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D Sommariva

Publications and source records attributed to D Sommariva.

At least 19 recordsLinked to original sources
PubMed2002

Atorvastatin increases HDL cholesterol in hypercholesterolemic patients. Evidence of a relationship with baseline HDL cholesterol.

BACKGROUND AND AIM: It has been reported that atorvastatin increases high-density lipoprotein cholesterol (HDL-C) more in patients with low than in those with high baseline HDL-C levels. This may have a biological explanation, but also suggests a statistical artifact known as the regression to the mean. METHODS AND RESULTS: Atorvastatin 10 mg/day led to a 4% increase in HDL-C after two months in 67/121 patients with hypercholesterolemia (55%), who had lower baseline HDL-C levels than the patients in whom HDL-C did not increase. In the patients with baseline HDL-C below the median, HDL-C significantly increased whereas no change was observed in patients with baseline HDL-C above the median. The correlation coefficient between pre- and post-treatment HDL-C was 0.84, thus suggesting a regression to the mean. However, the regression artifact did not entirely explain the increase in HDL-C in patients with low baseline HDL-C or the lack of an increase in those with high baseline HDL-C. The adjusted mean increase was 5.4% in patients with low pretreatment HDL-C, and 2.4% in the patients with high pretreatment HDL-C. Multiple regression analysis with the changes in HDL-C as the dependent variable showed that baseline HDL-C and the changes in serum triglycerides independently contributed to the change in HDL-C levels. CONCLUSIONS: Atorvastatin 10 mg/day increases HDL-C more in patients with low pretreatment HDL-C levels, an effect that seems to be related to the hypotriglyceridemic activity of the drug.

Adult↗
PubMed2001

Effects of low doses of simvastatin and atorvastatin on high-density lipoprotein cholesterol levels in patients with hypercholesterolemia.

BACKGROUND: Simvastatin 40 to 80 mg/d has been found to increase high-density lipoprotein cholesterol (HDL-C) levels significantly more than atorvastatin at equipotent doses (ie, 20-80 mg/d). Data on the effects of lower doses of the 2 drugs on HDL-C levels are conflicting. OBJECTIVE: The purpose of this study was to investigate the effects of simvastatin 20 mg/d and atorvastatin 10 mg/d on HDL-C levels in patients with hypercholesterolemia. METHODS: Patients with primary hypercholesterolemia (total cholesterol [TC] >250 mg/dL) who were not taking any lipid-lowering agents and who were following a low-fat diet were randomized to receive 1 of 2 treatments: simvastatin 20 mg/d or atorvastatin 10 mg/d. Serum TC, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and HDL-C levels were measured using standard methods after 2 months of therapy. In a secondary analysis, lipids and lipoprotein cholesterol were measured after 1 year in patients who continued treatment. RESULTS: Of the 240 patients enrolled (108 men and 132 women; age range, 23-77 years, mean [SEM] 56.7 [0.69]), 235 completed the study. After 2 months of therapy, TC, LDL-C, and serum TG levels decreased significantly versus baseline in both groups (P < 0.001), with no significant differences between treatment groups. HDL-C levels increased by 9.0% (P < 0.001 vs baseline) in the simvastatin group and by 4.3% (P < 0.02) in the atorvastatin group. The difference between the 2 groups in the percentage increase in HDL-C was statistically significant (P < 0.05). In 113 patients who continued treatment, HDL-C levels at 1 year were still significantly higher than baseline levels in the simvastatin group (6.3%, P = 0.034), but not in the atorvastatin group (2.8%, P = 0.587). CONCLUSIONS: The findings from this study suggest that the HDL-C-increasing effect of simvastatin 20 mg is significantly greater than that of atorvastatin 10 mg. Since increasing HDL-C levels is thought to lower the risk for atherosclerosis and coronary heart disease, these results warrant further investigation.

Adult↗
PubMed2000

Serum lipoprotein profile in patients with cancer. A comparison with non-cancer subjects.

