Systemic sclerosis (SSc) shows variable clinical expression among different ethnic groups. Herein, we describe the clinical features, prevalence of organ involvement, and autoantibody profile in Mexican Mestizo SSc patients and we compare them with patients from other ethnic groups.We included 139 SSc patients. They underwent clinical evaluation and were tested for antinuclear antibodies (ANA), anticentromere antibodies (ACA), anti-topoisomerase I, anti-RNA polymerase III, anti-U1 RNP, anti-U3 RNP, anti-U11/U12 RNP, anti-Th/To, anti-PM-Scl, anti-Ku, antinucleosome, anti-double-stranded DNA (dsDNA), anti-Sm, anti-SSA, and anti-SSB antibodies. Female predominance (93.5%) was noted; 56.8% of patients had limited cutaneous SSc; 91% had peripheral vascular involvement; 70% had joint involvement; 27% had musculoskeletal damage; 66% had gastrointestinal involvement; 41% had interstitial lung disease; 32% had pulmonary arterial hypertension (PAH); 11% had cardiac involvement; and in 1.4% renal involvement was observed. Our patients showed lower frequency of renal crisis and higher frequency of PAH than patients from other ethnic groups; also they showed higher frequency of ACA than Japanese and African American patients, higher frequency of anti-topoisomerase I than Caucasian and African American patients, higher frequency of anti-PM-Scl and anti-Ku and lower frequency of anti-RNA Pol III than the other ethnic groups. High frequencies of antinucleosome (41%) and anti-dsDNA (63%) were identified. SSc-specific autoantibody frequencies are different in our patients and in those from other ethnic groups; associations of autoantibodies with clinical manifestations are confirmed in our patients. Ethnicity and the interaction of gene and environmental factors may influence the clinical picture and autoantibody profile in SSc patients.
The kidneys are organs that can be severely impaired by metabolic syndrome (MS). This is characterized by the association of various pathologies such as hypertension, dyslipidemia, and type-2 diabetes. Glycine, a nonessential amino acid, is known to possess various protective effects in the kidney, such as a decrease in the deterioration of renal function and a reduction of the damage caused by hypoxia. In a rat model of MS, the effect of glycine on the cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism was studied in isolated perfused kidney. MS was induced in Wistar rats by feeding them a 30% sucrose solution for 16 weeks. The addition of 1% glycine to their drinking water containing 30% sucrose, for 8 weeks, reduced high blood pressure, triglyceride levels, insulin concentration, homeostatis model assessment (HOMA) index, albuminuria, AA concentration in kidney homogenate, renal perfusion pressure, prostaglandin levels, PLA2 expression, and COX isoform expression, compared with MS rats that did not receive the glycine supplement. Glycine receptor expression decreased significantly with MS, but glycine treatment increased it. The results suggest that in the MS model, 1% glycine treatment protects the kidney from damage provoked by the high sucrose consumption, by acting as an anti-inflammatory on the COX pathway of AA metabolism in kidney.
Prevalence of metabolic syndrome and progression of nephropathy depend on sex. We examined a protective effect of estradiol against nephropathy in metabolic syndrome through the modulation of the arachidonic acid metabolism by activating the 5-lipoxygenase and cytochrome p450 4A pathways. 28 female Wistar rats were divided into four groups of seven animals each: control, intact metabolic syndrome, ovariectomized metabolic syndrome, and metabolic syndrome ovariectomized plus estradiol. Blood pressure, body weight, body fat, triglycerides, insulin, HOMA-index, albuminuria, and TNF-α were increased in ovariectomized metabolic syndrome rats (p < 0.001). The perfusion pressure in isolated kidneys of ovariectomized metabolic syndrome rats in presence of 4 μg of arachidonic acid was increased. The inhibitors of the arachidonic acid metabolism Baicalein, Miconazole, and Indomethacin in these rats decreased the perfusion pressure by 57.62%, 99.83%, and 108.5%, respectively and they decreased creatinine clearance and the arachidonic acid percentage. Phospholipase A2 expression in the kidney of ovariectomized metabolic syndrome rats was not modified. 5-lipoxygenase was increased in metabolic syndrome ovariectomized rats while cytochrome p450 4A was decreased. In conclusion, the loss of estradiol increases renal damage while the treatment with estradiol benefits renal function by modulating arachidonic acid metabolism through the 5-lipoxygenase and cytochrome p450 4A pathways.
The role of the renin-angiotensin system (RAS) in blood pressure regulation in MS during aging is unknown. It participates in metabolic syndrome (MS) and aging regulating vascular tone and remodeling. RAS might participate in a compensatory mechanism decreasing blood pressure and allowing MS rats to reach 18 months of age and it might form part of therapeutical procedures to ameliorate MS. We studied histological changes and distribution of RAS receptors in aortas of MS aged rats. Electron microscopy images showed premature aging in MS since the increased fibrosis, enlarged endothelium, and invasion of this layer by muscle cells that was present in control 18-month-old aortas were also found in 6-month-old aortas from MS rats. AT1, AT2, and Mas receptors mediate the effects of Ang II and Ang 1-7, respectively. Fluorescence from AT2 decreased with age in control and MS aortas, while fluorescence of AT1 increased in aortas from MS rats at 6 months and diminished during aging. Mas expression increased in MS rats and remained unchanged in control rats. In conclusion, there is premature aging in the aortas from MS rats and the elevated expression of Mas receptor might contribute to decrease blood pressure during aging in MS.
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