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Biomedical subjects

A Lonardo

Publications and source records attributed to A Lonardo.

At least 19 recordsLinked to original sources
PubMed2006

Hepatitis C and steatosis: a reappraisal.

The overall prevalence of steatosis in patients with Hepatitis C virus (HCV) chronic infection is 55.5% (range 34.8-81.2%). This is a two to threefold increase compared with the prevalence of steatosis in chronic hepatitides because of other aetiologies and of the figures expected on the grounds of a steatosis-HCV chance association. HCV genotype 3 (HCV-3) has specific epidemiological features; furthermore, as compared with HCV-non-3 genotypes, it is associated with a higher prevalence (74.1%vs 47.9%, P < 0.01) and with more severe grades of steatosis (prevalence of grade 3 steatosis 29.6 vs 5.5 P < 0.01). Host and viral factors play a role, although to a variable extent, in the pathogenesis of HCV-3 and non-3 steatosis. HCV load and body mass index are associated with steatosis in HCV-3 and in HCV-non-3 patients respectively. Serum cholesterol levels and liver steatosis at baseline follow an inverse relationship in HCV infection. As hypocholesterolaemia corrects only in those sustained responders to antiviral treatment both in genotype 3 and in non-3 genotypes, the occurrence of a virally induced, acquired and reversible hypobetalipoproteinaemia seems plausible. Steatosis affects the natural course of HCV infection: it is associated with fibrosis, a possible mediator of increased risk to develop type 2 diabetes, it impairs the response to antiviral treatment in HCV-3 patients and might constitute a risk factor for the development of hepatocellular carcinoma. These observations indicate the need to evaluate the efficacy of combined antiviral and 'metabolic' approaches vs standard antiviral regimes in patients with steatosis and HCV chronic infection.

Antiviral Agents↗
PubMed2005

Review article: the metabolic syndrome and non-alcoholic fatty liver disease.

Metabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity. The liver is a target organ in metabolic syndrome patients in which it manifests itself with non-alcoholic fatty liver disease spanning steatosis through hepatocellular carcinoma via steatohepatitis and cirrhosis. Given that metabolic syndrome and non-alcoholic fatty liver disease affect the same insulin-resistant patients, not unexpectedly, there are amazing similarities between metabolic syndrome and non-alcoholic fatty liver disease in terms of prevalence, pathogenesis, clinical features and outcome. The available drug weaponry for metabolic syndrome includes aspirin, metformin, peroxisome proliferator-activated receptor agonists, statins, ACE (angiotensin I-converting enzyme) inhibitors and sartans, which are potentially or clinically useful also to the non-alcoholic fatty liver disease patient. Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non-alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance-related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non-alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non-alcoholic fatty liver disease.

Cardiovascular Diseases↗
PubMed2005

Review article: hepatic steatosis and insulin resistance.

Hepatic steatosis may be both an adaptive phenomenon and an example of lipotoxicity. Its prevalence ranks in the same order of magnitude of insulin resistance in the general population. Studies support the finding that hepatic steatosis is secondary to insulin resistance and not vice versa. A steatotic liver will further contribute to the development of insulin resistance through impaired clearance of insulin from the portal blood, creating a vicious cycle. Insulin resistance is the leading force in the pathogenesis and natural history of non-alcoholic fatty liver disease. Dysfunction of energetic homeostasis and the interaction of adiponectin, leptin and tumour necrosis factor-alpha are key events in the pathogenesis of steatosis and insulin resistance. Insulin resistance represents the frame within which hepatic and extrahepatic non-alcoholic fatty liver disease-related clinical manifestations are to be anticipated and interpreted.

Adenosine Triphosphate↗
PubMed2002

Fasting insulin and uric acid levels but not indices of iron metabolism are independent predictors of non-alcoholic fatty liver disease. A case-control study.

