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Ulcerating Ileocolitis in Severe Amatoxin Poisoning.

Hilty MP, Halama M, Zimmermann AK, Maggiorini M, Geier A - Case Rep Gastrointest Med (2015)

Bottom Line: The absence of discernible alternative etiologies such as infectious agents makes a causal relationship between the ulcerating ileocolitis and the amatoxin poisoning likely.Diarrhea and varying abdominal pain persisted over several weeks and clinical follow-up after six months showed a completely symptom-free patient.The case presented highlights the importance to consider the possibility of rare complications of Amanita intoxication in order to be able to respond to them early and adequately.

View Article: PubMed Central - PubMed

Affiliation: Medical Intensive Care Unit, University Hospital of Zurich, Rämistrasse 100, 8091 Zurich, Switzerland.

ABSTRACT
Amatoxin poisoning is still associated with a great potential for complications and a high mortality. While the occurrence of acute gastroenteritis within the first 24 hours after amatoxin ingestion is well described, only very few descriptions of late gastrointestinal complications of amatoxin poisoning exist worldwide. We present the case of a 57-year-old female patient with severe amatoxin poisoning causing fulminant but reversible hepatic failure that on day 8 after mushroom ingestion developed severe abdominal pain and watery diarrhea. Ulcerating ileocolitis was identified by computed tomography identifying a thickening of the bowel wall of the entire ileum and biopsies taken from the ileum and large bowel revealing distinct ileitis and proximally accentuated colitis. The absence of discernible alternative etiologies such as infectious agents makes a causal relationship between the ulcerating ileocolitis and the amatoxin poisoning likely. Diarrhea and varying abdominal pain persisted over several weeks and clinical follow-up after six months showed a completely symptom-free patient. The case presented highlights the importance to consider the possibility of rare complications of Amanita intoxication in order to be able to respond to them early and adequately.

No MeSH data available.


Related in: MedlinePlus

Biopsy of the cecum, showing rarefication and atrophy of the crypts, dilation of the lumina with intraluminal cell detritus (∗), and fibrosis of the lamina propria. Epithelial cells present reactive, respectively, regeneratory nuclear atypia in the context of inflammation (40x magnification); for details see the inset (200x magnification).
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fig2: Biopsy of the cecum, showing rarefication and atrophy of the crypts, dilation of the lumina with intraluminal cell detritus (∗), and fibrosis of the lamina propria. Epithelial cells present reactive, respectively, regeneratory nuclear atypia in the context of inflammation (40x magnification); for details see the inset (200x magnification).

