By means of a screening based on genotyping of patients with low plasma enzymatic activity, the prevalence of FD in our population of HCM is 1% (0.9% in men and 1.1% in women). This diagnosis is relevant, because it allows the identification of disease carriers that might benefit from enzyme replacement therapy.

Most of the previous studies dealing with the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the synthesis of inflammatory mediators involved in joint damage have been done in cells cultured in vitro or in blood cells from patients treated for short periods of time. In this work we have evaluated the long-term effect of aceclofenac, a new NSAID, and diclofenac on the production of a series of inflammatory mediators by blood cells from 30 patients with severe knee osteoarthritis. Both aceclofenac and diclofenac significantly inhibited prostaglandin E2 (PGE2) synthesis by blood mononuclear and polymorphonuclear cells after 180 days of treatment. However, no clear effect was noted on leukotriene B4 (LTB4) and platelet activating factor (PAF) production. The generation of O-2 by polymorphonuclear cells, stimulated with FMLP, was decreased after 15 days of treatment with both drugs, but reached normal values after 180 days. Interleukin-1 beta (IL-1 beta) production decreased significantly at 180 days with both drugs in the group of high producer patients. In a few (n = 3) patients with high basal mononuclear cell tumor necrosis factor alpha (TNF alpha) production, this also decreased on treatment for 180 days with the NSAIDs. In the remaining low TNF alpha-producing patients, TNF alpha production tended to increase. Interleukin-6 (IL-6) synthesis was not affected by aceclofenac while it was diminished by diclofenac. The decrease in IL-6 in all treated patients was significantly correlated with a worsening of the clinical condition. On the whole, these data could afford a pathogenetic basis for the long-term employment of these drugs in patients with inflammatory conditions.

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Acute toxoplasmosis was induced in mice, and interferon (IFN) production in serum and by spleen cells was evaluated during the infection period. Interferon was characterized by acid-treatment and anti-IFN-alpha/beta neutralization. In order to verify the correlation between the unusual aspects of the IFN production and the induction of immunosuppression, splenocyte mitogen responsiveness was investigated concomitantly to IFN synthesis. The activity of Toxoplasma-induced serum IFN-alpha/beta increased gradually throughout all post-infection days, but IFN-gamma was not detected in the systemic circulation at any time during the infection. It was also observed that IFN-alpha/beta production and the capacity to produce IFN-gamma by spleen cells were closely and inversely correlated. As the infection progressed, more IFN-alpha/beta was produced, and the ability of spleen cells to produce IFN-gamma decreased. The observation that Toxoplasma-infected mice were concomitantly immunosuppressed (as documented by mitogen unresponsiveness and defective IFN-gamma production) in direct correlation to IFN-alpha/beta production, suggests that such IFN-alpha/beta production is an important factor associated with acute toxoplasmosis-induced immunosuppression.

No abstract