Seminarios de la Fundación Espa?ola de Reumatología最新文献

The aims, structure and content of postgraduate training programs in rheumatology remain under the domain of national authorities. Data comparing training standards in rheumatology among different countries are scarce but suggest marked variability at a structural level and possibly in the competencies acquired during the training. However, a certain degree of harmonization throughout Europe would support the free movement of medical specialists within the European Union and would help guarantee minimum quality standards. The Rheumatology Section of the European Union of Medical Specialists (EUMS) has generated European recommendations for training in rheumatology but the general opinion is that their inclusion in the national curricula has been slow and limited.

Mature B cells emerge from the bone marrow and continue to diversify their immunoglobulin genes through 2 antigen-dependent processes known as somatic hypermutation and class switch recombination. These processes require AID, a DNA-editing enzyme. Although both processes predominantly occur in germinal center B cells engaged in a T cell-dependent (TD) antibody response against protein antigens recent, evidence shows that B cells receive additional help from invariant natural killer T cells, dendritic cells, and various granulocytes, including neutrophils, eosinophils, and basophils. These innate immune cells enhance TD antibody responses by delivering B-cell helper signals whether in germinal centers, postgerminal lymphoid centers, or the bone marrow. In addition to enhancing and complementing the B-cell helper activity of canonical T cells, invariant natural killer T cells, dendritic cells, and granulocytes can deliver T cell-independent B-cell helper signals at the mucosal interface and in the marginal zone of the spleen to initiate rapid innate-like antibody responses. In this review, we discuss recent advances in the role of innate cells in B-cell helper signals and in antibody diversification and production.

Cogan syndrome (CS) is typified by nonsyphilitic interstitial keratitis and Meniere-like auditory involvement. It can present atypically with other ocular and audiovestibular symptoms and associated systemic manifestations. Its name derives from the author who first described the disease. CS affects adults of both sexes, with a mean age of 30 years. The prevalence is higher in Caucasians. The pathogenesis of this syndrome is unknown, but is probably the result of an autoimmune mechanism triggered by an infection. The diagnosis is mainly clinical, using the criteria established by Haynes et al. in 1980 for “typical CS” and “atypical CS”. A differential diagnosis should be performed with other systemic diseases that cause similar eye and inner ear manifestations. The course is variable and deafness is a common complication. Prompt treatment and its maintenance are the basis of a favorable outcome.

Tuberculosis (TB) is one of the infectious diseases with a larger number of cases, especially in low-income countries. Despite having an effective treatment, its control is difficult due to the characteristics of the bacterium and the transmission mechanism of the disease. The microbiological diagnosis establishes the etiology and confirms the disease. It is based on specific staining microscopy, mycobacterial culture, especially liquid media, and gene amplification, when the suspicion is moderate to high. It is always necessary to identify positive cultures, since in the recent years an increase in non-tuberculous Mycobacteria (NMT), with different TB treatment, has been observed. The treatment of resistant cases is complicated and also limited due to the lack of alternative drugs. Therefore, systematic susceptibility testing should be performed on all patients with positive isolates. The screening of the mutations associated with resistance provides information in 2-3 days instead of 3-4 weeks. It is indicated in previously treated patients, contacts with resistant cases, in clinical failures or recurrences, and in patients originating from countries with a high incidence of TB.

New diagnostic tests are needed to improve the current limitations of these tests, such as the sensitivity and slow growth rate of Mycobacterium tuberculosis.

Although gout is a highly prevalent disease with significant clinical repercussions, it continues to a chronic disease with very low treatment adherence. The stigma associated with the disease, lack of treatment observance and others related to the physician and clinical practice are the most striking, specially the tendency for these patients to be managed in primary care, a certain lack of interest, and the low priority given to teaching among rheumatologists, as well as variation in adherence to recommendations established in clinical practice guidelines. Optimization strategies include improving the quality of prescriptions for specific drugs, being aware of patients’ perceptions of the disease, being proactive against lack of treatment adherence, and applying a comprehensive approach to treatment. The strong involvement of rheumatologists in the treatment of this disease is essential to achieve the desired results.

Interstitial lung disease (ILD), or diffuse infiltrative lung disease, includes a heterogeneous group of processes characterized by the appearance of an inflammatory reaction in the alveolar wall, triggered by different antigens.

This group represents a spectrum of diseases with distinct causes; furthermore, there is confusing variation in the use of nomenclature.

The imaging method of choice in the evaluation and diagnosis of ILD is high-resolution computed tomography (HRCT), as it confirms the presence of lung disease and establishes the correct diagnosis of associated complications. However, the definitive diagnosis of these diseases requires consistency between the clinical and pathological findings. The radiologic images obtained by HRCT in this group of diseases are highly useful, especially to avoid unnecessary biopsies. For these reasons, clinicians should be familiar with the basic radiologic patterns associated with this special group of lung diseases: septal, reticular, nodular, ‘ground glass’, cystic, and condensation. This article describes the characteristics and presentation of these patterns and reviews some of the most frequent ILD, with special emphasis on their main radiological patterns.

On the basis of advances in imaging, neural anatomic findings, new discoveries in chemical mediation of chronic pain, the development of precision diagnostic and therapeutic injection techniques, and reported non-operative treatment successes, has facilitated the expansion of minimally invasive techniques in the management of pain.

Described interventional techniques as minimally invasive procedures including percutaneous precision needle placement, with placement of drugs in targeted areas or ablation of targeted nerves; and some surgical techniques such as laser or endoscopic diskectomy, intrathecal infusion pumps and spinal cord stimulators, for the diagnosis and management of chronic, persistent or intractable pain.

Multiple therapeutic interventional techniques with reasonable evidence that are commonly applied are epidural injections including adhesiolysis, facet joint interventions, sacroiliac joint interventions, and implantable therapies. The rest of procedures performed in Pain Units have a more limited recommendation levels.

Synovial fibroblasts (SF) or fibroblast-like synoviocytes are the major resident cellular component of joint synovial membrane. Numerous studies support the hypothesis that SF play an important role in the pathogenesis of rheumatoid arthritis (RA). In the RA synovial membrane, SF increase in number (hyperplasia) and exhibit an altered phenotype that persists in culture in the absence of external stimuli. These abnormalities are associated with the activation of specific signalling pathways that promote cell growth and the expression of multiple factors such as cytokines, chemokines, growth factors, adhesion molecules, and matrix degradation enzymes. The activation and expansion of SF appear to contribute to the recruitment, retention and activation of inflammatory cells, new blood vessel formation (angiogenesis), and bone and cartilage destruction. The relative contribution of SF to these processes is very important in animal models but has not been determined in human RA due to the lack of treatment interventions specifically targeting these cells. The identification of the molecular pathways involved in the altered phenotype of rheumatoid SF and their pathophysiological contribution are the basis for the development of new therapeutic alternatives for chronic inflammation and joint damage not targeting the immune system.