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The Journal of Clinical Endocrinology & Metabolism 90(1):575580

Copyright 2005 by The Endocrine Society
doi: 10.1210/jc.2004-0825

CLINICAL CASE SEMINAR

Giant Insulinoma: Case Report and Review of
the Literature
Elizabeth A. Mittendorf, Yao-Chang Liu, and Christopher R. McHenry
Department of Surgery, Uniformed Services University of the Health Sciences (E.A.M.), Bethesda, Maryland 20762; and
Departments of Pathology (Y.-C.L.) and Surgery (C.R.M.), MetroHealth Medical Center, Case Western Reserve University
School of Medicine, Cleveland, Ohio 44109
An insulinoma is a rare pancreatic endocrine tumor that is
typically sporadic, solitary, and less than 2 cm in diameter.
Fewer than 5% of insulinomas are larger than 3 cm. Ninety
percent or more of all insulinomas are benign. Larger tumors
are more likely to be malignant. We report a case of a giant
pedunculated insulinoma, measuring 9 cm in diameter and
weighing 100 g, with amyloid deposits accounting for 70% of
the tumor volume. At the time of operation, no local invasion

or metastatic disease was identified. On pathological evaluation, the tumor was classified as an insulinoma of uncertain
biological behavior. In addition to describing the clinical presentation and operative findings, criteria for determining malignancy are outlined, a detailed pathological description is
presented, and the 2000 World Health Organization Classification for Pancreatic Endocrine Neoplasms is reviewed.
(J Clin Endocrinol Metab 90: 575580, 2005)

ANCREATIC ENDOCRINE TUMORS are rare lesions,

with a reported incidence of four cases per 1 million
patient-yr (1). Of these lesions, insulinomas are the most
common. The majority of patients diagnosed with an insulinoma are between 30 and 60 yr of age, with women accounting for 59% (2, 3). Most insulinomas are sporadic in
origin. In two series, 7.6% and 12% of patients with insulinoma had multiple endocrine neoplasia type I syndrome (1,
4) Insulinomas are more likely to be multiple in patients with
multiple endocrine neoplasia type I (1, 4).
Patients with insulinoma have symptoms of hypoglycemia resulting from neuroglycopenia and increased catecholamine release. Neuroglycopenic symptoms are most
common, including anxiety, dizziness, lightheadedness,
personality changes, unusual behavior, confusion, incoherence, blurred vision, seizures, and coma. Sympathoadrenal signs and symptoms, such as palpitations, tremulousness, diaphoresis, and tachycardia, may also be
present and are due to catecholamine release in response
to low serum glucose levels (5). Surgical excision is the
treatment of choice and is curative in most cases. At the
time of surgery, the majority of these lesions are found to
be solitary, equally distributed throughout the pancreas,
and less than 2 cm in diameter. In a review of the experience at University of Michigan, Pasieka et al. (6) reported
that 24% were less than 1 cm, 42% were 12 cm, 30% were
23 cm, and only 4% larger than 3 cm. Those that are larger
than 3 cm are more likely to be malignant, with local

invasion or metastases to the peripancreatic lymph nodes

and liver. We report a patient with a 9-cm insulinoma
comprised of a disproportionate amount of amyloid without evidence of local invasion or metastatic disease. The
case review was approved by the institutional review
board at MetroHealth Medical Center.
Case Report

A 65-yr-old woman was seen in the emergency department with the acute onset of lightheadedness, chills, diaphoresis, palpitations, and shakiness. A serum glucose level
determined in the Emergency Department was 28 mg/dl
(1.55 mmol/liter; normal range, 68 110 mg/dl; 3.7 6.1
mmol/liter). She was given 10% dextrose iv, and her symptoms resolved. The patient reported that she had experienced
similar symptoms, but of lesser severity, for approximately
3-yr duration. She typically experienced the symptoms from
1000 1300 h during the day, although she was occasionally
awakened at night with symptoms. She also reported a recent
20-lb weight gain. She denied any galactorrhea or visual
changes. She was discharged from the emergency department, and her work-up was completed as an out-patient.
Her past medical history was significant for osteoporosis
and hypercholesterolemia, for which she was taking Fosamax and Lipitor. She also reported intermittent hypertension. She had previously undergone a total abdominal hysterectomy and bilateral salpingooophorectomy for a benign
ovarian mass and a lumpectomy and radiation therapy for
breast cancer. Her family history was remarkable for a
daughter with hypothyroidism and a maternal grandmother
who had diabetes mellitus. Her father died at age 45 yr of
Brights disease, and her mother died at age 43 yr of a cerebral
hemorrhage. There was no family history of hyperparathyroidism, ulcer disease, or hypoglycemia.