Mentions: A 57-year-old female patient presented on day 3 after ingestion of approximately 200 g of self-collected mushrooms with a history of severe gastroenteritis beginning on day 1 and lasting through admission. On the day of admission, she became increasingly weak, providing her with the reason to seek medical attention. Otherwise, the patient had no medical record of any significance. The patient presented with stable cardiovascular and pulmonary function, afebrile, with diffuse abdominal tenderness and lively bowel sounds. There were no mushroom residues available for examination by an expert, but Amanita phalloides intoxication, which was highly compatible with the description of the patient and the clinical course, was proven via detection of α-amanitin in the urine using ELISA (Buehlmann Laboratories, Schonenbuch, Switzerland) with a maximal concentration of 42.2 μg/L on admission on day 3. Directly on admission, intravenous silibinin (Legalon SIL, Rottapharm, Monza, Italy) and acetylcysteine (Fluimucil 10%, Zambon Pharma, Milan, Italy) and multiple dose oral activated charcoal therapy were initiated at the intensive care unit according to current guidelines [9]. Silibinin was administered intravenously at 20 mg/kg per day for three days after a loading dose of 5 mg/kg; acetylcysteine was administered intravenously at 150 mg/kg over 1 hour, followed by 12.5 mg/kg over 4 hours and 6.25 mg/kg over 16 hours. At admission on day 3, liver enzymes were already elevated, reaching maximum on day 4 with alanine aminotransferase levels of 6894 U/L, aspartate aminotransferase of 5232 U/L, and lactate dehydrogenase of 10596 U/L. Alkaline phosphatase and γ-glutamyl transferase levels remained normal. As a measure of liver function, factor V activity was nondetectable on day 4, with factor II activity at 29% (60–150) and factor VII activity at 25% (60–150); the international normalized ratio (INR) was 2.7. Fortunately, liver function improved without further interventions on day 7 (Table 1). The patient initially also presented with renal failure. Renal ultrasonography studies were normal; however a calculated fractional excretion of urea of 65% hinted at an intrarenal pathology. Renal failure was completely reversible by day 4 without need for renal replacement therapy. On day 8, however, the patient developed severe abdominal pain, tenderness on examination with signs of peritonitis especially in the lower right quadrant, accompanied by watery diarrhea and an elevation of inflammatory parameters. Cardiovascular and pulmonary function remained stable. Abdominal computed tomography showed a thickening of the bowel wall of the entire ileum and no other pathologies. On day 12 after mushroom ingestion gastrointestinal biopsies were taken from the ileum and the large bowel; see Figures 1 and 2. Diagnostic findings were most prominent in the mucosa of the ileum and the cecum and decreased towards the rectum. The mucosa of the ileum showed, in addition to acute cryptitis and ulcerating inflammation with fibrinoleukocytic exudate (pseudomembranes), regenerating changes of the epithelium. Acute erosive and ulcerating inflammatory changes together with a rarefication and atrophy of crypts, fibrosis of the lamina propria, and regenerating epithelial changes were most prominent in the cecum. These findings of a distinct ileitis and proximally accentuated colitis are not specific. Architectural and regenerating epithelial changes and fibrosis indicate a sustained or previous damage of the mucosa. Screening for Clostridium difficile toxin using ELISA as well as cultures for Clostridium difficile and Salmonella, Shigella, and Campylobacter species remained negative. With supportive therapy, gastrointestinal symptoms as well as inflammatory markers showed a tendency to regression so that the patient could be dismissed in good shape on day 17 after ingestion of Amanita. Diarrhea and varying abdominal pain persisted over several weeks thereafter. Clinical follow-up after six months showed a completely symptom-free patient.


Ulcerating Ileocolitis in Severe Amatoxin Poisoning.

Hilty MP, Halama M, Zimmermann AK, Maggiorini M, Geier A - Case Rep Gastrointest Med (2015)

Biopsy of the cecum, showing rarefication and atrophy of the crypts, dilation of the lumina with intraluminal cell detritus (∗), and fibrosis of the lamina propria. Epithelial cells present reactive, respectively, regeneratory nuclear atypia in the context of inflammation (40x magnification); for details see the inset (200x magnification).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555452&req=5

