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Nausea, vomiting, abdominal pain, high eosinophils--help!
My 20-year-old daughter has been ill with vomiting, severe abdominal pain, 20-pound weight loss, shortness of breath, malaise, fatigue and a high eosinophil count (34.8). This has been going on for over two months. About 45 minutes after eating, she cannot stand the pain, is nauseated, and vomits. She has had an endoscopy, colonoscopy, enteroclysis, CT scan with barium, a small bowel follow through (SBFT), head MRI, ultrasound of gallbladder and pancreas, chest x-ray, and also blood tests. The obly unusual blood finding is high TIBC, high eosinophils, borderline anemia with hematocrit at 33, and high prolactin. The SBFT showed two strictures in the small intestine, but the enteroclysis and colonoscopy showed nothing. Interestingly, she has shortness of breath and was just put on Advair. I have put her on a restrictive diet, given her Benadryl and, of course, she takes the Advair daily which has a steroid in it. Her eosinophils were skyhigh at 34.8. Her muscles also ache. Docs cannot seem to find what is wrong. Could her asthma, which developed at the same time as the belly problems and the other symptoms, be related to the abdominal problems? Since on the above medications, she does feel a little better but is still sickly and very small at 106 pounds. Certain foods, i.e., fatty foods, tomatoes, oranges (acidic fruits), meats (especially red meats) bother her. Any ideas? Are doctors missing something here? She is so pale and sickly feeling. Also, she only has a bowel movement about every seven to eight days and her belly is distended. Thanks so much for any advice.
To answer your question of "can asthma be related or caused from something else", yes it can. If she has Acid Reflux (GERD) it can cause you to be asthmatic. I have the reflux so bad that when it hits, it goes all the way up into my throat and ears and the pain is so bad, it locks my jaw. Acid relfux can cause you to feel like "something is stuck in your throat or your air way is closing up". I take prilosec everyday. If I miss a dose, boy do I pay! Take her to a good Gastro doctor and have them run some tests. I had my gallbladder taken out years ago, have had trouble with the sphincter of Odie not opening up and had to have it cauterized open. It was causing sever pain, nausea and vomiting and weight loss. They can check that through a scope down the throat and blood work to see if bile and amalase levels are high. What my doctor did was put a stint in for a month to see how that did and then took it out and cauterized it open all thru a scope down the throat procedure. Made a world of difference and the only thing I had wrong right after the procedure was a sore throat for a few days.
While browsing GI forum I came across your question. I have several suggestions.
1. What color are her stools and do they float and do they leach out fat (oil)?
An Anwers to one of your questions about Celiac Disease is that the best way of DX is biopsy of small bowel done on the endoscopy.
It is a small bowel malabsorption, not large.
From my own recent experience I would first say Asthma can come from Gastric reflux disease. She has many symptoms of malabsorption from, at this point, an unknown cause but the Eosinophilia usually means allergies. Some of her symptoms sounds like food allergies reactions. I would ask you doctor to try GASTROCROM three times a day, 1/2 prior to her meals and see if you see a change. From everything I have read About IgE levels, even if you find the allergy the level may never go down.
2. Take her to a BIG facility that deals with the unknown and rare disease. example John Hopkins.
1. What color are her stools and do they float and do they leach out fat (oil)?
An Anwers to one of your questions about Celiac Disease is that the best way of DX is biopsy of small bowel done on the endoscopy.
It is a small bowel malabsorption, not large.
From my own recent experience I would first say Asthma can come from Gastric reflux disease. She has many symptoms of malabsorption from, at this point, an unknown cause but the Eosinophilia usually means allergies. Some of her symptoms sounds like food allergies reactions. I would ask you doctor to try GASTROCROM three times a day, 1/2 prior to her meals and see if you see a change. From everything I have read About IgE levels, even if you find the allergy the level may never go down.
