Combined effects of MSU crystals injection and high fat-diet feeding on the establishment of a gout model in C57BL/6 mice

Abstract Objective: Gout is characterized by inflammatory arthritis with hyperuricaemia and deposition of monosodium urate (MSU) crystals in the joints. Several animal models have been proposed based on MSU crystals injection or high-fat diet feeding; however, neither hyperuricaemia model nor acute gout model can effectively reflect clinical features of gout. This study aimed to assess the effectiveness of a compound gout model induced by the combination of MSU crystals injection and high-fat diet feeding. Methods: The compound gout model was induced by high-fat diet feeding per day and the intraplantar injection of MSU crystals (1 mg) into the footpad of each mouse every 10 days. Serum uric acid, foot swelling and pain analyses were performed at days 22, 32 and 42. Gout inflammation, serum proinflammatory cytokines and gut microbiota analyses were performed only at day 42. Results: Compared to hyperuricaemia model or acute gout model, the compound gout model showed little advantages of elevating serum uric acid, causing foot swelling and gout inflammation, while it caused more severe serum inflammation and gut microbiota dysbiosis. Severe serum inflammation in the compound gout model could be reflected by the increased levels of IL-1 α, IL-4, IL-6, IL-10, IL-12p40, IL-12p70, IFN-γ, KC, MCP-1 and MIP-1β. In addition, the compound gout model induced more alterations in the gut microbiota, including increasing levels of Desulfovibrio and Parasutterella. Conclusion: The injection of MSU and feed of high-fat diet have a combined effect on elevating serum inflammation and causing gut microbiota disorders in the process of establishing a gout model.(AU)

Clinical characteristics and risk factors for gout flare during the postsurgical period

Abstract Objectives: To evaluate the clinical features and risk factors for gout flare during postsurgical period in patients who were previously diagnosed with gout. Methods: Seventy patients who had histories of gout and had been consulted in the rheumatologic clinic before surgery under general anesthesia were included. Clinical characteristics of patients who developed a postsurgical gout flare were compared with those of patients who did not develop gout flare. Results: Among 70 patients, 31 (44.3%) developed gout flare during the postsurgical period. Mean intervals from surgery to gout flare was 3.7 days. Flares tended to involve monoarticular joints (61.3%) and affect lower extremity joints (83.9%). Knee joints (26%) and foot joints except the first metatarsophalangeal (MTP) joint (26%) were more frequently involved than the first MTP joint (13%). Presurgical uric acid level ≥ 9 mg/dL (OR 3.77, 95% CI 1.28-11.10, p = 0.016) and amount of uric acid changes between before and after surgery (OR 1.62, 95% CI 1.21-2.18, p = 0.001) were risk factors for postsurgical gout flare. Taking allopurinol reduced the risk of postsurgical gout flare (OR 0.15, 95% CI 0.05-0.45, p = 0.001). Operation time, amount of blood loss during surgery, and surgery site were not significantly associated with postsurgical gout flare. Conclusions: Adequate uric acid control before surgery could prevent the postsurgical gout flare.

A case of gout secondary to primary myelofibrosis / 北京大学学报(医学版)

A 52-year-old man was referred to our department with a 2-year history of polyarthritis. He was diagnosed as gout due to acute arthritis of bilateral feet dorsum 2 years ago,but he didn't receive any standard treatment. 1 year ago,there were more and more joints evolved during the gout attack, and many subcutaneous nodules occurred. When he presented to our clinic 1 month ago,the urate acid level was as high as 715 μmol/L. Moreover, we could find bone erosion in the X rays of his hand and foot,as well as synovitis,double contour sign and tophus on the ultrasound examination. The diagnosis of gout was clearly and definitely. However, he had leukocytosis and thrombocytosis for 4 years in the past history, and the urate acid level was only 400 μmol/L at that time. He also had well-controlled hypertension. The family history was unremarkable. Furthermore, we found megalosplenia on his physical examination. The bone marrow examination showed myelofibrosis and JAK2 V617F gene was positive. He was diagnosed as primary myelofibrosis and treated with interferon-α, together with urate acid-lowing therapy (febuxostat 60 mg once daily). Following-up for 1 year,the dosage of febuxostat decreased to 40 mg once daily, and the patient didn't have gout attack again, some of the tophus diminished, and the urate acid level ranged from 400 to 500 μmol/L. Gout is a common disease in clinical practice,usually combined with metabolic syndrome,chronic renal failure and specific drugs using (diuretic and calcineurin inhibitors). However,it is relatively rare to see gout associated with myeloproliferative diseases, including polycythemia vera, primary thrombocythemia, primary myelofibrosis and chronic myelocytic leukemia. In these diseases, the turnover of nucleic acids is greatly augmented, and an excess of purine metabolites, including uric acid, is released. In the natural course of gout, the appearance of tophus from the first onset of arthritis usually takes several years. This patient only had one traditional risk factor, but his urate acid level was remarkably high and he developed tophus in a short term. After treatment of primary myelofibrosis, the symptom of gout partially alleviated. Careful physical examination and medical history taking lead to the diagnosis of secondary gout, which should be reminded in the daily practice.