The association of cancer with low serum total cholesterol is well established. Less clear is the relationship of cancer with the cholesterol distribution among the different lipoprotein classes. Conflicting results have been reported on low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and serum triglyceride levels in different types of tumor. Total serum cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and serum triglycerides were analyzed in 530 patients with newly diagnosed cancer (97 with hematological malignancies, 92 with tumor of the lung, 108 of the upper digestive system, 103 of colon, 32 of breast, and 98 of the genitourinary system) and in 415 non-cancer subjects. Anthropometric (body mass index) and biochemical (serum albumin) indices of nutritional status were also determined in all subjects. Total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, serum albumin, and body mass index were significantly lower in cancer than in non cancer-subjects. The lowest values of total cholesterol, low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol were recorded in patients with hematological malignancies and the highest in patients with breast tumor. All the cancer groups, with the exception of women with breast cancer, showed significantly lower total cholesterol, low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol than age- and sex-matched non-cancer subjects. Multiple regression analysis with low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and triglycerides as dependent variables and sex, age, body mass index, albumin, and cancer (dummy variable) as independent variables, showed that cancer was independently associated with low levels of low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol and with high values of serum triglycerides. Total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, serum triglycerides, body mass index and serum albumin were significantly lower in patients with metastatic than in patients with non-metastatic solid tumor. The significant difference in low-density lipoprotein-cholesterol and serum triglycerides between patients with metastatic and non-metastatic cancer was lost when lipoprotein cholesterol and serum triglyceride levels were adjusted for nutritional variables. The lipid profile in cancer patients is characterized by low low-density lipoprotein-cholesterol, low high-density lipoprotein-cholesterol and relatively high serum triglycerides. The abnormality is a common feature of both hematological and solid tumors and is not entirely explained by poor nutrition.

Adult↗
PubMed1999

Lowering effects of four different statins on serum triglyceride level.

OBJECTIVES: The main effect of statins is the decrease of serum level of low-density lipoprotein (LDL) cholesterol, due to the inhibition of intracellular cholesterol biosynthesis which brings about an upregulation of LDL receptors. A minor effect is the decrease of serum triglycerides. The present study was undertaken to verify whether all statins are effective in reducing serum triglycerides and whether their effect on triglycerides is related to the LDL cholesterol lowering activity. METHODS: Of 197 hypercholesterolaemic patients on stable low-fat low-cholesterol diet, 49 were put on atorvastatin 10 mg per day, 48 on fluvastatin 40 mg per day, 50 on pravastatin 20 mg per day and 50 on simvastatin 10 mg per day. RESULTS: After 2 months, mean percentage change in serum triglycerides and LDL cholesterol resulted to be significantly different among the four treatment groups, whereas the ratio between the percentage decrease in serum triglycerides and that of LDL cholesterol (Deltatriglyceride/DeltaLDL cholesterol ratio) was not significantly different. Only baseline serum triglycerides resulted to be significantly associated with Deltatriglycerides/DeltaLDL cholesterol ratio. All statins are then effective in decreasing triglyceride levels. CONCLUSION: The lack of a significant difference in Deltatriglycerides/DeltaLDL cholesterol ratio among the treatment groups suggests that the more effective the statin is in decreasing LDL cholesterol, the more it will also be in decreasing serum triglycerides.

Adult↗
PubMed1998

Accuracy of calculated serum low-density lipoprotein cholesterol for the assessment of coronary heart disease risk in NIDDM patients.

OBJECTIVE: To evaluate the accuracy of LDL cholesterol calculated with Friedewald's equation in the assessment of cardiovascular risk in NIDDM patients. RESEARCH DESIGN AND METHODS: The calculation of LDL cholesterol according to Friedewald's formula was compared with the measurement of LDL cholesterol separated by ultracentrifugation in 151 NIDDM patients with fairly good metabolic control (HbA1c < or =10%) and in 405 nondiabetic subjects. RESULTS: Measured and calculated LDL cholesterol was found to be well correlated in both diabetic (r = 0.95) and nondiabetic (r = 0.97) subjects. Compared with measured LDL cholesterol, the calculated LDL cholesterol differed by > or =10% in 34% of samples from diabetic patients and in 26% of samples from nondiabetic subjects (chi(2) = 3.885, P < 0.05). The percentage of error increased when the serum triglyceride (TG) level was > or =200 mg/dl (2.26 mmol/l) and when the ratio of VLDL cholesterol to TG was <0.20 or >0.29 in both groups of subjects. Although the percentage of error from calculated LDL cholesterol was greater in diabetic than in nondiabetic subjects because of the greater prevalence of hypertriglyceridemia in the former group, the misclassification of coronary heart disease risk, according to the cutoff points of the National Cholesterol Education Program (NCEP), was similar in the two groups (25% in diabetic and 22% in nondiabetic subjects). In both groups of patients, the misclassification of coronary heart disease risk was higher when calculation of LDL cholesterol produced values near the cutoff points. CONCLUSIONS: Although accuracy in the estimation of LDL cholesterol is less than ideal, Friedewald's equation seems to be of value in the correct assignment of coronary heart disease risk classes in the great majority of diabetic as well as nondiabetic subjects. Caution must be exercised for subjects in whom calculated LDL cholesterol is close to the cutoff points of the NCEP guidelines.