BACKGROUND: Non-alcoholic fatty liver disease is a common reason for hepatological consultation and may herald severe hepatic and extra-hepatic disease. The aetiopathogenesis of this condition is an area of increasing interest. AIM: To evaluate anthropometric and biochemical factors associated to non-alcoholic fatty liver disease in a case-control study. Methods. Demographic and biochemical data of 60 consecutive patients with bright liver absent-to-low alcohol consumption, no evidence of viral, genetic and autoimmune diseases, were compared to those of 60 age- and gender-matched historical controls without fatty liver by univariate and multiple logistic regression analysis. RESULTS: Patients were more often hypertriglyceridaemic, obese and diabetic than controls (p<.01). Mean values of alanine transaminase, gammaglutamyltranspeptidase, triglycerides, uric acid, fasting and log insulin, transferrin percent saturation and ferritin were significantly higher in the patients, while transferrin and quantitative insulin sensitivity check index, a quantitative insulin sensitivity index, were lower. No iron storage was found in those who underwent liver biopsy At univariate analysis the relative risk for non-alcoholic fatty liver disease significantly increased (p<0. 05) with increasing body mass index, fasting insulin, alanine transaminase, uric acid, triglycerides and gammaglutamyltranspeptidase; it decreased with increasing transferrin and quantitative insulin sensitivity check index. Multiple logistic regression analysis disclosed only fasting insulin and uric acid to be independent predictors of non-alcoholic fatty liver disease (p<0.05). CONCLUSIONS: Fasting insulin and serum uric acid levels indicating insulin resistance, but not indices of iron overload, are independent predictors of non-alcoholic fatty liver disease.

Case-Control Studies↗
PubMed2001

Phenotypic expression of familial hypobetalipoproteinemia in three kindreds with mutations of apolipoprotein B gene.

We report the clinical phenotype in three kindreds with familial heterozygous hypobetalipoproteinemia (FHBL) carrying novel truncated apolipoprotein Bs (apoBs) of different sizes (apoB-8.15, apoB-33.4 and apoB-75.7). In D.A. kindred, we found three carriers of a C-deletion in exon 10 leading to the synthesis of apoB-8.15 not detectable in plasma. They showed steatorrhea and fatty liver. In N.L. kindred, the proband is heterozygous for a nonsense mutation in exon 26, leading to the formation of apoB-33.4. He had premature cerebrovascular disease and fatty liver; two apoB-33.4 carriers in this kindred showed only fatty liver. In B.E. kindred, the proband is heterozygous for a T-deletion in exon 26, which converts tyrosine at codon 3435 into a stop codon, resulting in apoB-75.7. The proband, a heavy alcohol drinker, had steatohepatitis, whereas his teetotaller daughter, an apoB-75.7 carrier, had no detectable fatty liver. This study suggests that: i) fatty liver invariably develops in FHBL carriers of short and medium-size truncated apoBs (< apoB-48), but its occurrence needs additional environmental factors in carriers of longer apoB forms; ii) intestinal lipid malabsorption develops only in carriers of short truncated apoBs, which are not secreted into the plasma; and iii) cerebrovascular disease due to premature atherosclerosis may occur even in FHBL subjects.

Adult↗
PubMed2000

A study of fatty liver disease and plasma lipoproteins in a kindred with familial hypobetalipoproteinemia due to a novel truncated form of apolipoprotein B (APO B-54.5).

BACKGROUND/AIMS: Familial hypobetalipoproteinemia (FHBL) is a co-dominant disorder characterized by reduced plasma levels of low-density lipoproteins. It can be caused by mutations in the gene encoding apolipoprotein B-100 (apo B), leading to the formation of truncated apo Bs which have a reduced capacity to export lipids from the hepatocytes as lipoprotein constituents. Case reports suggest the occurrence of liver disease in FHBL, but there are no studies of liver involvement in FHBL with defined apo B gene mutations. The presence of fatty liver disease was investigated in a large FHBL kindred. METHODS: Plasma lipoprotein and apolipoprotein analysis, liver function tests, and apo B gene sequence were performed in 16 members of a FHBL kindred. The presence of fatty liver was assessed by ultrasound and computed tomography scanning. RESULTS: The proband, a non-obese heavy drinker male with hypobetalipoproteinemia, had steatohepatitis with fibrosis. He was heterozygous for a novel non-sense mutation of apo B gene producing a truncated apo B of 2745 amino acids (designated apo B-54.5, having half the size of normal apo B-100). Seven other members of his kindred carried apo B-54.5. Although all of them were hypolipidemic, their lipid levels showed a large inter-individual variability not accounted for by polymorphisms of genes involved in apo B metabolism. Four carriers (two heavy drinkers and two teetotallers), irrespective of their plasma lipid levels, had ultrasonographic evidence of fatty liver. In the other four carriers no evidence of fatty liver was found. CONCLUSIONS: In this kindred apo B-54.5 predisposes to fatty liver, which however may require some additional factors to become clinically relevant.

