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Objective: Current risk algorithms do not accurately predict cardiovascular disease (CVD) risk in rheumatoid arthritis (RA). An area of interest is that of single-nucleotide polymorphisms (SNPs), of which several have been associated with CVD in the general population. We investigated whether these SNPs are associated with CVD in RA and whether SNPs could improve CVD risk prediction in RA., Methods: Sixty SNPs were genotyped in 353 patients with RA. Logistic and Cox regression analyses were performed to identify SNPs that were associated with CVD (n = 99). A prediction model with clinical variables was made. SNPs were added to investigate the additional predictive value. Both models were internally validated. External validation was done in a separate cohort (n = 297)., Results: rs3184504, rs4773144, rs12190287, and rs445925 were significantly associated with new CVD. The clinical prediction model consisted of age, sex, body mass index, systolic blood pressure, high-density lipoprotein cholesterol (HDLc), and creatinine, with an area under the curve (AUC) of 0.74 (P = 0.03). Internal validation resulted in an AUC of 0.76 (P < 0.01). A new model was made including SNPs and resulted in a model with rs17011666 and rs801426, age, total cholesterol, and HDLc, which performed slightly better with an AUC of 0.77 (P < 0.01). External validation resulted in a good fit for the clinical model, but a poor fit for the SNP model., Conclusion: Several SNPs were associated with CVD in RA. Risk prediction slightly improved after adding SNPs to the models, but the clinical relevance is debatable. However, larger studies are needed to determine more accurately the additional value of these SNPs to CVD risk prediction algorithms., (© 2024 The Author(s). Arthritis Care & Research published by Wiley Periodicals LLC on behalf of American College of Rheumatology.)

Loss of income and out-of-pocket expenditures are important causes of financial hardship in many patients with cancer, even in high-income countries. The far-reaching consequences extend beyond the patients themselves to their relatives, including caregivers and dependents. European research to date has been limited and is hampered by the absence of a coherent theoretical framework and by heterogeneous methods and terminology. To address these shortages, a task force initiated by the Organisation of European Cancer Institutes (OECI) produced 25 recommendations, including a comprehensive definition of socioeconomic impact from the perspective of patients and their relatives, a conceptual framework, and a consistent taxonomy linked to the framework. The OECI task force consensus statement highlights directions for future research with a view towards policy relevance. Beyond descriptive studies into the dimension of the problem, individual severity and predictors of vulnerability should be explored. It is anticipated that the consensus recommendations will facilitate and enhance future research efforts into the socioeconomic impact of cancer and cancer care, providing a crucial reference point for the development and validation of patient-reported outcome instruments aimed at measuring its broader effects., Competing Interests: Declaration of interests WvH reports grants from Koningin Wilhelmina Fonds (KWF), European Cancer League for European Fair Pricing Network (EFPN) project, and OECI; and consulting fees from Raad voor de Rechtspraak. VPR reports grants from KWF, EFPN, OECI, and the National Health Care Institute. JMV reports grants from EFPN. OSL reports support for attending meetings and travel from the Catalan Institute of Oncology (ICO). EA reports a grant from the Norwegian Directorate of Health; and leadership roles on the scientific board of the Norwegian Cancer Association, the advisory board of the Frisch Centre, and the Faculty of Medicine board elected among academic employees. AE reports support for attending meetings and travel from ICO. NF reports support for the present manuscript and for attending meetings from EFPN and OECI; and a budget-based action grant from EU HORIZON. IK reports a leadership role as a patient advocate at the Institute for Gastroenterological Tumors of Croatia (IGET). SS reports a leadership role at Connect Norway. RS is supported by City Cancer Challenge. SV reports a leadership role at IGET. All other authors declare no competing interests., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Interleukin 12 (IL-12) is a proinflammatory cytokine composed by two chains, p40 and p35, that plays a key role in the promotion of a Th1 immune response in the gastrointestinal mucosa. An enhanced expression of IL-12 mRNA in gastric mucosa has been reported in individuals infected by Helicobacter pylori. The aim of our study was to assess whether a functional polymorphism located at position 1188 (A-->C) of the IL-12 p40 (IL12B) gene is associated with the susceptibility and clinical features of peptic ulcer disease. Genotyping of 184 unrelated white Spanish patients with peptic ulcer and 107 healthy controls was performed by polymerase chain reaction and restriction fragment length polymorphism. Helicobacter pylori status and nonsteroidal antiinflammatory drugs use were studied in patients and controls. There were no significant differences in carriage, genotype, and allele frequencies of the IL-12 p40 gene polymorphism between patients with peptic ulcer and controls. Moreover, no differences were found with respect to the localization of the ulcer, Helicobacter pylori status, nonsteroidal antiinflammatory drug use, age, sex, bleeding episodes, and family history of peptic ulcer. Our data reveal that the IL12B 1188 (A-->C) gene polymorphism is not involved in defining the genetic basis of the susceptibility to and final outcome of peptic ulcer disease.

