can completely reduce the activity of the disease in nearly two-thirds of the patients. In the remainder, who suffer from breakthrough disease, the condition of the patient worsens, and secondline therapies must be used. The second-line drug natalizumab exhibits almost double efficacy of the first-line drugs, but also have less favourable adverse effects. As a severe side-effect for instance, natalizumab carries the risk of the development of progressive multifocal leucoencephalopathy (PML), caused by a polyoma virus, the JC virus. There are three major risk factors for PML: an anti-JCV antibody status, a long duration of natalizumab treatment and prior immunosuppressant therapy. The lowest-risk group (1:14 286) comprises of patients who are anti-JCV antibody-negative, in whom the prior immunosuppressant use and duration of natalizumab therapy do not influence the risk of PML. With no prior immunosuppressant treatment, the incidence of PML increases to 1 in 192 patients after 2 years among those who are anti-JCV antibody-positive. These data may lead the physician to decide to discontinue natalizumab treatment. The half-life of natalizumab is three months; during this time other therapies can not be administered and the patients encounter the rebound effect: as the patients receiving natalizumab therapy displayed a high disease activity before treatment, the rebound effect can lead to relapses. After the termination of natalizumab secondline disease-modifying therapy with fingolimod may be introduce; no PML cases occur in response to fingolimod treatment. In the large majority of patients taking natalizumab who do not develop PML, this drug is highly effective and can prevent the progression of MS. The benefit of therapy and the risk of PML must be considered on an individual basis, with regard to the disease activity, the progression and the MRI activity, before natalizumab therapy is implemented.]

Hypertension and nephrology

MAY 20, 2012

[Gender differencies in coronary reactivity in angiotensin II hypertension rat model]


[It is known that hypertension shows several gender specific elements both in pathogenesis and in therapy. Understanding this phenomenon may bring us closer to individualized therapy. That was the reason why we examined process of hypertensive adaptation on the level of small intramural coronary arteries. 10-10 male and female Sprague-Dawley rats were used in this study. Animals received osmotic pumps in anaesthesia, which emitted 100 ng/bwkg/min angiotensin II acetate for four weeks. After four weeks treatment, animals were sacrified and heart weights were measured. We isolated intramural, small branches of the left anterior descendant coronary artery, placed them into vessel chamber and tested biomechanical properties and pharmacological reactivity. Heart weight and wall thickness were higher in females comparing to males. However, basal vascular tone and thromboxane-mediated vasoconstriction were elevated in males. Bradykinin relaxation was bigger in females. In female animals inward eutrophic remodeling was found, while in males increased wall stress and elastic moduli dominated the adaptation process. In conclusion, initial steps of angiotensin II mediated hypertension induced markedly gender dependent alterations.]

Clinical Neuroscience

SEPTEMBER 23, 2011

[New antiepileptic drugs, and therapeutic considerations]


[Epilepsy is not a singular disease, but a variety of disorders. It is affects up to 0.5% of the population. Over the past decade, the researchers have been made great advances in the field of epilepsy. These have been accompanied by the licensing of a great number of antiepileptic drugs. However, despite these efforts, up to 15-20% of patients have refractory epilepsy. The novel antiepileptic drugs must suit several requirements: higher efficacy, especially in resistant cases, better tolerability, and improved pharmacokinetic properties. Recently, three new drugs have been introduced for the medication. The retigabine is a carbamic derivate, and the anticonvulsive properties are largely due to its ability to prolong the opening of neuronal voltage-gated potassium Kv7.2 and Kv7.3 channels. The lacosamide is a functionalized amino acid, and selectively enhances voltage-gated sodium channel slow inactivation. The eslicarbazepine acetate is a new member of the dibenzazepine family, and blocks the fast inactivated voltage-gated sodium channel. All three of them differ from the foregoing agents in several important ways, including new mechanism of action (retigabine, lacosamide), or pharmacokinetics (eslicarbazepine acetate). These novel anticonvulsants appears to be a safe and effective addition to the armamentarium for the treatment of patients with refractory epilepsy. However, it must take some new approaches into consideration, in the therapeutic algorithm.]

