Noninvasive markers would be useful for the assessment of portal hypertension (PH) and esophageal varices (EV) in patients with cirrhosis. The aim of our study was to evaluate the performance of the indocyanine green (ICG) retention test as a noninvasive marker of PH and EV, measured against the gold standards (hepatic venous pressure gradient [HVPG] measurement and upper endoscopy). We prospectively enrolled patients with compensated cirrhosis referral to our unit. All patients underwent laboratory tests, abdominal ultrasound, upper gastrointestinal endoscopy, HVPG measurement, and the ICG 15-minute retention (ICG-r15) test. We evaluated the sensitivity and specificity of the ICG retention test and other noninvasive tools for the diagnosis of PH and EV. Ninety-six consecutive Child-Pugh A patients (67 male and 29 female; 60.3 6 11.8 years of age) were enrolled. Seventy-four patients had clinically significant portal hypertension (CSPH), of whom 59 had severe portal hypertension (SPH). ICG-r15 and Lok index were independently related to the presence of both CSPH and SPH, whereas ICG-r15 and INR were related to EV. ICG-r15 values (<6.7% and <6.9%, respectively) were able to rule out the presence of CSPH and SPH (LR 2 0.15 and 0.14); ICG-r15 <10% provided a 97.8% sensitivity (LR 2 0.042) for the exclusion of EV and a 100% sensitivity (LR 2 0.0) for large EV. Conclusion: The ICG-r15 test is an effective tool for assessment of PH in patients with compensated cirrhosis. Although this would not replace endoscopy, the ICG-r15 appears able to identify patients with advanced liver disease in which endoscopy is mandatory as well as rule out the presence of EV in patients with compensated cirrhosis. (HEPATOLOGY 2014;59:643-650) H istological and hemodynamic alterations occurring in the course of chronic liver disease (CLD) are characterized by progressive deposition of extracellular matrix (ECM), leading to liver tissue fibrogenesis and intra-and extrahepatic vascular changes. Capillarization of hepatic sinusoids as well as development of intrahepatic shunts and neoangiogenesis lead to increased intrahepatic resistance to blood flow.1,2 Both architectural and dynamic alterations (activation of myofibroblasts and hepatic stellate cells), together with increased portal blood flow resulting from splanchnic vasodilatation, lead to the development of portal hypertension (PH).The presence of PH is commonly observed in patients with liver cirrhosis. Development of PH significantly increases the risk of complications, such as

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The main purpose of the present study was to determine whether constructional apraxia is due to a visual perceptual disorder in right but not in left brain-damaged patients. In order to resolve this question, 36 normal controls and 73 brain-damaged patients with lesions restricted to the right (N = 30) or to the left (N = 43) cerebral hemisphere were given a graphomotor and a multiple choice version of the Benton Visual Retention Test. The graphomotor version of the V.R.T. was used as a test of constructional praxis, whereas the multiple choice version of the V.R.T. was used as a test of visual form discrimination. No difference was found between right and left brain-damaged patients with respect to incidence and severity of visuo-constructive and of visuo-perceptive disabilities. Contrary to the hypothesis, the relationship between perceptual and praxic tasks was higher in left than in right brain-damaged patients. The high level of correlation found between graphomotor and perceptual scores within the left hemispheric group was due chiefly to the poor performances obtained on both tasks by aphasic patients. These findings are interpreted as suggesting that the basis for visuoconstructive disturbances is a perceptual disorder, independently of the hemispheric side of lesion. The contrasting results of our intercorrelational study and of analogous studies reported in neuropsychological literature are interpreted as being due to sampling differences, in the absence of clearcut qualitative or quantitative differences between visuo-constructive disabilities of right and left brain-damaged patients.

Objective patients presenting with melena and nondiagnostic esophagogastroduodenoscopy are usually investigated with colonoscopy and if negative, with small bowel capsule endoscopy. In this pilot study, we tested feasibility and performance of panenteric capsule endoscopy (PCE) in patients presenting with melena and negative esophagogastroduodenoscopy. Methods Between January and December 2018, consecutive patients presenting with melena, clinically significant bleeding and negative esophagogastroduodenoscopy were invited to undergo PCE by swallowing PillCam Colon 2 (Medtronic Inc., Dublin, Ireland). PCE results, further diagnostic or therapeutic examinations, rebleeding rates at 30 days and 12 months were recorded. Results Out of 128 patients with melena, 23 had negative esophagogastroduodenoscopy. Of them, 12 (8 female, mean age 76 years) underwent PCE, which allowed complete small bowel and colonic evaluation in 12 (100%) and 11 (91.7%) patients, respectively. The small bowel and colon cleansing were adequate in 100 and 83.3%, respectively. No PCE-related complications were observed. The PCE diagnostic yield was 83.3%: significant findings were located in the small bowel, colon or both in 5 (41.7%), 4 (33.3%) and 1 (8.3%) patients, respectively. Device-assisted enteroscopy was performed in 6 (50%) patients. Thirty days and 1 year rebleeding rates were 0 and 18.1%, respectively. Conclusions In this proof-of-concept study, PCE was feasible and safe in patients with melena and negative esophagogastroduodenoscopy, identifying the bleeding site in 83% of patients. PCE lead to small bowel therapeutic interventions in 50% of patients, thus avoiding unnecessary standard colonoscopy. Further large prospective randomized studies investigating this strategy are warranted.

