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10.7 · Diabetic Nephropathy
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Signs on Plain Radiographs and CT
The bladder shade is seen surrounded by radiolucent
line due to air within the wall that may give cobblestone
appearance due to the wall trabeculation
(pathognomonic;
. Fig. 10.7.7 ).
. Fig. 10.7.7 Plain radiography of the bladder of a patient
with emphysematous cystitis that shows radiolucent air within
the bladder wall ( arrowheads )
431
k Signs on US
1. Classical pyelonephritis is seen as an area of parenchymal
hyperechogenicity with low vascular ow (checked by
Doppler and power Doppler sonography). ickening of
the renal edges can be seen, with loss of di erentiation
between the cortex and the medulla.
2. Emphysematous pyelonephritis will show signs on
classical pyelonephritis plus multiple intraparenchymal
echogenic foci due to the presence of gas. e condition
is bilateral in 10 % of cases.
3. Multiple hypoechoic intraparenchymal lesions may be
seen due to abscesses formation.
Signs on CT
1. In classical pyelonephritis, there is enlarged
edematous kidney, delayed renal enhancement,
wedge-shaped areas of decreased attenuation,
Gerota’s fascia thickening, and obstruction of the
renal tubules by debris impairing contrast excretion
that results in “striated” appearance of the kidney
(
. Figs. 10.7.8 and 10.7.9 ).
2. In emphysematous pyelonephritis, there are
gas-density lesions within the renal parenchyma with
or without multiple abscesses that are seen as cystic
lesions with rim contrast enhancement.
10
Emphysematous Pyelonephritis
Pyelonephritis is a bacterial infection of the renal parenchyma
that results in tubulointerstitial in ammation and usually
results from ascending infection of the bladder (e.g., via vesico-
ureteric re ux ). Emphysematous pyelonephritis is an acute necrotizing pyelonephritis characterized by gas formation within
the renal parenchyma and the perirenal tissues. Emphysematous
pyelonephritis is a surgical emergency that is seen almost exclusively in poorly controlled diabetic female > 50 years of age
(90 % of cases). If medical intervention is delayed, mortality can
reach up to 80 %. e causative organisms include E. coli ,
Klebsiella pneumoniae , and Pseudomonas species.
Signs on Radiographs
Plain radiographs show signs of radiolucent air within
the renal shades (pathognomonic).
. Fig. 10.7.8 Axial CT postcontrast illustration that shows the
diff erent manifestations of pyelonephritis on CT postcontrast
images

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Chapter 10 · Diabetology
a
. Fig. 10.7.9 Plain ( a ) and axial CT image postcontrast ( b ) of a patient with xanthogranulomatous pyelonephritis showing a stone
impacted in the renal pelvic ( arrowhead in a and b ) and fatty infi ltration of the renal parenchyma ( arrow in b )
b
10
Xanthogranulomatous Pyelonephritis
Xanthogranulomatous pyelonephritis is a rare condition characterized by chronic UTI that causes replacement of the renal
parenchyma by lipid- lled microphages due to in ammation
and renal calculus (80 % of cases). e causative organisms of
xanthogranulomatous pyelonephritis include Proteus species
(most common) and Staphylococcus aureus . Patients usually
complain of multiple genitourinary symptoms more than 6
month in duration (40 % of cases), which include renal colic,
fever, malaise, weight loss, anorexia, and persistent urosepsis.
Signs on Plain Radiographs
Radiographs typically show staghorn calculus with
enlarged renal shade (
Signs on Ultrasound
Xanthogranulomatous pyelonephritis has a diff use and a
focal form. In the diff use form , the kidney shows
nephromegaly (<12 cm in diameter), multiple calyceal
dilatation (multiple cystic formations), renal pelvis
dilatation, and stone formation within the kidney. In the
focal form , a lesion is confi ned to one part or pole of the
kidney, usually occurring in women and children, and may
not present fi ndings similar to those of the diff use form.
Signs on CT
Typically, there is a stone in the ureter of the aff ected
kidney (often staghorn), with signs of fatty lesions within
the renal parenchyma ( you must see these two
combinations before you diagnose xanthogranulomatous
pyelonephritis ) (
. Fig. 10.7.8a ).
. Fig. 10.7.8b ).
Selected References
Browne RFJ, etal. Imaging of urinary tract infection in the
adult. Eur Radiol. 2004;14:E168–83.
