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7 results on '"A. J.L. Ferrari"'

1. Aspectos de imagem do xantoma do tendão calcâneo na ultrassonografia e ressonância magnética

Author

Eloy de Ávila Fernandes, Eduardo Henrique Sena Santos, Tatiana Cardoso de Mello Tucunduva, Antonio J.L. Ferrari, and Artur da Rocha Correa Fernandes

Subjects
Xantoma, Tendão calcâneo, Ultrassonografia, Ressonância magnética, Diseases of the musculoskeletal system, RC925-935
Abstract

O xantoma no tendão calcâneo é uma doença rara e tem uma alta associação com hiperlipidemia primária. O diagnóstico precoce é fundamental para o início do tratamento e para alterar o curso da doença. Os exames de imagem podem auxiliar nesse diagnóstico. Este estudo relata o caso de um homem de 60 anos apresentando nódulos indolores nos cotovelos e tendões calcâneos, sem crises típicas de gota, acompanhado no ambulatório de doenças microcristalinas da Unifesp para esclarecimento diagnóstico. Os testes laboratoriais solicitados apresentavam dislipidemia. Ultrassom (US) mostrou espessamento difuso dos tendões calcâneos com áreas hipoecoicas. Ressonância magnética (RM) mostrou espessamento difuso dos tendões, com áreas de sinal intermediário e padrão reticulado no interior. Os exames de imagem mostraram aspectos relevantes no diagnóstico de xantoma, auxiliando no diagnóstico diferencial.

Published
2015
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4. NONSTEROIDAL ANTI-INFLAMMATORY DRUGS AND PROSTAGLANDINS

Author

P. Branigan, D. Van Linthoudt, Schumacher Hr, D. G. Baker, L. Morrone, and A. J.L. Ferrari

Subjects
Pharmacology, medicine.drug_class, business.industry, medicine.medical_treatment, Inflammation, General Medicine, Anti-inflammatory, stomatognathic diseases, Diclofenac, Oral administration, medicine, Pharmacology (medical), Tumor necrosis factor alpha, medicine.symptom, business, Misoprostol, Saline, medicine.drug, Prostaglandin E
Abstract

The objective of this study was to determine the effects of orally administered misoprostol and diclofenac on inflammation caused by particulates in the rat subcutaneous air-pouch model. Subcutaneous air pouches were formed in male Sprague-Dawley rats. The animals were premedicated by gavage with either saline, diclofenac, misoprostol, or both diclofenac and misoprostol. The air pouches were injected with either polymethyl methacrylate particles or monosodium urate crystals, and the pouch fluids were obtained at 1, 6, 24, 48, and 72 h. Leukocyte influx, tumor necrosis factor, neutral metalloprotease activity, and prostaglandin E(2) levels were measured. It was determined that leukocyte influx was inhibited by diclofenac in the acute inflammation caused by monosodium urate crystals only. In all animals receiving diclofenac, prostaglandin E(2) (PGE(2)) levels were reduced, whereas tumor necrosis factor levels were elevated. The elevation of tumor necrosis factor was prevented by the addition of misoprostol. It is concluded that the oral administration of diclofenac or misoprostol can affect levels of specific mediators involved in particulate-induced inflammation in the subcutaneous air pouch.

Published
1996
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7. Nonsteroidal Anti-Inflammatory Drugs and Prostaglandins: Their Interactions and Effects on the Particulate-Induced Inflammatory Process Implicated in Joint Implant-Loosening and on Monosodium Urate Crystal-Induced Inflammation

Author

A. J.L., Ferrari, D., Van Linthoudt, L., Morrone, P., Branigan, H. R., Schumacher, and D. G., Baker

Abstract

The objective of this study was to determine the effects of orally administered misoprostol and diclofenac on inflammation caused by particulates in the rat subcutaneous air-pouch model. Subcutaneous air pouches were formed in male Sprague-Dawley rats. The animals were premedicated by gavage with either saline, diclofenac, misoprostol, or both diclofenac and misoprostol. The air pouches were injected with either polymethyl methacrylate particles or monosodium urate crystals, and the pouch fluids were obtained at 1, 6, 24, 48, and 72 h. Leukocyte influx, tumor necrosis factor, neutral metalloprotease activity, and prostaglandin E(2) levels were measured. It was determined that leukocyte influx was inhibited by diclofenac in the acute inflammation caused by monosodium urate crystals only. In all animals receiving diclofenac, prostaglandin E(2) (PGE(2)) levels were reduced, whereas tumor necrosis factor levels were elevated. The elevation of tumor necrosis factor was prevented by the addition of misoprostol. It is concluded that the oral administration of diclofenac or misoprostol can affect levels of specific mediators involved in particulate-induced inflammation in the subcutaneous air pouch.

Published
1996

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