First Published Online November 2, 2004

Abbreviation: HPF, High powered field.
JCEM is published monthly by The Endocrine Society (http://www.
endo-society.org), the foremost professional society serving the endocrine community.

575

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Mittendorf et al. Giant Insulinoma

TABLE 1. Laboratory studies

Glucose [mg/dl (mol/liter)]

Insulin (pmol/liter)
C Peptide (pmol/liter)
Proinsulin (pmol/liter)
24-h urine for sulfonylureas
Antiinsulin antibodies

12-h fast

18-h fast

20-h fast

70 (3.9)
288.6
1660
36.2
Negative
Negative

47 (2.6)
402.6
1820

42 (2.3)
342.6
1260

Threshold levels for diagnosis of hyperinsulinism in patients with

hypoglycemia of 45 mg/dl or less recommended by Service (20) are:
insulin (by immunoradiometric assay), 36 pmol/liter; C peptide,
200 pmol/liter; and proinsulin, 5 pmol/liter.

The physical examination was unremarkable. She was a well

developed and well nourished woman, with no nipple discharge and a normal visual field exam. Her abdomen was soft
and nontender, with no palpable masses or organomegaly.
The results of her subsequent laboratory evaluation are
detailed in Table 1. Of note, the patient was observed in an
office setting after cessation of any oral intake at 2000 h the
night before the office visit. The first, second, and third glucose, insulin, and C peptide levels represent values obtained
after 12, 18, and 20 h of fasting. A diagnosis of insulinoma
was made, and a computed tomogram of the abdomen was
obtained. Spiral axial 1-mm collimated images were obtained
through the pancreas in early arterial phase after a 100-cc
injection of iv contrast. Oral contrast material was also administered. A large, heterogeneous enhancing mass associated with the distal tail of the pancreas (Fig. 1) was identified.
There was no associated lymphadenopathy. The liver appeared normal.
At operation, a 9 6.5 4-cm pedunculated tumor,
weighing 100 g, was resected from the tail of the pancreas
(Fig. 2). There was no evidence of gross invasion, abnormal
lymph nodes, or liver metastases. Pathological evaluation
revealed a well differentiated insulinoma with extensive

FIG. 1. Computed tomographic image

of the abdomen, demonstrating a large
heterogeneous enhancing insulinoma
arising from the tail of the pancreas.

amyloid deposition occupying approximately 70% of the

tumor volume (Fig. 3A). The amyloid was confirmed by a
Congo Red stain as well as by demonstration of apple green
birefringence under polarized light. The protein component
of the amyloid was islet amyloid polypeptide, otherwise
known as amylin. The tumor had more than 2% Ki-67-positive cells/10 high powered fields (HPF; Fig. 3B), and less
than one mitosis per 10 HPF. There was no local or microscopic vascular invasion. On electron microscopy, the amyloid deposits consisted of a disordered meshwork of nonbranching rigid fibrils (Fig. 3C). Immunohistochemical
studies using an immunoperoxidase method revealed that
nearly all of the neoplastic cells were strongly positive for the
neuroendocrine markers synaptophysin (Fig. 4A) and chromogranin. In addition, 50% of the tumor cells were positive
for insulin (Fig. 4B), 30% for pancreatic polypeptide (Fig. 4C),
15% for glucagon, and 5% for somatostatin. The tumor was
classified as an insulinoma of uncertain biological behavior
based on the 2000 World Health Organization Classification
for Pancreatic Endocrine Neoplasms (Table 2).
The patient reported complete resolution of her symptoms. Her postoperative course was complicated by a low
output pancreatic fistula, which closed 1 wk after surgery.
She developed hyperglycemia in the postoperative period,
with serum glucose levels as high as 303 mg/dl (16.8 mmol/
liter; normal range, 3.7 6.1 mmol/liter). At her 6-wk followup, her fasting blood glucose and insulin levels were 120
mg/dl (6.66 mmol/liter) and 95.4 pmol/liter (normal range,
6 144 pmol/liter), respectively. A routine follow-up computed tomogram of the abdomen was obtained 6 months
postoperatively and showed no evidence of recurrent disease.
Discussion