Demertzis J, etal. State of the art: imaging of renal infections.
Emerg Radiol. 2007;14:13–22.
Jung DC, etal. Renal papillary necrosis: review and compari-
son ndings at multi-detector row CT and intravenous
urography. Radiographics. 2006;26:1827–36.
Marzano MA, etal. Early renal involvement in diabetes mellitus:
comparison of renal Doppler US and radioisotope evaluation
of glomerular hyper ltration. Radiology. 1998;209:813–7.
Rodriguez-de-Velasquez A, etal. Imaging the e ects of dia-
betes on the genitourinary system. Radiographics.
1995;15:1051–68.
10.8 Lipomatosis
Lipomatosis is a benign condition characterized by proliferation of noncapsulated mature adipocytes. Similar conditions
include lipoblastomatosis, which is de ned as proliferation of
noncapsulated immature adipocytes, and liposarcoma which
is de ned as proliferation of neoplastic adipocytes.
Di erentiation between the three clinical entities requires
histopathological conformation.
Lipomatosis, lipoblastomatosis, and liposarcoma can
arise from any part of the body. Lipomatosis of certain areas
within the body can present with signi cant clinical symptoms, which radiological modalities can identify e ciently.
is topic discusses some of the well-known symptomatic
lipomatosis conditions within the body.
Intestinal Lipomatosis
Intestinal lipomatosis is a rare benign condition characterized
by the formation of multiple polypoid masses within the interior
intestinal lumen composed of mature fatty tissues (lipomas).

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10
Intestinal lipomas can be seen as normal variant commonly a ecting the ileocecal valve, duodenum, or the cecum.
Most cases of intestinal lipomatosis lesions involve solitary
lipoma; multiple intestinal lipomatosis is a very rare condition. When multiple intestinal lipomatosis occurs, they are
frequently involving the ileum (39 %) and the jejunum
(13 %). Simultaneous presence of diverticulosis is a frequent
feature.
Patients with intestinal lipomatosis typically present with
recurrent attacks of abdominal pain, melena, anemia, and
lower GI bleeding Abdominal pain is attributed to recurrent
attacks of intussusception, while melena and lower GI bleeding are attributed to ulceration of the lipomas caused by
a
intussusception. Laboratory investigations o en show anemia and hypercholesterolemia.
k Signs on Barium Enteroclysis
1. Typically, there are multiple, sharply demarcated, intraluminal lling defects con ned to the wall of the intestinal
lumen caused by the lipomas (. Fig. 10.8.1 ).
2. Multiple intestinal diverticula may be seen.
k Signs on CT
1. Single or multiple intraluminal intestinal lipomas with
typical fat density can be detected in any part of the gastrointestinal tract (. Figs. 10.8.1 and 10.8.2 ).
b
. Fig. 10.8.1 Axial CT image ( a ) and colonic enema image ( b ) that shows ileocecal lipoma ( white arrowhead in a ) and cecal lipoma ( black arrowhead in b )
a
. Fig. 10.8.2 Axial ( a ) and coronal ( b ) abdominal CT postcontrast images that show duodenal intraluminal lipoma ( arrowhead in a and b )
b

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Chapter 10 · Diabetology
10
2. Intussusception may be found, especially if the CT is
performed during the acute attack.
Pelvic Lipomatosis
Pelvic lipomatosis is a rare benign condition characterized by
fat proliferation around the bladder, prostate, and rectum
producing characteristic radiographic appearance that simulates a pelvic neoplasm. e incidence of pelvic lipomatosis is
0.6–1.7 cases per 100,000 populations. e condition has a
male predominance, a ecting males of black origin (60 %) in
their fourth and h decades. Symptoms are relatively mild
and include urinary frequency, constipation, and occasionally low-grade fever.
Signs on IVU and CT
The bladder shows a banana shape with displacement
anterosuperiorly out of the true pelvis due to the fat
proliferation around it and below it (
Diff erential diagnoses include pelvic hematoma and
psoas muscle compression.
. Fig. 10.8.3 Intravenous pyelogram that shows elongated
bladder shape due to pelvic lipomatosis ( arrowheads )
. Fig. 10.8.3 ).
Epidural Lipomatosis
Epidural lipomatosis is a rare condition which is characterized by proliferation of the fat in the epidural space leading to
cord compression and displacement within the spinal canal.
