Leukocytosis, specifically granulocytosis in malignancy is a common finding with various etiologies. Graulocytosis associated with esophageal cancer has not commonly been reported in case reports in the United States. Furthermore, granulocyte colony stimulating factor (G-CSF) producing tumors have been associated with a variety of cancers. However, G-CSF producing esophageal tumors are rare. The diagnosis is established through serum G-CSF levels and immunohistochemistry staining of tumor cells. Here, we report a case of a 72-year-old woman with persistent granulocytosis leading to the diagnosis of esophageal squamous cell carcinoma (ESCC). Although, our case did not report serum G-CSF levels, we strongly suspect it to be the underlying etiology in our case. Additionally, through our missed opportunity, we hope to emphasize and increase awareness of G-CSF producing ESCC.
INTRODUCTION:
Proton pump inhibitors (PPIs) are used to suppress acid production and to promote hemostasis, which significantly reduces the risk of rebleeding in upper gastrointestinal bleeding [1]. Accumulating evidence indicates an association between PPIs and thrombocytopenia in patients treated for upper gastrointestinal bleeds [2-4].
CASE DESCRIPTION/METHODS:
A 38-year-old male with no significant past medical history presented to the hospital complaining of coffee ground emesis, hematochezia, dark stools and three episodes of syncope in the setting of daily naproxen use for one month. Vital signs revealed orthostasis without tachycardia or hypotension. Physical exam revealed a soft, non-tender, non-distended, abdomen with normoactive bowel sounds. Rectal exam was positive for melena but negative for hemorrhoids or any palpable masses. Initial laboratory workup was significant for a hemoglobin of 7.8, platelet count of 163, and BUN of 27. Intravenous (IV) PPI was administered for management of suspected bleeding PUD. The patient received packed red blood cells (PRBCs) with appropriate response to transfusion. Upper endoscopy revealed a pre-pyloric non-bleeding ulcer that was successfully treated. A significant drop in platelet count was noted on hospital day four which continued to decrease from 163 to 107. PPI route of administration was changed from IV to oral, resulting in an increase in platelet count to 116 by hospital day 7.
DISCUSSION:
PPIs are widely used for the treatment of PUD, GERD, Barrett esophagus, esophagitis, and gastritis. As the main medication used in the treatment of upper gastrointestinal bleeding, it is crucial to understand the effect of PPI therapy on platelets. Literature review suggests an association between thrombocytopenia and the use of PPIs [2-4]. However, further studies are needed to establish a direct association between PPIs and thrombocytopenia. In our case, thrombocytopenia was noted on hospital day 3 of PPI infusion. Route of administration of PPI was changed from IV to oral and thrombocytopenia improved steadily. Although the exact mechanism linking PPI therapy to thrombocytopenia remains unknown, it is important to be aware of this possibility. Close monitoring of platelet count is recommended upon initiation of PPI therapy.
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