We report a case of a giant insulinoma measuring 9 cm and

weighing 100 g. It was pedunculated and attached to the tail

Mittendorf et al. Giant Insulinoma

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577

FIG. 2. Excised insulinoma, measuring 9.0 6.5 4.0 cm.

of the pancreas, rather than within the gland. The tumor

expressed multiple hormones, including glucagon, pancreatic polypeptide, and somatostatin, in addition to insulin, a

phenomenon that is often reported with pancreatic endocrine neoplasms (79). There was no evidence of local invasion or metastases to the regional lymph nodes or liver. The

FIG. 3. Microscopic features of the excised insulinoma. A, Tumor cells in a broad anastomosing trabecular pattern within a background of
abundant pink homogeneous amyloid (400 magnification); B, immunoperoxidase stain for Ki-67 cells, demonstrating three tumor cells with
positive nuclear staining pattern (200 magnification); C, electron micrograph, demonstrating rigid, nonbranching filaments of amyloid
measuring 710 mm in diameter.

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Mittendorf et al. Giant Insulinoma

FIG. 4. Histological sections of the insulinoma with immunohistochemical

demonstration of almost all the tumor
cells with immunoreactivity to the neuroendocrine marker synaptophysin (A),
50% of the tumor cells with immunoreactivity to insulin antibody (B), 30% of
the tumor cells with immunoreactivity
to pancreatic polypeptide antibody (C),
and none of the tumor cells with immunoreactivity for calcitonin (D; control).

majority of patients with insulinomas have lesions that are

12 cm in size, with 96% being less than 3 cm (6). The mean
tumor size of insulinomas found in three of the largest reported series was 1.5 cm, with a range of 0.17.0 cm (3, 10,
11).
The large size and weight of the tumor was related to the
unusually extensive proportion of amyloid. Amyloid deposits have been demonstrated in more than 50% of insulinomas,
but not to the extent present in our patients tumor (12, 13).
The major component of the amyloid of an insulinoma is a
37-amino acid polypeptide known as islet amyloid polypeptide or amylin. Islet amyloid polypeptide has been observed
within the tumor cells and the stroma surrounding the islet
cells of patients with an insulinoma as well as in the stroma
surrounding the islet cells of patients with insulinomas and
patients with type II diabetes mellitus (12, 13). Overexpression of islet amyloid polypeptide, with aberrant processing
and secretion by abnormal -cells of the insulinoma, is postulated to be the cause of amyloidogenesis (13).

Tumors larger than 3 cm raise concern for malignancy. The

diagnosis of malignancy is based on the presence of metastases to the liver or regional lymph nodes or gross evidence
of local invasion. In a review of malignant insulinomas, Danforth et al. (14) identified 62 cases: 17 from the NIH and 45
others reported in the literature. Thorough pathological data
were available for 14 of the patients treated at the NIH. The
average tumor size was 4.7 0.6 cm. There were 11 lesions
more than 3 cm in diameter, including two that were 7.0 cm
and one that was 9.0 cm. Data regarding tumor size were
available for 25 of the 45 cases found in their literature review, and the average size in this group was 7.1 0.8 cm (14).
Additional review of the world literature identifies only
three reported cases of insulinomas more than 9 cm in size,
all of which were benign by traditional criteria (1517).
In addition to the large tumor size, more than 2% of the tumor
cells/HPF were Ki-67-positive cells. Measurement of the percentage of Ki-67 cells provides an assessment of the tumors
proliferative index. The patients tumor was classified as an

