RESUMO
An acute attack of gouty arthritis is one of the most painful experiences reported throughout medical history. Therefore it is paramount to initiate appropriate therapy quickly in order to terminate the acute phase. This goal can be achieved with non-steroidal anti-inflammatory agents, colchicine, or corticosteroid-based therapies. Rarely, because of contraindications to these agents, only symptomatic treatment can be given until the attack subsides. The next step is to lower the serum urate level below the limit of solubility (i.e., below 40.8 mmol/L, or 6.8mg/dL) which reduces recurrences and begins to return the total body urate pool to normal. This equally important goal can be achieved by uricosuric agents or xanthine oxidase inhibitors, although the latter is generally favored. Allopurinol is the agent most commonly preferred because of its safety profile and ease of use, but there are known serious allergic reactions and untoward side effects that occasionally require discontinuation. Febuxostat, a xanthine oxidase inhibitor, and pegylated uricase are new agents under development and may be beneficial in these situations or when other comorbid conditions prevent the use of conventional treatments. Alcohol and dietary consumption are also related to hyperuricemia and acute gout. Recently beer, wine, and liquor were studied and the risk of gout varied according to the alcohol ingested. Furthermore, recent data sheds light on important dietary modifications that may help in the treatment of gout, and dispels certain beliefs about protein ingestion and the occurrence of acute gout. As we learn more about the associated conditions of hypertriglyceridemia, hypertension, and the metabolic syndrome, it may allow the tailoring of medical regimens that directly prevent or reduce recurrent attacks of gouty arthritis. There are specific approved treatments for these common comorbidities that have parallel effects of lowering serum urate levels. These recent findings may be especially important for treating refractory cases. While patient education remains a cornerstone to ensure compliance, other quality indicators for the management of this disease have been reported and should guide the clinician in the treatment of gout and result in improved care.
Assuntos
Artrite Gotosa/tratamento farmacológico , Hiperuricemia/tratamento farmacológico , Corticosteroides/uso terapêutico , Hormônio Adrenocorticotrópico/uso terapêutico , Anti-Inflamatórios não Esteroides/uso terapêutico , Colchicina/uso terapêutico , Humanos , Hiperuricemia/diagnóstico , Transplante de Órgãos , Cooperação do Paciente , Fatores de Risco , Prevenção Secundária , Uricosúricos/uso terapêutico , Xantina Oxidase/antagonistas & inibidoresRESUMO
The investigations used to diagnose an inflammatory muscle disease include history and physical examination, evaluation of serum levels of enzymes derived from skeletal muscle, electromyography, magnetic resonance imaging, and muscle histology. The evaluation of patients who may have noninflammatory myopathy includes, but is not limited to, these methods. Additional tools that may be useful include measurements of additional biochemistries, the forearm ischemic exercise test, magnetic resonance spectroscopy, and special tests on muscle tissue. Reports published in the past year have improved and expanded our understanding of the numerous noninflammatory myopathies and how these tools can be used more effectively.
Assuntos
Doenças Musculares/diagnóstico , Adulto , Biópsia , Criança , Ensaios Enzimáticos Clínicos , Creatina Quinase/sangue , Diagnóstico Diferencial , Feminino , Humanos , Lactente , Espectroscopia de Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/enzimologia , Músculo Esquelético/patologia , Doenças Musculares/metabolismo , Doenças Musculares/patologia , Fatores de TempoRESUMO
Metabolic myopathies are the result of genetic defects that cause disordered energy metabolism. These diseases can cause a variety of myopathic syndromes and can become clinically manifest at any age. Recent advances in the understanding of the molecular and metabolic bases for these diseases have resulted in expanded clinical descriptions, recognition of additional entities, and development of new therapeutic approaches.
Assuntos
Miopatias Mitocondriais/fisiopatologia , Humanos , Miopatias Mitocondriais/etiologia , Miopatias Mitocondriais/terapiaAssuntos
Supressores da Gota/uso terapêutico , Gota/tratamento farmacológico , Gota/metabolismo , Cooperação do Paciente , Educação de Pacientes como Assunto , Anti-Inflamatórios/uso terapêutico , Anti-Inflamatórios não Esteroides/uso terapêutico , Gota/prevenção & controle , Conhecimentos, Atitudes e Prática em Saúde , Humanos , Esteroides , Fatores de Tempo , Uricosúricos/uso terapêuticoRESUMO
Ideally, primary care physicians can successfully manage cases of arthritis in a manner that obviates the need for reconstructive surgery. However, that is not always possible. When surgical intervention is believed to be of potential benefit, the primary care physician needs to enlist the help of a surgeon and other health professionals to determine the best approach. Primary care physicians should take an active role in preoperative planning, perioperative management, and rehabilitation. The unique characteristics of the patient's specific type of arthritis and use of medications must be carefully considered. This approach should optimize the chances for a successful outcome.
