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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

Remission of Nausea and Vomiting with Prednisone. One cycle shown. Nausea was graded by patient from 0 (absent) to 10 (constant/severe). "P" indicates where prednisone was initiated. Prednisone dose is provided in mg/day in parenthesis on x-axis. After prednisone was initiated and maintained at 10–20 mg/day, the patients cyclical vomiting was aborted for the next 2 years of follow up. Body weight, total protein, and albumin levels improved, while eosinophilia was absent.
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Figure 3: Remission of Nausea and Vomiting with Prednisone. One cycle shown. Nausea was graded by patient from 0 (absent) to 10 (constant/severe). "P" indicates where prednisone was initiated. Prednisone dose is provided in mg/day in parenthesis on x-axis. After prednisone was initiated and maintained at 10–20 mg/day, the patients cyclical vomiting was aborted for the next 2 years of follow up. Body weight, total protein, and albumin levels improved, while eosinophilia was absent.

Mentions: Our patient was started on prednisone (40 mg po once daily). Also at that time she was started on a proton pump inhibitor (lansoprazole 30 mg daily) for esophageal reflux which greatly improved her reflux symptomatology. Prednisone induced a dramatic remission in her symptoms and induced a feeling of well being. There was reversal of the protein losing enteropathy as well as improvements in eosinophilia and serum levels of total protein and albumin. The cyclical vomiting episodes were aborted (one such cycle is shown in Figure 3. On prednisone, these cycles were completely abolished in the subsequent months). However, given the severe adverse effects of steroids including mood swings and weight gain, the patient opted for alternative therapies. She was started on azathioprine (Imuran®) at 50 mg/day and was quickly able to taper down to a maintainence dose of prednisone of 2 mg/day. She has remained on azathioprine for over 1 year with excellent benefits. It is likely that the combination of prednisone and azathiprine was more effective in this patient than either alone or 6-mercaptopurine. While it was likely that mescalamnine induced an allergic reaction or in when administered concomitantly with 6-mercaptopurine, induced toxic side effects, the discontinuation of mescalamine had no beneficial effects on the eosinophilia or vomiting in this patient [56,57]. It is likely that the patient may have had a very low activity of thiopurine methyltransferase (TPMT) but this was not measured in the patient at the time of the study [58].


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

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

Remission of Nausea and Vomiting with Prednisone. One cycle shown. Nausea was graded by patient from 0 (absent) to 10 (constant/severe). "P" indicates where prednisone was initiated. Prednisone dose is provided in mg/day in parenthesis on x-axis. After prednisone was initiated and maintained at 10–20 mg/day, the patients cyclical vomiting was aborted for the next 2 years of follow up. Body weight, total protein, and albumin levels improved, while eosinophilia was absent.
© Copyright Policy
Related In: Results  -  Collection

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Figure 3: Remission of Nausea and Vomiting with Prednisone. One cycle shown. Nausea was graded by patient from 0 (absent) to 10 (constant/severe). "P" indicates where prednisone was initiated. Prednisone dose is provided in mg/day in parenthesis on x-axis. After prednisone was initiated and maintained at 10–20 mg/day, the patients cyclical vomiting was aborted for the next 2 years of follow up. Body weight, total protein, and albumin levels improved, while eosinophilia was absent.
Mentions: Our patient was started on prednisone (40 mg po once daily). Also at that time she was started on a proton pump inhibitor (lansoprazole 30 mg daily) for esophageal reflux which greatly improved her reflux symptomatology. Prednisone induced a dramatic remission in her symptoms and induced a feeling of well being. There was reversal of the protein losing enteropathy as well as improvements in eosinophilia and serum levels of total protein and albumin. The cyclical vomiting episodes were aborted (one such cycle is shown in Figure 3. On prednisone, these cycles were completely abolished in the subsequent months). However, given the severe adverse effects of steroids including mood swings and weight gain, the patient opted for alternative therapies. She was started on azathioprine (Imuran®) at 50 mg/day and was quickly able to taper down to a maintainence dose of prednisone of 2 mg/day. She has remained on azathioprine for over 1 year with excellent benefits. It is likely that the combination of prednisone and azathiprine was more effective in this patient than either alone or 6-mercaptopurine. While it was likely that mescalamnine induced an allergic reaction or in when administered concomitantly with 6-mercaptopurine, induced toxic side effects, the discontinuation of mescalamine had no beneficial effects on the eosinophilia or vomiting in this patient [56,57]. It is likely that the patient may have had a very low activity of thiopurine methyltransferase (TPMT) but this was not measured in the patient at the time of the study [58].

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