Background. Myostatin is a regulator of muscle size. To date, there have been no published studies focusing on the relation between myostin levels and myopenia in rheumatoid arthritis (RA). Objective. Evaluate the value of serum myostatin as a biomarker of cachexia and low skeletal muscle mass (LSMM) in RA patients, along with whether high serum myostatin is associated to these conditions after adjusting for potential confounders. Methods. This cross-sectional study included 161 female RA patients and 72 female controls. In the RA group, we assessed several potential risk factors for LSMM and rheumatoid cachexia. Dual-energy X-ray absorptiometry was used to quantify the skeletal muscle mass index (SMMI) (considering kg/m²) and the presence of rheumatoid cachexia (a fat-free mass percentile and fat mass percentile of the reference population). Serum myostatin concentrations were determined by ELISA. To identify a cut-off for high serum myostatin levels, we performed ROC curve analysis. Multivariable logistic regression analysis was used to identify the risk factors for LSMM and rheumatoid cachexia. The risk was expressed as odds ratios (ORs) and their 95% confidence intervals (95% CIs). Results. Compared to the controls, the RA group had a higher proportion of LSMM and exhibited high serum myostatin levels ( ). ROC curve analysis showed that a myostatin ng/mL was the most efficient cut-off for identifying rheumatoid cachexia (sensitivity: 53%, specificity: 71%) and LSMM (sensitivity: 43%, specificity: 77%). In the multivariable logistic regression, RA with high myostatin levels (≥17 ng/mL) was found to increase the risk of cachexia ( , 95% CI: 1.24-6.29; ) and LSMM ( , 95% CI: 1.17-7.89; ). Conclusions. High serum myostatin levels increase the risk of LSMM and rheumatoid cachexia. We propose that high myostatin levels are useful biomarkers for the identification of patients in risk of rheumatoid cachexia and myopenia.

The use of complementary therapies is highly prevalent among patients with rheumatoid arthritis (RA). Nevertheless, the use of complementary medicine could involve problems in the following of scientifically accepted treatments. To date, there is limited information regarding the association of nonconventional therapies with problems regarding compliance with the treatment. Therefore, the objective of this study was to identify whether the utilization of complementary therapies is associated with a high risk of problems regarding therapeutic adherence to conventional synthetic disease-modifying anti-rheumatic drugs (cs-DMARDs) in RA patients. A survey was performed with RA patients in an outpatient rheumatology clinic in a university hospital; the use of complementary therapies, as well as their type, was identified. To assess problems with therapeutic adherence, we used the four-item Morisky–Green scale. A comprehensive assessment of clinical and therapeutic characteristics was performed. Univariable and multivariable models were performed to identify the risk of problems with therapeutic adherence in users of complementary therapies. In total, 250 RA patients were included; 92% used complementary therapies. Of them, the most frequently used were herbal medicine (65%), homeopathy (64%), and cannabis and its derivatives (51%). In the univariable logistic regression analysis, the factors associated with problems in the therapeutic adherence to cs-DMARDs were age (p = 0.019), the presence of other comorbidities (p = 0.047), and the use of complementary therapies (p = 0.042). After controlling for potential confounders, the use of complementary therapies increased the risk of problems with therapeutic adherence to cs-DMARDs (adjusted OR = 2.84, 95% CI = 1.06–7.63, p = 0.037). We concluded that the use of complementary therapies increases the risk of problems with therapeutic adherence. Therefore, for physicians and healthcare professionals, the early identification of the use of nonconventional therapies in their RA patients is required, followed by a directed discussion with their patients about the risks and benefits to which they could be exposed to complementary therapies.

Background and Objectives: According to the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3), sepsis is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. The increased presence of free radicals causes an increase in oxidative stress. Vitamin C is an essential water-soluble vitamin with antioxidant activity and immunoregulatory effects that plays a potential role in the treatment of bacterial infections. Our aim was to evaluate the effectiveness of adding vitamin C to the conventional treatment of sepsis to decrease its mortality rate. Materials and Methods: In a prospective cohort study, we included patients with a diagnosis of sepsis and a SOFA score ≥ 9 who were evaluated in an Intensive Care Unit at a secondary-care hospital. According to the intensive care specialist, they were treated using two different strategies: Group 1—patients with sepsis treated with conventional treatment without vitamin C; Group 2—patients with sepsis with the addition of vitamin C to conventional treatment. Results: We included 34 patients with sepsis. The incidence of mortality was 38%, and 47% of patients used vitamin C as an adjuvant to the basic treatment of sepsis. In the basal analyses, patients treated with use of vitamin C compared to patients treated without vitamin C required less use of glucocorticoids (75% vs. 100%, p = 0.039). At follow-up, patients treated without vitamin C had higher mortality than patients treated with vitamin C as an adjuvant for the treatment of sepsis (55.6% vs. 18.8%, p = 0.03). We observed that the use of vitamin C was a protective factor for mortality in patients with sepsis (RR: 0.54, 95% CI: 0.31–0.96, p = 0.03). Conclusions: The use of vitamin C as an adjuvant to treatment decreases the risk of mortality by 46% in patients with sepsis and SOFA ≥ 9 compared to patients treated without vitamin C as an adjuvant to sepsis.

