Cervical spine radiculopathy epidemiology: systematic review

Background and objective: Cervical spine radiculopathy (CSR) is a disabling condition that has significant negative impacts on a person's mental health, physical functioning and social participation. Research has reported variable CSR incidence and prevalence among different populations. To date, no systematic review has been completed investigating the prevalence or incidence of CSR; therefore, our objective was to determine the incidence and/or prevalence of CSR in adults. Design and method: A systematic review was conducted including searches of PubMed (MEDLINE), EMBASE and CINAHL from inception to February 25, 2020. Studies including data on incidence and/or prevalence of CSR were included. Methodological quality was assessed using a modified Hayden, Cote and Bombardier appraisal checklist. Data were analysed narratively. Results: Nine low- to high-quality studies were included in the final review. Incidence ranged between 0.832 and 1.79 per 1,000 person-years from two high-quality and one low-quality study. Prevalence values ranged from 1.21 to 5.8 per 1,000 from four medium- to high-quality studies. Prevalence values of 1.14% [95% confidence interval (CI): 0.45–1.82] and 1.31% (95% CI: 0.66–1.96) for males and females, respectively, were reported from one medium-quality study. One medium-quality study reported an unadjusted prevalence value of 6.3% for males and females. Conclusions: This is the first systematic review investigating the epidemiology of CSR in an adult population. This review reports a variable incidence rate and prevalence of CSR among specific populations; however, this was based on nine studies. There is a priority to investigate CSR epidemiology across other populations globally and standardising CSR diagnostic criteria

A capillary blood ammonia bedside test following glutamine load to improve the diagnosis of hepatic encephalopathy in cirrhosis

<p>Abstract</p> <p>Background</p> <p>Hepatic encephalopathy (HE) is a frequent and severe complication of cirrhosis. A single determination of ammonia in venous blood correlates poorly with neurological symptoms. Thus, a better biological marker is needed.</p> <p>Aim</p> <p>To make a diagnosis of HE, we explored the value of ammonia in capillary blood, an equivalent to arterial blood, measured at bedside following an oral glutamine challenge.</p> <p>Methods</p> <p>We included 57 patients (age 56 yrs; M/F: 37/20) with cirrhosis (alcoholic = 42; MELD score 13.8 [7-29], esophageal varices = 38) and previous episodes of HE (n = 19), but without neurological deficits at time of examination, and 13 healthy controls (age 54 yrs). After psychometric tests and capillary (ear lobe) blood ammonia measurements, 20 gr of glutamine was administered orally. Tests were repeated at 60 minutes (+ blood ammonia at 30'). Minimal HE was diagnosed if values were > 1.5 SD in at least 2 psychometric tests. Follow-up lasted 12 months.</p> <p>Results</p> <p>The test was well tolerated (nausea = 1; dizziness = 1). Patients showed higher values of capillary blood ammonia over time as compared to controls (0'-30'-60 minutes: 75, 117, 169 versus 52, 59, 78 umol/L, p < 0.05). At baseline, 25 patients (44%) had minimal HE, while 38 patients (67%) met the criteria for HE at 60 minutes (chi²: p < 0.01). For the diagnosis of minimal HE, using the ROC curve analysis, baseline capillary blood ammonia showed an AUC of 0.541 (CI: 0.38-0.7, p = 0.6), while at 60 minutes the AUC was 0.727 (CI: 0.58-0.87, p < 0.006). During follow-up, 18 patients (31%) developed clinical episodes of HE. At multivariate analysis, the MELD score (1.12 [1.018-1.236]), previous episodes of HE (3.2[1.069-9.58]), but not capillary blood ammonia, were independent predictors of event.</p> <p>Conclusions</p> <p>In patients with cirrhosis and normal neurological examination, bedside determination of ammonia in capillary blood following oral glutamine load is well tolerated and achieves a better diagnostic performance for minimal HE than basal capillary ammonia levels. However, capillary blood ammonia is a poor predictor of development of clinically overt HE.</p

Abdominal Surgery in Patients With Idiopathic Noncirrhotic Portal Hypertension: A Multicenter Retrospective Study

