Background: Increased gallstone prevalence and incidence in cirrhosis have already been reported in different series, including a limited number of patients with cirrhosis.Objective: To evaluate the frequency of gallstones and related risk factors in a large series of patients with cirrhosis. Patients and Methods:The cross-sectional study involved 1010 patients with cirrhosis related to alcohol abuse, chronic viral infection, or miscellaneous causes (42%, 48%, and 10%, respectively) in Child class A, B, or C (48%, 36%, and 16%, respectively). In the longitudinal study gallstone development was monitored ultrasonographically in 618 patients free of gallstones at enrollment. Results:The overall prevalence of gallstone(s) was 29.5% and increased significantly with age without differences according to sex or cause of cirrhosis. Multiple logistic regression analysis showed that only Child classes B and C were significantly related to a higher risk of gallstone (odds ratio, 1.63 for class C vs class A and 1.91 for class B vs class A; P = .001). During a mean ± SD follow-up of 50 months ± 9 months, 141 (22.8%) of 618 patients developed gallstone(s), with an estimated cumulative probability of 6.5%, 18.6%, 28.2%, and 40.9% at 2, 4, 6, and 8 years, respectively. Multivariate analysis showed that Child class (hazard ratio, 2.8 for class C vs class A and 1.8 for class B vs class A; P = .002 and P = .001, respectively) and high-body mass index (hazard ratio, 1.31; P = .04) carried a significantly greater risk of gallstone formation. Conclusion:Cirrhosis per se represents a major risk factor for gallstones whose prevalence and incidence were far higher than those reported in a general population from the same area.

Gastric carcinoids are rare tumors of the stomach. Gastric carcinoid type 1 is associated with chronic atrophic gastritis, and because of a low metastatic potential, is the most benign type. Death from metastatic disease has been reported in only three patients in a review including 724 cases. The present report refers to a 60-year-old man who was affected by type 2 diabetes mellitus and pernicious anemia and died from metastatic gastric carcinoid type 1. In 1998, a well-differentiated 1.2 cm gastric neuroendocrine tumor, immunoreactive for chromogranin A, with a Ki-67 index less than 2% and with infiltration to the submucosal layer was diagnosed and enucleated. In 2002, a new well-differentiated gastric endocrine tumor 6 mm in size with a Ki-67 of approximately 2% was detected, and endoscopic ultrasound confirmed it to be limited to the submucosal layer. The patient refused antrectomy and started long-acting somatostatin analog (lanreotide) in 2005 when the Ki-67 index was 7%, but he stopped the treatment after 4 months. In 2007, despite previous endoscopic stability, endoscopic ultrasound showed an infiltrating gastric lesion of 7 cm. At surgery, the disease appeared to be extended to the liver and to the peritoneum (well-differentiated endocrine carcinoma, Ki-67 40%) with both hepatic and massive peritoneal metastases. A regimen of somatostatin analog was soon restarted; however, the disease continued to spread, and the patient died 6 months later. Overall, despite their generally benign course, type 1 gastric carcinoids may have malignant potential, a finding that should be considered when planning the medical workup of these patients.

Primary intestinal lymphangiectasia (PIL) is a protein-losing enteropathy characterized by tortuous and dilated lymph channels of the small bowel. The main symptoms are bilateral lower limb edema, serosal effusions, and vitamin D malabsorption resulting in osteoporosis. We report here a case of long-lasting misdiagnosed PIL with a peculiar liver picture, characterized by a very high stiffness value at transient elastography, which decreased with clinical improvement. The complex interplay between lymphatic and hepatic circulatory system is discussed. (HEPATOLOGY 2014;60:759-761) Case PresentationA 52-year-old woman presented with chronic bilateral lower limb edema, ascites, and small pleural effusion which had been previously misdiagnosed as liver cirrhosis. The patient's medical history was notable for hypothyroidism, iron deficiency anemia, and osteoporosis. Laboratory tests showed hypoproteinemia (33 g/ L), severe hypoalbuminemia (12 g/L), and low serum immunoglobulins (IgG 1.05 g/L, IgA 0.41 g/L, IgM 0.75 g/L).Abdominal ultrasound and computed tomography (CT) scan demonstrated hepatomegaly with irregular margins, mild portal vein dilation, and splenomegaly (Fig. 1A). A small amount of fluid in the Douglas space and bilateral pleural effusions were detected. In addition, transient elastography (FibroScan; Echosens, Paris, France) revealed highly elevated hepatic stiffness (34.8 kPa; interquartile range [IQR] 4.3 kPa; success rate 100%), consistent with the hypothesis of cirrhotic liver disease. Nevertheless, liver histology showed a normal liver pattern with no signs of fibrosis, steatosis, or inflammatory infiltrate (Fig. 1C,D). Viral, autoimmune, and toxic hepatitis were ruled out.Upper endoscopy showed small white spots scattered on duodenal mucosa with histologic evidence of markedly dilated villous lymphatics and a moderate inflammatory infiltrate consistent with a diagnosis of PIL (Fig. 1B).Following 1 month of a low-fat diet associated with medium-chain triglycerides supplementation, the cornerstone of PIL management, serous effusions resolved and lymphedema improved. Interestingly, during the follow-up, liver stiffness showed a progressive decrease (to 26.6 and 14.3 kPa after 1 and 6 months, respectively; Fig. 2).

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