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

The Vogt-Koyanagi-Harada (VKH) disease, formerly known as uveomeningitic syndrome, is a bilateral diffuse granulomatous panuveitis associated with exudative retinal detachment, which can be accompanied by central nervous system involvement, dermatological and auditory alterations.

Its name derives from the authors who first described the disease. It affects adults of both genders, between 20 and 50 years old, with darkly pigmented races prevalence. This inflammatory syndrome is probably the result of an autoimmune mechanism, influenced by genetic factors.

The evolution of the disease is divided into four clinical stages: prodromal, acute uveitic, convalescent and chronically recurrent. The diagnosis is mainly clinical, using the criteria established by the American Society of Uveitis (AUS) posted in the year 2001. Differential diagnosis must be done with sympathetic ophthalmopathy, primary B cell lymphoma, posterior scleritis, and uveal effusion syndrome. An early and maintained treatment is the basis of a favorable outcome.

Temporal arteritis is a vasculitis of the medium and large vessels that affects the extracranial branches of the carotid artery. This condition is characterized by a combination of focal inflammation causing arterial stenosis or occlusion and systemic inflammation manifested as polymyalgia rheumatica, constitutional symptoms and changes in laboratory tests. The only feature of giant cell arteritis (GCA) that is not controversial is its classification as the first medical emergency in ophthalmology. Visual loss occurs in up to a fifth of patients.

Prompt recognition of the disease and early initiation of therapy can prevent loss of vision in the affected eye or new visual deficits in the contralateral eye. The treatment of GCA is based on daily glucocorticoid administration, which should be started urgently in patients with incipient visual symptoms (diplopia or amaurosis fugax). The duration of glucocorticoid therapy is unpredictable and adverse effects are common. The aim of treatment is mainly to prevent the progression of visual loss.

Synovial fluid eosinophilia is defined as the presence of eosinophils, irrespective of quantity, in the synovial fluid and is a rare finding that is probably underestimated. The pathogenesis of this entity remains incompletely understood. Secondary and idiopathic forms have been described. Idiopathic forms are those not associated with systemic or rheumatic inflammatory disease or associated with chronic non-inflammatory rheumatic diseases. Idiopathic forms can be divided into pure or pseudoallergic forms when they occur in patients with an atopic background and/or intensely positive dermographism. Both forms are usually monoarthritis of the large joints with a substantial component of joint effusion but few inflammatory signs. Synovial fluid usually contains between 2,000 and 10,000 leukocytes/mm³, with a variable percentage of eosinophils. Although a major form (>10% eosinophils) and a minor form (<10% eosinophils) have been distinguished, both seem to have the same significance in terms of clinical manifestations and prognosis. Peripheral eosinophilia (>600 eosinophils/mm³) is a rare association and is not usually severe. Symptoms resolve within a few days without specific therapy and recurrences occur in approximately half of patients. Non-steroidal anti-inflammatory drugs are usually sufficient to control symptoms. Synovial fluid eosinophilia has not been associated with the development of new joint deformities nor has it been described as a chronic form of arthritis.

Cardiovascular disease has become the leading cause of mortality in patients with systemic lupus erythematosus (SLE). Accelerated atherosclerosis is considered one of the most important mechanisms implicated in the high cardiovascular (CV) mortality associated with SLE. Atherosclerosis in SLE patients arises from an interaction among classical CV risk factors, inflammatory mediators and factors specific to SLE itself. Consequently, calculating CV risk in these patients is central to decision-making on treatment to prevent CV disease. However, although Systematic COronary Risk Evaluation (SCORE) is recommended by The European League against Rheumatism (EULAR) experts and is widely used by rheumatologists for CV assessment in patients with rheumatoid arthritis and other forms of inflammatory arthritis, CV risk in SLE patients cannot be adequately evaluated with widely used charts for stratifying CV risk. Due to the lack of specific charts, assessment of traditional CV risk factors (smoking, blood pressure, diabetes, body mass index and lipid profile) and the use of validated imaging techniques to detect subclinical atherosclerosis have been proposed for the assessment of vascular disease in SLE patients. Among these techniques, calculating the intima-media thickness of the common carotid arteries measured in the far wall and the presence of plaques in the carotid system have become commonly used indicators of subclinical atherosclerosis. To a certain extent, the use of these methods allows individualized CV assessment and consequently a more useful management strategy, which can decrease CV mortality in SLE patients.

Lupus erythematosus (LE) is an autoimmune inflammatory disease that includes a broad spectrum of manifestations, ranging from systemic disease (systemic lupus erythematosus [SLE]) to purely cutaneous forms (cutaneous lupus erythematosus [CLE]).

Cutaneous involvement occurs in 90% of patients with SLE.

Based on morphological and histopathological features, CLE can be divided into three categories: chronic CLE, subacute CLE and acute CLE.

The precise etiology of LE is not fully understood, but the disease occurs when environmental factors, drugs and infectious agents trigger an abnormal immune response in an individual with predisposing genetic factors.

To assess cutaneous involvement, several scores have been developed over the years. A recent study, called CLASI (Cutaneous Lupus Erythematosus Disease Area and Severity Index), staged mucocutaneous damage and disease activity separately, allowing assessment of therapeutic response to be standardized.

The management of CLE is challenging. Although treatment traditionally consists of photoprotection, topical steroids and antimalarial agents, these measures are sometimes ineffective in subgroup of patients, giving rise to what is called resistant CLE.

This article reviews the topical and systemic treatment options, both the classical and new treatment alternatives currently available.

Science and technology parks (STPs) were first set up in Silicon Valley in California (USA) in the 1950s. These parks were established in the context of the concepts and models of entrepreneurial universities. Triple helix theory adds a third mission to entrepreneurial universities, namely to transfer knowledge and technology to industry and society in general. Currently, far from being a single model, the complexity of the components and models of STPs have increased.

Current STPs consist of sources of knowledge—such as universities, research institutes—spin-offs, technology and innovative companies and specialized capital. These entities are public-private partnerships that encourage interaction and synergy among the park's tenants. STP networks include all the innovation system agents located in a specific territory. Therefore, these hybrid spaces between science, technology and industry are, in many countries, public policy tools for economic and social development.

Neuropathic pain syndromes are a challenge for professionals working in the field of pain. Although major advances have been made in both diagnostic and analgesic treatment in recent years, satisfactory pain relief is achieved in less than 50% of patients, despite well-indicated treatment. The prevalence in the population is about 6-8% and the distress produced by pain is so intense that it leads to a loss of quality of life and significant functional limitation. The possibility of etiopathological treatment is greatly complicated by the enormous physiopathological complexity of pain, the various mechanisms underlying the various symptoms, both spontaneous and evoked, and the co-occurrence of several mechanisms in the same patient. Diagnosis of neuropathic pain is aided by the patients’ symptoms and questionnaires such as the Neuropathic Pain Diagnostic Questionnaire (DN4), a fairly accurate tool to measure neuropathic pain. Another problem in neuropathic pain is when, how and with what this type of pain should be treated. There are numerous publications on the topic. The treatment of neuropathic pain is itself multidisciplinary, given the comorbidity, the frequency of advanced age in these patients, and the anxiety and depression caused by pain. There is a wide diversity of techniques, types of treatment, combinations, and drug dosages. We review consensus treatments, and emphasize the emerging treatments that represent future therapeutic options: capsaicin and lidocaine patches, cannabinoids and botulinum toxin.