In patients with idiopathic noncirrhotic portal hypertension (INCPH), data on morbidity and mortality of abdominal surgery are scarce. We retrospectively analyzed the charts of patients with INCPH undergoing abdominal surgery within the Vascular Liver Disease Interest Group network. Forty‐four patients with biopsy‐proven INCPH were included. Twenty‐five (57%) patients had one or more extrahepatic conditions related to INCPH, and 16 (36%) had a history of ascites. Forty‐five procedures were performed, including 30 that were minor and 15 major. Nine (20%) patients had one or more Dindo‐Clavien grade ≥ 3 complication within 1 month after surgery. Sixteen (33%) patients had one or more portal hypertension–related complication within 3 months after surgery. Extrahepatic conditions related to INCPH (P = 0.03) and history of ascites (P = 0.02) were associated with portal hypertension–related complications within 3 months after surgery. Splenectomy was associated with development of portal vein thrombosis after surgery (P = 0.01). Four (9%) patients died within 6 months after surgery. Six‐month cumulative risk of death was higher in patients with serum creatinine ≥ 100 μmol/L at surgery (33% versus 0%, P < 0.001). An unfavorable outcome (i.e., either liver or surgical complication or death) occurred in 22 (50%) patients and was associated with the presence of extrahepatic conditions related to INCPH, history of ascites, and serum creatinine ≥ 100 μmol/L: 5% of the patients with none of these features had an unfavorable outcome versus 32% and 64% when one or two or more features were present, respectively. Portal decompression procedures prior to surgery (n = 10) were not associated with postoperative outcome. Conclusion: Patients with INCPH are at high risk of major surgical and portal hypertension–related complications when they harbor extrahepatic conditions related to INCPH, history of ascites, or increased serum creatinine

Resident liver progenitor cells: Proofs of their contribution to human liver regeneration.

Whether the epithelial cell response (named "ductular reaction") observed in chronic situations is only a marker of severity of liver disease or plays a role in liver cell regeneration remains under debate. However, recent cell tracking experiments provide a robust argument for the differentiation of those cells in an animal model of chronic liver disease and indicate that the situation could be similar in humans (Deng et al. 2018). Thanks to three other human studies (Lin et al., 2010; Yoon et al. 2011; Lanthier et al. 2015), we believe that epithelial cells give rise to subsequent peribiliary intermediate hepatocytes and create fully functional adjacent hepatocytes that may be beneficial for human liver regeneration

SPINK1, macrophages et cellules progénitrices du foie: de nouvelles pistes pour stimuler la régénération dans l'hépatite alcoolique?

Cet article discute des nouveaux facteurs de bon pronostic identifiés dans l’hépatite alcoolique. Outre la prolifération des hépatocytes - phénomène évident mais pouvant être compromis en cas d’atteinte sévère du foie -, la prolifération des cellules progénitrices est désormais associée à un meilleur pronostic. Le rôle des macrophages hépatiques et de facteurs de croissance comme l'HGF, ou de prolifération comme le SPINK1 ou le TWEAK, est également discuté

Letter: the value of quality liver biopsy before initiation of corticosteroids for severe alcoholic hepatitis

We believe that it is essential to determine the presence of alcoholic steatohepatitis (ASH) on a histological basis not only for cases of diagnostic uncertainty but in all patients with severe (clinical) alcoholic hepatitis (AH) before starting corticosteroid treatment. In the absence of histological confirmation of ASH (10%–20% of cases), such treatment should not be initiated

Liver progenitor cells and therapeutic potential of stem cells in human chronic liver diseases.

Liver progenitor cells, thought to reside in the terminal bile ductules (canals of Hering) at the interface between portal tracts and liver lobule, proliferate during severe hepatic injury. They may contribute to hepatocyte regeneration, or even take over this role if the liver injury is severe and associated with an impairment of hepatocyte proliferation. They represent promising targets in an attempt to stimulate liver regeneration in chronic diseases. Recent studies on liver progenitor cell recruitment in response to injury in chronic viral hepatitis B, hepatitis C, alcoholic and non-alcoholic liver diseases are presented in this review, as well as clinical trials in which stem cells are administered as a therapeutic intervention to promote liver regeneration. Liver progenitor cell expansion is part of the disease process itself and may contribute to disease severity, mainly related to fibrosis. As the majority of these progenitor cells tend to acquire a biliary phenotype, their role in liver repair and improvement in liver function remains to be addressed. Present data on stem cell therapy are heterogeneous in terms of methods and endpoints; thus, results need to be carefully examined prior to drawing a conclusion on possible benefits

Severe immune-mediated drug-induced liver injury linked to ibandronate: a case report

Ibandronate is a widely used bisphosphonate with no previously well documented hepatotoxicity. We report the first case of ibandronate-related hepatotoxicity and, to our knowledge, the first case of immune-mediated drug-induced liver injury (DILI) related to bisphosphonates