When the proliferation occurs at the end of the spinal cord,
cauda equina syndrome can develop. Patients o en present
with radicular pain and spinal claudication due to cord compression. ere is o en a history of chronic systemic steroid
therapy or Cushing’s syndrome.
Signs in CT and MRI
There is hypertrophic epidural fat pressing and fl attening
of the spinal cord. On axial images, Y-shaped compressed
dural sac (very characteristic).
Encephalocraniocutaneous Lipomatosis
Syndrome (Haberland Syndrome)
Encephalocraniocutaneous lipomatosis (ECCL) is nonhereditary, congenital, neurocutaneous (phakomatosis) syndrome characterized by unilateral cutaneous hamartoma of
the scalp with ipsilateral ophthalmologic and neurological
malformations. Most reported cases are sporadic.
Cutaneous lesions of ECCL include nevus psiloliparus;
multiple small, popular, or polypoid cutaneous lipomatous
nodules usually present on the face and eyelid in a unilateral
distribution; a scar-like lesions; and café au lait spots. Nevus
psiloliparus is a term used to describe a lipomatous scalp
lesion causing head asymmetry. e lipomatous scalp hamartoma is always devoid of hair (alopecia areata). Jaw odontomas can be found.
Ocular abnormalities are always present and include epibulbar choristoma, desmoids tumor of the sclera, persistent
hyaloids vessels, ectopia lentis, cataract, and colobomas.
Cerebral manifestations include porencephalic cysts ipsilateral to the lipomatous scalp (major manifestation), causing
hydrocephalus and brain atrophy. Seizures may be found,
with spasticity of the contralateral limb.
e diagnostic features of ECCL include :
1. Unilateral lipomatous hamartoma of the scalp with ipsi-
lateral ocular abnormalities
2. Ipsilateral porencephalic cysts with cerebral atrophy
3. Cranial asymmetry
4. Marked developmental delay and mental retardation
5. Seizures
6. Spasticity of the contralateral limb
Signs on Plain Radiographs
1. Skull asymmetry
2. Jaw odontomas

10.8 · Lipomatosis
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10
Signs on MRI
1. Scalp lipoma with ipsilateral porencephalic cyst and
brain atrophy. The porencephalic cyst is classically
located in the parieto-occipital region.
2. Cerebral calcifi cations.
3. Hydrocephalus.
4. Partial agenesis of the corpus callosum may be seen.
5. Intracranial lipoma (especially in the CP angle) may
be found.
Lipomatous Hypertrophy of the Interatrial
Septum
Lipomatous hypertrophy of the interatrial septum (LHIS) is a
rare condition de ned as fatty deposits within the interatrial
septum with a thickness more than 2cm.
Although the LHIS is detected incidentally and usually
asymptomatic, it can rarely cause atrial brillation, atrial premature contractions, and atrioventricular block as a consequence of involvement of the atrial wall and atrioventricular
conduction pathway. An abnormal P wave con guration in
leads II and III and aVF named “dome and dip” have been
described in some patients with LHIS.
Di erential diagnosis of LHIS in CT and MRI includes
interatrial lipoma and atrial myxoma. Atrial myxoma is
gelatinous tumors with 90 % of cases are seen in adult women
between 30 and 60 years of age. It is the most common primary cardiac neoplasm in adults (50 % of cardiac neoplasms).
Most cases are sporadic, and patients usually present with
CNS symptoms, fatigue, arthralgia, fever, anemia, and weight
loss; however, 20 % of myxomas are asymptomatic.
Signs on CT and MRI
1. The interatrial septum is seen diff usely replaced by
fatty tissue (hypodense in CT and high T1 signal
intensity on MRI;
from the upper and/or lower part of the interatrial
septum with typical sparing of the foramen ovale,
giving the lesion a characteristic dumbbell shape .
2. Associated features include increased pericardial and
mediastinal fat.
3. On CT, cardiac myxoma typically appears as a
heterogeneous mass with a narrow base attachment
located in the interatrial septum at the area of fossa
ovalis (90 % of cases). Eighty percent of cases arise in
the left atrium and 10 % in the right atrium.
Calcifi cation is frequently seen. On MRI, myxoma is
seen as a high signal intensity lesion on T2W images.
Heterogeneous enhancement is seen on both CT and
MRI.
