In addition to LDL, Lp(a) can be quantitatively eliminated from plasma in an extracorporeal LDL-apheresis procedure based on precipitation with heparin at pH 5.12. The rates of return of post-apheresis Lp(a) and LDL-cholesterol concentrations to baseline levels were investigated in six individuals with familial hypercholesterolaemia (one homozygote, five heterozygote) and one normolipaemic individual. The first-order disappearance constants (kappa) were derived for LDL and Lp(a) according to Apstein et al. The kappa values for LDL in the homozygous FH and the normolipaemic individual were 0.082 and 0.43 respectively while the heterozygous FH patients had kappa values intermediate between the two (median 0.231; range 0.116-0.261). The first-order disappearance constants of Lp(a) did not correlate with those of LDL. The homozygous FH and normolipaemic individuals had Lp(a) kappa values of 0.158 and 0.199 respectively; the corresponding values in the heterozygous FH patients were: median 0.142; range 0.045-0.179.

The recent elucidation of the structure of apo(a), the characteristic apoprotein of the lipoprotein Lp(a), has revealed a high homology to human plasminogen [6, 8]. This similarity provides a tentative link between the plasma lipoproteins and the clotting system and may give further insight into the role of Lp(a) in atherosclerosis [2]. Numerous studies have demonstrated a strong association between high levels of Lp(a) and coronary heart disease [1, 3, 10]. Furthermore, there is an additive effect of LDL and Lp(a) such that the relative risk for angiographically documented coronary artery disease at Lp(a) concentrations of 30 mg/dl and greater increases from twofold to fivefold when LDL are also elevated [1]. Whereas both LDL and Lp(a) levels can be lowered by neomycin and niacin [4], bile-acid resins such as cholestyramine do not affect Lp(a) concentrations [11]. The HMG-CoA reductase inhibitors, have proven to be extremely effective in lowering plasma LDL and apo B levels [5, 9], presumably through inhibition of intracellular cholesterol synthesis with a concomitant increase in the livers LDL receptors [7]. In order to establish whether Lp(a) levels are also After a wash-out phase of 4 weeks in which all previous lipid-lowering therapy, with the exception of diet, was stopped, serum total cholesterol, LDL-cholesterot, apoB and Lp(a) concentrations were determined. Total cholesterol was measured with an enzymatic test kit, (Boehringer, Mannheim), LDL-cholesterol by a specific precipitation method (Quantolip-LDL, Immuno, Heidelberg), apoB by rate nephelometry and Lp(a) with a specific non-competitive ELISA. All individuals were administered a single daily dose of 10 mg Simvastatin for 6 weeks and this was then raised to 20 mg once daily for a further 6 weeks. Lipid and lipoprotein parameters betbre and after therapy are summarised in table 1. Simvastatin caused a significant reduction in mean total cholesterol (32%), LDL-cholesterol (38%) and apoB (26%) concentrations. No consistent effect was observed on serum Lp(a) concentrations and both the mean and median remained unchanged after 12 weeks treatment. These results confirm that Lp(a) levels are not altered by increasing the LDL-receptor activity.

Tuberculosis (TB) has been described in association with different malignancies including Hodgkin's disease. However, the association with primary pulmonary Hodgkin's disease (PPHD) is hardly reported in literature and in teenage is quite exceptional. We report a case of an 11 years old boy in whom the diagnosis of tuberculosis preceded and delayed the diagnosis of PPHL.

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