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1.
Physiol Rep ; 11(8): e15657, 2023 04.
Artigo em Inglês | MEDLINE | ID: mdl-37078370

RESUMO

Pemphigus Vulgaris (PV) is a blistering autoimmune disease caused by autoantibodies against desmoglein 1 and 3. Treatment options are limited to corticosteroids and immunosuppressants. The myotoxic effect of glucocorticoids is a fact that has been elucidated. So, the development of efficacious treatment approaches to combat muscle wasting is of great importance. Considering the adverse effect of glucocorticoid therapy in pemphigus patients and altered muscle metabolism, this study aimed to investigate the effect of l-carnitine supplementation which can be useful in combating muscle-wasting impact of glucocorticoid therapy. In this randomized double-blind placebo-controlled trial 44 pemphigus patients aged from 30 to 65 years, receiving glucocorticoid therapy were selected to evaluate the suitability of l-carnitine (LC) as an anti-wasting substance. Patients were randomly divided into two groups to receive 2 g/d l-carnitine or placebo for 8 weeks; serum markers of muscle metabolism (IGF-1, creatine kinase, myogenin, myostatin) was evaluated before and after the l-carnitine supplementation. Paired T-test was used to analyze the differences between variables before and after the intervention. Therefore, the student's t-test was performed to find any differences in baseline characteristics and dietary intakes between the trial groups. LC intake led to a significant rise in serum IGF-1 and a reduction in CK and myostatin levels compared to baseline (p < 0.05) but there were no significant inter-group differences in IGF-1 and CK levels; There was also a significant reduction in myostatin level in LC group (p < 0/05). Myogenin levels decreased in both LC and placebo groups but the decrease in the placebo group was significant (p = 0/008); it means LC prevent the myogenin decreasing trend in the LC group compared to placebo. In conclusion, LC supplementation beneficially changes the level of IGF-1 and myostatin and improves muscle metabolism and regeneration in PV patients.


Assuntos
Carnitina , Pênfigo , Humanos , Adulto , Pessoa de Meia-Idade , Idoso , Carnitina/uso terapêutico , Glucocorticoides/efeitos adversos , Pênfigo/tratamento farmacológico , Fator de Crescimento Insulin-Like I , Miogenina , Miostatina , Atrofia Muscular/tratamento farmacológico , Músculos , Método Duplo-Cego , Suplementos Nutricionais
2.
Crit Rev Food Sci Nutr ; 62(11): 3023-3041, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-33356467

RESUMO

PURPOSE: This systematic review and meta-analysis aimed to investigate the effect of zinc supplementation on immune factors in randomized controlled trials. METHODS: A comprehensive search was done in PubMed, Scopus, Web of Science, Embase, and Cochrane databases up to December 2020. We used standard and weighted mean differences and 95% confidence intervals for net changes in selected parameters of immune responses. Subgroup analysis was used to find heterogeneity. RESULT: Overall, 35 RCTs comprising 1995 participants were eligible for this meta-analysis. There was a significant reduction of circulating CRP (WMD: -32.4; 95% CI: -44.45 to -19.62, p < 0.001), hs-CRP (WMD: -0.95; 95% CI: -1.01 to -0.89, p < 0.001), Neutrophil levels (SMD: -0.46; 95% CI: -0.90 to -0.01, p = 0.043), following zinc supplementation. CD4 level also increased significantly, (WMD: 1.79; 95% CI: 0.57 to 3, p = 0.004). Zinc supplementation had no significant effect on WBC (SMD: -0.66; 95% CI: -1.67 to 0.36, p = 0.204), lymphocyte (WMD: 1.86; 95% CI: -0.86 to 4.58, p = 0.181), monocyte levels (SMD: -0.16; 95% CI: -0.07 to 0.39, p = 0.167), CD3 (SMD: 0.37; 95% CI: -0.49 to 1.22, p = 0.399). CONCLUSION: Zinc supplementation decreased the CRP, hs-CRP and TNF-α, IL-6, neutrophil and increased CD3 and CD4 level significantly.


Assuntos
Proteína C-Reativa , Zinco , Adulto , Biomarcadores/análise , Proteína C-Reativa/análise , Suplementos Nutricionais , Humanos , Fatores Imunológicos , Inflamação , Ensaios Clínicos Controlados Aleatórios como Assunto , Zinco/farmacologia
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