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Biomedical subjects

B Delisse

Publications and source records attributed to B Delisse.

5 recordsLinked to original sources

Multiple sclerosis, interferon beta and clinical thyroid dysfunction.

The objective of this study was to investigate frequency and presentation of clinical thyroid dysfunction in patients treated with interferon beta (IFN-beta). We have collected the cases of clinical thyroid dysfunction in 700 consecutive patients receiving IFN-beta for multiple sclerosis (MS). Five patients (four women, one man) treated with IFN-beta1b developed hyperthyroidism. Three of them have secondary progressive MS, and two have relapsing-remitting MS. It was necessary to stop IFN-beta in three cases; these patients still require carbimazole after several months. In the two other cases, hyperthyroidism disappeared spontaneously. Two patients (one man and one woman) treated with IFN-beta1a developed hypothyroidism. One of them required l-thyroxine. Lastly, an increased thyroid volume without modification of thyroid hormones plasma levels was discovered in a patient receiving IFN-beta1a. Among patients treated with IFN-beta, clinical thyroid dysfunction is much rarer than laboratory thyroid dysfunction. However, this side-effect is sometimes severe.

Adult↗

Quality of life in multiple sclerosis: influence of interferon-beta1 a (Avonex) treatment.

BACKGROUND: Numerous data argue for initiating treatment with interferon-beta (IFN-beta) at an early stage in multiple sderosis (MS). The consequences of its use may negatively influence the MS patient's quality of life (QoL). OBJECTIVE: To evaluate the QoL of MS patients before and after a one-year period of treatment with IFN-beta1a (Avonex). PATIENTS AND METHODS: QoL was assessed using the SF-36 in 121 relapsing-remitting MS patients. We compared QoL before and after treatment and with data from a normal population. We also studied the possible influence of disease progression on the SF-36 scores. RESULTS: One hundred six patients completed the study (87%). Compared to a normal population, patients were, at baseline, worse off for all QoL scales, varying from a minimum decrease of 0.73 SD in mental health, to a maximum decrease of 1.55 SD in general health. After treatment, we found no significant changes in any of the QoL scores, except for physical function, where we noted a slight but significant decrease (p = 0.03). Furthermore, there was no significant change either in the physical component summary (PCS) or mental component summary (MCS). The 'reported health transition' item was significantly improved compared to baseline (p = 0.001). At indusion, significant correlations were found between EDSS scores and scores of physical function (p < 0.001), role - physical (p < 0.01), general health and social function (both p < 0.01), and with the PCS (p < 0.01). Patients with dinical relapses and/or disability progression had a more significant decease in physical function (p < 0.05) and also in social function (p < 0.05). CONCLUSION: The QoL, assessed by the SF-36 scale, is correlated with disability in MS. IFN-beta1a treatment (Avonex) has no negative effect on MS patient's QoL.

Adjuvants, Immunologic↗

[Hereditary parkinsonism-dystonia syndrome of juvenile onset with diurnal fluctuations].

Symptoms of fluctuating dystonia developed in 4 subjects of the same family during childhood or adolescence. In the 2 sisters, these symptoms were initially or subsequently associated with signs of parkinsonism, whereas in the 2 brothers they disappeared, spontaneously in at least 1 case, and signs of parkinsonism appeared later after a free interval. Anticholinergic agents and L-Dopa proved very effective against all extrapyramidal signs. These cases are similar to those gathered by Nygaard et al. in 1988 under the term "Dopa-responsive dystonia". Yet laboratory data seem to confirm that the common physiological mechanism is a disorder of tetrahydrobiopterin metabolism. Serum and urinary biopterin levels were lowered in our 4 cases but were normal in an unaffected sister. However, like the subjects affected this third sister showed a decrease of platelet serotonin which was taken as being a consequence of aromatic aminoacid hydroxylation defect due to tetrahydrobiopterin deficiency.

Adolescent↗