Assuntos
Artrite/cirurgia , Prótese Articular , Humanos , Prótese Articular/efeitos adversos , Educação de Pacientes como Assunto , Cuidados Pós-Operatórios , Complicações Pós-Operatórias , Cuidados Pré-Operatórios , Fatores de RiscoRESUMO
The term metabolic myopathy refers to a heterogeneous group of conditions that have in common abnormalities of muscle energy metabolism that result in skeletal muscle dysfunction. Most recognized metabolic myopathies are considered primary, represent inborn errors of metabolism, and are associated with known or postulated defects that affect the ability of muscle fibers to maintain adequate ATP concentrations. Traditionally, these diseases are grouped into abnormalities of glycogen, lipid, purine, and mitochondrial biochemistry. This discussion reviews the basic metabolic pathways that regulate normal muscle function; recent observations involving glycogen storage diseases, carnitine deficiency states, and myoadenylate deaminase deficiencies; and lastly, newer techniques available to assess patients with myopathic disorders.
Assuntos
Erros Inatos do Metabolismo/metabolismo , Doenças Musculares/metabolismo , HumanosRESUMO
Ten years ago, we studied the clinical and radiographic manifestations of gout in 60 patients and described 3 patterns of disease. To determine the consequences of management over a 10-year period, we recently reassessed the 39 available patients of this population. We found that although reduced tophaceous deposition on physical examination correlated with normalization of the serum urate concentration, no correlation existed between radiographic changes and mean serum urate concentrations. Progression of gouty changes on radiography reflected progressive deformity on physical examination. We have described the radiographic changes that occurred in a well-characterized population of subjects with gout over 10 years and determined that serum urate concentrations alone may not provide an effective means of monitoring the progression of tophaceous disease in bone.
Assuntos
Alopurinol/uso terapêutico , Artrite Gotosa/tratamento farmacológico , Probenecid/uso terapêutico , Ácido Úrico/sangue , Idoso , Idoso de 80 Anos ou mais , Artrite Gotosa/sangue , Artrite Gotosa/diagnóstico por imagem , Humanos , Pessoa de Meia-Idade , Radiografia , Punho/diagnóstico por imagem , Punho/patologiaRESUMO
Despite an increase in the number of rheumatologists in clinical practice over the past 15 years, the outcome for patients with rheumatoid arthritis (RA) remains relatively poor. The poor prognosis for patients with this disease is due to a lack of effective therapies. Better therapies will be developed only after the cause and pathogenesis of RA are better understood. Although the precise cause is unknown, a variety of evidence indicates that RA results from the presentation of a relevant antigen to an immunogenetically susceptible host. This report reviews recognized potential antigens and known genetic variables affecting the immune response, as well as the various cellular and humoral immune responses that result from the antigen-host interaction. More successful therapy for RA will most certainly result from a better understanding of the pathobiology of the disease.
Assuntos
Artrite Reumatoide/etiologia , Formação de Anticorpos , Artrite Reumatoide/imunologia , Artrite Reumatoide/terapia , Citocinas/fisiologia , Suscetibilidade a Doenças , Previsões , Antígenos HLA/análise , Humanos , Imunogenética , Linfócitos/fisiologiaRESUMO
We measured 5'-nucleotidase (5NT) activity in synovial fluid from 159 patients with various diagnoses. The activity of 5NT was compared with activities of nucleotide pyrophosphohydrolase, alkaline and neutral phosphatases, and adenosine deaminase, in the same samples. Higher levels of 5NT activity occurred in synovial fluid from osteoarthritic joints than from joints of patients with gout, pseudogout, or rheumatoid arthritis. The highest levels of 5NT activity were found in synovial fluid from patients with Milwaukee shoulder syndrome and from osteoarthritis patients in whom deposition of calcium-containing crystals was also present.
Assuntos
5'-Nucleotidase/metabolismo , Artrite Reumatoide/enzimologia , Cálcio/metabolismo , Líquido Sinovial/enzimologia , Adenosina Desaminase/metabolismo , Idoso , Idoso de 80 Anos ou mais , Fosfatase Alcalina/metabolismo , Cristalização , Feminino , Gota/enzimologia , Humanos , Masculino , Pessoa de Meia-Idade , Osteoartrite/enzimologia , Monoéster Fosfórico Hidrolases/metabolismo , Pirofosfatases/metabolismoAssuntos
Adenosina Desaminase/deficiência , Osteocondrodisplasias/etiologia , Inibidores de Adenosina Desaminase , Animais , Cartilagem/efeitos dos fármacos , Cartilagem/enzimologia , Cartilagem/patologia , Sobrevivência Celular/efeitos dos fármacos , Desoxiadenosinas/farmacologia , Modelos Animais de Doenças , Técnicas In Vitro , Camundongos , Osteocondrodisplasias/enzimologia , Osteocondrodisplasias/patologia , Pentostatina/farmacologia , SuínosRESUMO
Deoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro-osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxy-adenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro-osseous dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.