Cholesterol, LDL↗
PubMed1997

Association of alcohol consumption with HDL subpopulations defined by apolipoprotein A-I and apolipoprotein A-II content.

OBJECTIVE: To investigate the relationship between alcohol intake and serum level of high-density lipoprotein (HDL) subfractions defined on the basis of their apolipoprotein A-I and A-II content (LpA-I and LpA-I: A-II). DESIGN: Observational study. SETTING: Institute of Internal Medicine and Medical Physiopathology, IRCCS Maggiore Hospital, University of Milan. SUBJECTS: One hundred healthy males with a mean age of 42 +/- 11.1 y, selected among blood donors. RESULTS: Both LpA-I and LpA-I:A-II were significantly higher in men drinking more than 30 g a day of alcohol than in non-drinkers (LpA-I: difference between means 6.5 mg/dL, 95% C.I. 1.14-11.9; LpA-I:A-II difference between means 11.5 mg/dL, 95% C.I. 0.52-22.5). The association of alcohol consumption with LpA-I and LpA-I:A-II levels was independent from age, body mass index, physical activity, serum triglycerides and diet composition. CONCLUSIONS: Alcohol consumption is associated with an increase of serum levels of both LpA-I and LpA-I:A-II particles and this may, at least in part, explain the reduced cardiovascular morbidity observed in subjects drinking moderate amounts of alcoholic beverages. SPONSORSHIP: Supported by grants from Ricerca Corrente Ospedale Maggiore di Milano IRCCS, Milan Italy.

Adult↗
PubMed1996

Serum cholesterol levels in patients with cancer. Relationship with nutritional status.

Epidemiological surveys indicate an inverse relationship between cancer occurrence and serum cholesterol. Low serum cholesterol might be either a risk factor for cancer or the effect of factors associated with cancer itself, such as biological properties of malignant cells, tumor mass, and poor nutritional status. We have measured serum cholesterol in 975 selected patients admitted to our hospital; 496 (272 males, 224 females) had solid tumors and 479 (253 males, 226 females) had non-neoplastic diseases. Serum cholesterol was positively correlated with body mass index, serum albumin, hemoglobin, and cholinesterase in both cancer and non-cancer subjects. Cholesterol was significantly lower in cancer patients than in age- and sex-matched non-cancer subjects. After adjustment for nutritional variables (analysis of covariance), the difference in cholesterol level between cancer and non-cancer subjects lost statistical significance in all but patients with tumors of the upper gastrointestinal tract. No difference was found in adjusted mean serum cholesterol between cancer patients subdivided according to the extension of the tumor was defined by the TNM system. In patients with solid tumors, serum cholesterol seems to be more related to the nutritional status than the presence and extension of cancer.

Aged↗
PubMed1996

The effect of simvastatin on HDL cholesterol in hyperlipidemic patients. Evidence of a relationship with the changes in serum triglyceride level.