Clinical Neuroscience

MARCH 10, 2005

[Application of the Multiple Sclerosis Functional Composite in Debrecen]


[Introduction - The Multiple Sclerosis Functional Composite (MSFC) has been recommended by the National Multiple Sclerosis Society as a new clinical outcome measure. It is based on measurements in three clinical dimensions: leg function/ambulation (timed 25-foot walk), arm function (9-hole peg test), and cognitive function (paced auditory serial addition test). Scores on component measures are converted to standard scores (Z-scores) that reflect patient performance. This method has not yet been introduced into routine clinical practice. Patients and method - MSFC calculation was applied to 17 patients with relapsing-remitting multiple sclerosis (age mean: 37.4±10.8 years; duration of the disease: 5.5±4.9 years, EDSS: 2.7±1.4) seen at the neuroimmunological outpatient clinic to evaluate its usefulness and its correlation with the traditionally applied Expanded Disability Status Scale (EDSS) and with patient-reported quality of life. Fifteen patients received immunomodulatory treatment (interferon beta and glatiramer acetate). MSFC and EDSS were measured at 0, 3, 6, 9, 12, 18 months, and questionnaires on quality of life were filled in by the patients at 0, 6, 12, 18 months of follow- up. Results - The prospective study confirmed a strong correlation between EDSS and MSFC (Spearman correlation test, p=0.03, 0.004, 0.002, 0.004, 0.0008, 0.002; R=-0.54, -0.66, -0.68, -0.65, -0.73, -0.69) in multiple sclerosis. The MSFC was more sensitive to clinical changes than EDSS. The extent of changes on the two scales correlated only after 18 months (p<0.005, R=-0.65). The arm/hand function was the most sensitive measure for disease progression. There was no correlation between the quality of life and either of the two other clinical parameters. Conclusion - MSFC is a simple method, suitable for followup of multiple sclerosis patients in everyday clinical practice.]

Clinical Neuroscience

DECEMBER 10, 2004

[Immunomodulatory treatment in multiple sclerosis ]


[During the past decade, several disease-modifying agents have been established and have become available for the treatment of multiple sclerosis. The disease-modifying agents could be grouped into immunomodulatory and immunosuppressive therapies altering the long-term course of multiple sclerosis. Therapy is now available for relapsing-remitting, secondary progressive and progressive-relapsing multiple sclerosis. Different disease-modifying agents became also available for the treatment of relapsing-remitting multiple sclerosis in Hungary which makes the therapeutic decision difficult. This overview might help to give an answer for different questions in the management of multiple sclerosis: Which agent to choose? When to initiate the therapy? Which dose to apply? Are the drugs safe? How long to treat the patients with immunomodulatory drugs? We give a review from the literature to assess the efficacy of disease-modifying therapies and to compare the data from phase three trials of interferon β1b, two preparations of interferon β1a or glatiramer acetate for the treatment of multiple sclerosis. We analyzed the efficacy and safety of these agents on physical, inflammatory and cognitive measures of disease activity. Comparison of study results indicated similar effects of immunomodulatory agents on relapse-related and inflammatory measures in relapsing multiple sclerosis. Interferon β1a slowed the progression of disability in relapsing multiple sclerosis. One interferon β1a preparation (intramuscularly injected) demonstrated efficacy in slowing progression of cognitive dysfunction. The interferons reduced relapses at early phase of secondary progressive multiple sclerosis, but their efficacy have not yet been proven in the later phase of secondary progressive multiple sclerosis without relapses. Mitoxantrone demonstrated efficacy in slowing the progression of disability in secondary progressive multiple sclerosis. All of the disease modifying agents are safe and tolerable, if the indication is correct and the patients are strictly controlled.]

Clinical Neuroscience

JANUARY 20, 2009

[Neuroprotection in Parkinson’s disease and other neurodegenerative disorders: preclinical and clinical findings]


[The authors summarized the evidence supporting neuroprotection based on the data available in the literature. In vivo and in vitro studies have indicated that many compounds can decrease neurodegeneration, excitotoxicity, oxidative stress, protein aggregation, disturbance of Ca2+ homeostasis and compensate the energy impairment. Selegiline, rasagiline, dopamine agonists and other molecules (ubiquinone, kynurenic acid, tocopherol, creatine, glatiramer acetate) exert neuroprotective effects in preclinical studies. Much less clinical data are available regarding neuroprotection in different neurological disorders. In this review, such preclinical and clinical evidences are summarized.]