Publications by authors named "Hassan H Salama"

3 Publications

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Schistosomal myeloradiculopathy due to Schistosoma mansoni: Report on 17 cases from an endemic area.

Ann Indian Acad Neurol 2011 Apr;14(2):107-10

Department of Neurosurgery, Mansoura University, Egypt.

Background: After malaria, schistosomiasis is the second most prevalent tropical disease. The prevalence of oviposition in CNS of infected persons varies from 0.3 to 30%. The conus medullaris is a primary site of schistosomiasis, either granulomatous or acute necrotizing myelitis.

Objective: To report the clinical, radiological, and laboratory results of spinal cord schistosomiasis (SCS) and to design proper therapeutic regimens.

Materials And Methods: Seventeen patients (13 males and four females) with SCS were enrolled between 1994 and 2009 at Mansoura University Hospitals. Their median age at diagnosis was 19 years (13-30 years). Independent neurological, radiological, and laboratory assessments were performed for both groups, excluding pathological confirmation that was done earlier in eight patients (Group 1). In the group 2 (nine patients), indirect hemagglutination (IHA) test for bilharziasis in blood and cerebrospinal fluid (CSF) was performed. Higher positive titer in CSF than serum indicated SCS plus induction of antibilharzial and corticosteroid protocols for 12 months with a three-year follow-up.

Results: Rate of neurological symptoms of granulomatous intramedullary cord lesion was assessed independently in 16 cases and acute paraparesis in one case. All patients in group 2 had positive IHA against Schistosoma mansoni with median CSF and serum ranges 1/640 and 1/320, respectively. Seven patients (41.18%) had complete recovery, eight patients (47.06%) showed partial recovery, and no response was reported in two patients (11.76%) (P = 0.005). There was no recorded mortality in the current registry.

Conclusions: Rapid diagnosis of SCS with early medical therapies for 12 months is a crucial tool to complete recovery.
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http://dx.doi.org/10.4103/0972-2327.82796DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3141472PMC
April 2011

Blocking effects of serum reactive antibodies induced by glatiramer acetate treatment in multiple sclerosis.

Brain 2003 Dec 22;126(Pt 12):2638-47. Epub 2003 Aug 22.

Multiple Sclerosis Research Unit, Department of Neurology, Baylor-Methodist Multiple Sclerosis Center, Baylor College of Medicine, Houston, Texas, USA.

Glatiramer acetate (GA) is a treatment option for multiple sclerosis. Although its mechanism of action remains unclear, evidence has emerged supporting the role of GA as an immunomodulatory drug that regulates T-cell function. It has been demonstrated that long-term GA treatment induces a serum antibody response; however, the functional properties of these 'reactive antibodies' are unknown. It has been speculated that GA-induced antibodies may have a blocking effect that can inhibit the immunologic activity of GA. This study was conducted to determine whether serum antibodies induced by GA treatment can block the in vitro immunoregulatory effects of GA on T-cell proliferation and cytokine production. Forty-two patients with relapsing-remitting multiple sclerosis who were treated with GA for 1-5 years were examined for GA antibody titres using enzyme-linked immunoabsorbent assay (ELISA). Thirty-three percent of patients developed high antibody titres [antibody binding index (ABI) = 16-64] and 14% had low antibody titres (ABI = 4) after 1 year on treatment. Results showed that purified GA antibodies blocked the stimulatory effects of GA on GA-specific T-cell lines of Th0 cytokine profile. The increase in interleukin-10 (IL-10) and IL-4 levels and the decrease in IL-12 and tumour necrosis factor-alpha levels, normally seen with GA stimulation, were reversed in the presence of GA antibodies. The study has important implications in our understanding of the potential role of high-titre GA antibodies in the treatment of multiple sclerosis.
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http://dx.doi.org/10.1093/brain/awg269DOI Listing
December 2003

Effects of combination therapy of beta-interferon 1a and prednisone on serum immunologic markers in patients with multiple sclerosis.

Mult Scler 2003 Feb;9(1):28-31

Multiple Sclerosis Research Unit, Department of Neurology, Baylor-Methodist Multiple Sclerosis Center, Houston, TX 77030, USA.

Beta-interferon (beta-IFN) has a proven treatment effect on relapsing-remitting multiple sclerosis (MS), presumably through its regulatory properties on T-cell activation and cytokine production. This paper examines whether combination therapy of beta-IFN with prednisone would enhance immunoregulatory effects of beta-IFN by measuring serum levels of selected proinflammatory cytokines and soluble T-cell activation markers associated with MS. The selected markers were analyzed in MS patients treated with beta-IFN alone (n = 22) and beta-IFN combined with a low daily dose of prednisone (n = 33), as compared with those in 27 healthy controls at baseline and at a three-month interval for one year. The study confirmed that beta-IFN treatment inhibited serum levels of tumor necrosis factor-alpha (TNFalpha) and intracellular adhesion molecule-1 (ICAM-1) in patients with MS. However, combination therapy did not significantly enhance the inhibitory effect of beta-IFN treatment on the production of TNFalpha, interleukin (IL)-12, IL-2R, and ICAM-1, while the addition of prednisone antagonized the effect of beta-IFN on up-regulation of IL-10 and soluble CD95. No difference in the occurrence of binding antibodies to beta-IFN was found between the two treatment groups. The findings are important for the understanding of the role of combination therapy in the treatment of MS.
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http://dx.doi.org/10.1191/1352458503ms865oaDOI Listing
February 2003