The main effect of simvastatin is the decrease of serum cholesterol due to the reduction of LDL. A decrease of serum triglycerides and an increase of HDL-C are commonly observed during the treatment. The reduction of triglycerides is accounted for by the increased catabolism of apo B-containing lipoproteins whereas the mechanisms bringing about the increase of HDL-C are still unknown. We treated 318 patients with primary hyperlipidemia (227 with phenotype IIa and 91 with phenotype IIb) with simvastatin 10 mg a day and after 6 weeks we found a mean 3% increase in HDL-C. HDL-C increased only in about half of the patients and the patients in whom HDL-C increased had baseline higher serum triglycerides and had a greater hypotriglyceridemic response than patients in whom HDL-C did not increase. Accordingly, HDL-C increased in type IIb patients who experienced a greater change in triglycerides than type IIa patients, in whom HDL-C did not increase significantly. Apo A-I levels did not change and apo A-I/HDL-C ratio significantly decreased. At a daily dose of 40 mg, administered to 51 treatment-resistant patients, simvastatin produced a marginally greater decrease in serum cholesterol and LDL-C, but not in serum triglycerides and HDL-C, than at the daily dose of 10 mg. An increase in HDL-C was associated with a reduction in serum triglycerides. The decrease in apo A-I/HDL-C ratio suggests that the increase in HDL-C after simvastatin must be regarded as an enrichment of the cholesterol core of HDL particles. The effect is likely to be due to the decrease of the serum concentration of VLDL bringing about a reduction of cholesterol transfer from apo A-I to apo B-containing lipoproteins.

Adult↗
PubMed1995

Effects of bezafibrate and of 2 HMG-CoA reductase inhibitors on lipoprotein (a) level in hypercholesterolemic patients.

Lp(a) level is relatively stable in each individual and is mainly under genetic control. Attempts made to lower Lp(a) with pharmacological means gave conflicting results. In order to further evaluate the effect of hypocholesterolemic drugs on Lp(a) level, 66 patients with primary hypercholesterolemia were selected. The vast majority of the patients had Lp(a) concentration at the low end of the range of distribution, 7 had undetectable Lp(a) levels and only 2 had Lp(a) higher than 30 mg/dl. No relationship was found between Lp(a) level and serum and lipoprotein lipids. In 12 patients serum cholesterol was well controlled by diet alone and the patients continued the diet for up to 8 months. The other patients were randomly subdivided into 3 groups of therapy. The first group received slow release bezafibrate 400 mg once a day, the second one pravastatin 20 mg once a day and the third one simvastatin 10-40 mg once a day. Drug therapy lasted for 8 months. At the end of the period, 22 of 29 patients treated with the 2 HMG-CoA reductase inhibitors had Lp(a) higher than baseline. The difference was statistically significant in both groups of patients. No significant change in Lp(a) was observed in diet and in bezafibrate group. Serum and LDL cholesterol significantly decreased in all the 3 drug groups. The increase in Lp(a) after the 2 HMG-CoA reductase was small enough to have negligible effects on cardiovascular risk, but raises the problem of the role of LDL receptor in the catabolism of Lp(a).

Adult↗
PubMed1995

Effect of bezafibrate on HDL with APO A-I and APO A-II and on HDL with APO A-I without APO A-II in hyperlipidaemic patients.

On the basis of apoprotein composition, high-density lipoprotein (HDL) particles may be subdivided into two main subpopulations defined by the presence in the lipoprotein molecule of apo A-I (Lp A-I) and of both apo A-I and apo A-II (Lp A-I:A-II). The effect of slow-release bezafibrate 400 mg a day on Lp A-I and Lp A-I: A-II was evaluated in 34 hyperlipidaemic patients (19 with hypercholesterolaemia and 15 with hypertriglyceridaemia). Seventeen patients on low-fat low-cholesterol diet only were taken as the reference group. In the reference group, no change in HDL-C, apo A-I, apo A-II, Lp A-I and Lp A-I:A-II occurred during the 3 months of observation. In patients on bezafibrate, HDL-C, apo A-I and apo A-II significantly increased. Lp A-I:A-II increased by 33% in hypercholesterolaemic and by 29% in hypertriglyceridaemic patients. Lp A-I decreased by 15% in hypercholesterolaemic patients and did not change significantly in hypertriglyceridaemic patients. This differential effect of bezafibrate on apo-A-defined HDL subpopulations in hypertriglyceridaemia and in hypercholesterolaemia is in accord with previous studies on the effect of the drug on HDL subfractions defined by their density.

Apolipoprotein A-I↗
PubMed1993

Effect of three fibrate derivatives and of two HMG-CoA reductase inhibitors on plasma fibrinogen level in patients with primary hypercholesterolemia.