A case of Gerstmann syndrome following a trauma is presented. After one month the patient showed the four symptoms of the Gerstmann syndrome associated with slight visual memory and constructional praxis deficits. Eight months later, however, he showed only dyscalculia, dysgraphia, right-left disorientation and finger agnosia, in accordance with selective damage of the left angular gyrus revealed by CT scan. The findings seems to support the existence and the localizing value of Gerstmann syndrome.

BackgroundUrsodeoxycholic acid (UDCA) administration in intrahepatic cholestasis of pregnancy (ICP) induces bile acids (BA) efflux from the foetal compartment, but the molecular basis of this transplacental transport is only partially defined.AimTo determine if placental breast cancer resistance protein (BCRP), able to transport BA, is regulated by UDCA in ICP.Methods32 pregnant women with ICP (14 untreated, 34.9±5.17 years; 18 treated with UDCA - 25 mg/Kg/day, 32.7±4.62 years,) and 12 healthy controls (33.4±3.32 years) agreed to participate in the study. Placentas were obtained at delivery and processed for membrane extraction. BCRP protein expression was evaluated by immunoblotting techniques and chemiluminescence quantified with a luminograph measuring emitted photons; mRNA expression with real time PCR. Statistical differences between groups were evaluated by ANOVA with Dunn’s Multiple Comparison test.ResultsBCRP was expressed only on the apical membrane of the syncytiotrophoblast. A significant difference was observed among the three groups both for mRNA (ANOVA, p = 0.0074) and protein (ANOVA, p<0.0001) expression. BCRP expression was similar in controls and in the untreated ICP group. UDCA induced a significant increase in placental BCRP mRNA and protein expression compared to controls (350.7±106.3 vs 100±18.68% of controls, p<0.05 and 397.8±56.02 vs 100±11.44% of controls, p<0.001, respectively) and untreated ICP (90.29±17.59% of controls, p<0.05 and 155.0±13.87%, p<0.01).ConclusionOur results confirm that BCRP is expressed only on the apical membrane of the syncytiotrophoblast and show that ICP treatment with high dose UDCA significantly upregulates placental BCRP expression favouring BA efflux from the foetal compartment.

The nyctohemeral pattern of serum luteinizing (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) in eight patients with myotonic dystrophy (MD) was studied. Gonadotropin patterns were classified as adult, pubertal or infantile. Six patients showed an adult pattern, whereas two had a pubertal or infantile pattern. A normal pattern of PRL secretion was found in seven patients and a blunted sleep-related hormonal increase was observed in one. Impaired hypothalamic control of pituitary secretion in MD is proposed as the cause for these findings.

Mild to moderate autoimmune thrombocytopenia (AITP) is a common finding in patients receiving interferon-based antiviral treatment, due to bone marrow suppression. Here we report the case of a patient with chronic genotype 1b hepatitis C virus (HCV) infection treated with pegylated-interferon alpha-2a, ribavirin and telaprevir for 24 wk; the patient developed severe AITP three weeks after treatment withdrawal. We performed a systematic literature search in order to review all published cases of AITP related to HCV antiviral treatment. To our knowledge, this is the second case of AITP observed after antiviral treatment withdrawal. In most published cases AITP occurred during treatment; in fact, among 24 cases of AITP related to interferon-based antiviral treatment, only one occurred after discontinuation. Early diagnosis of AITP is a key factor in order to achieve an early interferon discontinuation; in the era of new direct antiviral agents those patients have to be considered for interferon-free treatment regimens. Prompt prescription of immuno-suppressant treatment (i.e., corticosteroids, immunoglobulin infusion and even rituximab for unresponsive cases) leads to favourable prognosis in most of cases. Physicians using interferon-based treatments should be aware that AITP can occur both during and after treatment, specially in the new era of interferon-free antiviral treatment. Finally, in the case of suspected AITP, presence of anti-platelet antibodies should be checked not only during treatment but also after discontinuation.