RESUMEN
76-year-old female patient, with past medical history of relapsing-remitting multiple sclerosis manifested by retrobulbar optic neuritis in both eyes with an interval of one year between the first episode in the left eye and the one in the right eye and after three decades of remission, who consulted due to bilateral blurred and foggy vision. Subsequently, several differential diagnoses where ruled out. Diagnosis of bilateral anterior and intermediate uveitis with occlusive vasculitis attributed to a new relapse episode of multiple sclerosis was made, as the association between multiple sclerosis and intermediate uveitis is known, though the causal association is still questioned. This case shows how multiple sclerosis may only manifest with ocular involvement and exemplifies the broad spectrum of manifestations and complications, taking into account that ischemic areas from vasculitis and other comorbidities led to macular edema and unfortunately, prognosis became poorer. The complex course of the case enables emphasizing the responsibility role of the ophthalmologists in such systemic entities that may compromise the eye, in which suspicion of the disease and an adequate timing management approach is essential.
RESUMEN
Numerous studies have found polymorphisms in the lipoprotein lipase (LPL) gene to be associated with the risk of coronary artery disease (CAD), implicating LPL in the development of atherothrombotic disease. It remains controversial, however, whether LPL acts in a pro- or anti-atherogenic fashion. We quantitated activity and concentration of LPL in post-heparin plasma from 194 male patients undergoing coronary angiography. HDL cholesterol was significantly associated with LPL activity quartiles (1.09+/-0.26 the highest vs. 0.96+/-0.25 mmol/l the lowest quartile, P<0.01). There was also a trend towards higher total (5.61+/-1.33 vs. 5.16+/-1.44 mmol/l, P=0.059) and LDL cholesterol (3.92+/-1.39 vs. 3.46+/-1.06 mmol/l, P=0.09) with higher LPL activity. In contrast, measures of CAD extent showed no differences between LPL quartiles (P>0.30 for prior myocardial infarction, number of diseased vessels, Gensini and extent scores). Additionally, there was no difference in LPL activity (CAD: n=158, 168+/-70 nmol/ml/min, no CAD: n=36, 180+/-89 nmol/ml/min, P=0.47) or concentration (280+/-121 ng/ml and 288+/-111 ng/ml, P=0.72) between patients with and without CAD. Our data show that, in spite of an association with lipoprotein parameters, LPL in post-heparin plasma is unrelated to the presence or the extent of CAD. Therefore, lipoprotein lipase determination in plasma does not appear to be a useful marker in the assessment of CAD risk.
