Two patients with ectopic liver are described. In one patient, a small ectopic liver attached to the gastric serosa developed hepatocellular carcinoma (HCC). The preoperative diagnosis was an ␣-fetoprotein (AFP)-producing carcinoma and a malignant ulcer of the stomach. Total gastrectomy and esophago-jejunostomy were performed. The tumor that measured 4 ؋ 2 ؋ 2 cm contained an AFP-producing HCC and normal liver tissue. In another patient who had alcoholic cirrhosis, ectopic liver on the serosa of the gallbladder was found to have the same histological changes as the mother liver. A survey of the literature disclosed more than 20 cases in which HCC developed outside the liver; the liver did not have HCC. By contrast, there was only one report on HCC occurring in the liver in the presence of a noncancerous, relatively large accessory liver lobe. Because ectopic liver does not have a complete vascular and ductal system as a normal liver, it is perhaps functionally handicapped and more prone to hepatocarcinogenesis. (HEPATOLOGY 1999;29:57-61.)

Compared to incidence in Hispanic and European populations, PACG was more common among South Brazilians, whereas the POAG rates were similar. The rate of undiagnosed glaucoma was almost 90%. The higher POAG prevalence in the population self-reported as nonwhite may affect the estimation of glaucoma in Brazil, as more than 40% of the population self-report their race as nonwhite.

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BackgroundLong QT syndrome causes ventricular tachyarrhythmias and sudden death. Recently, a short QT interval has also been shown to be associated with an increased risk of tachyarrhythmia and sudden death. However, the prevalence of short QT syndrome is not well‐known.HypothesisThe aim of this study was to assess the distribution of corrected QT intervals (QTc) and prevalence of short QT syndrome.MethodsThis study comprised 12,149 consecutive subjects who received a consultation at Kanazawa University Hospital, Kanazawa, Japan, and had an electrocardiogram (ECG) between February 2003 and May 2004. Of these subjects, 1,165 subjects were excluded because of inappropriate ECGs, while the remaining 10,984 subjects had their last‐recorded ECGs analyzed.ResultsThe QTc values showed a nearly normal distribution (408 ± 25 msec1/2), and were significantly longer in females (412 ± 24 msec1/2) than in males (404 ± 25 msec1/2) (p < 0.05). Among 5,511 males, 69 subjects (1.25%) exhibited QTc < 354 msec1/2 (2 standard deviations [SDs] below the mean in males), and among 5,473 females, 89 subjects (1.63%) exhibited QTc < 364 msec1/2 (2 SDs below the mean in females). Only 3 subjects (0.03% in all subjects and 0.05% in males) exhibited QTc < 300 msec1/2, however, none had clinical symptoms of short QT syndrome.ConclusionsShort QT syndrome may be very rare. Copyright © 2008 Wiley Periodicals, Inc.

Cancer has a non-negligible prevalence in patients with acute coronary syndrome undergoing percutaneous coronary intervention, with a major risk of cardiovascular events and bleedings. Moreover, these patients are often undertreated from clinical despite medical therapy seems to be protective. Registration:The BleeMACS project (NCT02466854).

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Background-The STA gene encodes emerin and is one of the genes that is affected in Emery-Dreifuss muscular dystrophy (EDMD). Although it has been reported that EDMD caused by the STA gene mutation is associated with X-linked recessive inheritance, the genotype-phenotype correlations, with special reference to cardiac manifestations, are not well defined. Methods and Results-We identified 16 carriers (7 male and 9 female) with a nonsense mutation in exon 6 of the STA gene in 2 EDMD families. Pacemakers were required for treatment of bradyarrhythmias in all 7 male carriers and in 2 of the 9 female carriers. In addition, 2 of the 9 female carriers displayed atrial fibrillation. In these 2 families, 3 males without pacemaker implantation, who were not tested genetically, had died suddenly. In these family members, the majority of carriers with the mutation had not been clinically diagnosed as having EDMD before genetic testing because of extremely mild or nonexistent skeletal myopathy. Conclusions-EDMD