In order to evaluate the effects of hypocholesterolemic drugs on plasma fibrinogen concentration, six groups of subjects with primary hypercholesterolemia have been put on treatment with diet alone or diet plus fenofibrate (100 mg t.i.d.), slow release bezafibrate (400 mg once a day), gemfibrozil (600 mg b.i.d.), simvastatin (20 mg once a day) or pravastatin (20 mg once a day) respectively. After 1 month of therapy, plasma fibrinogen significantly decreased by 9% and 15% in fenofibrate and bezafibrate groups respectively and increased by 19% in gemfibrozil treated patients. After 4 months of therapy the changes were -16% with fenofibrate, -10% with bezafibrate and +20% with gemfibrozil. No significant changes were observed in patients treated with diet alone, simvastatin or pravastatin. The fibrinogen lowering effect of fenofibrate and bezafibrate does not seem to be related to the hypolipidemic activity of the drugs.

Adult↗
PubMed1993

[The effects of chronic cilazapril treatment on sympathetic vasomotor tonus: a spectral analysis study of pressure variability].

Animal experiments suggest that an important component of the antihypertensive effects of ACE inhibitors might derive from an inhibition of the sympathetic vasomotor tone. We addressed this problem on 22 mildly hypertensive subjects (48 +/- 2 years; arterial pressure 151 +/- 3/95 +/- 1 mmHg), in whom sympathetic vasomotor tone was non invasively inferred by the power of the low frequency component (0.1 Hz) of the spontaneous oscillations of systolic arterial pressure (LFSAP), during placebo and after 4 weeks of treatment with a new ACE inhibitor, cilazapril, 5 mg per os oid. LFSAP was computed at rest and during physical (active orthostatism) and mental (computerized attentional test and mental arithmetic) stimuli capable of enhancing sympathetic drive. Cilazapril treatment reduced resting arterial pressure to 128 +/- 3/80 +/- 2 mmHg, without affecting heart rate (78 +/- 2 and 74 +/- 2 b/min, respectively). The increases in LFSAP produced by standing were significantly greater during placebo than during active treatment (delta LFSAP = 10 +/- 3 and 5 +/- 2 mmHg2, respectively). These data suggest that an important reduction of sympathetic vasomotor tone accompanies the antihypertensive effects of chronic ACE-inhibitor treatment.

Blood Pressure↗
PubMed1992

Effects of slow release bezafibrate on the lipid pattern and on blood glucose of type 2 diabetic patients with hyperlipidaemia.

Ninety-eight type 2 diabetic patients with hyperlipidaemia in stable metabolic control with diet alone (41) or diet plus hypoglycaemic agents (57) were divided into two groups: group 1 was put on treatment with slow release bezafibrate 400 mg a day, while group 2 was considered as control. In group 1, after 1 month of bezafibrate, serum triglycerides fell by 47% and cholesterol by 13%. HDL cholesterol showed a non-significant trend toward an increase. Fasting blood glucose significantly decreased by 6%, fructosamine and glycated haemoglobin by 5%. During OGTT, the area under the curve of both serum C-peptide and blood glucose showed a trend toward a decrease after bezafibrate. However, the difference did not reach statistical significance. Thirty-six patients continued the treatment with the drug for 4 months and 23 for 8 months, without further changes of the lipid pattern and glycaemic control. In the control group no significant variation of the lipid levels occurred and diabetic control slightly worsened during the study. Bezafibrate has been proved to be effective in the treatment of hyperlipidaemia in type 2 diabetic patients. The drug seems moreover to improve glycaemic control. The mechanism by which bezafibrate produces this latter effect remains to be elucidated, though an increase of peripheral insulin sensitivity might be suggested.

Aged↗
PubMed1992

Effects of bezafibrate on biosynthesis of cholesterol and on degradation of native and acetylated low-density lipoproteins in incubated human monocytes.