4. Unlike LHIS, interatrial septum lipoma is seen as
localized well-defi ned (capsulated) fatty lesion.
. Fig. 10.8.4 ). The fatty tissue derives
. Fig. 10.8.4 Axial CT image of the heart shows lipomatosis
of the interatrial septum ( arrowhead )
Selected References
Al-Me y O, et al. e multiple manifestations of the
Encephalocraniocutaneous lipomatosis syndrome. Child’s
Nerv Syst. 1987;3:132–4.
Andaç N, et al. Fat necrosis mimicking liposarcoma in a
patient with pelvic lipomatosis. CT ndings. J Clin
Imaging. 2003;27:109–11.
Ayan K, etal. Lipomatous hypertrophy of the interatrial sep-
tum. Int J Cardiovasc Imaging. 2005;21:659–61.
Bodas A, etal. Intestinal lipomatosis in a 10-year-old girl. Eur
J Pediatr. 2008;167:601–2.
Bogaert J, etal. Esophageal lipomatosis: another consequence
of the use of steroids. Eur Radiol. 2000;10:1390–4.
Church PA, etal. Computed tomography and ultrasound in
diagnosis of pelvic lipomatosis. Urology. 1979;14(6):631–3.
Fitoz S, etal. Intracranial lipoma with extracranial extension
through foramen ovale in a patient with encephalocraniocutaneous lipomatosis syndrome. Neuroradiology.
2002;44:175–8.
Gawel J, et al. Encephalocraniocutaneous lipomatosis. J
Cutan Med Surg. 2003;7(1):61–5.
Haloi AK, etal. Facial in ltrative lipomatosis. Pediatr Radiol.
2006;36:1159–62.
Hauber K, etal. Encephalocraniocutaneous lipomatosis: a
case with unilateral odontomas and review of the literature. Eur J Pediatr. 2003;162:589–93.
Heyer CM, etal. Lipomatous hypertrophy of the interatrial
septum: a prospective study of incidence, imaging ndings, and clinical symptoms. Chest. 2003;124:2068–73.
Komagata T, etal. Extensive lipomatosis of the small bowel
and mesentery: CT and MRI ndings. Radiat Med.
2007;25:480–3.
Parazzini C, et al. Encephalocraniocutaneous lipomatosis:
complete neuroradiologic evaluation and follow-up of
two cases. AJNR Am J Neuroradiol. 1999;20:173–6.
Pugliatti P, etal. Lipomatous hypertrophy of the interatrial
septum. Int J Cardiol. 2008;130:294–5.

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Soles R, etal. MR of laryngeal and scrotal involvement in mul-
tiple symmetrical lipomatosis. Eur Radiol. 1997;7:946–8.
Türkavtan A, etal. Di use in ltrating abdominal lipomato-
sis. Eur J Radiol Extra. 2008;67:15–7.
Xanthos T, etal. Lipomatous hypertrophy of the interatrial
septum: a pathological and clinical approach. Int J Cardiol.
2007;121:4–8.
Yakabe S, etal. Jejunal lipomatosis with diverticulosis: report
of a case. Jpn J Surg. 1998;28:846–9.
7 . Late dumping syndrome : this is a pathological situation
10.9 Hypoglycemia
Hypoglycemia is de ned as plasma glucose concentration
less than 45mg/dL and commonly develops when rate of glucose uptake by peripheral tissue exceeds the capacity of the
liver glucose output.
Patients with hypoglycemia typically presents with fea-
tures due to low glucose supply to the brain ( neuroglycope-
nia ) and increased catecholamine secretion
( counter - regulatory response ). Neuroglycopenia manifesta-
tions include altered mental status, aggressiveness, seizures,
diplopia, and maybe coma. In contrast, counter- regulatory
response manifestations include anxiety, tachycardia, and
sweating. e most common causes of hypoglycemia include:
1 . Brittle diabetes : it is a pathological condition characterized
by recurrent sever hypoglycemia and/or ketoacidosis. It is
seen mostly in type 1 diabetics who have had diabetes
more than 10 years. Brittle diabetes is characterized by
negligible insulin secretion and absent glucagon and
adrenalin response to hypoglycemia.
