RESUMEN
BACKGROUND: It has been suggested that the presence of chronic immunoinflammatory rheumatic disease (CIRD) may be a factor that increases the likelihood of developing hypogonadism syndrome, and conversely, the presence of uncompensated testosterone deficiency may predispose to a greater risk of developing or more severe course of ICRD. AIM: To study the incidence of hypogonadism in men with rheumatoid arthritis (RA) and evaluate its impact on the course of RA and concomitant diseases. MATERIALS AND METHODS: A one-time continuous study included 170 men with RA who were undergoing inpatient treatment at the Federal State Budgetary Institution NIIR named after. V.A. Nasonova. Patients were assessed for total testosterone levels and subsequently divided into subgroups with normal (>12 nmol/l) and reduced levels. An intergroup comparison was carried out on the main indicators used in clinical rheumatological practice to assess the stage, activity and other medical and demographic characteristics of RA, as well as the state of purine and carbohydrate metabolism. A correlation analysis was performed between the level of total testosterone and some clinical and laboratory parameters. RESULTS: The frequency of detected testosterone deficiency in the study group was 24.1%. Significant correlations were noted between the level of total testosterone and body mass index (r=-0.29), the level of blood uric acid (r=-0.19) and C-reactive protein (r=-0.18). Patients with hypogonadism compared to the group with normal testosterone levels were characterized by higher body mass index (29.3±5.6 vs 26.3±4.0 kg/m2; p<0.001), glucose levels (6.95±7 .85 mmol/l vs 5.42±1.13 mmol/l; p=0.034) and uric acid (354.6±110.7 vs 317.5±84.8 µmol/l; p=0.03) blood. In addition, patients with hypogonadism were more likely to suffer from obesity (41.6% vs 15.7%; p=0.001) and diabetes mellitus (21.6% vs 10.2%; p=0.075) without a statistically significant difference, and also had higher ESR (46.5±42.2 vs 31.0±30.9 mm/h; p=0.012). A more frequent occurrence of anemia was noted in hypogonadism (32.4% vs 16.7%; p=0.041). CONCLUSION: Testosterone levels and the presence of hypogonadism were not associated with the stage and activity of RA, however, testosterone deficiency was accompanied by a more frequent development of overweight and obesity, and a deterioration in purine and carbohydrate metabolism.
Asunto(s)
Artritis Reumatoide , Hipogonadismo , Testosterona , Humanos , Masculino , Testosterona/sangre , Testosterona/deficiencia , Artritis Reumatoide/sangre , Artritis Reumatoide/complicaciones , Artritis Reumatoide/epidemiología , Persona de Mediana Edad , Hipogonadismo/sangre , Hipogonadismo/epidemiología , Adulto , AncianoRESUMEN
AIM: To clarify the association between HLA-DRB1 and TNFα (-308G>A) genes polymorphism and joint destruction/further progression during 12 months of the follow-up period (FUP) in patients with early (<6 months), active, predominantly antibodies to cyclic citrullinated peptide (ACCP) and rheumatoid factor (RF)-positive rheumatoid arthritis (RA) treated according to "Treat to target" strategy. MATERIALS AND METHODS: The study included 85 patients with early RA and duration of symptoms <6 months. All patients were initially assigned to subcutaneous methotrexate (MTX) with rapid dose escalation to 20-25 mg/week. Combination MTX + biological therapy, mainly adalimumab, was used when MTX was ineffective. Joint destruction was assessed by Sharp-Van der Heijde modification scoring method at baseline and after 12 months FUP. Real time polymerase chain reaction (PCR-RT) was used for TNFα gene polymorphism (-308G>A) genotyping. Low resolution PCR-RT with subsequent sequence-based typing of *04 were performed to study HLA-DRB1 gene polymorphism. The HLA-DRB1*01, *04:01, *04:04, *04:05, *04:08, *10 alleles were categorized as SE+ (Shared Epitope) alleles. RESULTS: As for TNFα gene polymorphism, it was demonstrated that the number of narrowings and total Sharp score values were almost twice as high at baseline in GG genotype carriers as compared to GA genotype carriers (Ñ<0,005, and Ñ<0,004 respectively). Similar association was found after 12mo FUP. The progression of joint destruction, assessed as the change (∆) in the number of erosions, joint space narrowings and the total score, was statistically significantly associated with HLA-DRB1*(SE) genotypes: the carriers of SE (SE+/SE+) double-dose had more advanced progression as compared to (SE+/SE-)/(SE-/SE-) carriers (Ñ<0,028, Ñ<0,019, Ñ<0,035 respectively). CONCLUSION: Our data suggest that HLA-DRB1 (SE+) gene and TNFα (-308G>A) polymorphisms are associated with the progression of radiographic joint destruction in early, active RA patients managed according to "Treat to target" stratagy.