fig2: Biopsy of the cecum, showing rarefication and atrophy of the crypts, dilation of the lumina with intraluminal cell detritus (∗), and fibrosis of the lamina propria. Epithelial cells present reactive, respectively, regeneratory nuclear atypia in the context of inflammation (40x magnification); for details see the inset (200x magnification).
Mentions: A 57-year-old female patient presented on day 3 after ingestion of approximately 200 g of self-collected mushrooms with a history of severe gastroenteritis beginning on day 1 and lasting through admission. On the day of admission, she became increasingly weak, providing her with the reason to seek medical attention. Otherwise, the patient had no medical record of any significance. The patient presented with stable cardiovascular and pulmonary function, afebrile, with diffuse abdominal tenderness and lively bowel sounds. There were no mushroom residues available for examination by an expert, but Amanita phalloides intoxication, which was highly compatible with the description of the patient and the clinical course, was proven via detection of α-amanitin in the urine using ELISA (Buehlmann Laboratories, Schonenbuch, Switzerland) with a maximal concentration of 42.2 μg/L on admission on day 3. Directly on admission, intravenous silibinin (Legalon SIL, Rottapharm, Monza, Italy) and acetylcysteine (Fluimucil 10%, Zambon Pharma, Milan, Italy) and multiple dose oral activated charcoal therapy were initiated at the intensive care unit according to current guidelines [9]. Silibinin was administered intravenously at 20 mg/kg per day for three days after a loading dose of 5 mg/kg; acetylcysteine was administered intravenously at 150 mg/kg over 1 hour, followed by 12.5 mg/kg over 4 hours and 6.25 mg/kg over 16 hours. At admission on day 3, liver enzymes were already elevated, reaching maximum on day 4 with alanine aminotransferase levels of 6894 U/L, aspartate aminotransferase of 5232 U/L, and lactate dehydrogenase of 10596 U/L. Alkaline phosphatase and γ-glutamyl transferase levels remained normal. As a measure of liver function, factor V activity was nondetectable on day 4, with factor II activity at 29% (60–150) and factor VII activity at 25% (60–150); the international normalized ratio (INR) was 2.7. Fortunately, liver function improved without further interventions on day 7 (Table 1). The patient initially also presented with renal failure. Renal ultrasonography studies were normal; however a calculated fractional excretion of urea of 65% hinted at an intrarenal pathology. Renal failure was completely reversible by day 4 without need for renal replacement therapy. On day 8, however, the patient developed severe abdominal pain, tenderness on examination with signs of peritonitis especially in the lower right quadrant, accompanied by watery diarrhea and an elevation of inflammatory parameters. Cardiovascular and pulmonary function remained stable. Abdominal computed tomography showed a thickening of the bowel wall of the entire ileum and no other pathologies. On day 12 after mushroom ingestion gastrointestinal biopsies were taken from the ileum and the large bowel; see Figures 1 and 2. Diagnostic findings were most prominent in the mucosa of the ileum and the cecum and decreased towards the rectum. The mucosa of the ileum showed, in addition to acute cryptitis and ulcerating inflammation with fibrinoleukocytic exudate (pseudomembranes), regenerating changes of the epithelium. Acute erosive and ulcerating inflammatory changes together with a rarefication and atrophy of crypts, fibrosis of the lamina propria, and regenerating epithelial changes were most prominent in the cecum. These findings of a distinct ileitis and proximally accentuated colitis are not specific. Architectural and regenerating epithelial changes and fibrosis indicate a sustained or previous damage of the mucosa. Screening for Clostridium difficile toxin using ELISA as well as cultures for Clostridium difficile and Salmonella, Shigella, and Campylobacter species remained negative. With supportive therapy, gastrointestinal symptoms as well as inflammatory markers showed a tendency to regression so that the patient could be dismissed in good shape on day 17 after ingestion of Amanita. Diarrhea and varying abdominal pain persisted over several weeks thereafter. Clinical follow-up after six months showed a completely symptom-free patient.

Bottom Line: The absence of discernible alternative etiologies such as infectious agents makes a causal relationship between the ulcerating ileocolitis and the amatoxin poisoning likely.Diarrhea and varying abdominal pain persisted over several weeks and clinical follow-up after six months showed a completely symptom-free patient.The case presented highlights the importance to consider the possibility of rare complications of Amanita intoxication in order to be able to respond to them early and adequately.

View Article: PubMed Central - PubMed

Affiliation: Medical Intensive Care Unit, University Hospital of Zurich, Rämistrasse 100, 8091 Zurich, Switzerland.

ABSTRACT
Amatoxin poisoning is still associated with a great potential for complications and a high mortality. While the occurrence of acute gastroenteritis within the first 24 hours after amatoxin ingestion is well described, only very few descriptions of late gastrointestinal complications of amatoxin poisoning exist worldwide. We present the case of a 57-year-old female patient with severe amatoxin poisoning causing fulminant but reversible hepatic failure that on day 8 after mushroom ingestion developed severe abdominal pain and watery diarrhea. Ulcerating ileocolitis was identified by computed tomography identifying a thickening of the bowel wall of the entire ileum and biopsies taken from the ileum and large bowel revealing distinct ileitis and proximally accentuated colitis. The absence of discernible alternative etiologies such as infectious agents makes a causal relationship between the ulcerating ileocolitis and the amatoxin poisoning likely. Diarrhea and varying abdominal pain persisted over several weeks and clinical follow-up after six months showed a completely symptom-free patient. The case presented highlights the importance to consider the possibility of rare complications of Amanita intoxication in order to be able to respond to them early and adequately.

No MeSH data available.


Related in: MedlinePlus