The effects of bezafibrate on 14C-acetate incorporation into non-saponifiable lipids and on degradation of native and acetylated [125I] low-density lipoproteins (LDL) in cultured human monocytes has been evaluated. The presence of bezafibrate in the incubation medium resulted in a decrease of labelled acetate incorporation into non-saponifiable lipids. In parallel with the decrease in sterol synthesis, bezafibrate produced an increase in total and specific degradation of native low-density lipoproteins, whereas the degradation of acetylated low-density lipoproteins was not affected by the drug. These data, though obtained with concentrations of bezafibrate in the incubation medium greater than those encountered in ordinary therapeutic conditions, support the hypothesis that bezafibrate inhibits cholesterol biosynthesis and increases removal of low-density lipoproteins by activating the specific receptor pathway.

Bezafibrate↗
PubMed1989

Inhibition of cholesterol biosynthesis in freshly isolated blood mononuclear cells from normolipidemic subjects and hypercholesterolemic patients treated with bezafibrate.

Bezafibrate was given for 15 days at a dose of 200 mg t.i.d. to 4 normolipidemic subjects, to 5 patients with putative heterozygous familial hypercholesterolemia, and to 6 patients with primary hypercholesterolemia of the non-familial type. At the end of the treatment, the rate of incorporation of labelled acetate into non-saponifiable lipids in freshly isolated blood mononuclear cells decreased in all subjects. On the average, acetate incorporation decreased by 31% in cells from normolipidemic subjects, 41% in cells from familial, and 45% in cells from non-familial hypercholesterolemia patients. Results of the present study suggest that the lowering effect of bezafibrate on serum cholesterol is mainly due to the inhibition of cholesterol synthesis through the suppression of HMG-CoA reductase as was demonstrated in rat hepatocytes and in cultured human blood mononuclear cells.

Adult↗
PubMed1988

Changes in serum and lipoprotein lipids, and apolipoprotein B and A-I, in patients with different types of primary hyperlipoproteinaemia treated with gemfibrozil.

Gemfibrozil was given at the dose of 600 mg twice daily to 16 type IIa, 13 type IIb and 11 type IV hyperlipoproteinaemic patients for four months. At the end of the fourth month of therapy low-density lipoprotein (LDL) cholesterol decreased on the average by 18% in type IIa, by 11% in type IIb and increased by 37% in type IV patients. Very-low-density lipoprotein (VLDL) cholesterol and triglycerides fell by 57% in type IIb and by 58% and 76% respectively in type IV subjects. High-density lipoprotein (HDL) cholesterol rose in all groups of patients owing to the increase of the HDL2 subfraction. However, in type IIa the change did not reach the level of statistical significance. Apoprotein B decreased in type IIa and in type IIb patients and apoprotein A-I significantly increased in type IIb and IV patients. The individual changes in total VLDL and LDL lipids and in apoprotein B could be related to their pretreatment level. The cholesterol triglyceride ratio significantly increased in LDL and HDL fractions and the effect was greater in the subgroup of patients with the greatest abnormality in lipoprotein lipid composition. On the whole the differential effects of gemfibrozil on serum lipoprotein concentration and composition in the various types of hyperlipoproteinaemia can be regarded as a trend toward a normalization and may be explained by the multiple effects of the drug on lipid metabolism.

Adolescent↗
PubMed1986

Autoantibodies to the low density lipoprotein receptor in a subject affected by severe hypercholesterolemia.

We studied a 32-yr-old man with a benign paraproteinemia (IgA) affected by severe nonfamilial hypercholesterolemia. In vitro experiments demonstrated that lipoprotein-deficient serum (LPDS) from the patient inhibited the binding of low density lipoprotein (LDL) to human skin fibroblasts cultured in vitro (up to 70%) whereas LPDS from controls had no effect. Removal of IgA from the patient's serum by immunoprecipitation with mono-specific antisera abolished the inhibition of LDL binding. IgA isolated from the serum of the patient by affinity chromatography inhibited, in a dose-dependent manner, the binding of LDL to human skin fibroblasts in vitro, thus showing an IgA-mediated effect. Ligand-blotting experiments demonstrated that the paraprotein directly interacts with the LDL receptor, thus inhibiting the binding of the lipoprotein. Treatment of the receptor protein with reducing agents blocked the interaction of the antibody with the LDL receptor. From these data we speculate that this autoantibody may be responsible for the severe nonfamilial hypercholesterolemia of the patient.

Adult↗