Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Common presentations of gastrointestinal bleeding include hematemesis, melena, and history of dizziness, fatigue, or syncope; yet, bleeds may present in many uncommon ways. This review discusses two cases of gastrointestinal bleeds (GIBs) in middle-aged female patients who presented with anemia and recurrent unexplained GIBs. Both patients were misdiagnosed for several years before the cause of their bleeding was established. Dieulafoy lesion is said to be rare, although its precise incidence is difficult to establish due to its anatomically inaccessible location, small size, and lack of symptoms prior to presentation. This condition can result in gastrointestinal hemorrhage and quickly pose life-threatening complications. Gastrointestinal stromal tumors (GISTs) are likewise difficult to diagnose due to their location in the submucosa and lack of good diagnostic tools. Depending on tumor size, location, and spread, GISTs can have a poor prognosis even with early intervention. By presenting the two cases, this review aims to bring attention to Dieulafoy lesion and GIST as arguably not-so-rare but potentially fatal sources of GIBs. Especially troublesome is the uncommon complication of GIST to perforate and the elusive nature of Dieulafoy lesions that require diligent evaluation. For these reasons, both should be considered in the differential diagnosis in patients with recurrent unexplained GIBs and anemia.
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PMID:Introducing GIST and Dieulafoy - Think of Them in GI Bleeding and Anemia. 3198 5

A 17-year-old boy presented with fatigue, hypoxia, palpitations, and anemia (hemoglobin 3.5 g/dL). The search for the etiology of the bleeding began with a Meckel scan. A photopenic region in the gastric body and a region of abnormal tracer uptake in the right midabdomen were unexpected findings. Further investigation with ultrasound and computed tomography revealed a gastric mass, which proved to be a gastrointestinal stromal tumor at pathology. The right-sided tracer uptake resulted from stasis in the collecting system of a malpositioned right kidney, a cause of false uptake in a Meckel scan.
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PMID:Gastric Gastrointestinal Stromal Tumor Incidentally Detected With Meckel Scintigraphy. 3214 88

Positron emission tomography (PET) using 2-deoxy-2-[18 F]fluoro-D-glucose ([18 F]FDG), a marker of energy metabolism and cell proliferation, is routinely used in the clinic to assess patient response to chemotherapy and to monitor tumor growth. Treatment with some tyrosine kinase inhibitors (TKIs) causes changes in blood glucose levels in both non-diabetic and diabetic patients. We evaluated the interaction of several classes of TKIs with human glucose transporter-1 (hGLUT-1) in FaDu and GIST-1 cells by measuring [3 H]2-deoxy-D-glucose ([3 H]2-DG) and [3 H]FDG uptake. Uptake of both was inhibited to varying extents by the TKIs, and representative TKIs from each class showed competitive inhibition of [3 H]2-DG uptake. In GIST-1 cells, [3 H]FDG uptake inhibition by temsirolimus and nilotinib was irreversible, whereas inhibition by imatinib, gefitinib, and pazopanib was reversible. Molecular modeling studies showed that TKIs form multiple hydrogen bonds with polar residues of the sugar binding site (i.e., Q161, Q282, Q283, N288, N317, and W388), and van der Waals interactions with the H-pocket site. Our results showed interaction of TKIs with amino acid residues at the glucose binding site to inhibit glucose uptake by hGLUT-1. We showed that inhibition of hGLUT-1 by TKIs could alter glucose levels in patients treated with TKIs, leading to hypoglycemia and fatigue, although further studies are required to evaluate roles of other SLC2 and SLC5 members. In addition, TKIs could affect tumor [18 F]FDG uptake, increasingly used as a marker of tumor response. hGLUT-1 inhibition by TKIs may have implications for routine [18 F]FDG-PET monitoring of tumor response in patients.
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PMID:Tyrosine kinase inhibitors reduce glucose uptake by binding to an exofacial site on hGLUT-1: Effects on 18 F-FDG PET uptake. 3327 34


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