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Eosinophilia in a patient with cyclical vomiting: a case report.

Copeland BH, Aramide OO, Wehbe SA, Fitzgerald SM, Krishnaswamy G - Clin Mol Allergy (2004)

Bottom Line: CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis.This was associated with extreme weakness and cachexia.CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms.

View Article: PubMed Central - HTML - PubMed

Affiliation: P,O, Box 70622, Department of Internal Medicine, Division of Allergy and Immunology, East Tennessee State University, Johnson City, TN 37614, USA. bhcopelandII@aol.com

ABSTRACT
BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.

No MeSH data available.


Related in: MedlinePlus

Pathology of eosinophilic gastritis. In the presence of an inciting event, inflammatory cells like T-cells and mast cells are activated to produce a host of eosinophilic cytokines that regulate eosinophil biology, activation, recruitment, and survival. Once in the gastric mucosa, eosinophils can orchestrate tissue damage by releasing toxic proteins like eosinophil cationic protein, major basic protein, eosinophil peroxidase, and eosinophil derived neurotoxin. With mucosal injury, vomiting, diarrhea, cachexia, and peripheral edema ensue.
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Figure 2: Pathology of eosinophilic gastritis. In the presence of an inciting event, inflammatory cells like T-cells and mast cells are activated to produce a host of eosinophilic cytokines that regulate eosinophil biology, activation, recruitment, and survival. Once in the gastric mucosa, eosinophils can orchestrate tissue damage by releasing toxic proteins like eosinophil cationic protein, major basic protein, eosinophil peroxidase, and eosinophil derived neurotoxin. With mucosal injury, vomiting, diarrhea, cachexia, and peripheral edema ensue.

Mentions: The diagnosis of eosinophilic gastritis was most compatible with the presentation of our patient. Her history of nausea and vomiting associated with weight loss and lower extremity edema are recognized features of the disease. Although cyclical vomiting has not been described as a typical feature of eosinophilic gastritis, this was the presenting feature in our patient. Initially some of these symptoms could have been contributed to her ulcerative colitis which can also be associated with eosinophilic infiltration but not to the degree and severity seen in this patient. The peripheral edema was most likely secondary to the protein losing enteropathy, hypoalbuminemia, and cachexia (Figure 2).


Eosinophilia in a patient with cyclical vomiting: a case report.

Copeland BH, Aramide OO, Wehbe SA, Fitzgerald SM, Krishnaswamy G - Clin Mol Allergy (2004)

Pathology of eosinophilic gastritis. In the presence of an inciting event, inflammatory cells like T-cells and mast cells are activated to produce a host of eosinophilic cytokines that regulate eosinophil biology, activation, recruitment, and survival. Once in the gastric mucosa, eosinophils can orchestrate tissue damage by releasing toxic proteins like eosinophil cationic protein, major basic protein, eosinophil peroxidase, and eosinophil derived neurotoxin. With mucosal injury, vomiting, diarrhea, cachexia, and peripheral edema ensue.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC425596&req=5

Figure 2: Pathology of eosinophilic gastritis. In the presence of an inciting event, inflammatory cells like T-cells and mast cells are activated to produce a host of eosinophilic cytokines that regulate eosinophil biology, activation, recruitment, and survival. Once in the gastric mucosa, eosinophils can orchestrate tissue damage by releasing toxic proteins like eosinophil cationic protein, major basic protein, eosinophil peroxidase, and eosinophil derived neurotoxin. With mucosal injury, vomiting, diarrhea, cachexia, and peripheral edema ensue.
Mentions: The diagnosis of eosinophilic gastritis was most compatible with the presentation of our patient. Her history of nausea and vomiting associated with weight loss and lower extremity edema are recognized features of the disease. Although cyclical vomiting has not been described as a typical feature of eosinophilic gastritis, this was the presenting feature in our patient. Initially some of these symptoms could have been contributed to her ulcerative colitis which can also be associated with eosinophilic infiltration but not to the degree and severity seen in this patient. The peripheral edema was most likely secondary to the protein losing enteropathy, hypoalbuminemia, and cachexia (Figure 2).

Bottom Line: CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis.This was associated with extreme weakness and cachexia.CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms.

View Article: PubMed Central - HTML - PubMed

Affiliation: P,O, Box 70622, Department of Internal Medicine, Division of Allergy and Immunology, East Tennessee State University, Johnson City, TN 37614, USA. bhcopelandII@aol.com

ABSTRACT
BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.

No MeSH data available.


Related in: MedlinePlus