RESUMEN
BACKGROUND: Plantar fasciitis (PF) is one of the most common causes of foot pain. Work can involve factors that may predispose to foot pain. AIMS: To systematically review the evidence of the association between weight bearing (walking or standing) and PF among workers. METHODS: Literature search of relevant indexing databases from inception to May 2012, grey literature, websites of relevant organizations and reference lists for all identified articles. Two reviewers independently selected studies for full review, assessed methodological quality and graded evidence. Findings were summarized qualitatively. RESULTS: Four studies were included; all were assessed as high or unclear risk of bias. Three studies were case-control studies; two used clinic populations and one used volunteers. The other study was cross-sectional involving the workforce of an assembly plant. A number of associations between PF and risk factors were identified including sex, obesity, foot biomechanics and job factors (e.g. job tenure). Two case-control studies and the cross-sectional study found an association with weight bearing, but the assessment of weight bearing varied (e.g. time on feet, time walking or standing). There was low-quality evidence to confirm a causal relationship (Royal College of General Practitioners (RCGP) * grade). CONCLUSIONS: This systematic review found low-quality evidence of an association between PF and weight-bearing tasks such as walking and standing on hard surfaces. The only occupations specifically identified as having higher risk were those associated with the engine assembly plant. Further research is required to fully determine the association between weight bearing and PF.
Asunto(s)
Fascitis Plantar/epidemiología , Obesidad/epidemiología , Enfermedades Profesionales/epidemiología , Salud Laboral , Estudios Transversales , Fascitis Plantar/diagnóstico , Fascitis Plantar/etiología , Humanos , Obesidad/complicaciones , Enfermedades Profesionales/diagnóstico , Enfermedades Profesionales/etiología , Postura , Factores de Riesgo , Factores de Tiempo , Soporte de PesoRESUMEN
We describe a 38-year-old patient with relapsing remitting multiple sclerosis who subsequently develops systemic sclerosis following a course of interferon B-1a injections. This rare association between MS and systemic sclerosis is interesting due to the added factor of beta interferon therapy prior to the onset of the systemic sclerosis. It is also important, as more patients are treated with interferon B-1a for multiple sclerosis, this is a potential association.
Asunto(s)
Factores Inmunológicos/efectos adversos , Interferón beta/efectos adversos , Esclerosis Múltiple Recurrente-Remitente/tratamiento farmacológico , Esclerodermia Limitada/inducido químicamente , Adulto , Femenino , Humanos , Interferón beta-1aAsunto(s)
Granulomatosis con Poliangitis/patología , Enfermedades Musculares/patología , Ciclofosfamida/administración & dosificación , Ciclofosfamida/uso terapéutico , Quimioterapia Combinada , Granulomatosis con Poliangitis/complicaciones , Granulomatosis con Poliangitis/tratamiento farmacológico , Humanos , Inmunosupresores/administración & dosificación , Inmunosupresores/uso terapéutico , Inyecciones Intravenosas , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Enfermedades Musculares/complicaciones , Enfermedades Musculares/tratamiento farmacológico , Quimioterapia por Pulso , Resultado del TratamientoRESUMEN
Accumulating evidence indicates that the interdomain B regions of ZAP-70 and Syk play pivotal roles in the coupling of T-cell antigen receptor (TCR) stimulation to the activation of downstream signaling pathways. The interdomain B region of ZAP-70 contains at least three candidate sites of tyrosine phosphorylation. In this report, we identify Tyr319 as a functionally important phosphorylation site in the ZAP-70 interdomain B region. TCR crosslinkage triggered a rapid increase in the phosphorylation of Tyr319 in Jurkat T cells. Although mutation of Tyr319 to Phe had no effect on the tyrosine kinase activity of ZAP-70, the resulting ZAP(Y319-->F) mutant failed to reconstitute TCR-dependent Ca2+ mobilization, Ras activation, CD69 expression and NFAT-dependent transcription in ZAP-70-deficient Jurkat cells. These defects were correlated with reduced tyrosine phosphorylation of phospholipase C (PLC)-gamma1 and the LAT adapter protein in the ZAP(Y319-->F)-expressing cells. On the other hand, ZAP(Y319-->F)-expressing cells displayed normal increases in SLP-76 phosphorylation and ERK activation during TCR stimulation. Phosphorylation of Tyr319 promoted the association of ZAP-70 with the SH2 domains of two key signaling molecules, Lck and PLC-gamma1. These studies suggest that Tyr319 phosphorylation is required for the assembly of a ZAP-70-containing signaling complex that leads to the activation of the PLC-gamma1- and Ras-dependent signaling cascades in antigen-stimulated T cells.