2 . Endocrine and metabolic diseases : like Addison’s disease,
congenital adrenal hyperplasia, familial fructose and
galactose intolerance ( Dormandy ’ s syndrome ),
pluriglandular insu ciency syndrome ( Falta syndrome ),
and pituitary insu ciency. Pluriglandular ine ciency
syndrome is a disease characterized by failure of more
than one gland, usually the thyroid and pituitary.
3 . Medications : like weight gain-reducing agents,
sulfonylurea, and alcohol. Alcohol induces hypoglycemia
especially postprandial due to stimulation of beta cells to
produce insulin. Also, alcohol can inhibit
gluconeogenesis especially in fasting people or
malnourished individuals.
4 . Autoimmune hypoglycemia : this is uncommon cause of
hypoglycemia that arises due to autoantibodies that bind
and activate insulin receptors.
5 . Paraneoplastic syndrome : this is seen with tumors that
secret insulin-like growth factor (e.g., hepatoma ).
6 . Insulin autoimmune syndrome ( Hirata disease ): this is a
relatively rare disease characterized by recurrent attacks
of postprandial and/or fasting hypoglycemia without
evidence of exogenous insulin administration due to the
presence of high titers of IgG insulin autoantibodies
(IAA). Hirata disease is seen between 60 and 70 years of
age and has a striking association with HLA-DR4. e
disease has a high incidence among Asian population
8 . Insulinoma : this is a benign pancreatic islet cell tumor
main categories: reactive (acute) hypoglycemia and
symptoms of prolonged hypoglycemia. Acute hypoglycemic
symptoms include nervousness, palpitation, trembling, and
weakness. Symptoms of prolonged hypoglycemia, on the
other hand, include disturbances in consciousness, headache,
visual disturbance, convulsions, and behavioral disturbances.
e behavioral disturbances include manic episodes,
personality change, negativism, and severe depression that
may cause the patient to seek psychiatric help.
Characteristically, the acute and chronic hypoglycemic
symptoms are interspersed with symptom-free periods but
tend to increase in frequency and severity. Exercise and
fasting usually intensify the symptoms, although the patient
is frequently unaware of the relationship. Late morning or
early a ernoon attacks are common.
hypoglycemia by measuring fasting blood glucose on three
mornings, high levels of serum proinsulin levels, and elevated
concentration of serum C-peptide (a peptide that connects
alpha and beta chains of proinsulin). Ultrasound and MRI
represents the rst radiological approach for insulinoma
detection. CT and angiography should be reserved for negative and/or doubtful cases.
9 . Congenital hyperinsulinism ( persistent hyperinsulinemic
compared to the rest of the world. Patients present with
hypoglycemic attacks more than 1 month and less than 3
month in duration. Eighty- ve percent of patients have
spontaneous remission. Up to 43 % of patients of Hirata
disease develop the disease a er intake of medications
that contains sul ydryl compounds for a period of time.
Examples of medications that predispose to Hirata
disease include glutathione, captopril, methimazole,
penicillamine, α-interferon, and loxoprofen sodium.
seen a er gastric or intestinal surgeries. e patient
presents with signs of hypoglycemia 1 to 3 h a er eating
due to inappropriate high insulin secretion stimulated by
secretin hormone, which is released from the gut due to
the presence of hyperosmolar food form the stomach.
that secretes insulin and arises from beta cells of islets of
Langerhans. e peak age of onset is in young adulthood.
Most cases are sporadic; however, it may occur in
multiple endocrine neoplasia (MEN) syndrome type 1.
Insulinoma is classically suspected by Whipple ’ s triad ,
described as symptoms associated with fasting or
exercise; the symptoms are associated with hypoglycemia
(serum glucose level <50mg/dL), and the symptoms are
relieved by glucose intake or administration.
Hypoglycemic symptoms of insulinoma falls into two
Laboratory diagnosis can be con rmed by demonstrating
hypoglycemia of infancy ): this is a rare disorder
characterized by excessive, glucose-independent insulin
secretion in the neonatal period, causing severe attacks of
recurrent hypoglycemia. Congenital hyperinsulinemia
(CHI) is formerly known as nesidioblastosis , and it has an
annual incidence of 1/30,000 live births.

10.9 · Hypoglycemia
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ere are two forms of CHI: focal and di use. Focal CHI
is characterized by the presence of small endocrine lesion in
the pancreas composed of hyperplastic but apparently normal islets of Langerhans. is lesion should not be confused
with insulinoma, because the cells are hyperplastic not neoplastic. In contrast, di use CHI is characterized by di use
proliferation of hyperplastic islets within the pancreas.
