CASE STUDY TABLE 14-1.1 Serum lipoprotein concentrations differ between adult
LABORATORY RESULTS men and women, primarily as a result of differences in
sex hormone levels, with women having, on average,
ANALYTE PATIENT VALUE REFERENCE RANGE higher HDL cholesterol levels and lower total cholesterol
Na ⫹
151 135–143 mEq/L and triglyceride levels than men.56 The difference in total
K⫹
4.5 3.0–5.0 mEq/L cholesterol, however, disappears after menopause as es-
trogen decreases.57 Men and women both show a ten-
Cl⫺ 106 98–103 mEq/L
dency toward increased total cholesterol, LDL choles-
CO2 content 13 22–27 mmol/L terol, and triglyceride concentrations with age. HDL
Total protein 5.7 6.5–8.0 g/dL cholesterol concentrations generally remain stable after
Albumin 1.6 3.5–5.0 g/dL the onset of puberty and do not drop in women with the
onset of menopause. General adult reference ranges are
Ca2⫹ 7.9 9.0–10.5 mg/dL
shown in Table 14-3.
Cholesterol 210 140–200 mg/dL Circulating levels of total cholesterol, LDL choles-
Uric acid 6.2 3.5–7.9 mg/dL terol, and triglycerides in young children are generally
Creatinine 2.5 0.5–1.2 mg/dL much lower than those seen in adults.58 In addition, con-
centrations do not significantly differ between boys and
BUN 95 7–25 mg/dL
girls. HDL cholesterol levels for both boys and girls are
Glucose 88 75–105 mg/dL
Total bilirubin 1.2 0.2–1.0 mg/dL
Alkaline 27 7–59 IU/L TABLE 14-3 ADULT REFERENCE RANGES
phosphatase FOR LIPIDS
Lactate 202 90–190 IU/L ANALYTE REFERENCE RANGE
dehydrogenase
Total cholesterol 140–200 mg/dL
Aspartate 39 8–40 IU/L
HDL cholesterol 40–75 mg/dL
transaminase
LDL cholesterol 50–130 mg/dL
Amylase 152 76–375 IU/L
Triglyceride 60–150 mg/dL
340 PART 2 ■ CLINICAL CORRELATIONS AND ANALYTIC PROCEDURES
hyperlipoproteinemia is a holdover from a lipoprotein typ- 2. Why do you think the triglycerides are abnormal?
If she takes hormonal therapy like estrogen she will has high triglyceride,
ing system developed by Fredrickson et al.101 that is oth- 3. What is the primary disease exhibited by this pa-
erwise generally no longer used. The disease results from tient’s laboratory data?
an accumulation of cholesterol-rich VLDL and chylomi- She has low albumin, Increased lipids, Low albumin, then it is nephrotic syndrome.
tri high, Hyper lipidemia, Hypo albuminemia.
cron remnants as a result of defective catabolism of those
CASE STUDY TABLE 14-4.1
particles. The disease is associated with the presence of a
LABORATORY RESULTS
relatively rare form of apo E, called apo E2/2. Individuals
with type III will frequently have total cholesterol values PATIENT REFERENCE
of 200–300 mg/dL (5–8 mmol/L) and triglycerides of ANALYTE VALUES RANGE
300–600 mg/dL (3–7 mmol/L). To distinguish them from Na⫹⫹ 149 135–143 mEq/L
other forms of combined hyperlipoproteinemias, it is first K⫹⫹ 4.5 3.0–5.0 mEq/L
necessary to isolate the VLDL fraction with ultracentrifu- ⫺
Cl 120 98–103 mEq/L
gation. A ratio derived from the cholesterol concentration
in VLDL to total serum triglycerides will be greater than CO2 content 12 22–27 mmol/L
⬎0.30 in the presence of type III hyperlipoproteinemia. If Total protein 5.7 6.5–8.0 g/dL
the VLDL fraction is analyzed by agarose electrophoresis, Albumin 2.3 3.5–5.0 g/dL
the particles will migrate in a broad  region, rather than 2⫹
Ca 7.6 9.0–10.5 mg/dL
in the normal pre- region. Definitive diagnosis requires a
determination of apo E isoforms by isoelectric focusing or Cholesterol 201 140–200 mg/dL
DNA typing, resulting in either apo E2/2 homozygosity or, Uric acid 15.4 3.5–7.9 mg/dL
rarely, apo E mutation or deficiency. Treatment does not Creatinine 4.5 0.5–1.2 mg/dL
totally rely on a diagnosis because these patients, as those
BUN 87 7–25 mg/dL
with other dyslipidemias, can be treated with niacin, gem-
fibrozil, HMG-CoA reductase inhibitors, or just a low-fat Glucose 88 75–105 mg/dL
diet. Because of the cholesterol-enriched composition of Total bilirubin 1.3 0.2–1.0 mg/dL
these particles, use of the Friedewald equation102 to calcu- Triglycerides 327 65–157 mg/dL
late LDL cholesterol levels will result in an underestima-
Lactate 200 90–190 IU/L
tion of VLDL cholesterol and, therefore, an overestimation
dehydrogenase
of LDL cholesterol, compared with beta-quantification.103
Aspartate 45 8–40 IU/L
Lipoprotein(a) Elevation transaminase
Amylase 380 76–375 IU/L
Elevations in the serum concentration of Lp(a), espe-
cially in conjunction with elevations of LDL, increase the
risk of CHD and CVD.104,105 Higher Lp(a) levels have
been observed more frequently in patients with CHD
than in normal control subjects,106 although prospective with the coagulation factor, plasminogen,109 it has been
studies have not conclusively determined this positive proposed that it competes with plasminogen for fibrin
association.107 Lp(a) are variants of LDL with an extra binding sites, thus increasing plaque formation.110,111
apolipoprotein, called apo (a); the size and serum con- Most LDL-lowering drugs have no effect on Lp(a) con-
centrations of Lp(a) are largely genetically deter- centration, even when LDL cholesterol is significantly
mined.108 Because apo (a) has a high degree of homology lowered. The two drugs shown to have some effect are
CHAPTER 14 ■ LIPIDS AND LIPOPROTEINS 347