Benzbromarone is a uricosuric drug that has been used in the treatment of gout over the last 30 years. Due to its potent inhibition of the dominant apical (luminal) urate exchanger in the human proximal tubule URAT1, it reduces the urate reabsorption, diminishing serum urate levels and therefore preventing gout flares. Through several clinical trials, Benzbromarone has been proved effective and safe, inclusive in patients with chronic kidney disease and as combination therapy with allopurinol. Due to hepatotoxicity reports, it was withdrawn from the European market by the manufacturer, however many authors have questioned the product's withdrawal due to a lack of clinical evidence in order to support its hepatotoxicity. Benzbromarone is still available in several European countries, New Zealand, Brazil and several other countries. Despite the product's marketing over more than 20 years after the first hepatotoxicity reports, we have found only five reports in our literature search, and no prospective or retrospective study correlating hepatotoxicity with benzbromarone use. Benzbromarone is a safe and effective molecule for the treatment of gout. However, due to in vitro and in vivo data related to hepatotoxicity, it is prudent to prescribe it with some caution, especially for patients with an already known liver condition.

INTRODUÇÃO: A Espondilite Anquilosante (EA) é uma doença inflamatória crônica que acomete o esqueleto axial. Cursa com dor e incapacidade funcional. Para medir o impacto da EA na vida dos pacientes são utilizados questionários que avaliam a atividade da doença (BASDAI); a incapacidade funcional (BASFI); e a qualidade de vida (ASQoL). A Fibromialgia (FM) é uma das causas mais comuns de dor generalizada e pode coexistir com outras doenças; pode ser avaliada por meio do questionário de impacto da Fibromialgia (FIQ). Há poucos estudos demonstrando correlações entre FM e EA. O presente estudo obteve dados referentes ao perfil epidemiológico de pacientes com EA e FM e avaliou a prevalência de FM em portadores de EA. Avaliou-se a interferência da FM nos escores dos testes BASDAI, BASFI e ASQoL. PACIENTES E MÉTODO: Foram incluídos 71 pacientes portadores de EA diagnosticados de acordo com os critérios modificados de Nova York. Avaliação clínica, funcional e aplicação dos testes BASDAI, BASFI e ASQoL foram realizados. Os pacientes com diagnóstico de FM foram avaliados com o FIQ. RESULTADOS: Onze pacientes preencheram os critérios para FM, observando-se assim uma prevalência de 15% de FM entre os pacientes com EA, sendo mais frequente entre as mulheres (3,8:1). A idade de início da doença (EA) foi de 27,5 anos. O antígeno HLA-B27 foi positivo na grande maioria (80,4%). Comparando-se as médias dos testes BASDAI, BASFI e ASQoL, verificou-se que os valores são significativamente superiores (P < 0,01) entre os pacientes com FM. Concluiu-se que a coexistência da FM pode piorar os aspectos de atividade na EA, a incapacidade funcional e a qualidade de vida INTRODUCTION: Ankylosing spondylitis (AS) is a chronic inflammatory disease that affects the axial skeletal system, causing pain and functional incapacity. To measure the impact of AS on patient's life, questionnaires are used to assess disease activity (BASDAI); functional incapacity (BASFI); and quality of life (ASQoL). Fibromyalgia (FM) is one of the most common causes of generalized pain and can coexist with other diseases; it can be assessed by the Fibromyalgia Impact Questionnaire (FIQ). Few studies have demonstrated correlations between FM and AS. The present study obtained data regarding the epidemiologic profile of patients with AS and FM and evaluated the prevalence of FM in patients with AS. The FM influence on BASDAI, BASFI and ASQoL test scores was assessed. PATIENTS AND METHOD: A total of 71 patients with AS, diagnosed according to the modified New York criteria, were studied. Clinical and functional assessment was performed and BASDAI, BASFI and ASQoL tests were applied. Patients with a diagnosis of FM were evaluated through the FIQ. RESULTS: Eleven patients met the criteria for FM; thus a FM prevalence of 15% was observed among the patients with AS. FM was more prevalent among women (3.8:1). Age at disease onset (AS) was 27.5 years. The HLA-B27 antigen was positive in most of them (80.4%). When comparing BASDAI, BASFI and ASQoL test means, it was observed that values are significantly higher (P < 0.01) among patients with FM. We concluded that the coexistence of FM can worsen AS activity aspects, as well as functional incapacity and quality of lif