Apolipoproteins↗
PubMed2000

Are there any sex differences in fatty liver? A study of glucose metabolism and body fat distribution.

BACKGROUND AND AIMS: Fatty liver is a common condition found more often in males. Whether sex differences affect its development is presently unknown. The hypothesis that glucose metabolism alterations or central body fat distribution are gender-related in fatty liver was investigated. METHODS: Overall 199 consecutive subjects seen in the Division of Internal Medicine and Gastroenterology, Modena City Hospital, were enrolled. In the main arm of the present study, 44 men with sonographic fatty liver and 47 controls without, and 18 women with and 19 without fatty liver had their body mass index (an index of overall adiposity), hepatobiliary serum enzymes, serum cholesterol and triglycerides determined. All underwent oral glucose tolerance tests (estimated through the glucose area under the curve with the trapezoidal method). In the ancillary arm study, 17 other men with and 14 without, and 11 other women with and 29 without fatty liver had anthropometric measurements of body fat distribution (waist/hip, waist/height and skinfold thickness). RESULTS: Following statistical evaluation including univariate and multivariate analyses (main study), elevated body mass index was found to be an independent predictor of fatty liver in either sex. Glucose area under the curve and a central-type body fat distribution (ancillary study) predicted FL only in women. CONCLUSIONS: Fatty liver could be gender-related in the present series.

Body Mass Index↗
PubMed1999

Fatty liver and nonalcoholic steatohepatitis. Where do we stand and where are we going?

BACKGROUND: Fatty liver (FL) is the most common liver disease but its clinical significance remains elusive. Nonalcoholic steatohepatitis (NASH) is increasingly recognized as a cause of liver failure, sometimes recurring following transplantation. Recent data on both conditions are critically reviewed. METHODS: A Medline search of the medical literature (1990 to September 1998) and cross-references was performed. RESULTS: FL most commonly affects middle-aged men with obesity, altered glucose metabolism, hyperlipidemia, and hypertension. The link between biology of HCV, iron metabolism and FL should be addressed. Prospective studies should also quantify the rate and the factors involved in the progression of FL to NASH. The clinical spectrum of NASH is currently broader than it was initially recognized. Diagnosis of FL and NASH may involve ultrasonography, liver biopsy, and recognition of related conditions. Treatment of these conditions must be tailored according to patient's features. CONCLUSIONS: The clinical significance of FL is incompletely understood at present. The relationship, if any, of FL and the metabolic syndrome should be carefully investigated.

Fatty Liver↗
PubMed1999

Ischaemic necrotizing pancreatitis after cardiac surgery. A case report and review of the literature.

Ischaemia is a rare but often lethal aetiology of pancreatitis. A 67-year-old man underwent aortocoronary by-pass. Postoperatively, he developed atrial fibrillation and possibly acute myocardial infarction. Later, he had acute pancreatitis and underwent laparotomy for purulent peritonitis due to a ruptured pancreatic abscess. Cholesterolosis was found but no gallstones. The postoperative period was heavily complicated and the patient eventually died due to multiorgan failure. The occurrence of ischaemic pancreatitis should be more readily suspected in patients with abdominal symptoms following surgery that induces ischaemia of the pancreas. It is possible that delay in diagnosis accounts for the high death rate of such postoperative complication.

Aged↗
PubMed1998

Isolated jejunal Crohn's disease in a young adult presenting as fever of unknown origin.