Urinary tract infections (UTIs) constitute one of the main complications in kidney recipients, increasing both morbidity and mortality. Due to the resurgence of antimicrobial resistance, new prophylactic approaches are being investigated. Nitrofurantoin is an antibiotic from the nitrofuran group that is effective against several Gram-negative and Gram-positive organisms; hence, there has been a resurgence in its prescription for treating MDR pathogens. Objectives: This study aims to assess the effectiveness of nitrofurantoin as an add-on to conventional therapy (amikacin + ceftriaxone or cefotaxime) for the treatment of urinary tract infections in kidney recipients. Methods: In a prospective cohort study, we included patients who received a kidney in a tertiary-care hospital. According to the intensive care specialist, group 1 patients were treated with the conventional prophylactic treatment plus nitrofurantoin as an add-on. Group 2 patients were treated only with the conventional prophylactic treatment. They were followed-up for 3 months, and the incidence of urinary tract infections was reported. Results: The UTI incidence for group 1 at 3 months was 20.6%, and for group 2, it was 20.0%; no statistical difference between treatments was observed (p = 0.9). The most commonly isolated pathogens were E. coli (28.5) and K. pneumonie (28.5%). The factor most associated with developing a UTI was female gender (aHR: 7.0; 95% IC 2.3–20.9, p < 0.001). Conclusions: In our cohort study, nitrofurantoin as an add-on in conventional therapy did not prove to be effective in preventing UTI development; therefore, other treatment options should be considered as a part of prophylactic treatment.

Background: Every year, 1.5 million women worldwide experience menopause and the associated changes that cause disability and dysfunction. There are multiple treatments focused on the symptoms; hormone replacement therapy (HRT) may be one that helps us reduce these changes. Objectives: the objective of this work was to assess the relationship between skeletal muscle mass and bone mineral density in postmenopausal women using hormone replacement therapy. Methods: Study design: cross-sectional study. A systematic assessment of clinical charts from postmenopausal women using hormone replacement therapy. Differences between low muscle mass and low bone mineral density were assessed; linear regression models were calculated to estimated the effect of body mass index, length of menopause, age, presence of comorbidities, physical activity and muscle mass have over those variables. Results: Bone mineral density was heavily influenced level of body mass index (aẞ: 0.015, 95% CI, 0.010, 0.019, p<0.001) and age (aẞ: -0.006, 95% CI, -0.010, -0.002, p=0.002); while muscle mass changes were associated with body mass index (aẞ: 0.548, 95% CI, 0.456, 0.640, p<0.001) and Age (aẞ: -0.081, 95% CI, -0.155, -0.006, p=0.034) Conclusions: The use of Hormone replacement therapy does not have a relation with the levels of muscle mass neither bone mineral density in postmenopausal women.

Rheumatoid arthritis (RA) is a highly prevalent chronic inflammatory rheumatic disorder leading to functional impairment and sequels. The search for new biomarkers helping in detecting RA subjects of high risk of functional disability is required. Studies showing high follistatin levels in RA have been described; however, none of them have placed focus on the role of follistatin as marker of deteriorated functionality. We aim to identify whether follistatin concentrations could be a potential biomarker of physical disability and disease activity in RA patients. Fifty-seven female RA subjects and 20 age–gender-matched controls were included in a cross-sectional evaluation. An assessment of clinical characteristics, grip strength, gait speed, and muscle mass was conducted. In RA subjects, disability was assessed using HAQ-DI and active disease using the DAS28-ESR. Follistatin levels were measured by ELISA. We compared (a) RA + functional disability and (b) RA + preserved physical function. Serum follistatin levels were increased in RA subjects compared to controls (175 ± 119 vs. 133 ± 47; p = 0.030). Follistatin levels correlated with deteriorated physical function levels (r = 0.491; p < 0.001) and severe activity (r = 0.344; p = 0.009). The RA + functional disability group, as compared to the RA + preserved physical function group, had higher serum follistatin levels (218 ± 159 vs. 141 ± 59; p = 0.030), lower grip strength (7.9 ± 4.6 vs. 14.5 ± 5.1; p < 0.001), reduced gait speed (0.77 ± 0.20 vs. 0.92 ± 0.20; p = 0.010), as well as higher proportions of tender joints ≥4 (48% vs. 16%; p = 0.008), and higher disease activity scores (3.8 ± 1.5 vs. 2.8 ± 1.2; p = 0.008). We concluded that higher follistatin levels are associated with physical functional impairment and the severity of disease activity in women with RA. Future studies are required to evaluate whether these follistatin levels can be related to other outcomes such as labor disability, hospitalization, and falls.