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1.
Immun Inflamm Dis ; 11(11): e1079, 2023 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-38018591

RESUMO

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and debilitating lung disease characterized by irreversible scarring of the lungs. The cause of IPF is unknown, but it is thought to involve a combination of genetic and environmental factors. There is no cure for IPF, and treatment is focused on slowing disease progression and relieving symptoms. AIMS: We aimed in this review to investigate and provide the latest insights into IPF management modalities, including the potential of Saracatinibas a substitute for current IPF drugs. We also investigated the therapeutic potential of Sotatercept in addressing pulmonary hypertension associated with IPF. MATERIALS AND METHODS: We conducted a comprehensive literature review of relevant studies on IPF management. We searched electronic databases, including PubMed, Scopus, Embase, and Web of science. RESULTS: The two Food and Drug Administration-approved drugs for IPF, Pirfenidone, and Nintedanib, have been pivotal in slowing disease progression, yet experimental evidence suggests that Saracatinib surpasses their efficacy. Preclinical trials investigating the potential of Saracatinib, a tyrosine kinase inhibitor, have shown to be more effective than current IPF drugs in slowing disease progression in preclinical studies. Also, Sotatercept,a fusion protein, has been shown to reduce pulmonary vascular resistance and improve exercise tolerance in patients with PH associated with IPF in clinical trials. CONCLUSIONS: The advancements discussed in this review hold the promise of improving the quality of life for IPF patients and enhancing our understanding of this condition. There remains a need for further research to confirm the efficacy and safety of new IPF treatments and to develop more effective strategies for managing exacerbations.


Assuntos
Hipertensão Pulmonar , Fibrose Pulmonar Idiopática , Estados Unidos , Humanos , Hipertensão Pulmonar/tratamento farmacológico , Hipertensão Pulmonar/etiologia , Qualidade de Vida , Fibrose Pulmonar Idiopática/tratamento farmacológico , Fibrose Pulmonar Idiopática/diagnóstico , Fibrose Pulmonar Idiopática/metabolismo , Progressão da Doença
2.
Ann Med Surg (Lond) ; 85(6): 2821-2832, 2023 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-37363482

RESUMO

Multiple sclerosis (MS) and myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) share the symptom of fatigue, and might even coexist together. Specifically focusing on genetics, pathophysiology, and neuroimaging data, the authors discuss an overview of the parallels, correlation, and differences in fatigue between MS and ME/CFS along with ME/CFS presence in MS. Studies have revealed that the prefrontal cortex and basal ganglia regions, which are involved in fatigue regulation, have similar neuroimaging findings in the brains of people with both MS and ME/CFS. Additionally, in both conditions, genetic factors have been implicated, with particular genes known to enhance susceptibility to MS and CFS. Management approaches for fatigue in MS and ME/CFS differ based on the underlying factors contributing to fatigue. The authors also focus on the recent updates and the relationship between MS and sleep disorders, including restless legs syndrome, focusing on pathophysiology and therapeutic approaches. Latest therapeutic approaches like supervised physical activity and moderate-intensity exercises have shown better outcomes.

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