A 27-yr-old man was referred for fever, weight loss, fatigue, and occasional mild epimesogastric pain without diarrhea or vomiting. Laboratory tests were suggestive of an active inflammatory disease but serological, bacteriological, viral searches, markers of autoimmunity, and neoplasia were all negative. The following were also negative: ultrasonography; conventional x-rays; CT scans; esophagogastroduodenoscopy, pancolonoscopy with ileoscopy; cytohistology including duodenum and ileocolon. Empiric antibiotic regimens failed to control the temperature. Small bowel enema disclosed multiple proximal jejunal strictures. Jejunoscopy revealed erythema, friability, linear ulcerations, stenosis, and dilation in the proximal jejunum. Multiple directed biopsies showed inflammatory changes devoid of any specific features. The patient received steroid treatment and his temperature normalized. Six months later, he was readmitted on account of intestinal subocclusion that was managed conservatively. A few days later urgent laparotomy was performed with peritoneal lavage, repair of double perforated proximal jejunal ulcers, and stricturoplasty. Surgical jejunal biopsy confirmed the results of enteroscopic biopsies. The patient is presently without fever, in the absence of steroid treatment. There have been no reports of cryptogenic fever due to isolated jejunal Crohn's disease in the recent literature. Our patient's clinical picture resembled disease as seen in older children and adolescents, in whom it is a difficult diagnosis owing to the absence of diarrhea. In adults with Crohn's disease isolated jejunal involvement represents approximately 1% of cases. A thorough small bowel investigation is warranted in young adults with cryptogenic fever and low serum protein levels, even in the absence of major gastrointestinal complaints.

Adult↗
PubMed1997

The bright liver syndrome. Prevalence and determinants of a "bright" liver echopattern.

BACKGROUND: "Bright" liver at ultrasonography predicts fatty liver. AIM: To assess prevalence and predictors of a bright liver. METHODS: Prevalence arm--Prospective collection of records of unselected patients undergoing liver ultrasound. Protocol arm--A sample of patients with bright liver underwent routine laboratory investigations, liver tests, HBsAg (EIA) and anti-HCV (ELISA). Equipment--Grey scale real-time scanner. Bright liver diagnosed through the liver-kidney contrast. Statistics--Student's t-test; chi-square test; one-way analysis of variance; stepwise multiple logistic regression analysis, forward and backward. RESULTS: Prevalence arm--72 out of 363 (19.8%) cases had bright liver. Protocol arm--100 cases underwent laboratory evaluation. No difference was found in mean values of fasting plasma glucose, LDL cholesterol, apo A, Lp(a), uric acid, total bilirubin, GOT, GPT, AP, GGT, and serum bile acids or in the prevalence of serum HBsAg and anti-HCV in bright liver vs control groups. Univariate analysis showed body mass index, age, total cholesterol triglycerides, apo B, albumin, HDL cholesterol to be significantly different between cases and controls. However, the last 2 variables dropped out when logistic regression analysis was applied. CONCLUSIONS: 1. Roughly 20% of Italian patients undergoing US for routine clinical practice will have a bright liver. 2. Body mass index, age, serum cholesterol, triglycerides, and apo B levels are the independent predictors of a bright liver.

Aged↗
PubMed1996

Fatty liver in heterozygous hypobetalipoproteinemia caused by a novel truncated form of apolipoprotein B.

Fatty liver has been anecdotally associated with heterozygous hypobetalipoproteinemia. The aim of this study was to characterize the molecular defect in a subject with heterozygous hypobetalipoproteinemia (low-density lipoprotein cholesterol, 52 mg/dL; apolipoprotein [apo] B, 15 mg/dL) and otherwise unexplained fatty liver. Plasma lipoproteins were separated by ultracentrifugation, and apo B was analyzed by electrophoresis and immunoblotting. A fragment of genomic DNA corresponding to the 5' end of exon 26 of the apo B gene was amplified by polymerase chain reaction and sequenced. The plasma lipoproteins of the proband contained, besides normal apo B-100, a 200-kilodalton truncated apo B whose size suggested the presence of a mutation in exon 26 of the apo B gene. The nucleotide sequence of a fragment of the 5' end of exon 26 revealed that the proband was a heterozygote for a 14-nucleotide deletion, producing a frameshift resulting in a premature stop codon at residue 1768. This truncated apo B was named apo B-38.95. The proband's father was a carrier of the same mutation. Fatty liver in this subject with familial heterozygous hypobetalipoproteinemia most likely results from the inability of apo B-38.95 to export lipids from hepatocytes into the blood stream. Heterozygous hypobetalipoproteinemia should be considered in a hypolipidemic subject with an otherwise unexplained fatty liver.

Adult↗