PMC10105505_01
Endoscopic aspects of duodenum (upper row) and colon (lower row). The duodenum displays diffuse edema and loss of normal folding
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F1
A similar appearance with remarkable loss of the normal folds was observed in the duodenum (Figure 1, upper row). On the other hand, ileocolonoscopy findings (few colon diverticula) were irrelevant (Figure 1, lower row).
Gastric antral mucosa with heavy lymphoplasmacytic infiltration and intraepithelial lymphocytosis. Collagen deposits are lacking (HE; 100x)
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F2
Helicobacter pylori microorganisms and collagen deposits were not identified (Figure 2).
Duodenal mucosa with severe villous atrophy, subepithelial collagen deposits, and superficial epithelial detachment (HE; 100 x)
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F3
Duodenal mucosa biopsies disclosed moderate villous atrophy without crypt hyperplasia, superficial epithelium detachment, increased lymphoplasmacytic inflammatory infiltration, and mild to moderate collagen subepithelial deposits with a thickness of 6-7 micro (Figure 3).
Ileum mucosa with severe villous atrophy, subepithelial collagen deposits, and superficial epithelial detachment (HE; 400x)
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F4
Terminal ileum mucosa biopsies showed morphological alterations similar to the ones described in the duodenum (Figure 4).
Ileum mucosa. Trichrome stain disclosed the key histological finding of collagen in the subepithelial region (400x)
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F5
Masson trichrome stain confirmed collagen subepithelial deposits (Figure 5).
Pathological examination of the hepatic lesion. (a) revealed brownish pigment in hepatocytes (hematoxylin and eosin staining, bar = 100 mum). At higher power, the granular brown pigment was present within hepatocytes, and Kupffer cells (b), and hematopoietic tissue proliferated in the sinusoids, comprising erythroid and myeloid precursors (c) (bar = 50 mum)
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F6
No intraepithelial lymphocytosis was observed (Figure 6).