1296 AJR:204, June 2015
Quantifcation of Bone Marrow
Involvement in Treated Gaucher
Disease With Proton MR
Spectroscopy: Correlation With
Bone Marrow MRI Scores and
Clinical Status
Diego Jaramillo
1,2
Maria A. Bedoya
1
Dah-Jyuu Wang
1
Andres H. Pena
3
Jorge Delgado
1
Camilo Jaimes
4
Victor Ho-Fung
1,2
Paige Kaplan
5, 6
Jaramillo D, Bedoya MA, Wang DJ, et al.
1
Department of Radiology, The Children’s Hospital of
Philadelphia, 34th St and Civic Center Blvd, Philadelphia,
PA 19104. Address correspondence to D. Jaramillo
(jaramillo@email.chop.edu).
2
Department of Radiology, Perelman School of Medicine,
University of Pennsylvania, Philadelphia, PA.
3
Department of Radiology, SUNY Stony Brook University
Hospital, Stony Brook, NY.
4
Department of Radiology, Massachusetts General
Hospital, Boston, MA.
5
Section of Metabolic Disease, The Children’s Hospital of
Philadelphia, Philadelphia, PA.
6
Department of Pediatrics, Perelman School of Medicine,
University of Pennsylvania, Philadelphia. PA.
Pediatric Imaging • Original Research
AJR 2015; 204:1296–1302
0361–803X/15/2046–1296
© American Roentgen Ray Society
Keywords: bone marrow, Gaucher disease, MRI, MR
spectroscopy
DOI:10.2214/AJR.14.13563
Received July 23, 2014; accepted after revision
September 21, 2014.
D. Jaramillo has received a research grant from Genzyme
Corporation, a Sanofi Company, to enable this pilot study
to be done. P. Kaplan is a member of the Advisory Board
for Gaucher Disease and Mucopolysaccharidosis, which
is supported by Genzyme; she has received honoraria in
this capacity and for giving lectures, which have been
independently prepared.
Symptoms and signs include chronic fatigue,
frequent nose bleeds, prolonged bleeding or
bruising, hepatomegaly, splenomegaly, skel-
etal compromise, poor growth in childhood,
and delayed pubertal development [ 1–3].
Skeletal compromise is observed in 70–
100% of the patients with type 1 GD, and it
includes a wide range of clinical and radio-
logic findings such as chronic bone pain,
bone crisis, bone marrow infiltration, Erlen-
meyer flask deformity, lytic lesions, osteo-
sclerosis, osteonecrosis, fractures, and low
bone density (measured with dual-energy x-
ray absorptiometry [DEXA]) [2, 3].
The enzyme that is deficient or absent, re-
sulting in GD, is replaced by an analog of the
human enzyme β-glucocerebrosidase and is
produced by recombinant DNA. The enzyme is
administered IV every 2 weeks usually at doses
N
onneuropathic type 1 Gaucher
disease (GD) is an autosomal-re-
cessive inherited disease caused
by a deficiency or absence of
β-glucocerebrosidase (β-glucosidase). It can
manifest at any age, but 66% of patients
manifest symptoms of GD during the first 2
decades of life. The highest prevalence of
type 1 GD is in Ashkenazi Jews, but it affects
all ethnic groups [ 1]. The phenotype is char-
acterized by painless splenohepatomegaly;
infiltration of bone marrow by lysosome-en-
gorged macrophages (Gaucher cells) and
secondary damage to bone (osteonecrosis
from bone marrow vascular compression and
altered osteoclastic and osteoblastic function
through defective paracrine regulation); and
hypersplenism with variable low hemoglobin
levels, platelet levels, and WBC counts.
OBJECTIVE. The objective of our study was to use proton MR spectroscopy (MRS) to
quantitatively evaluate bone marrow infiltration by measuring the fat fraction (FF) and to
compare the FF with semiquantitative bone marrow MRI scores and clinical status in chil-
dren treated for type 1 Gaucher disease (GD).
SUBJECTS AND METHODS. Over a 2-year period, we prospectively evaluated 10
treated GD patients (six males, four females; median age, 15.1 years) and 10 healthy age-
matched control subjects (five males, five females; median age, 15.3 years) using 3-T proton
MRS of L5 and the femoral neck. Water and lipid AUCs were measured to calculate the FF.
Two blinded pediatric musculoskeletal radiologists performed a semiquantitative analysis of
the conventional MR images using the bone marrow burden score and modified Spanish MRI
score. We evaluated symptoms, spleen and liver volumes, platelet levels, hemoglobin levels,
and bone complications.
RESULTS. In the femur, the FF was higher in the control subjects (median, 0.71) than
the GD patients (0.54) ( p = 0.02). In L5, the difference in FF—higher FF in control subjects
(0.37) than in GD patients (0.26)—was not significant ( p = 0.16). In both groups and both re-
gions, the FF increased with patient age ( p < 0.02). Semiquantitative scores showed no dif-
ferences between control subjects and treated GD patients ( p > 0.11). Eight of 10 GD patients
were asymptomatic and two had chronic bone pain. The median age of patients at symptom
onset was 4.0 years, the median age of patients at the initiation of enzyme replacement thera-
py was 4.3 years, and the median treatment duration was 10.2 years. Hemoglobin level, plate-
let count, and liver volume at MRI were normal. Mean pretreatment spleen volume (15.4-fold
above normal) decreased to 2.8-fold above normal at the time of MRI ( p = 0.01).
CONCLUSION. Proton MRS detected FF differences that were undetectable using con-
ventional MRI; for that reason, proton MRS can be used to optimize treatment of GD patients.
Jaramillo et al.
Proton MRS to Quantify Bone Marrow
Involvement in GD
Pediatric Imaging
Original Research
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