TABLE 2. Clinicopathological classification of endocrine tumors of the pancreas

1. Well-differentiated endocrine tumor
A. Benign behavior: confined to the pancreas, nonangioinvasive, 2 cm in size,a 2 mitoses, and 2% Ki-67-positive cells/HPF
a) Functioning: insulinoma
b) Nonfunctioning
B. Uncertain behavior: confined to the pancreas, 2 cm in size or angioinvasive, 2 mitoses and 2% Ki-67-positive cells/HPF
a) Functioning: gastrinoma, insulinoma, VIPoma, glucagonoma, somatostatinoma or inappropriate syndromeb
b) Nonfunctioning
2. Well-differentiated endocrine carcinoma
Low grade malignancy with gross local invasion and/or metastases
a) Functioning: gastrinoma, insulinoma, glucagonoma, VIPoma, somatostatinoma, or inappropriate syndrome
b) Nonfunctioning
3. Poorly differentiated endocrine carcinoma
High grade malignant (small to intermediate cell) carcinoma
VIPoma, Vasoactive intestinal peptide-secreting tumor.
2 cm in size implies near to 100% probability of benign behavior; 3 cm implies 90% probability of benign behavior.
b
Inappropriate hormone syndromes, such as Cushings syndrome due to ectopic ACTH production, acromegaly or gigantism, and hypercalcemia.
a

Mittendorf et al. Giant Insulinoma

insulinoma of uncertain biological behavior according to the

2000 World Health Organization Classification for Pancreatic
Endocrine Neoplasms. This new clinicopathological classification of neuroendocrine tumors was adopted because it combines an assessment of the clinical syndrome as well as tumor
morphology.
In devising this new classification system, it was recognized that classic histopathological criteria, such as atypia,
were of limited value in predicting the behavior of neuroendocrine tumors of the pancreas. Several new histopathological criteria were considered: 1) tumor size; 2) local invasion;
3) structural atypia with prevalence of broad solid areas; 4)
necrosis; 5) cellular atypia with high nuclear cytoplasmic
ratio, irregular distribution of chromatin, and prominent nucleoli; 6) more than two mitoses per 10 HPF; 7) more than 2%
Ki-67-positive tumor cells; 8) perineural or angioinvasion; 9)
cellular dedifferentiation, as assessed by loss of chromogranin A immunoreactivity; and 10) nuclear p53 protein accumulation detected by immunohistochemistry (18). Our patients tumor displayed the favorable finding of fewer than
one mitosis per 10 HPF; however, the finding of more than
2% Ki-67-positive tumor cells indicates an increased risk of
malignant behavior; therefore, the tumor was classified as an
insulinoma of uncertain biological behavior. Despite new
histopathological criteria, there are no conclusive histological
criteria or histochemical markers that reliably predict biological behavior, and the definitive diagnosis of malignant
insulinoma is still based on the presence of metastases or
gross evidence of local invasion (2).
Our patient displayed several characteristics typical for
insulinomas. She admitted to a 3-yr history of symptoms
similar to those that prompted her presentation to the emergency department. It is not uncommon for patients to have
symptoms for several months to years before diagnosis, in
part because the diagnosis is not entertained by clinicians.
This is presumed to be due to the rarity of pancreatic endocrine tumors.
In 1935, Whipple and Franz (19) described a triad of clinical findings that were unique to patients with insulinoma:
symptoms of hypoglycemia, a plasma glucose level of 45
mg/dl (2.5 mmol/liter) or less when symptoms of hypoglycemia occurred, and relief of symptoms with the administration of glucose. More recently, Service (20) recommended
the following biochemical criteria to establish a diagnosis of
insulinoma in the absence of renal insufficiency: an insulin
level of 36 pmol/liter or more as measured by RIA or of 18
pmol/liter or more as measured by an immunochemiluminescence assay, a C peptide level of 200 pmol/liter or more,
and a proinsulin level of 5 pmol/liter or more in a patient
with a serum glucose level of 45 mg/dl (2.5 mmol/liter) or
less, a negative plasma sulfonylurea screen (including repaglinide), and negative insulin antibodies. Vezzosi et al. (21),
using a modern insulin-specific immunoradiometric assay,
have documented insulin levels below 18 pmol/liter in patients with symptomatic hypoglycemia of 45 mg/dl or less
from small insulinomas. They concluded that insulin levels
are dependent on the assay employed and its cross-reactivity
with proinsulin, and they emphasized that concomitant measurement of C peptide levels is mandatory for establishing a