Symptoms are nonspeci c and include feeding problems,
irritability, and lethargy; if the condition is not treated properly or the diagnosis is delayed, permanent brain damage and
atrophy may result. Laboratory investigations typically show
hypoglycemia, hyperinsulinemia, hypoketosis, and hypofatty acidemia. e hypoglycemia is persistent and recurrent.
Hypertrophic cardiomyopathy and gastroesophageal re ux
are common in patients with CHI for unknown cause.
Diagnosis of CHI can be further con rmed by 18 F- uorodopa
PET scan. Surgery is reserved for medically uncontrolled
hypoglycemia and involves local excision in focal CHI or
subtotal pancreatectomy in di use CHI.
437
Signs on Chest Radiographs
Solitary fi brous tumor is detected as a sharply
demarcated, lobulated mass attached to the chest wall
with or without opacifi cation of the hemithorax. On
sequential chest radiographs, the tumor can change its
position with changes in posture, a feature often referred
to as dancing tumor .
Signs on US and Doppler Sonography
The majority of insulinomas are seen as hypoechoic
pancreatic nodule with a surrounding capsule. On
Doppler sonography, numerous intratumoral vascular
spots (spots pattern) may be seen typical of
neuroendocrine pancreatic tumors due to
hypervascularity.
10
D i ff erential Diagnoses and Related Diseases
1 . Doege - Potter syndrome : this is a term used to describe
recurrent attacks of hypoglycemia in a patient with
malignant solitary brous tumor due to secretion of
insulin-like growth factor 2 by the tumor cells. Solitary
brous tumor (SFT) is a relatively rare tumor that arises
typically from the pleura and the upper respiratory tract.
e tumor is locally aggressive, usually is > 8cm in size,
and with a broad base of attachment to the pleura. Distant
metastases may be seen. Patients with SFT usually present
with chest pain, shortness of breath, hemoptysis, and
attacks of hypoglycemia with nervousness and irrational
behavior. e hypoglycemia associated with SFT is seen
in < 5 % of cases and is attributed to the secretion of
insulin-like growth factor 2 (IGF-2). IGF-2 is a peptide
hormone primarily made in the liver, while insulin is
synthesized as a prohormone from beta cells in the
pancreas. IGF circulate at nanomolar concentrations
bound to IGF binding proteins, which are also
manufactured by the liver. Free IGFs constitute up to 1 %
of the circulating pool and have a half-life of approx.
10min. Some tumors, like SFT, produce excessive amount
of a prohormone form of IGF-2 o en referred to as “Big
IGF-2.” Big IGF-2 causes hypoglycemia mainly by
transporting glucose into muscles, inhibiting
gluconeogenesis in the liver and lipolysis in adipose
tissues. e optimal time to detect high serum levels of
IGF-2 is during the hypoglycemic attack.
2 . Somogyi e ect : it is a condition characterized by
nocturnal hypoglycemia that is followed by morning
hyperglycemia due to counter-regulatory hormonal
response. Somogyi e ect arises due to high insulin or
oral hypoglycemic medications therapy. It is diagnosed
by detecting hypoglycemia mainly 2 to 3a.m. in the
morning in a patient on diabetes medications.
Signs on CT, MRI, and PET
1. Insulinoma is part of islet of Langerhans cells, a
group of tumors that can be small to the extent that
they are usually not seen by imaging techniques. In
imaging islets of Langerhans cell tumors, the
following points should be considered: (a) there are
no specifi c CT features if insulinoma is less 3 cm,
which is found in 70 % of insulinoma cases
(high-density iodinated contrast material (e.g., 400 or
350 iodine concentration ) may be needed to
distinguish the tumor from the rest of the enhanced
pancreatic parenchyma, since neuroendocrine
tumors are highly vascular tumors); (b) insulinoma
may contain calcium; and (c) angiography and portal
venous sampling can be used to localize the lesion.
Ten percent of insulinomas are malignant, and
criteria of malignancy include local invasion and/or
metastasis. To image insulinoma, the arterial phase
should be taken very early (e.g., at 18 s) to detect the
early enhancement of the tumor, typically in the tail
of the pancreas or the gastrinoma triangle . Imaging in
the regular arterial phase of 20–25 s can miss the
tumors because of their rapid washout phenomenon
(
. Fig. 10.9.1 ).