2. Take her to a BIG facility that deals with the unknown and rare disease. example John Hopkins.
You know I was just doing some research for my own problems and I remember seeing something that might relate to your problems. It may be a long shot but check this out:
Eosinophilic Gastroenteritis
Background: Eosinophilic gastroenteritis (EGE) is an uncommon disease characterized by (1) the presence of abnormal GI symptoms; (2) eosinophilic infiltration in 1 or more areas of the GI tract, defined as 20 or more eosinophils per high-power field; (3) the absence of an identified cause of eosinophilia; and (4) the exclusion of eosinophilic involvement in organs other than the gut.Pathophysiology: The etiology of EGE is unknown, and the pathogenesis is poorly understood. EGE is thought to be a disorder of the GI tract, in which various inflammatory stimuli may trigger an eosinophilic infiltration of the GI tract. These, in turn, cause tissue damage by degranulation and cytokine release, ie, major basic proteins (eosinophilic cationic proteins), that may directly damage the GI tract wall. Examples of stimuli that have been thought to have an incriminating role in triggering this inflammation include food allergens, immunologic disorders, and, possibly, undiscovered infections.Frequency:
In the US: The disease is rare, and the incidence is difficult to estimate. However, since the description of EGE by Kaijser in 1937, more than 280 cases have been reported in the medical literature.
Internationally: Although cases have been reported worldwide, the exact incidence of EGE is unclear. A confounding factor is lack of diagnostic precision. Mortality/Morbidity:
Death from EGE has been reported only rarely.
Morbidity includes malnutrition and intestinal obstruction and perforation. Race:
Cases of EGE are reported mostly in Caucasians, with some cases occurring in Asians.
Sex:
A slight male preponderance has been reported.Age:
Patients present clinically in the third to fifth decades of life, but the disease can affect any age group, from infancy through the seventh decade. CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
History: Patients may have various clinical presentations depending on the region of the GI tract involved and the depth of the bowel wall involvement. The disease most often involves the stomach and the small bowel. Symptoms include, but are not limited to, the following:
Abdominal pain
Intermittent epigastric pain
Anorexia
Bloating
Postprandial nausea, vomiting
Weight loss
Diarrhea
Ankle edema
Dysphagia
MelenaPhysical: EGE can be classified according to the layer of the GI tract involved; however, mixed forms do occur.
The most prevalent form is mucosal and submucosal layer involvement.
Patients present with colicky abdominal pain, nausea, vomiting, diarrhea, and weight loss.
Approximately 50% of patients have a history of atopy (hayfever, asthma, food allergy). In children, a history of allergy is even more common.
The condition may be associated with protein-losing enteropathy, iron-deficiency anemia, or malabsorption.
Children and adolescents can present with growth retardation, delayed puberty, or amenorrhea.
Patients with muscle layer involvement typically present with pyloric or intestinal obstruction.
The eosinophilic involvement often is localized to the stomach but can involve small bowel.
Cramping and abdominal pain associated with nausea and vomiting occur frequently.
Food allergy and past history of allergy are less common in these patients than in patients with mucosal layer disease.
Involvement of the serosal layer is the least common form of the disease.
The entire GI wall usually is involved.
These patients typically present with eosinophilic ascites.
Serosal and visceral peritoneal inflammation leads to leakage of fluids.
A history of allergy appears to be common in this group.Causes: The cause or mechanism of eosinophilic infiltration is not known.
Patients with EGE have elevated immunoglobulin E (IgE) and eosinophilia of tissue and blood. An imbalance in the T-cell paradigm causing an increase in the production of interleukins (IL) 3, 4, and 5 and cytokines has been postulated as the cause of IgE synthesis and eosinophilia.
In one study, immunohistochemistry detected IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 in the granule matrix of eosinophils, the release of which is thought to be involved in the perpetuation of intestinal eosinophil infiltration and inflammation. DIFFERENTIALS
Lab Studies:
CBC count with differential
Peripheral blood eosinophilia is found in 20-80% of cases.
Average count is 2000 eosinophils (eos) per microliter in patients with mucosal layer involvement, 1000 eos/mcL in patients with muscular layer involvement, and 8000 eos/mcL in patients with serosal involvement.
Mean corpuscular volume
Iron-deficiency anemia may be evident.
Serum albumin may be low, especially in patients with mucosal layer involvement.
Although usually unnecessary, fecal protein loss can be measured by measuring alpha1-antitrypsin in a 24-h feces collection.
This test is used to identify the inability to digest and absorb proteins in the GI tract.