Objective. To profile a sample of gouty patients treated with allopurinol, benzbromarone, or a combination of these two drugs and to describe the impact of this therapy in reducing uric acid levels.Methods. An observational, transversal study was performed. We evaluated 48 patients diagnosed with gout who were seen at the Outpatient Rheumatology Clinic of the Federal University of Paraná between January 2009 and November 2010. Clinical data, creatinine serum levels, and basal and posttreatment levels of serum urates, transaminases, and bilirubins were recorded. Uric acid levels were measured in a 24-hour urine sample. Patients were divided into three groups: patients given only allopurinol (A), only benzbromarone (B), and both in combined therapy (A + B).Results. The average age of these patients was 56.6 ± 11.4 years, varying from 35 to 81 years. The entire patient group experienced a significant drop in serum urate levels, from 8.5 ± 1.8 mg/dL (0.472 ± 0.1 mmol/L) to 6.7 ± 2.1 mg/dL (0.372 ± 0.116 mmol/L) (P<0.001), regardless of the prescribed medication. The number of patients taking both drugs whose serum uric acid values fell within normal range (men <7 mg/dL (0.38 mmol/L) and women <6 mg/dL (0.33 mmol/L)) was 85.7% (6/7) while this value for the group taking benzbromarone alone was 75% (3/4) and for the group taking allopurinol alone this number was 51.8% (14/27).Conclusions. The therapeutic combination of benzbromarone and allopurinol significantly decreased serum urate levels in patients with gout when compared to individual use of each of these agents. This finding is especially important in treating patients who cannot control hyperuricemia with monotherapy. Benzbromarone alone or in combination with allopurinol has an important clinical role in controlling hyperuricemia in patients with gout.

Over time, clinicians have become increasingly comfortable embracing the prescription of biosimilars—highly similar versions of innovator or reference biological agents—for their patients with inflammatory diseases. Although a switch from a reference product to a licensed biosimilar version (or vice versa) is a medical decision robustly supported by the stepwise accumulation of clinical trial evidence concerning comparable safety, immunogenicity, and efficacy between these products, a switch from one biosimilar to another biosimilar of the same reference product, or a cross-switch, is not. Similarity among biosimilars of a reference product is not a regulatory agency concern and therefore is unlikely to be investigated in randomized controlled trials in the foreseeable future. Yet in clinical practice, across a diverse range of patients, the option to cross-switch from one biosimilar to another can and does arise for valid reasons such as convenience or tolerability issues, or driven by third parties (e.g., payers). In the absence of clinical trial data, clinicians must attempt to objectively evaluate the emerging real-world cross-switching evidence within the context of what is known about the science underpinning a designation of biosimilar. That knowledge then needs to be integrated with what clinicians know about their patients and their disease on a case-by-case basis. This review aims to consolidate relevant emerging real-world data and other key information about biosimilar-to-biosimilar cross-switching for prescribing clinicians. In the absence of clear clinical guidelines addressing this topic at present, this review may serve to facilitate discretionary and educated treatment decision making.

Etanercept was the first tumour necrosis factor alpha antagonist approved in the USA for the treatment of rheumatoid arthritis, in 1998, and then for other diseases. With the etanercept patent set to expire in the EU in 2015, a number of etanercept copies have reached the production phase and are undergoing clinical trials, with the promise of being cheaper alternatives to the reference product. In a global scenario that is favourable to the entry of biosimilars, this article discusses the stage of development, manufacture, clinical trials and the regulatory process involved in the approval of etanercept biosimilars, compiling the literature data. Reducing treatment cost is the principal attraction for biosimilars to emerge in the global market. It is essential for the doctors’ decision on the prescription of these medications, as well as for payers, to have clearly defined studies of clinical equivalence, quality, and safety in order to better evaluate the various copies of etanercept. The authors discuss the need to harmonize different national regulations and the introduction of effective pharmacosurveillance systems for prompt recognition of adverse effects in copies of biopharmaceuticals that differ from those found in the reference products.