13 research outputs found

    Relationship between disease severity and pituitary axis function.

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    <p>Data are <i>ÎČ</i> coefficient<i>s</i> of the linear regression. The multivariate linear regression model adjusted for age, sex, neuroleptic treatment, IGFBP3 when IGF-1 was in the model, and BMI when GH was in the model.</p>*<p><i>p</i>≀0.10.</p>**<p><i>p</i>≀0.05.</p>***<p><i>p</i>≀0.01.</p><p>GH, growth hormone; IGF-1, insulin-like growth factor-I; ACTH, adrenocorticotropic hormone; TSH, thyroid stimulating hormone; FT3, free triiodothyronine; FT4, free total thyroxine; LH, luteinizing hormone; FSH, follicle-stimulating hormone; TT, testosterone; TFC, total functional capacity.</p>†<p>Only males were included (110 patients).</p>─<p>Only patients not taking neuroleptics were included (96 patients).</p

    Levels of pituitary and peripheral hormones according to HD stage and comparatively to controls.

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    <p>An orange arrow: early increase in hormone concentration compared to controls. A green arrow: increase in hormone concentration related to an exogenous factor (neuroleptic treatment or stress). A blue arrow: late decrease in hormone concentration related to disease severity. GH, growth hormone; IGF-1, insulin-like growth factor-I; TSH, thyroid stimulating hormone; FT3, free triiodothyronine; ACTH, adrenocorticotropic hormone; LH, luteinizing hormone; FSH, follicle-stimulating hormone; TT, testosterone.</p

    Relationship between body mass index and clinical and hormonal disturbances.

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    <p>Data are <i>ÎČ</i> coefficients (<i>p</i> value) of the linear regression.</p>1<p>adjusted for age and sex.</p>2<p>multivariate analysis including age, sex, and parameters significant in the univariate analysis.</p>*<p><i>p</i>≀0.10.</p>**<p><i>p</i>≀0.05.</p>***<p><i>p</i>≀0.01.</p><p>BMI, body mass index; GH, growth hormone; IGF-1, insulin-like growth factor-I; ACTH, adrenocorticotropic hormone; TSH, thyroid stimulating hormone; FT4, free total thyroxine; FT3, free triiodothyronine.</p

    SCD indices are higher in ALS patients than in control subjects.

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    <p>(A) Palmitoleate to palmitate ratio (16:1/16:0) in serum and blood cells from ALS patients (ALS) and control subjects (CT). (B) Oleate to stearate ratio (18:1/18:0) in serum and blood cells from ALS patients (ALS) and control subjects (CT). *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 (Mann-Withney test, n = 48).</p

    Blood cell 16:1/16:0 ratio correlates with disease progression and affects survival of ALS patients.

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    <p>Correlation between 16:1/16:0 and 18:0/18:1 ratios and disease duration (A, E) at blood collection or ALSFRS-R slope (B, F), determined as the decline of the score over a period of six months starting at the point of blood collection. Correlation coefficients (r) and <i>p</i>-values are indicated. n.s., non-significant <i>p</i>-value (Spearman test, n = 111). Based on the median ratio of the population, ALSFRS-R decline is shown in patients with low or high 16:1/16:0 ratio (C), and in patients with low or high 18:1/18:0 ratio (G). *<i>p</i><0.05 (Mann-Withney test). (D, H) Kaplan-Meier curves of survival in the subgroups of patients as above. Survival was the interval between the point of blood collection and death. <i>P</i>-values are indicated (Gehan-Breslow-Wilcoxon test, n = 117).</p

    Pairwise comparisons of effectiveness during the treatment period.

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    <p>Adjusted difference (line minus column) in mean change per year ± standard error.</p><p>SDMT: Symbol digit modality test.</p><p>*<i>P<0.05.</i></p><p>† Scores were reversed if necessary (change under risperidone minus the change under dibenzodiazepines  =  −0.41); the mean evolution of TFC was greater with dibenzodiazepines than with risperidone.</p
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