Lipoprotein abnormalities in patients with asymptomatic acute porphyria.

There have been discrepancies in reports of total cholesterol and low density lipoprotein (LDL)-cholesterol levels in patients with acute porphyria. Some studies have found that acute porphyria patients have increased levels while others do not. The aim of this study has been to evaluate the lipid profile in a series of patients with acute porphyria, in order to help clarify these differences. Serum lipoprotein levels were studied in 30 patients (25 women and five men; age:38+/-10 years) with asymptomatic acute porphyria. Controls were 30 healthy volunteers matched for age and gender. For 13 patients and 15 controls, lipoprotein lipase and hepatic lipase activities were determined. Patients exhibited increased levels of total-cholesterol, LDL-cholesterol, high density lipoprotein (HDL)-cholesterol and apolipoprotein (apo)-A1 compared with controls (P4 mmol/l in 15 patients (50%). Levels of total triglycerides, very low density lipoprotein (VLDL)-triglycerides, VLDL-cholesterol, apo-B and lipoprotein(a) were similar in patients and controls. The hepatic lipase activity tended to be lower in patients than controls (33.8+/-17.7 vs. 50.4+/-23.0 pkat/ml; P=0.05). In conclusion, in patients with asymptomatic acute porphyria an increase of total and LDL-cholesterol was found. The cardiovascular risk conferred by this factor may be attenuated by increased HDL-cholesterol and apo-A1.

Lipoprotein changes in patients with chronic hepatitis C treated with interferon-alpha.

OBJECTIVE: The aim of this study was to evaluate the effects of interferon-alpha therapy on the lipid profile of patients with chronic hepatitis C. METHODS: In 36 consecutive patients with chronic hepatitis C, fasting lipoproteins were evaluated prospectively at baseline, 1, 3 and 6 months during interferon-alpha therapy and 3 months after the end of treatment. RESULTS: During interferon-alpha therapy, there was a progressive increase in total and very low density lipoprotein (VLDL)-triglycerides, VLDL-cholesterol and a sustained raise in apolipoprotein (apo) B. In parallel, there was a reduction in high density lipoprotein (HDL)-cholesterol and apo A1 levels. In contrast, total and low density lipoprotein (LDL)-cholesterol and lipoprotein (a) levels remained essentially unchanged during interferon-alpha therapy. Three patients developed chylomicronemia, two of them with severe hypertriglyceridemia, although none of them presented with pancreatitis. Chylomicronemia and severe hypertriglyceridemia were more common in patients with basal triglycerides above 200 mg/dl. Nineteen patients responded to interferon-alpha therapy, but their lipid profile did nor differ from that of nonresponders. Three months after the end of interferon-alpha therapy lipid changes subsided, although VLDL and HDL-cholesterol and apo B did not reach basal levels. CONCLUSION: In patients with chronic hepatitis C, interferon-alpha therapy is associated with an increase of total and VLDL-triglycerides, VLDL-cholesterol and apo B, and a decline of HDL-cholesterol and apo A1. The development of chylomicronemia and severe hypertriglyceridemia in some cases makes mandatory a close monitoring of triglycerides during interferon-alpha therapy, particularly among patients with increased triglycerides at baseline.

Lipoprotein alterations in patients with HIV infection: relation with cellular and humoral immune markers.

In order to determine lipid abnormalities in serum in HIV-infected patients and their relation with humoral and cellular immunological changes. Ninety HIV-infected patients without acute inflammatory or malignant disease have been studied. Thirty healthy HIV-negative subjects constituted the control group. As compared with controls, patients with CD4 + lymphocytes > 400 x 10(6)/l had higher triglycerides and lower high density lipoprotein (HDL)-cholesterol and apolipoprotein (apo)-A1. Lipoprotein comparison by groups of patients according to CD4 + cell counts showed a decrease of HDL-cholesterol in patients with CD4 + cells < or = 200 x 10(6)/l. When CD4 + lymphocyte counts were < 50 x 10(6)/l, total and very low density lipoprotein (VLDL)-triglycerides and VLDL-cholesterol were increased and HDL and low density lipoprotein (LDL)-cholesterol and apo-A1 were decreased. Interferon (IFN)-alpha, beta2-microglobulin and tumor necrosis factor (TNF)-alpha were correlated positively with total and VLDL-triglycerides and negatively with HDL-cholesterol. In conclusion, lipoprotein changes in patients with HIV-infection are related with humoral and cellular immune markers. A decrease of HDL-cholesterol and apo-A1 and an increase of triglyceride levels could be considered as markers of disease progression.

Lipoprotein abnormalities in long-term stable liver and renal transplanted patients. A comparative study.

Hyperlipidemia is a common feature after organ transplantation. Most studies have evaluated the lipid profile in recipients of a particular graft, usually renal. In the present work, we studied the lipid profiles of 30 long-term stable liver transplant patients (LTP) and compared their pattern with 40 long-term stable renal transplant patients (RTP) matched for gender, age, and time from transplantation. There were no significant differences between both groups in body mass index, serum glucose, serum creatinine, or urinary protein excretion. In contrast, RTP had higher pre-transplant total cholesterol and triglycerides, received higher doses of steroids (both average and cumulative) and had higher cycosplorine blood levels. After a mean time of 60 months after transplantation, RTP exhibited higher levels of total serum cholesterol (226 +/- 26 vs. 180 +/- 39 mg/dl; p = 0.000 002) and low-density lipoprotein (LDL) cholesterol (152 +/- 22 vs. 112 +/- 37 mg/dl; p = 0.00001). In contrast, there were no differences between RTP and LTP in high density lipoprotein (HDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, total triglycerides, VLDL triglycerides, or lipoprotein (a) [Lp(a)]. By univariate analysis in the whole group, renal graft, prednisone daily dose, cyclosporine blood levels, pre-transplant cholesterol, and triglycerides were associated with increased post-transplant cholesterol levels. By multivariate analysis, prednisone daily dose was the only independent variable predicting increased post-transplant serum cholesterol levels. The present data show that hypercholesterolemia is more frequent among RTP than among LTP. In addition, our data suggest that corticosteroid therapy, rather than the transplanted organ, may be the major contributor to this difference.

Lipid abnormalities in stable liver transplant recipients--effects of cyclosporin, tacrolimus, and steroids.

Dyslipidemia is common after liver transplantation, but the underlying mechanisms are largely unknown. We studied the lipid profile of 27 liver transplant recipients randomized to received either cyclosporin (CyA, n = 14) or tacrolimus (n = 13) and compared them with 20 healthy, matched controls. Before transplantation, patients presented low total and low-density lipoprotein (LDL) cholesterol (as compared to controls) that increased shortly, i.e., 3 months, after transplantation. Eighteen months post-transplantation, total and LDL cholesterol levels decreased to pre-transplant values but tended to remain higher in CyA-treated patients. However, at that time, prednisone treatment was more prevalent among CyA-treated than tacrolimus-treated patients and fully accounted for the difference in cholesterol levels. Indeed, regardless of therapy, patients not receiving prednisone exhibited lower cholesterol levels than prednisone-treated patients and controls. We conclude that prednisone therapy, rather than CyA or tacrolimus immunosuppression, seems to be the major determinant of increased cholesterol levels.