Vol.2, No.7, 432-435 (2013) Case Reports in Clinical Medicine
http://dx.doi.org/10.4236/crcm.2013.27113
Role of abdominal CT in predicting the diagnosis of
insulin resistant diabetes abbreviated title:
Diagnosing insulin resistant diabetes on
abdominal CT
Cynthia Tan1, Aruna V ade1, Jennifer Orrico1, Julius Griauzde1, Terrence C. Demos1,
Alaleh Mazhari2, Mary Ann Emanuele2
1Departments of Radiology, Loyola University Medical Center, Maywood, USA;
2Department of Endocrinology, Loyola University Medical Center, Maywood, USA; Email: [e-mail], [e-mail]
Received 26 June 2013; revised 29 July 2013; accepted 20 August 2013
Copyright © 2013 Cynthia Tan et al. This is an open access article distributed under the Creative Commons Attribution Li-
cense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
ABSTRACT
We report a diagnosis of diabetes type 2 sug-
gested by diffuse omental infiltration seen on
computed tomography which resolved following
treatment. There have been reports of increased
macrophage infiltration in the omental fat of dia-
betic patients which we believe is identifiable by
CT. To our knowledge, the diagnosis of diabetes
with CT has not yet been report ed. Diabe tes ty pe
2 is commonly a clinical diagnosis. However,
undiagnosed diabetic patients may present with
nonspecific manifestations and CT may be or-
dered as part of the initial evaluation. We pre-
sent a case in which diabetes type 2 was sug-
gested by diffuse omental infiltration.
Keywords: Omental Infiltration; Diabetes
1. INTRODUCTION
The obesity epidemic is increasing at an alarming rate.
Health complications from obesity have dramatically
impacted patients’ quality of life and health care. Obesity
has been strongly associated with many diseases, espe-
cially insulin resistant type 2 diabetes. Patients with dia-
betes type 2 are defined as either not producing enough
insulin or being insu lin resistant. Prior to developing type
2 diabetes, most are prediabetic as determined by ele-
vating fasting plasma glucose levels that are greater than
normal (100 mg/dl) but less than 126 mg/dl. By accu-
rately identifying patients who have not yet been diag-
nosed with diabetes, we may be able to provide early
initiation of treatment. Type 2 diabetes has been strong ly
associated with central obesity [1]. Current research has
shown preferential macrophage infiltration of omental fat
different from subcutaneous fat in Type 2 diabetic pa-
tients [2,3]. Chronic low-grade inflammation caused by
macrophage infiltration of the omentum inhibits forma-
tion of mature adipocytes alters their function [4,5].
Though much research has been done focusing on body
mass index and quantification of visceral fat by CT and
MR using volumetric assessment of visceral fat, there
has been no study addressing the alteration in visceral fat
density as shown by CT or MR imaging in patients with
insulin resistant Type 2 diabetes [6,7]. We present a pa-
tient who presented to the emergency department with
abdominal pain. Abdomen pelvis CT showed diffuse in-
filtration of omental fat and diabetes was suggested as a
possibility. Subsequ ently, the patient was proven to have
Type 2 diabetes.
2. CASE REPORT
A previously healthy 49-year-old white male pre-
sented to the emergency department with abdominal pain.
This pain had been intermittent every day for several
months and was described as needle-like with radiation
to the thighs and groin. On review of systems, the patien t
reported urinary frequency and a 20 pound weight loss
over the prior year, currently weighing 130 pounds. His
BMI was 19.8. Abdomen pelvis CT with intraveno us and
oral contrast material showed diffuse increased density
and stranding of the omentum and a 1 cm hypodense
liver lesion (Figure 1). No other abnormalities were seen.

C. Tan et al. / Case Reports in Clinical Medicine 2 (2013) 432-435 433
Based on the finding of omental fat infiltration without
any other abdominal pa thology, the possibility of Type 2
diabetes was suggested. Same day laboratory results fol-
lowing the abdominal CT revealed elevated blood glu-
cose (417 un its) and HbA1c (11.5), which were co mpati-
ble with insulin resistant diabetes (diabetes mellitus type
2). His lipid profile was normal. Autoimmune antibody
titre for glutamic acid decarboxylase, islet cell and insu-
lin antibodies was negative. Metformin (500 mg twice a
day) and glipizide (5 mg daily) were started. One month
later, follow up liver protocol CT to evaluate the liver
lesion showed no omental infiltration and a stable he-
patic hemangioma (Figure 2). Over the period of two
and a half years of treatment the patient gained 32
pounds, his blood glucose level was normal and HbA1c
level had dropped to 6.7.
3. DISCUSSION
In the US, 23.6 million adults are estimated to have
diabetes. Zhang et al. have estimated that one-fourth of
these patients remain undiagnosed. The National Health
and Nutrition Examination Survey is a random stratified
survey used to identify adults who have elevated fasting
Figure 1. Contrast enhanced axial CT scan of
the abdomen shows diffuse increased density
and stranding of the omentum (arrow).