The normal value is 0-54 mg/dL. Patients with EGE have elevated alpha1-antitrypsin in their feces.
Obtain a stool sample (minimum 2-g portion). Keep it refrigerated.
Protein loss also can result in a low level of quantitative immunoglobulins.
The erythrocyte sedimentation rate (ESR) and serum IgE level can be elevated.
Obtain 3 separate stool specimens to rule out parasitic infection. Perform a wet mount or stain smear.
Mild-to-moderate steatorrhea is present in approximately 30% of patients. This can be measured by qualitative and quantitative stool tests.Imaging Studies:
Radiographically, EGE does not have a pathognomic appearance. Radiographic changes are variable, nonspecific, and/or absent in at least 40% of patients.
Gastric folds can be enlarged, with or without nodular filling defects.
Valvular conniventes may be thickened and flattened. Strictures, ulceration, or polypoid lesions may occur.
In EGE involving the muscle layer, localized involvement of the antrum and pylorus may occur, causing narrowing of the distal antrum and gastric retention. The small intestine also may be dilated, with an increase in the thickness of the folds. Prominent mucosal folds also may be observed in the colon.
Rarely, diffuse esophageal narrowing or achalasialike motor abnormalities may occur.
Further studies include ultrasound and CT scans.
Ultrasound and CT scans may show thickened intestinal walls and, sometimes, localized lymphadenopathy.
Ascitic fluid usually is detected in patients with serosal layer involvement.Other Tests:
Exploratory laparotomy may be indicated, especially in patients with serosal EGE.Procedures:
Endoscopy and biopsy
Due to possible sampling error, when performing endoscopy, obtain at least 6 biopsy specimens from normal and abnormal areas of the bowel.
Grossly prominent mucosal folds, hyperemia, ulceration, or nodularity may be apparent.
In patients with esophageal or colonic symptoms, obtain additional biopsy specimens from the relevant sites to aid in diagnosis. Gastroesophageal reflux can cause tissue eosinophilia in the distal esophagus.
Patients with serosal disease present with ascites. Abdominal paracentesis demonstrates a sterile fluid with a high eosinophil count. Pleural effusion also may be present. Laparoscopy may show hyperemia and/or nodularity of the GI wall.Histologic Findings: Histopathology usually demonstrates increased numbers of eosinophils (often >50 eos per high-power field) in the lamina propria. Large numbers of eosinophils often are present in the muscularis and serosal layers. The localized eosinophilic infiltrates may cause crypt hyperplasia, epithelial cell necrosis, and villous atrophy. The gross appearance of EGE upon endoscopy shows erythematous, friable, nodular, and, often, ulcerated mucosa. Diffuse enteritis with complete loss of villi, submucosal edema, infiltration of the GI wall, and fibrosis may be apparent. Mast cell infiltrates and hyperplastic mesenteric lymph nodes infiltrated with eosinophils may be present. Due to errors in sampling or to mucosal sparing, 10% of mucosal biopsies are not helpful for diagnosis. TREATMENT Section 6 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
If you go to emedicine and pull this up and has more information and other similar diseases. Good Luck...
Eosinophilic Gastroenteritis
Background: Eosinophilic gastroenteritis (EGE) is an uncommon disease characterized by (1) the presence of abnormal GI symptoms; (2) eosinophilic infiltration in 1 or more areas of the GI tract, defined as 20 or more eosinophils per high-power field; (3) the absence of an identified cause of eosinophilia; and (4) the exclusion of eosinophilic involvement in organs other than the gut.Pathophysiology: The etiology of EGE is unknown, and the pathogenesis is poorly understood. EGE is thought to be a disorder of the GI tract, in which various inflammatory stimuli may trigger an eosinophilic infiltration of the GI tract. These, in turn, cause tissue damage by degranulation and cytokine release, ie, major basic proteins (eosinophilic cationic proteins), that may directly damage the GI tract wall. Examples of stimuli that have been thought to have an incriminating role in triggering this inflammation include food allergens, immunologic disorders, and, possibly, undiscovered infections.Frequency:
In the US: The disease is rare, and the incidence is difficult to estimate. However, since the description of EGE by Kaijser in 1937, more than 280 cases have been reported in the medical literature.
