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Background and aims Nonalcoholic fatty liver disease (NAFLD) and impaired lung function share similar risk factors and phenotypes, such as obesity and type 2 diabetes. The study is an updated meta-analysis to evaluate the association between NAFLD and impaired lung function. Methods A total of 696 articles were identified with mention of NAFLD and lung function (or pulmonary function testing) in MEDLINE, EMBASE, and Scopus. After de-duplication, 455 articles were screened, 18 underwent full-text review. Five studies met our review and inclusion criteria with an interrater reliability kappa score of 1. Results Five studies with a total of 118 118 subjects (28.4% with NAFLD) were included. The cross-sectional studies supported a statistically significant relationship between decreased pulmonary function tests and NAFLD. There was no association observed with obstructive lung pattern. One of the longitudinal studies revealed an association with increased rate of decline in forced vital capacity in patients with NAFLD and FIB4 score ≥1.30 (−21.7 vs. −27.4 mL/year, P = 0.001 in males, −22.4 vs. −27.9 mL/year, P = 0.016 in females). The second longitudinal study revealed that patients with impaired pulmonary function had an increased hazard ratio of developing NAFLD dependent on the severity of pulmonary impairment. Conclusions This is the first systematic review that supports an association of NAFLD with decreased (restrictive) lung function. The estimated severity of liver fibrosis correlates with the rate of progression of restrictive lung function. There are also data showing that patients with impaired lung function have a higher risk of developing NAFLD.

INTRODUCTION: Gastric variceal bleeding occurs in 15–50% of patients with non-cirrhotic portal venous thrombosis but can also occur in cases of splenic vein thrombosis (SVT) due to the formation of isolated gastric varices (IGV). We present the first reported case of a page kidney causing splenic vein compression, thrombosis, and subsequent gastric variceal bleeding. CASE DESCRIPTION/METHODS: A 31-year-old stuntman presented with epigastric pain and worsening exertional dyspnea over 3 weeks. History was notable for melena and anemia with no reported ulcers on endoscopy. On admission, he had hemoglobin of 4.1 g/dl with severe iron deficiency and elevated reticulocyte count. There was no serologic evidence of hepatic or renal disease. A computed tomography (CT scan) of the abdomen revealed a large left-sided perirenal collection consistent with page kidney, splenomegaly and decreased caliber of the mid and distal splenic vein suggestive of nonocclusive SVT. His liver was normal. Initial endoscopy revealed an IGV type 1 and mild portal hypertensive gastropathy (Figure 1). CT angiography did not reveal a splenorenal shunt to pursue a balloon retrograde transvenous obliteration (BRTO). While admitted, he developed hematemesis and worsening anemia. Ultimately, underwent IR splenic vein stenting with a bare-metal stent and subsequent decompression of the gastric varices with brisk flow of the portal vasculature (Figure 2). DISCUSSION: Gastric varices are classified primarily by location with most involving the gastroesophageal junction due to portal hypertension. The incidence of bleeding is highest in IGV, typically associated with SVT. Common etiologies of SVT include pancreatitis, malignancy or trauma. Our case described an extrinsic splenic vein compression and subsequent thrombosis due to a sub-capsular renal hematoma possibly of unclear etiology. Treatment for GV often depends on local expertise, but commonly consists of cyanoacrylate injection, banding (especially in type 1 gastro-esophageal varices), transjugular intrahepatic portosystemic shunt (TIPS) placement, BRTO, and even splenectomy. More recently, in cases of IGV due to isolated SVT, splenic vein stenting has been increasingly utilized. In our case, TIPS would not address the pre-hepatic portal hypertension and cyanoacrylate was not available. Splenic vein stenting was thus chosen to decompress the IGV with excellent response seen on subsequent follow-up (Figure 1).