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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 ~ p.23 ~ 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. 2011 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 ~ p.24 ~ 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. ~ p.25 ~ 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 ~ p.26 ~ 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. ~ p.27 ~