Internationally: Although cases have been reported worldwide, the exact incidence of EGE is unclear. A confounding factor is lack of diagnostic precision. Mortality/Morbidity:
Death from EGE has been reported only rarely.
Morbidity includes malnutrition and intestinal obstruction and perforation. Race:
Cases of EGE are reported mostly in Caucasians, with some cases occurring in Asians.
Sex:
A slight male preponderance has been reported.Age:
Patients present clinically in the third to fifth decades of life, but the disease can affect any age group, from infancy through the seventh decade. CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
History: Patients may have various clinical presentations depending on the region of the GI tract involved and the depth of the bowel wall involvement. The disease most often involves the stomach and the small bowel. Symptoms include, but are not limited to, the following:
Abdominal pain
Intermittent epigastric pain
Anorexia
Bloating
Postprandial nausea, vomiting
Weight loss
Diarrhea
Ankle edema
Dysphagia
MelenaPhysical: EGE can be classified according to the layer of the GI tract involved; however, mixed forms do occur.
The most prevalent form is mucosal and submucosal layer involvement.
Patients present with colicky abdominal pain, nausea, vomiting, diarrhea, and weight loss.
Approximately 50% of patients have a history of atopy (hayfever, asthma, food allergy). In children, a history of allergy is even more common.
The condition may be associated with protein-losing enteropathy, iron-deficiency anemia, or malabsorption.
Children and adolescents can present with growth retardation, delayed puberty, or amenorrhea.
Patients with muscle layer involvement typically present with pyloric or intestinal obstruction.
The eosinophilic involvement often is localized to the stomach but can involve small bowel.
Cramping and abdominal pain associated with nausea and vomiting occur frequently.
Food allergy and past history of allergy are less common in these patients than in patients with mucosal layer disease.
Involvement of the serosal layer is the least common form of the disease.
The entire GI wall usually is involved.
These patients typically present with eosinophilic ascites.
Serosal and visceral peritoneal inflammation leads to leakage of fluids.
A history of allergy appears to be common in this group.Causes: The cause or mechanism of eosinophilic infiltration is not known.
Patients with EGE have elevated immunoglobulin E (IgE) and eosinophilia of tissue and blood. An imbalance in the T-cell paradigm causing an increase in the production of interleukins (IL) 3, 4, and 5 and cytokines has been postulated as the cause of IgE synthesis and eosinophilia.
In one study, immunohistochemistry detected IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 in the granule matrix of eosinophils, the release of which is thought to be involved in the perpetuation of intestinal eosinophil infiltration and inflammation. DIFFERENTIALS
Lab Studies:
CBC count with differential
Peripheral blood eosinophilia is found in 20-80% of cases.
Average count is 2000 eosinophils (eos) per microliter in patients with mucosal layer involvement, 1000 eos/mcL in patients with muscular layer involvement, and 8000 eos/mcL in patients with serosal involvement.
Mean corpuscular volume
Iron-deficiency anemia may be evident.
Serum albumin may be low, especially in patients with mucosal layer involvement.
Although usually unnecessary, fecal protein loss can be measured by measuring alpha1-antitrypsin in a 24-h feces collection.
This test is used to identify the inability to digest and absorb proteins in the GI tract.
The normal value is 0-54 mg/dL. Patients with EGE have elevated alpha1-antitrypsin in their feces.
Obtain a stool sample (minimum 2-g portion). Keep it refrigerated.
Protein loss also can result in a low level of quantitative immunoglobulins.
The erythrocyte sedimentation rate (ESR) and serum IgE level can be elevated.
Obtain 3 separate stool specimens to rule out parasitic infection. Perform a wet mount or stain smear.
Mild-to-moderate steatorrhea is present in approximately 30% of patients. This can be measured by qualitative and quantitative stool tests.Imaging Studies:
Radiographically, EGE does not have a pathognomic appearance. Radiographic changes are variable, nonspecific, and/or absent in at least 40% of patients.
Gastric folds can be enlarged, with or without nodular filling defects.
Valvular conniventes may be thickened and flattened. Strictures, ulceration, or polypoid lesions may occur.
In EGE involving the muscle layer, localized involvement of the antrum and pylorus may occur, causing narrowing of the distal antrum and gastric retention. The small intestine also may be dilated, with an increase in the thickness of the folds. Prominent mucosal folds also may be observed in the colon.
