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Clinicopathological Conference
p.23A 39-Year-Old Man with Abdominal Pain,
Nausea, Vomiting and Diarrhea
M ICHAEL
JAKOBY, MD, MA, FACP
JAMES KUMAR, MD, MS, FACP
SHIVANI SHINDE, MD
Clinicopathological Conference
A 39-Year-Old Man with Abdominal Pain, Nausea, Vomiting and Diarrhea
A 39-Year-Old Man with Abdominal Pain,
Nausea, Vomiting and Diarrhea
SERIES EDITOR: MICHAEL JAKOBY, MD, MA, FACP
CO–EDITOR: JAMES KUMAR, MD, MS, FACP
CASE AUTHOR: SHIVANI SHINDE, MD
The following is an unusual case of gastrointestinal complaints from the monthly
Clinicopathological Conference (CPC) of the University of Illinois College of
Medicine. At this conference a clinical faculty member is presented with a case about
which he or she has no prior knowledge and then describes the clinical reasoning
required to reach a final diagnosis. This case was discussed November 2010.
Discussants
Chief Discussant: Robert Healy, MD
Gastroenterology: Charles Lansford, MD
Radiology: Juan Jimenez, MD
Pathology: Ike Uzoaru, MD
Case Presentation
A 39-year-old, African-American male presented to
the emergency department (ED) with abdominal pain,
nausea, vomiting and diarrhea of one-week duration.
The abdominal pain was located in the periumbilical
region, was cramping in nature and present for most
of the day, and was occasionally associated with “abdominal palpitations.” There were no aggravating or
alleviating factors. Patient reported passing one or two
nonbloody loose stools every day, and complained of
early satiety and an unintentional weight loss of twenty
pounds over the past three months. One month prior
to this presentation the patient experienced an episode
of nausea, vomiting and diarrhea that lasted three to
four days and was attributed to viral gastroenteritis.
The patient was not taking any prescription or overthe-counter medications and past medical and family
history were unremarkable. He did not drink alcohol,
smoke cigarettes or abuse illicit substances. Patient was
married and lived with his wife.
Discussion
Nausea, vomiting and abdominal pain
are common complaints of patients
presenting to the ED. Differential diagnoses are broad and include gastrointestinal, central nervous system,
metabolic, infectious and psychiatric
disorders, and medication side effects.
Careful review of the patient’s history
and detailed physical exam is needed to
exclude organic pathologies. One would
be quick to make a provisional diagnosis of viral gastroenteritis based on the
history, though the recent recurrence of
symptoms is concerning. Most importantly, weight loss raises a red flag and
demands a thorough assessment.
Case Presentation
The patient was alert and in no distress. Blood pressure
was 154/88 mmHg, pulse was 121, respiratory rate was
18 and temperature was 98°F. No scleral icterus, scleral
injection or conjunctival pallor was observed. There
were no lesions of the oropharynx and no palpable cervical lymph nodes. No goitrous thyroid enlargement
was appreciated. Cardiovascular examination confirmed tachycardia with regular rhythm and a poorly
localized systolic ejection murmur radiating across the
precordium. Lungs were clear to auscultation bilaterally. The abdomen was not distended but was tender
to deep palpation near the umbilicus. No guarding or
rebound tenderness was elicited. Bowel sounds were
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Carle Selected Papers
easily audible. No palpable abdominal organomegaly or
masses were appreciated. There were no masses on digital rectal exam, and stool was negative for occult blood.
A fine tremor was noted with arms extended, but cranial
nerves, muscle strength, sensation, gait and deep-tendon
reflexes were unremarkable. No rashes, bruises, jaundice
or hyperpigmentation were observed.
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Vol. 54, No. 2
Initial biochemistries and complete blood count results
are presented in Table 1. Notable only was the mild elevation in total serum calcium and total bilirubin. Computed tomography (CT) of the abdomen and pelvis did
not reveal any gastrointestinal pathology.
