R. Lanes et al., Cardiac mass and function, carotid artery intima-media thickness, and lipoprotein levels in growth hormone-deficient adolescents, J CLIN END, 86(3), 2001, pp. 1061-1065
The objective of our study was to evaluate whether cardiac mass and functio
n, carotid artery intima-media thickness, and serum lipid and lipoprotein(a
) levels are abnormal in adolescents with GH deficiency.
Young adults with childhood-onset and adulthood-onset GH deficiency have be
en found to have a higher cardiovascular risk, as manifested among other fa
ctors by reduced left ventricular mass, impaired systolic function, signifi
cant increase in arterial intima-media thickness, and dyslipidemia.
Twelve adolescents (seven males and five females) with GH deficiency (10 id
iopathic and 2 organic), with an age of 14.2 +/- 2.8 yr and a height of 140
.6 +/- 17.9 cm (height so score, -2.6 +/- 0.3), were studied. Six children
had received GH in the past but were off therapy for several years, whereas
six patients had never been treated with GH. Fasting blood samples were ob
tained for serum lipids and lipoprotein(a) analysis. Patients underwent tra
nsthoracic M-mode and two-dimensional echocardiographic evaluation for meas
urement of interventricular septal thickness, left ventricular posterior wa
ll thickness, and left ventricular mass, as well as left ventricular ejecti
on fraction at rest and pulmonary Venous flow velocities; carotid artery in
tima-media thickness was measured using high-resolution mode B ultrasound.
Seven GH-deficient (GHD) adolescents on GH at the time of the study and 19
healthy adolescents, all comparable for age, pubertal status, height, weigh
t, blood pressure, and pulse, participated in this study as controls.
Interventricular septal thickness (6.5 +/- 1.3 vs. 7.0 +/- 1.5 mm), left ve
ntricular posterior wall thickness (7.0 +/- 1.8 us. 7.5 +/- 2.0 mm), and le
ft ventricular mass after correction for body surface area (71.2 +/- 21.8 v
s. 70.7 +/- 18.0 g/m(2)) were similar in untreated GHD patients and healthy
controls. Similarly, the left ventricular ejection fraction at rest was si
milar in untreated GHD subjects and controls (70.0 +/- 0.7 vs. 70.0 +/- 0.6
%), as were the pulmonary venous flow velocities (0.54 +/- 0.16 vs. 0.55 +/
- 0.10 m/s for diastolic peak velocity; 0.51 +/- 0.16 vs. 0.50 +/- 0.09 m/s
for systolic peak velocity; and 0.19 +/- 0.06 vs. 0.19 +/- 0.05 m/s for at
rial reversal filling). Carotid artery intima-media thickness (0.60 +/- 0.0
2 mm and 0.59 +/- 0.02 mm for the right and left carotid arteries, respecti
vely) was also normal in our untreated GHD patients when compared with heal
thy controls. In addition, all echocardiographic measurements were similar
in GHD subjects on or off GH at the time of the study.
Low-density lipoprotein cholesterol levels were increased in untreated GHD
patients when compared with healthy controls (3.17 +/- 0.70 vs. 2.33 +/- 0.
36 mmol/L; P < 0.01), whereas total cholesterol, high-density lipoprotein c
holesterol, and triglyceride concentrations were similar to that of control
s. Total cholesterol levels were increased in our untreated GHD adolescents
when compared with GHD subjects receiving GH therapy at the time of the st
udy, while low-density lipoprotein cholesterol and triglyceride levels were
also elevated, although not significantly. Lipoprotein(a) levels were elev
ated in untreated GHD adolescents when compared with healthy controls, and
untreated GHD subjects had higher Lipoprotein(a) concentrations than GH-tre
ated patients.
GHD adolescents, regardless of whether or not they received GH therapy, do
not seem to show alterations in cardiac mass and function or early atherosc
lerotic changes. They must, however, be followed carefully because they alr
eady present cardiovascular risk factors such as dyslipidemia, which may in
crease their cardiovascular morbidity over time.