Comparison of Metabolic, Lifestyle and Mental Health Parameters in People with Diabetes and Relatives with and without Family Support.

Purpose: To analyze and compare metabolic, lifestyle and mental health parameters in relatives and people-with-T2DM (PDM) with and without support. Patients and Methods: We included 160 patients with <5 years of diagnosis of T2DM, without disabling complications, and non-smokers, attending a multidisciplinary program for diabetes control, and their accompanying relatives. If the patients or relatives abandoned the program, we contacted them and asked to take laboratory tests and answer surveys regarding anxiety, depression, and perception of their family support. Variables distribution was assessed with the Kolmogorov-Smirnov test. We used ANOVA or Kruskal Wallis Tests, according to variable distribution. Frequencies and percentages are used for categorical values and analyzed with a chi-square test. We separated the participants in four groups: relatives with and without support and PDM with and without support. Results: We included 160 participants, age 51±10, and 54.3% women. Total cholesterol (188±36 vs 204±43 vs 170±34 vs 181±35 mg/dL, p=0.001), LDL-cholesterol (113±35 vs 125±27 vs 101 ±30 vs 109±29, p=0.008), and non-HDL cholesterol (143±32 vs 154 ±30 vs 129±33 vs 135±35 mg/dL, p=0.010) were higher in the group without support. Although patients without family support had lower values, they did not achieve metabolic goals. Weight (75±17 vs 77±19 vs 74.2±10.5 vs 90.2±17.3 kg) and body mass index (28.9±4.8 vs 30.1±4.7 vs 27.4±3.3 vs 33±4.3 kg/m2) were higher in PDM without family support (p<0.001 for both). Conclusion: Support in PDM and their families is important in metabolic control. However, raising awareness among family members to screen for diabetes and changes in lifestyle are points to improve. Including the evaluation of social and family support will allow a more complete assessment to identify barriers to achieving goals.

Lung Function and Asthma Clinical Control in N-ERD Patients, Three-Year Follow-Up in the Context of Real-World Evidence.

Purpose: To describe the lung function and clinical control of asthma in patients with N-ERD during three years of medical follow-up using GINA guidelines. Methods: We evaluated 75 N-ERD and 68 asthma patients (AG). Clinical control, lung function, and asthma treatment were evaluated according to GINA-2014. We compared all variables at baseline and one, two, and three years after treatment. Results: At baseline, the N-ERD group had better basal lung function (LF) than the AG group (p<0.01), and the AG group used higher doses of inhaled corticosteroids than the N-ERD group (52.4% vs 30.5%, p=0.01) and short-term oral corticosteroid (OCS) use (52.4% vs 30.5%, p<0.01). Instead, N-ERD patients needed more use of leukotriene receptor antagonists (LTRA) (29.3% vs 5.9%, p<0.01). This group had better clinical control than the AG group (62.1% vs 34.1%, p<0.01). During the medical follow-up, the LF of the N-ERD group remained at normal values; however, these parameters improved in AG from one year (p<0.01). Likewise, there was a diminished use of high doses of ICS (52.4% vs 33%, p<0.05) and short-term OCS (67.6% vs 20.6%, p<0.01) in asthma patients. However, N-ERD patients still needed more use of LTRAs (p<0.02) during the study. In this context, one-third of N-ERD patients had to use a combination of two drugs to maintain this control. From the second year on, clinical control of asthma was similar in both groups (p>0.05). Conclusion: According to GINA guidelines, only one-third of patients with N-ERD can gradually achieve adequate lung function and good asthma control with a high ICS dosage. Only a very small portion of patients will require the continued use of a second medication as an LTRA to keep their asthma under control.

Neuroimmune Pathophysiology in Asthma.

Asthma is a chronic inflammation of lower airway disease, characterized by bronchial hyperresponsiveness. Type I hypersensitivity underlies all atopic diseases including allergic asthma. However, the role of neurotransmitters (NT) and neuropeptides (NP) in this disease has been less explored in comparison with inflammatory mechanisms. Indeed, the airway epithelium contains pulmonary neuroendocrine cells filled with neurotransmitters (serotonin and GABA) and neuropeptides (substance P[SP], neurokinin A [NKA], vasoactive intestinal peptide [VIP], Calcitonin-gene related peptide [CGRP], and orphanins-[N/OFQ]), which are released after allergen exposure. Likewise, the autonomic airway fibers produce acetylcholine (ACh) and the neuropeptide Y(NPY). These NT/NP differ in their effects; SP, NKA, and serotonin exert pro-inflammatory effects, whereas VIP, N/OFQ, and GABA show anti-inflammatory activity. However, CGPR and ACh have dual effects. For example, the ACh-M3 axis induces goblet cell metaplasia, extracellular matrix deposition, and bronchoconstriction; the CGRP-RAMP1 axis enhances Th2 and Th9 responses; and the SP-NK1R axis promotes the synthesis of chemokines in eosinophils, mast cells, and neutrophils. In contrast, the ACh-α7nAChR axis in ILC2 diminishes the synthesis of TNF-α, IL-1, and IL-6, attenuating lung inflammation whereas, VIP-VPAC1, N/OFQ-NOP axes cause bronchodilation and anti-inflammatory effects. Some NT/NP as 5-HT and NKA could be used as biomarkers to monitor asthma patients. In fact, the asthma treatment based on inhaled corticosteroids and anticholinergics blocks M3 and TRPV1 receptors. Moreover, the administration of experimental agents such as NK1R/NK2R antagonists and exogenous VIP decrease inflammatory mediators, suggesting that regulating the effects of NT/NP represents a potential novel approach for the treatment of asthma.