Table 1. Initial Laboratory Data
Variable
Value
Reference Range (Adults)
Hematocrit (%)
41.1
37–51
Hemoglobin (g/dl)
13.9
12–18
White-cell count (per mm3)6890
4000–11000
Differential count (%)
Neutrophils
51
50–70
Band forms
0
0–10
Lymphocytes
34
20–45
Monocytes
14
0–10
Eosinophils
1
0–5
Basophils
0
0–2
Metamyelocytes
0
0
Platelet count (per mm3)
Calcium (mg/dl)
10.6
8.5–10.5
Glucose (mg/dl)
90
60–99
BUN (mg/dl)
10
6–20
Creatinine (mg/dl)
0.95
0.50–1.20
TP (g/dl)
6.4
6.0–8.1
Albumin (g/dl)
3.6
3.2–5.5
Total Bilirubin (mg/dl)
1.2
0.2–1.0
Aspartate aminotransferase (IU/liter)
32
12–50
Alanine aminotransferase (IU/liter)
55
10–75
Alkaline phosphatase (IU/liter)
116
42–121
Sodium (mmol/liter)
139
135–145
Potassium (mmol/liter)
3.8
3.6–5.0
Chloride (mmol/liter)
104
101–111
CO2 (mmol/liter)
26.9
21–31
Amylase (U/liter)
66
25–125
Lipase (U/liter)
24
22–51
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Clinicopathological Conference
A 39-Year-Old Man with Abdominal Pain, Nausea, Vomiting and Diarrhea
Discussion
Discussion
Hypercalcemia in this setting might be blamed on dehydration secondary to nausea and vomiting; however, the overall
picture demands a detailed workup. The systolic murmur
would also need to be further evaluated; it is unclear if this
was a new finding. The absence of significant anatomic lesions on CT of the abdomen is reassuring though additional
studies, namely endoscopic evaluation, of the gastrointestinal tract are warranted.
The suppressed PTH with hypercalcemia rules out primary hyperparathyroidism which is the most common cause
of hypercalcemia in the ambulatory patient. This, however,
opens the likelihood of other causes of hypercalcemia, most
importantly malignancy. The extrinsic compression of
esophagus, a finding difficult to identify during a routine
EGD, suggests the presence of a mediastinal mass. Screening for hyperthyroidism is also indicated as the patient has
weight loss, gastrointestinal symptoms and extrinsic esophageal compression.
Case Presentation
The patient received supportive care for his symptoms and was discharged from the ED with significant
improvement of symptoms. He underwent esophagogastroduodenoscopy (EGD) that revealed extrinsic
compression in the area of proximal esophagus and
nonspecific gastritis. Gastric mucosal biopsies showed
superficial and patchy mild chronic inflammation. No
acute inflammation or cancerous cells were identified.
Additional workup of the patient’s esophageal findings
was planned, though his abdominal symptoms resolved spontaneously. Evaluation for causes of hypercalcemia revealed a suppressed serum intact parathyroid hormone (PTH) level (3 pg/mL, reference range
12–88). Simultaneously measured total serum calcium
was 10.6 mg/dL. A follow-up calcium level was also increased to 11 mg/dL.
Case Presentation
The patient experienced recurrence of abdominal
pain, nausea and vomiting and unintentionally lost 40
pounds in 6 months. Additionally, he complained of
heat intolerance, palpitations, anxiety, insomnia and
diminished exertional capacity. A CT of the chest (Figure 1) revealed diffuse, asymmetrical (left more than
right) and significant enlargement of the thyroid gland
as well as an enlarged thymus. Ultrasound of the neck
revealed an enlarged inhomogeneous gland with a
generalized increase in vascularity. Thyroid stimulating hormone (TSH) was 0.01 mIU/ml (0.4–4.00), free
T3 >2000 pg/dL (230–420), and free T4 >5.50 ng/dL
(0.61–1.2). Thyroid stimulating immunoglobulin (TSI)
was elevated at 244 (125 or less % baseline).
Figure 1. Contrast enhanced CT scan of the chest done after appropriate anti-thyroid therapy reveals a
grossly enlarged thyroid gland deviating the trachea and vascular structures of the neck and compressing
the esophagus.
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Carle Selected Papers
2011
Vol. 54, No. 2
Graves’ thyrotoxicosis was diagnosed, and the patient
was started on therapy with metoprolol and methimazole. Later, he developed exophthalmos and progressively worsening vision (blurring and double vision)
which prompted thyroidectomy. Surgical pathology of
the thyroid gland (Figure 2) was consistent with findings of Graves’ disease. The patient was started on Lthyroxine for management of post-surgical hypothyroidism. Graves’ ophthalmopathy improved after several
external beam radiation treatments.
thyrotoxicosis and manifests as increased
direct bilirubin, transaminases (ALT and
AST), and alkaline phosphatase.9,10 Isolated abdominal symptoms are rare as the
presenting complaints in cases of hyperthyroidism and the diagnosis may be delayed in the absence of other more typical
symptoms, such as heat intolerance, palpitations or tremor.
