The cause of PGCH is unknown and probably multifactorial; possibi

The cause of PGCH is unknown and probably multifactorial; possibilities include a virus,8,

9 drugs and herbal remedies,10 and autoimmune changes.11, 12 In addition, reports have been published about patients who have undergone liver transplantation.13, 14 Our patient received Pil-Food. Severe changes in liver function tests occurred, she was positive for antinuclear antibody autoreactivity, and a histological examination found abundant PF-01367338 nmr areas of multinucleate giant cells with marked periportal and parenchymal hepatocellular necrosis and inflammation. Because all the aforementioned alterations appeared during the long-term ingestion of Pil-Food [a composition developed by Synthelabo that contains D,L-methionine, GDC-0068 cost L-(+)-cysteine hydrochloride, L-cysteine, enzymes and animal protein hydrolysates, millet extract, calcium pantothenate, vitamin B2 phosphate, vitamin B6, biotin (vitamin H), and vitamin E] and a successful corticosteroid response was attained, we speculate that this hepatic autoreactivity could be related to the Pil-Food treatment.15, 16 Moreover, just like patients with drug-induced AIH,1 our patient did not require long-term immunosuppressive therapy. We believe that this case highlights (1) that the breakdown of immune tolerance by drugs is able to trigger liver autoreactivity and (2) that some cases of PGCH may present a rapid and effective response

to corticosteroid therapy instead of a fulminant or progressive course. Ricardo Moreno-Otero M.D.* ‡, Maria Trapero Marugán M.D.* ‡, Luisa García-Buey M.D.* ‡, Asunción García-Sancchez Adenosine M.D.†, * Digestive Diseases Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain, † Pathology Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid,

Madrid, Spain, ‡ Centro de Investigación Biomédica en Red, Instituto de Salud Carlos III, Madrid, Spain. “
“A 53 year-old man presented with a 5-month history of severe diarrhoea and abdominal cramping immediately occurring after tube feeding. The Percutaneous Endoscopic Gastrostomy (PEG) tube was inserted 2 years previously, for enteral feeding, following diagnosis of an oropharyngeal carcinoma. The patient had no signs or symptoms of peritonitis. The skin surrounding the tube was inflamed with brown odorous fluid exuding. Upon checking the tube position using upper endoscopy no inner bumper was seen within the stomach. A fistulogram through the feeding tube revealed typical haustration of the colon rather than expected gastric appearances (Figure 1A). CT confirmed misplacement, localizing the position of the bumper in the transverse colon (Figure 1B, arrow). A gastrocolic fistula could not be visualized. Colonoscopy showed the inner bumper located near the splenic flexure (Figure 2A).

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