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2017 ; 9
(5
): e1228
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Gastrointestinal Amyloidosis: Review of the Literature
#MMPMID28611935
Rowe K
; Pankow J
; Nehme F
; Salyers W
Cureus
2017[May]; 9
(5
): e1228
PMID28611935
show ga
Gastrointestinal amyloidosis (GIA), a protein deposition disorder, represents a
complex common pathway that encompasses multiple etiologies and presentations. It
represents a significant diagnostic and treatment challenge. The disease results
from the deposition of insoluble extracellular protein fragments that have been
rendered resistant to digestion. GIA can be acquired or genetic, and most
commonly results from chronic inflammatory disorders (AA amyloidosis),
hematologic malignancy (AL amyloidosis), and end-stage renal disease (Beta-2
amyloidosis). The deposition of these abnormal proteins interferes with
gastrointestinal tract (GI) organ structure and function, most notably in the
liver and small bowel. Presentation from GI involvement includes cirrhotic
sequelae, abdominal pain, malabsorption, and GI bleeding. Diagnosis hinges on
pathologic examination of affected tissue, with classic green birefringence under
polarized light. Abdominal fat pad and rectal mucosal biopsy have been described
as sites of higher sensitivity for diagnosis. Serum amyloid P scintigraphy is
near 90% sensitive for diagnosis of AA amyloidosis. Patients should be considered
for further evaluation to rule out additional organ involvement, notably cardiac
and renal. Treatment hinges on an adequate suppression of the predisposing
inflammatory disorder, or malignancy, followed by supportive therapy. Prognosis
varies depending on the etiology of the disease, with the AL subtype showing
worse outcomes, as well as those with hepatic involvement.
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