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Corina-Daniela Ene

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Articles signed on Romanian Journal of NEUROLOGY:

PROFILE IN GANGLIOSIDE ANTIBODIES IN BENIGN PROSTATIC HYPERPLASIA

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Romanian Journal of Neurology, Volume XV, No. 1, 2016
ISSN 1843-8148  |  e-ISSN 2069-6094
ISSN-L 1843-8148
DOI: 10.37897/RJN

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PROFILE IN GANGLIOSIDE ANTIBODIES IN BENIGN PROSTATIC HYPERPLASIA

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ABSTRACT

Molecular pathology of benign prostatic hyperplasia is multifactorial and involves endocrine, biochemical, immunological interactions. The mechanisms involved in the onset and progression of benign prostatic hyperplasia are: infections, older than 50 years, imbalances in hormones and neurotransmitters, inflammation, oxidative stress. It is estimated that an infectious etiology can be a cause of wrong immune response directed at the prostate. Inflammatory neuropathies often occur after infections with various microorganisms. It is also known, that the presence of microorganisms is heterogeneous in patients with benign prostatic hyperplasia.

In this paper we documented the antibody profile of anti-GM1, -GM2, -GM3, -GD1a, -GD1b, -GT1b, -GQ1b IgG and IgM type in 30 patients with benign prostatic hyperplasia and in 30 controls. The results showed an increasing anti-GD1a and anti-GQ1b titer in patients with benign prostatic hyperplasia compared to control. The authors suggest that a careful monitoring of the patients developing an endogenous anti-gangliosidic immune response is required in order to assess these antibodies as potential risk factors for neuropathy in patients with benign prostatic hyperplasia.

Keywords: benign prostatic hyperplasia, infection, gangliosides, anti-gangliosides antibodies, neuropathies

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INTERFERON ALPHA2B INDUCED DOPAMINE CHANGES IN CUTANEOUS MELANOMA PATIENTS

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Romanian Journal of Neurology, Volume XIV, No. 4, 2015
ISSN 1843-8148  |  e-ISSN 2069-6094
ISSN-L 1843-8148
DOI: 10.37897/RJN

Indexed

DOI - Crossref
Similarity Check by iThenticate, worldwide No 1 professional plagiarism checking system
DOAJ
Scopus
NLM Catalog
Ebsco Host - Medline
Google Academic
Semantic Scholar

HIGHLIGHTS

ICMJE- Recommendations

Read the Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly work in Medical Journals.

Promoting Global Health

The published medical research literature is a global public good. Medical journal editors have a social responsibility to promote global health by publishing, whenever possible, research that furthers health worldwide.

INTERFERON ALPHA2B INDUCED DOPAMINE CHANGES IN CUTANEOUS MELANOMA PATIENTS

and

ABSTRACT

Objective. The authors interest was focused on interferon impact on dopamine status and on the relation between negative emotional state and dopamine in melanoma patients. 
Methods. 60 patients diagnosed with malignant melanoma in 1st or 2nd clinical stage were included in the fi rst 56 days after surgical removal of the tumor in an observational prospective study. The patients were divided in 2 groups: group A that included 30 cases treated with 10MU interferon alpha2b/mp three times a week for one year and group B that included 30 cases with no adjuvant treatment. Urinary dopamine (ELISA) was evaluated before treatment with interferon alpha2b, after 1, 6, 12 months of treatment and after 6 months from the end of the treatment. Neuropsychiatric disorders were grouped according to their frequency in melanoma patients.
Results. Neuropsychiatric disorders associated with the treatment with interferon were: irritability, asthenia and fatigability, sleep disorders, anxiety, cognitive disorders, somatic symptoms. The treatment with interferon altered dopamine metabolism. Dopamine returned to the pretherapeutical values at six months after interferon was stopped. Patients with low levels of urinary dopamine had a high, statistically signifi cant risk of developing depression during interferon treatment (OR=2.647, IC=2.186-3.014, p=0.0216). 
Conclusions. Low dopamine might have a major role in the development of depression secondary to interferon treatment.

Keywords: dopamine, interferon alpha2b, melanoma, neuropsychiatric disorders

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