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579

diagnosis of insulinoma (21). In most patients with insulinoma, a diagnosis is established by a supervised fast during
which simultaneous measurements of glucose, insulin, and
C peptide are obtained. On presentation, our patient had a
serum glucose level of 28 mg/dl (1.55 mmol/liter) and typical symptoms of hypoglycemia that were relieved by iv
glucose. Subsequent biochemical indices obtained during a
20-h fast confirmed the diagnosis of insulinoma.
The imaging modalities used for localization of an insulinoma remain an area of debate. Clinicians who do not
routinely perform preoperative localization cite studies that
document a 30 35% failure rate with noninvasive imaging
studies and report that those tumors that are localized preoperatively are easily identified by palpation or intraoperative ultrasound (22). Intraoperative palpation and ultrasound are the gold standards for localizing an insulinoma,
with a reported success rate of 96 100%.
It is our practice to routinely perform a spiral computed
tomographic scan of the abdomen in patients with functional
pancreatic endocrine tumors. Although reported sensitivities
are suboptimal, ranging from 20 40%, valuable information
concerning the primary tumor location, the presence of metastatic disease, and potential resectability may be obtained (6,
10, 23). If liver metastases are identified, plans are made for
resection. In general, a wedge resection of hepatic metastases
is performed. Hepatic resection for metastatic neuroendocrine malignancies has been found to be safe and effective for
palliation (24). Because of the rarity of insulinomas and our
relative inexperience with intraoperative ultrasound, we
would perform hepatic venous insulin sampling after administration of intraarterial calcium to help localize an occult
insulinoma before proceeding with laparotomy. This technique is very sensitive in localizing insulinomas, which are
typically highly vascular, and has been reported to be positive in up to 75% of cases (25). Some centers use preoperative
endoscopic ultrasound, which has reported accuracy rates of
60 90% (26). Lesions in the tail may be missed using endoscopic ultrasound; however, these lesions are usually easily
identified intraoperatively (27). Approximately 40% of all
insulinomas are not localized preoperatively, and between
3% and 10% remain occult even after intraoperative palpation and the use of intraoperative ultrasound (3, 4).
In conclusion, this case report emphasizes some unusual
features of an insulinoma of which a clinician should be aware,
including an extremely large tumor size in the absence of definite features of malignancy; the inordinate deposition of amyloid, which accounted for 70% of the tumor volume; and the
pedunculated nature of the tumor, which arose from the surface
of the pancreas rather than from within the parenchyma. The
goal of treatment of a patient with an insulinoma is to identify
and excise the primary tumor and, when possible, all metastatic
disease. Follow-up computed tomographic scanning of the abdomen is recommended for insulinomas of uncertain behavior
to evaluate subsequent development of recurrent or metastatic
disease. In the absence of neuroglycopenic symptoms, it is our
approach to obtain a follow-up computed tomogram of the
abdomen at 6 and then 12 months. Thereafter, computed tomography is performed only if patients become symptomatic.

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J Clin Endocrinol Metab, January 2005, 90(1):575580

Acknowledgments
Received May 3, 2004. Accepted October 22, 2004.
Address all correspondence and requests for reprints to: Dr. Christopher R. McHenry, Department of Surgery, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, Ohio 44109. E-mail: cmchenry@
metrohealth.org.

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JCEM is published monthly by The Endocrine Society (http://www.endo-society.org), the foremost professional society serving the
endocrine community.