2. Pancreatic islet tumors (including insulinomas) can
be detected with high sensitivity by MRI enhanced
with mangafodipir trisodium. Mangafodipir
trisodium (Mn-DPDP) is a specifi c hepatobiliary
contrast that is taken up by the normal functioning
hepatocytes. Mn-DPDP causes also enhancement of
the normal pancreatic tissues but not the malignant
tissues. Consequently, after 15–30 min of intravenous
Mn-DPDP administration, the normal pancreatic
tissue will enhance, while malignant tissues will

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Chapter 10 · Diabetology
10
enhance in a lesser degree, causing the tumor to
appear less enhanced against an enhanced tissue
background. However, chronic pancreatitis fi brosis
and pseudotumor lesions of the pancreas may also
show low signal intensity, so interpretation with
clinical data is essential to establish the correct
diagnosis.
3. Brain MRI in children with neurological defi cits or
abnormalities due to hypoglycemia typically show
bilateral hyperintense signal intensity lesions seen on
T2W, FLAIR, and DW images in the parieto-occipital
region, known as hypoglycemia – occipital syndrome
(
. Fig. 10.9.2 ). Central pontine myelinolysis, delayed
myelination, leukomalacia, and ulegyria are also
reported to occur in diabetics and children with
congenital hyperinsulinemia.
4. Solitary fi brous tumor is detected on chest CT as a
dense lobulated mass with homogenous contrast
enhancement due to its rich vascular supply
(
. Fig. 10.9.3 ). The mass is typically attached to the
pleura. Large masses may show areas of necrosis and
inhomogeneous enhancement.
5. PET/CT scan with
18
F-fl uorodopa is used to detect the
hyperplastic islets in congenital hyperinsulinemia.
The sensitivity of
18
F-fl uorodopa PET in diagnosing
focal CHI is 92 % with specifi city of 100 %.
. Fig. 10.9.2 Axial, T2W-MR illustration that demonstrates the
MR fi ndings of patients with hypoglycemia–occipital syndrome
. Fig. 10.9.1 Coronal CT, arterial postcontrast image that
shows insulinoma detected as a highly enhanced tumor in the
body of the pancreas ( arrowheads )
. Fig. 10.9.3 Axial, postcontrast CT illustration that demonstrates
the CT fi ndings of patients with solitary fi brous tumor

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Selected References
Aliefendioglu D, etal. Long-term MRI ndings of a case with
persistent hyperinsulinemic hypoglycemia of infancy
(nesidioblastosis). Eur J Radiol Extra. 2006;60:79–84.
Bertolotto M, et al. Ultrasonography of the pancreas. 3.
Doppler imaging. Abdom Imaging. 2007;32:161–70.
Chamberlain MH, et al. Solitary brous tumor associated
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441
https://t.me/medicina_free
Infectious Diseases and Tropical
Medicine
11.1 Fever – 443
11.2 Giardiasis – 444
Diff erential Diagnoses and Related Diseases – 444
11.3 Amebiasis – 444
Intestinal Amebiasis – 445
Hepatic Amebiasis – 446
Thoracic Amebiasis – 447
Brain Amebiasis – 447
11.4 Leprosy (Hansen Disease) – 448
Skin Involvement – 448
Nerve Involvement – 448
Eye Involvement – 448
Mucosal Involvement – 449
Bone Involvement – 449
Post-therapy Leprosy – 449
1 1
11.5 Toxoplasmosis – 451
11.6 Brucellosis (Malta Fever) – 454
11.7 Neurocysticercosis – 455
11.8 Ascariasis – 458
Diff erential Diagnoses and Related Diseases – 458
11.9 Guinea Worm Disease (Dracunculiasis) – 459
11.10 Hydatid Cyst (Echinococcosis) – 461
Echinococcus granulosus Disease – 461
Grading of the Liver Lesions by E. granulosus – 461
Diff erential Diagnoses and Related Diseases – 465
Echinococcus alveolaris Disease – 465
© Springer International Publishing Switzerland 2017
J.A. Al-Tubaikh, Internal Medicine, DOI 10.1007/978-3-319-39747-4_11
Соседние файлы в папке Библиотека им академика М.И. Перельмана
