Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

Background and Aim: Idiopathic achalasia is a rare esophageal motor disorder. The disease state manifests local and systemic inflammation, and it appears that an autoimmune component and specific autoantibodies participate in the pathogenesis. The study aims to determine the prevalence of autoimmune and chronic inflammatory diseases in patients with achalasia and compare the results with those from patients with gastroesophageal reflux disease (GERD). Methods: It was a cross-sectional and included 114 patients with idiopathic achalasia and 114 age-matched and sex-matched control patients with GERD. Data on the presence of autoimmune and inflammatory diseases, the time of presentation, and any family history of autoimmune disease were obtained from the hospital's medical records. Results: Seventy three (64%) were female patients (mean age: 42.3 ± 15.5; median disease duration: 12 months). We identified the presence of autoimmune disease in 19 patients with achalasia (16.7%), hypothyroidism was the main diagnosis, and it was present in 52.6% of patients compared with 4.2% in controls. Thirteen of the 19 achalasia patients (68.4%) with autoimmune disease had history of familial autoimmunity. We identified 11 achalasia (9.6%) and 5 GERD patients (4.16%) with an inflammatory condition. Compared with the GERD, the achalasia group was 3.8 times more likely to have an autoimmune disease (95% CI: 1.47-9.83), 3.0 times more likely to have thyroidopathies (95% CI: 1.00-9.03), and 3.02 times more likely to suffer from any chronic inflammatory disease (95% CI: 1.65-6.20). Conclusions: The non-negligible number of patients with autoimmune diseases identified among the patients with idiopathic achalasia supports the hypothesis that achalasia has an autoimmune component.

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Dear Editor, Although dexamethasone is approved for the hyperinflammation treatment of hospitalised COVID-19 patients, nonhospitalised patients do not benefit from this therapy. 1 A potential drug for treating COVID-19 patients is polymerised type I collagen (PTIC). A downregulator of proinflammatory cytokines, adhesion molecules (ELAM-1, VCAM-1, and ICAM-1), cyclooxygenase (Cox)-1 enzyme and the collagenases expression through the modulation of transcription of factor NF-kB. [2][3][4][5][6] The intramuscular or subcutaneous administration of PTIC to patients with active RA (Phase II studies) improved the count of swollen joints and morning stiffness; 57% of patients achieved an ACR score of 50, and 30% had disease remission with this therapeutic combination. PTIC was safe and well-tolerated in long-term treatment, without adverse effects. [7][8][9] A double-blind, randomised, placebo-controlled clinical trial evaluated the PTIC intramuscular administration's safety and efficacy on hyperinflammation, oxygen saturation and symptom improvement in adult symptomatic COVID-19 outpatients (https://www.medrxiv.org/content/ 10.1101/2021.05.12.21257133v1).Eighty-nine participants with a confirmed COVID-19 diagnosis (mild to moderate disease) were included from August 31 to November 7, 2020, and followed for 12 weeks. Patients were randomly assigned to receive either 1.5 ml of PTIC intramuscularly every 12 h for 3 days and then every 24 h for 4 days (n = 45) or a matching placebo (n = 44) (sample size is describe in Methodology S1). Demographics, clinical characteristics, coexisting conditions and symptoms are described in Table 1. Ninety-eight per cent of patients in the PTIC group and 95.5% in the placebo group were analysed by the intention-to-treat principle (Figure S1). Of 89 patients at baseline, 64 (72%) were being treated with acetaminophen, 28 (31.5%) with acetylsalicylic acid, 5 (5.6%) with antivirals and 36 (40.4%) with antibiotics. The use of acetaminophen (71% vs. 73%), acetylsalicylic acid (27% vs. 39%), antivirals (7% vs. 5%) and antibiotics (40% vs. 41%) were similar in the PTIC andThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Idiopathic achalasia is a relatively infrequent esophageal motor disorder for which major histocompatibility complex (MHC) genes are well-identified risk factors. However, no information about HLA-achalasia susceptibility in Mexicans has previously been reported. We studied a group of 91 patients diagnosed with achalasia and 234 healthy controls with Mexican admixed ancestry. HLA alleles and conserved extended haplotypes were analyzed using high-resolution HLA typing based on Sanger and next-generation sequencing technologies. Admixture estimates were determined using HLA-B and short tandem repeats. Results were analyzed by non-parametric statistical analysis and Bonferroni correction. P-values < 0.05 were considered significant. Patients with achalasia had 56.7% Native American genes, 24.7% European genes, 16.5% African genes and 2.0% Asian genes, which was comparable with the estimates in the controls. Significant increases in the frequencies of alleles DRB1*14:54 and DQB1*05:03 and the extended haplotypes DRB1*14:54-DQB1*05:03 and DRB1*11:01-DQB1*03:01, even after Bonferroni correction (pC<0.05), were found in the achalasia group compared to those in the controls. Concluding, the HLA class II alleles HLA-DRB1*14:54:01 and DQB1*05:03:01 and the extended haplotype are risk factors for achalasia in mixed-ancestry Mexican individuals. These results also suggest that the HLA-DRB1*14:54-DQB1*05:03 haplotype was introduced by admixture with European and/or Asian populations.