Conclusion
Excess thyroid hormone increases bone resorption, leading to loss of both cortical and trabecular bone, though
loss of cortical bone density tends to exceed loss of trabecular bone volume.11 Increased bone turnover may
lead to increases in serum alkaline phosphatase level,
mild hypercalcemia and suppression of parathyroid hormone secretion. Bone turnover and circulating calcium
levels fall with successful treatment of hyperthyroidism.
Gastrointestinal symptoms in thyrotoxic
patients include anorexia, nausea, vomiting, weight loss and diarrhea.1,2 Excess
thyroid hormone may decrease gastric
emptying and trigger emesis centers in
the hypothalamus.3,4 Thyrotoxicosis also
increases the risks of gastritis, achlorhydria and peptic ulcer disease.5,6 Contrary
to popular belief, both diarrhea and constipation are observed in hyperthyroid patients.7,8 Therapy with beta-blockers usually improves symptoms within 24 hours.
Hepatic dysfunction is also common in
summary
This case demonstrates an uncommon presentation of
thyrotoxicosis. Screening for thyroid disorders should
be considered when patients have prolonged and unexplained gastrointestinal symptoms. Recognizing the
unusual clinical manifestations of hyperthyroidism may
result in timely diagnosis and treatment.
Figure 2. Low (A), medium (B) and high power (C) magnification of H&E stains of the excised thyroid
gland shows tall hyperplastic columnar epithelium. There are follicles with decreased colloid. Some colloids
demonstrate absorption droplets (scallops).
A
B
C
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Clinicopathological Conference
A 39-Year-Old Man with Abdominal Pain, Nausea, Vomiting and Diarrhea
Michael Jakoby, IV, MD, MA is an associate professor of
medicine and chief of the division of endocrinology at the
Southern Illinois University School of Medicine at Springfield, and the medical director of the Center for Diabetes and
Metabolic Health.
James Kumar, MD, MS, FACP is a hospitalist at Carle
Foundation Hospital, and the associate residency program
director at the University of Illinois College of Medicine at
Urbana-Champaign.
Shivani Shinde, MD is a hospitalist at Carle Foundation
Hospital, Urbana, IL.
References
1.Saeed-uz-Zafar M. The thyroid. In: Berk JE, ed. Bockus
Gastroenterology. Philadelphia, Pennsylvania: WB
Saunders;1985:4624-8.
2.Spaulding SW, Lippes H. Hyperthyroidism. Causes,
clinical features and diagnosis. Med Clin North Am
1985;69:937-51.
3.Parkin AJ, Nisbet AP, Bishop N. Vomiting due to
gastric stasis as the presenting feature in thyrotoxicosis.
Postgrad Med J 1981;57:405.
4.Rosenthal FD, Jones C, Lewis SI. Thyrotoxic vomiting.
Br Med J 1976;2:209-11.
5.Siurala H, Julkunen H, Lamberg BA. Gastrointestinal
tract in hyperthyroidism before and after treatment.
Scand J Gastroenterol 1966;1:79-85.
6.Garbat AL. The simultaneous occurrence of active
peptic ulcer and active hyperthyroidism. Mt Sinai J Med
1995;17:787-92.
7.Shirer JW. Hypermotility of the gastrointestinal tract in
hyperthyroidism. Am J Med Sci 1933;186:73-8.
8.Scarf M. Gastrointestinal manifestations of
hyperthyroidism. J Lab Clin Med 1936;21:1253-8.
9.Dooner HP, Parada J, Aliaga C. The liver in
thyrotoxicosis. Arch Intern Med 1967;120:25-32.
10.MacLagan NF, Rundle FF, Collard HB, Mills FH. Liver
function in thyrotoxicosis. Q J Med 1940;9:215-28.
11.Ross DS. Hyperthyroidism, thyroid hormone therapy
and bone. Thyroid 1994;4:319-26.
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