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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 )
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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.
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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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. 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
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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, etal. Imaging of urinary tract infection in the
adult. Eur Radiol. 2004;14:E168–83.
Demertzis J, etal. State of the art: imaging of renal infections.
Emerg Radiol. 2007;14:13–22.
Jung DC, etal. Renal papillary necrosis: review and compari-
son  ndings at multi-detector row CT and intravenous urography. Radiographics. 2006;26:1827–36.
Marzano MA, etal. 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, etal. 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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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
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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 2cm.
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, etal. Lipomatous hypertrophy of the interatrial sep-
tum. Int J Cardiovasc Imaging. 2005;21:659–61.
Bodas A, etal. Intestinal lipomatosis in a 10-year-old girl. Eur
J Pediatr. 2008;167:601–2.
Bogaert J, etal. Esophageal lipomatosis: another consequence
of the use of steroids. Eur Radiol. 2000;10:1390–4.
Church PA, etal. Computed tomography and ultrasound in
diagnosis of pelvic lipomatosis. Urology. 1979;14(6):631–3.
Fitoz S, etal. 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, etal. Facial in ltrative lipomatosis. Pediatr Radiol.
2006;36:1159–62.
Hauber K, etal. Encephalocraniocutaneous lipomatosis: a
case with unilateral odontomas and review of the litera­ture. Eur J Pediatr. 2003;162:589–93.
Heyer CM, etal. Lipomatous hypertrophy of the interatrial
septum: a prospective study of incidence, imaging  nd­ings, and clinical symptoms. Chest. 2003;124:2068–73.
Komagata T, etal. 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, etal. Lipomatous hypertrophy of the interatrial
septum. Int J Cardiol. 2008;130:294–5.
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Soles R, etal. MR of laryngeal and scrotal involvement in mul-
tiple symmetrical lipomatosis. Eur Radiol. 1997;7:946–8.
Türkavtan A, etal. Di use in ltrating abdominal lipomato-
sis. Eur J Radiol Extra. 2008;67:15–7.
Xanthos T, etal. Lipomatous hypertrophy of the interatrial
septum: a pathological and clinical approach. Int J Cardiol. 2007;121:4–8.
Yakabe S, etal. 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 45mg/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 <50mg/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.
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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.
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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.
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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 > 8cm 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. 10min. 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 3a.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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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, etal. 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
with hypoglycemia: an example of the Doege-Potter syn­drome. J  orac Cardiovasc Surg. 2000;119:185–7.
Das CJ, etal. MR imaging appearance of insulinoma in an
infant. Pediatr Radiol. 2007;37:581–3.
De Visschere PJL, etal. Brain injury due to persistent hyper-
insulinemic hypoglycemia of infancy. Eur J Radiol Extra. 2007;62:35–8.
Eser G, et al. Mangafodipir trisodium-enhanced magnetic
resonance imaging for evaluation of pancreatic mass and mass-like lesions. World J Gastroeneterol. 2006;12(10): 1603–6.
Hamoud AK.Mangan-enhanced MR, imaging for the detec-
tion and localization of small pancreatic tumors. Eur Radiol. 2004;14:923–5.
Hardy OT, etal. Diagnosis and localization of focal congeni-
tal hyperinsulinism by 18 F- uorodopa PET scan. J Pediatr. 2007;150:140–5.
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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