Figure 2. Contrast enhanced axial CT scan of the
abdomen one month after treatment for diabetes
shows no omental infiltration (arrow).
plasma glucose and have never been told they have dia-
betes. The prevalen ce of undiagnosed diabetics was mul-
tiplied by the Census Bureau popu lation in 2007. Care of
known diabetics is estimated to cost $174 billion per year
in higher medical costs and lose productivity [8]. Newly
diagnosed diabetics often develop complications linked
to diabetes including retinopathy, proteinuria, neuropathy,
arterial disease, cardiovascular disease, and coronary
heart disease [8]. A claims-based study suggested costs
of diabetes begins at least 8 years prior to diagnosis [8].
Since patients with undiagnosed diabetes were omitted
from the estimated cost, the total expense of diabetes is
likely much higher [8]. Estimated national medical costs
associated with undiagnosed diabetes depend on the es-
timated prevalence and the ratio of per capita health care
used by undiagnosed diabetics [8]. Impaired glucose tol-
erance has been positively correlated with obesity [9]. In
obese patients, central adiposity shows a strong associa-
tion with obesity-related metabolic syndromes including
insulin resistant diabetes [1]. Metabo lic syndromes affect
20% - 40% of US adults and are increasing in the preva-
lence of making it a leading public health issue [10].
Type 1 diabetes mellitus occurs in young patients who
have a lack of insulin and have normal or low BMI and a
normal lipid profile [11]. Some diabetic patients have
normal or low BMI, and normal lipid profile but have
latent autoimmune diabetes (LADA) [12]. They present
at an older age than individuals with Type 1 diabetic
patients and usually need insulin after initially respond-
ing to oral medication, usually within 2 - 3 years. Type 2
diabetes mellitus typically presents at an older age and is
due to insulin resistance in addition to relative insulin
deficiency or relative impairment of insulin secretion
[13]. However, now it is being documented in younger
patients due to th e rise in obesity. Type 2 diabetes melli-
tus patients usually have elevated BMI with other co-
morbidities including hyperten sion and dyslipid emia [13].
Maturity onset diabetes of the young (MODY) is an
autosomal dominant monogenetic form of diabetes. Pa-
tients present before the age of 25 years due to a domi-
nant genetic defect [14]. These patients do not have dia-
betes autoimmu ne antibodies. Our patient was diagno sed
with Type 2 diabetes despite his normal BMI and normal
lipid profile because of his negative autoimmune anti-
body titre and negative family histo ry of MODY.
Visceral or central body fat consists of fat in the
omentum and mesentery whereas subcutaneous fat is
extraperitoneal. Visceral fat is more metabolically active
than subcutaneous fat, not only in the degree of lipolytic
activity but also in the release of adipokines. Current
research indicates that macrophage infiltration preferen-
tially into omental fat and not subcutaneous fat is exag-
gerated by central obesity and is also associated with
clinical parameters of central obesity comorbidities [2 ,3].

C. Tan et al. / Case Reports in Clinical Medicine 2 (2013) 432-435
434
It has been shown that macrophage infiltration of the
omentum induces adipose tissue inflammation that re-
sults in dysfunction of ad ipose tissue by activatin g proin-
flammatory cytokines that in turn induce insulin resis-
tance, thus linking central obesity to Type 2 diabetes.
[15].
The greater omentum is a fatty peritoneal extension
from the stomach covering intra-abdominal organs [16].
The omentum serves to contain disease processes, how-
ever, it may also contribute to disease spread [16]. The
abdominal innervation clarifies clinical findings associ-
ated with omental abnormality. The parietal peritoneum
shares its somatic innervation with the anterior abdomi-
nal musculature and skin. A diseased omentum can thus
irritate the adjacent parietal peritoneum due to its close
proximity as well as its mobility. The anterio r abdominal
wall can therefore be the site of localized or diffuse ten-
derness, rigidity, and guarding. These nonspecific signs
and symptoms can mimic more ominous diseases such as
appendicitis, diverticulitis, peptic ulcer disease, chole-
cystitis, and pancreatitis. Omental infiltration is a non-
specific finding seen with diseased omentum and is as-
sociated with multiple etiologies including peritoneal
carcinomatosis, tuberculosis peritonitis, malignant peri-
toneal mesothelioma, pseudomyxoma peritonei, lym-
phomatosis, and cirrhosis with portal hypertension. Other
conditions which can demonstrate omental infiltration
include omental infarction, granuloma, hematoma, and
hernia. In cases where no etiology can be identified, as in
our patient, the diagnosis is idiopathic omental infiltra-
tion.
The evaluation of omental processes is primarily by
CT [16]. Approximately 10% of the population are esti-
mated to obtain a CT study during their lifetime, and a
total of 75 million scans are performed annually [17].
Currently, the utilization of CT to identify or follow up
idiopathic diffuse omental infiltration is not done. The
patient presented here had diffuse omental infiltration
indicated by the increased density of the omental fat
compared to subcutaneous fat. No underlying etiology
was found for this infiltration. Upon treatment for diabe-
tes with metformin and glipizide for one month, the
omental fat density returned to normal. He has responded
well to this treatment and has no t required insulin so far.
The CT finding o f diffuse omental infiltration with no
etiology should raise su spicion of insulin resistant diabe-
tes even in patients with normal or low BMI and normal
lipid profile. This can lead to earlier diagnosis and treat-
ment with reduction of comorbidities.
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