A 35-year-old Hispanic female was admitted for worsening upper abdominal pain, nausea, and vomiting. She had a past medical history of heartburn which was being treated with PPI. She was initially seen in the emergency department for worsening epigastric abdominal pain and was discharged home on daily omeprazole. She returned to her primary care clinic 2 months later complaining of similar symptoms while being on omeprazole. Since omeprazole was not effective, she was switched to esomeprazole. Two months later, she visited her home country of El Salvador and was evaluated for abdominal pain. Due to her persistent symptoms, cholecystectomy was performed, without much relief of her symptoms. Patient reported that she was unable to take the initially prescribed esomeprazole secondary to financial issues and was not on any acid-suppressing medications in the previous 2 months. Upper endoscopy was then performed and it showed multiple gastric ulcers. She was then started on pantoprazole. After returning to the United States, she continued to have pain and started taking nonsteroidal anti-inflammatory drugs (NSAIDs) for relief. Subsequently, she visited her primary care office with worsening of her pain associated with nausea and vomiting. During this clinic visit, she was switched to dexlansoprazole and was asked to come to the emergency department if she continued to have symptoms. She returned to the emergency department the next day for further evaluation of her worsening symptoms. On initial evaluation in the emergency department, she was afebrile and had stable hemodynamics. She endorsed severe abdominal pain and a 30-pound weight loss over the last year, but denied any hematemesis, melena, or hematochezia. Laboratory evaluation revealed white blood cell count of 26.5 x 103/mm3, hemoglobin 13.8 g/dl, and platelet count of 116 x 103/mm3. On review of laboratory data, patient's last platelet count checked 6 months priorly was normal (264 x 103/mm3) and had been obtained before the patient was started on a PPI for the first time. No other laboratory tests had been obtained until this recent emergency department visit. Therefore, the effect of PPI on the platelet count for the next 6 months after initiation of therapy was not available to us. Chemistry panel, liver function, urinalysis, and blood/urine cultures were negative. CT imaging of the abdomen and pelvis showed diffuse steatosis but was otherwise normal.
Gastroenterology was consulted and due to refractory abdominal pain, weight loss, and NSAID use, an upper endoscope was recommended. Additionally, intravenous esomeprazole twice daily was started. Her platelet count continued to drop, falling to 72 x 103/mm3 the next day and to 12 x 103/mm3 the day after. Hematology was consulted for the rapid drop in platelet count and the etiology was thought to be secondary to drug-induced thrombocytopenia, infection, or idiopathic thrombocytopenic purpura. Of note, the patient did not have any history of bleeding or clotting disorders. Additionally, there was no evidence of hemolysis on the peripheral blood smear and the patient was not coagulopathic. On review of medications, since there were no other drugs (except for one prophylactic dose of heparin) that could be attributed to thrombocytopenia, it was recommended to hold the PPI. The PPI was then stopped, and platelet count recovered to 99 x 103/mm3 within two days. Upper endoscope performed at that time revealed nonspecific gastritis. Biopsies were found to be negative for Helicobacter pylori infection. Due to the spontaneously improved platelet count, antibodies to heparin-platelet factor 4 complex were not checked to rule out heparin-induced thrombocytopenia. Since our patient's platelet count normalized after stopping PPI, this current episode of thrombocytopenia was deemed likely secondary to PPI use.
Our patient was subsequently discharged home, but continued to have persistent epigastric pain. She tried a H2 (histamine 2) receptor antagonist with minimal symptom relief. She was next seen in the Gastroenterology Clinic. At this time, the platelet count was 135 x 103/mm3. During this visit, the question of whether patient's thrombocytopenia was truly related to PPI use was revisited, given that heparin-induced thrombocytopenia was not ruled out. Since a PPI was warranted due to her persistent symptoms, the decision was made to restart dexlansoprazole with close follow-up. She ultimately got readmitted to the hospital 7 days later for persistent epigastric pain (while on PPI). This time the platelet count was found to have decreased further to 43 x 103/mm3. The platelet count continued to drop, similar to her prior admission while on PPI, with the lowest count being 10 x 103/mm3. PPI was held because of prior concern for PPI-induced thrombocytopenia. On this admission, our patient did not receive any heparin products and peripheral blood smear was not consistent with hemolysis. She did not receive any medications known to cause thrombocytopenia. Platelet count improved to 50 x 103/mm3 while off PPI and she was discharged home. Patient's symptoms improved on H2 antagonist, sucralfate, and pain control with morphine. On this admission, PPIs were listed as a drug allergy and documented in the patient's medical record. She was seen in the Gastroenterology Clinic after hospital discharge and it was noted that her symptoms were partially controlled on H2 antagonist, sucralfate, and scopolamine (which she received from her home country for control of nausea). Platelet count ultimately improved to 415 x 103/mm3. A complete pictorial description of our patient's platelet count is shown in Figure 1.