Chronic tophaceous gout in patients with psoriasis

Abstract: Psoriasis is a chronic inflammatory disease of multifactorial etiology influenced by genetic, immunological, and environmental factors. We report the case of a patient with psoriasis for more than 25 years who developed hyperuricemia and chronic tophaceous gout with unusual appearance. In psoriasis, hyperuricemia may occur by increased epidermal cell turnover, which accelerates purine metabolism and has uric acid as the product of its catabolism. The association of psoriasis with hyperuricemia can trigger the onset of gouty arthritis, and pose a greater risk of developing other inflammatory comorbidities. Therefore, it is important to periodically investigate uric acid levels in order to treat changes triggered by hyperuricemia.

Rhazes' prescriptions in treatment of Gout

Among the diseases that clinicians deal with, few do have a documented medical history that can be traced back to several centuries ago. A careful study of Rhazes' Treatments on Gout reveals a lot about the nature and therapy of gout. We managed to study the perceptions about pathogenesis, symptomatology, diagnosis, and treatment of gout that have changed over time. We also discussed some of the past and present fallacies regarding this disease. Rhazes provided a detailed description on the vital role of genetics and the relationship between the development of gout, an indulgent way of living, and tophi at a period of time between 1st and 6th centuries AD. This study showed that the findings of Rhazes about treatments of gout were consonant with modern medical theories

Gota familiar y nefropatía en una mujer joven: caso clínico / Familial gout and nephropathy in a young woman: clinical case

We report a 29 years old woman with a chronic tophaceous gout, whose disease started at the age of 18. On clinical examination, the blood pressure was elevated. The laboratory assessment showed a serum uric acid of 15 mg/dl, a urinary uric acid of 155 mg/24 h, a creatinine clearance of 59 ml/min/1.73 m2 and a uric acid excretion fraction off 1.3 per cent (normal 7 to 12 per cent). The clinical and laboratory features of this patient suggest the diagnosis of a familial juvenile gouty nephropathy

Gota e hiperuricemia / Gout and hyperuricemia

La lesión articular por microcristales de urato monosódico es la artritis mas frecuente en el sexo masculino entre los 40 y 60 años. Su presentación clínica clásica esta precedida por un estado morbido de hiperuricemia que debe ser adecuadamente reconocido y manejado. Una vez la gota se presenta clínicamente el papel del médico consiste no solo en tratar el episodio agudo sino en realizar un enfoque diagnóstico y terapéutico acorde con los parámetros internacionales, buscando un control sintomático rápido y seguro. Esta revisiàn incluye conceptos sobre la etiopatogenia, presentación clínica, criterios de diagnóstico y las diferentes opciones terapéuticas disponibles hoy en dia.

Hiperuricemia y gota postrasplante

Evaluamos la frecuencia y probable potegénesis de la hiperuricemia (HU) y la gota que se presentan en pacientes con trasplante renal: 163 recibieron ciclosporina (CS), azatioprina (AZA) y prednisolona (grupo CS), y 147 azotioprina y prednisolona (grupo AZA). La HU se presentó en 76 por ciento del grupos CS, frente a 25 por ciento de AZA (P<0.00001). Catorce pacientes presentaron uno a más episodios de gora, 12 de grupo CS y dos del AZA (P<0.00001); en estos pacientes predominó el sexo masculino (92 por ciento), la edad fue 36ñ8 y 36ñ4 años respectivamente (NS), y la función renal (expresada como creatinina sérica) fue igual en los dos grupos (1.6ñmg/dL). Los niveles séricos de ácido úrico mostraron correlación directa con el uso de diuréticos (r=0.48,P=0.001). La incidencia de HU fue de 15 veces más frecuente en el grupo CS, sugiriendo una interferencia de la CS en la depuración renal de los uratos. A los 24 meses de seguimiento, 70 por ciento de las HUs había desaparecido concomitantemente con la disminución de las dosis de CS. En conclusiónlla HU secundaria al empleo de la CS es un fenómeno transitorio y dependiente de la dosis, y su posible explicación es un defecto tubular en la depuración del ácido úrico

Compromiso osteoarticular asociado a Falciformismo / Osteoarticular involvement associated to sickle cell syndromes

Se reportan 6 pacientes con anemia falciforme (4 con Hb SS, 1 con Hb SC y 1 con Hb SB-talasemia), atendidos en el Hospital Nacional Cayetano Heredia entre 1983 y 1990, que presentaron diversas manifestaciones musculoesqueléticas en el curso de su evolución, resaltando dos casos de necrosis aséptica y un paciente con osteomielitis del fémur por Salmonella tiphy. se discuten los casos en relación a la literatura

Gota / Gout

Luego de hacer referencia al trastorno metabólico, en el curso del cual aparece la gota, el autor comienza por definir las cifras normales de uricemia y analiza el rol que sobre la misma juega la alimentación y otros factores. Recuerda la doble transferencia tubular del ácido úrico para explicar la acción a veces paradojal de muchas sustancias sobre la uraturia y la uricemia. Enumera y analiza los riesgos a que están sometidos los hiperuricémicos y termina con la clínica, los criterios diagnósticos y el tratamiento actualizado de la gota