Rarely, diffuse esophageal narrowing or achalasialike motor abnormalities may occur.
Further studies include ultrasound and CT scans.
Ultrasound and CT scans may show thickened intestinal walls and, sometimes, localized lymphadenopathy.
Ascitic fluid usually is detected in patients with serosal layer involvement.Other Tests:
Exploratory laparotomy may be indicated, especially in patients with serosal EGE.Procedures:
Endoscopy and biopsy
Due to possible sampling error, when performing endoscopy, obtain at least 6 biopsy specimens from normal and abnormal areas of the bowel.
Grossly prominent mucosal folds, hyperemia, ulceration, or nodularity may be apparent.
In patients with esophageal or colonic symptoms, obtain additional biopsy specimens from the relevant sites to aid in diagnosis. Gastroesophageal reflux can cause tissue eosinophilia in the distal esophagus.
Patients with serosal disease present with ascites. Abdominal paracentesis demonstrates a sterile fluid with a high eosinophil count. Pleural effusion also may be present. Laparoscopy may show hyperemia and/or nodularity of the GI wall.Histologic Findings: Histopathology usually demonstrates increased numbers of eosinophils (often >50 eos per high-power field) in the lamina propria. Large numbers of eosinophils often are present in the muscularis and serosal layers. The localized eosinophilic infiltrates may cause crypt hyperplasia, epithelial cell necrosis, and villous atrophy. The gross appearance of EGE upon endoscopy shows erythematous, friable, nodular, and, often, ulcerated mucosa. Diffuse enteritis with complete loss of villi, submucosal edema, infiltration of the GI wall, and fibrosis may be apparent. Mast cell infiltrates and hyperplastic mesenteric lymph nodes infiltrated with eosinophils may be present. Due to errors in sampling or to mucosal sparing, 10% of mucosal biopsies are not helpful for diagnosis. TREATMENT Section 6 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
If you go to emedicine and pull this up and has more information and other similar diseases. Good Luck...
Her strictures could be the result of inflammation secondary to an allergy to something since her eos are high....Now that she has asthma it seems to be an allergy of some sort...what did they say about her high prolactin...thats a little unusual...Personally i would change doctors..go to a medical center, bring the results with you...this doesnt seem normal and like you said waiting another month could be detrimental.
Thanks Ozark for the advice. I will check out the websites on Celiac disease and wheat allergies. It is just so hard to have someone so sick and the M.D.s keep putting it off. One doctor actually said it was in her head and she needed a complete psychological examination. If this was the case, I would be the first to take my daughter to a psychologist, but that is not the case. She is a well-rounded and grounded girl. Her blood tests are not off due to a psychological problem and one test showed strictures in her small intestine, which also could not be a psychological problem. Are there caring concerned physicians out there anymore who will stay with you and look for the unusual problems? Sorry to vent!
She had a blood test for celiac that came back negative, although I hear that the best way to diagnose Celiac is through a biopsy. She did have a biopsy when she had a colonscopy. This was at the ileocecal valve, but showed nothing. Do you know if a biopsy has to be at a certain site or can just one biopsy of the small or large intestine give the needed information. Her shortness of breath (SOB) cleared up with Advair, an asthma drug. If she does not take it twice a day, she is short of breath. I really do not know if that means she has asthma, or if the Advair is just helping the SOB and it could still be a symptom of another illness or problem. The doctors put her on Celexa (an antipressant for over two months) which did not help. They put her Bentyl for irritable bowel syndrome which did not help. Yesterday her CBC with differential came back with once again high eosinophils, high lymphocytes, low neutrophils, low red blood count, and low white blood count. The doctors only response is repeat the test in a month. But she is still ill, vomiting, nauseated, and losing weight. In a month she will be under 100 pounds, plus she wants to be back in college and enjoying life like a 20-year-old should be doing. I think they are missing something her. Could it be an unusual syndrome or disease, and if so what? Any ideas?
Also her low hematocrit could cause her to be a liitle short of breathe...how do they know whe has asthma?
Check on the web about wheat allergy or celiac diseases. This may be the cause...good luck
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