: Spondyloarthropathy (SpA) as observed in patients with idiopathic inflammatory bowel diseases is categorized according to the recently developed criteria of the European Spondylarthropathy Group, and belongs to a large complex of rheumatic disorders, encompassing ankylosing spondylitis, Reiter's disease, psoriatic arthritis, and reactive arthritis. It has been recognized for many years that patients with ulcerative colitis or Crohn's disease frequently have arthritic complications. The gastroenterologist should therefore carefully evaluate any symptom of peripheral or axial arthritis, in an attempt to provide an accurate diagnosis, to define a realistic prognosis, and to establish adequate therapy at an early stage. In this review, clinical and etiopathogenic aspects are analyzed, not only of patients with inflammatory bowel diseases and SpA, but also of patients developing arthritic symptoms after gastrointestinal bacterial infections (reactive arthritis). The significance of ileal mucosal inflammation as observed frequently in patients with SpA is discussed; the contribution of immunogenetic factors in the development of SpA, such as HLA-B27, is briefly reviewed. Finally, analysis is made of the different therapeutic options that are available at present.

The pepsinogen A isozymogen pattern in gastric mucosa is genetically determined and can be visualized in nondenaturating polyacrylamide gel electrophoresis of supernatants of sonified gastric mucosal biopsies by demonstrating proteolytic activity after converting pepsinogen into pepsin by acid. Pepsinogen isozymogens are present in very low concentrations in the blood but can now be demonstrated in serum by a newly developed immunoblotting procedure. This study investigated whether the serum pepsinogen A isozymogen pattern adequately reflects the pepsinogen A phenotype. Serum and gastric mucosal pepsinogen A isozymogen patterns were compared in 72 subjects from the routine endoscopy program. A close correlation was found between the relative intensities of the pepsinogen A isozymogens in the serum and the gastric mucosal patterns. Increasing the pepsinogen A release into the circulation by oral omeprazole did not affect the pepsinogen A patterns in the blood. It is concluded that the serum pepsinogen A pattern reflects the pepsinogen A phenotype in humans. In addition, no preferential release of a pepsinogen A isozymogen into the circulation was observed. Thus, immunoblotting of serum provides a new and reliable tool to study pepsinogen genetics in humans. Because a relationship was previously shown between specific pepsinogen A phenotypes and gastric malignancies in humans, serum pepsinogen A patterns may provide a tool to detect subjects who are at risk of gastric cancers.

The genetic polymorphism of group-specific component (GC) was investigated with isoelectric focusing in 351 homosexual men at risk for HIV infection, 96 male patients with AIDS, and 86 heterosexual controls. No significant differences in GC phenotype distribution were seen between controls and any of the at risk groups or patients, neither between HIV-Ab-positive/Ag-negative and HIV-Ab-positive/Ag-positive homosexual men nor between HIV-Ab-positive/Ag-positive homosexual men and AIDS patients, suggesting that the GC system is not involved in the infective susceptibility or progression of HIV infection to AIDS-related complex and AIDS.

The isozymogens PGA-3 and PGA-5 of human pepsinogen A were digested with endoproteinase Lys-C. The peptides were separated by reverse-phase HPLC. PGA-5 showed a peak strongly absorbing at 254 nm absent in PGA-3. Analysis of amino acid composition using the Pico-Tag methodology combined with DABITC-sequencing reveals the sequence Tyr-Phe-Pro-Gln-Trp-Lys (peptide 37-43 of the activation segment). This confirms a study at the DNA level by our group [16] suggesting a Glu greater than Lys mutation at position 43 in the activation segment of PGA-5. Furthermore, it is proposed that the number of genetic variants of PGA is higher than is actually seen by electrophoresis.