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Biomedical subjects

D Conte

Publications and source records attributed to D Conte.

At least 91 records · Page 5Linked to original sources
PubMed1998

Pattern of plasma cyclic nucleotides and related hormones in liver cirrhosis and hepatocellular carcinoma.

To evaluate the pattern of plasma cyclic adenosine 3',5'-monophosphate, cyclic guanosine 3',5'-monophosphate, atrial natriuretic factor and glucagon levels in different stages of chronic liver diseases, we measured these variables in 20 normal subjects, 25 patients with genetic hemochromatosis, associated with liver cirrhosis in 19 cases and not in six, eight patients with compensated and 15 with decompensated alcoholic or posthepatitic cirrhosis, and 12 with hepatocellular carcinoma. All variables were within the normal range in non-cirrhotic hemochromatotic patients. Cyclic adenosine 3',5'-monophosphate levels were within the normal range (9.5-15.7 nmol/l) in hemochromatotic cirrhotics and elevated in other patients. Cyclic guanosine 3',5'-monophosphate, atrial natriuretic factor and glucagon were above the normal ranges (1.92-5.91 nmol/l, 8.8-62.7 ng/l, and 39-165 ng/l, respectively) in most patients with cirrhosis both with and without hemochromatosis and in most individuals with hepatocellular carcinoma. Cyclic guanosine 3',5'-monophosphate correlated with atrial natriuretic factor in the former groups but not in the latter. These findings indicate that glucagon and atrial natriuretic factor hypersecretion is an early event in cirrhosis, regardless of its etiology. In hepatocellular carcinoma, the underlying cirrhosis may account for most hormonal and metabolic changes although cyclic guanosine 3',5'-monophosphate increases could also be due to the neoplastic process per se.

Adult↗
PubMed1998

[Respiratory variant of constrictive pericarditis. Report of 4 cases].

Constrictive pericarditis was diagnosed in four patients who presented respiratory impairment and pleural effusion, associated with right ventricular failure in two. The cause was probable tuberculosis in two cases, post-irradiation lesions in one and unknown in one. The diagnosis was suspected due to the normal heart volume and pathological electrocardiogram as well as the computed tomographic findings demonstrating pericardial morphology. Right catheterism confirmed the diagnosis: increased right ventricular telediastolic pressure with a dip plateau and equivalent pressures in the right atrium and ventricle. Early diagnosis allowed pericardectomy in two cases. In one case, the subacute epicardopericarditis regressed with corticosteroids and antituberculosis therapy.

Aged↗
PubMed1998

High prevalence but low pathogenicity of hepatitis G virus infection in Italian patients with genetic haemochromatosis.

BACKGROUND: Various environmental factors have been shown to hasten cirrhosis and hepatocellular carcinoma in patients with genetic haemochromatosis. AIM: To assess the prevalence and the role of the recently identified hepatitis G virus in 70 patients with genetic haemochromatosis in comparison with 40 patients with cryptogenic chronic hepatitis and 200 regular blood donors. PATIENTS: Six patients with genetic haemochromatosis (9%) had serum hepatitis B surface antigen, 14 (20%) had serum hepatitis C virus RNA. A liver biopsy was available in 66 patients with genetic haemochromatosis (43 with cirrhosis) and 40 with cryptogenic hepatitis (4 with cirrhosis). METHODS: Serum HGV-RNA was detected by a reverse transcriptase polymerase chain reaction using primers derived from the 5'-non-coding and non-structural-5A regions of the viral genome. Serum IgG antibodies against HGV were detected by enzyme-linked immunosorbent assay using a recombinant E2 protein of the virus envelope. RESULTS: The prevalence of serum HGV-RNA was higher in patients with cryptogenic hepatitis (n = 6, 15%) and genetic haemochromatosis (n = 6, 9%) than in donors (n = 3, 1.5%) (p = 0.0008 and p = 0.01, respectively). The corresponding figures for serum anti-HGV were 4 (10%), 16 (23%) and 10 (5%). The six haemochromatotic patients with serum HGV-RNA more often had parenteral exposure to blood (50% vs 5%, p < 0.001), and persistently elevated serum aminotransferases (100% vs 31%, p < 0.001) than the 64 non-viraemic patients. The six HGV-RNA seropositive patients with cryptogenic hepatitis were older than the 34 non-viraemic patients (56 vs 34 years, p < 0.05). CONCLUSIONS: The prevalence of serum markers of HGV infection in patients with genetic haemochromatosis is higher than in blood donors, but similar to that of patients with cryptogenic chronic hepatitis. However, HGV is not a cofactor of morbidity in patients with genetic haemochromatosis.

Adult↗
PubMed1998

Iron-related indexes in chronic alcoholics. Effect of alcohol withdrawal.

BACKGROUND: Increased serum transferrin saturation and ferritin levels have been reported in chronic alcoholics. AIM: To evaluate modifications in serum iron-related indexes in chronic alcohol abusers with and without cirrhosis, at enrolment and after complete alcohol withdrawal. PATIENTS: Fifty-one consecutive chronic alcohol abusers, 33 without and 18 with cirrhosis. METHODS: Liver function tests were performed and transferrin saturation percent and serum ferritin levels measured at time 0 and after 7 and 14 days of complete alcohol withdrawal. RESULTS: Duration of alcohol abuse was significantly longer in patients with cirrhosis than in those without (24 +/- 13 SD vs 18 +/- 13 SD years, p < 0.01). A concomitant increase in transferrin saturation percent and serum ferritin was found in 60% of the cirrhotics and 45% of the non cirrhotic group. During the observation period, transferrin saturation percent and serum ferritin fell significantly in both groups (from 59 +/- 33 SD to 36 +/- 22% SD, p < 0.05, and from 900 +/- 933 SD to 469 +/- 457 SD ng/ml, p < 0.01, in cirrhotics, and from 46 +/- 30 SD to 27 +/- 12% SD, p < 0.01, and from 702 +/- 602 SD to 340 +/- 29 SD ng/ml, p < 0.01, in non cirrhotics). CONCLUSIONS: Iron-related indexes increase with chronic alcohol abuse and return to normal rapidly after complete alcohol withdrawal. In chronic alcoholics the timing of determinations of iron-related indexes is crucial, and screening for possible concomitant genetic haemochromatosis must be postponed.

Adult↗
PubMed1997

Inappropriately high iron regulatory protein activity in monocytes of patients with genetic hemochromatosis.

In genetic hemochromatosis (GH), excess iron is deposited in parenchymal cells, whereas little iron is found in reticuloendothelial (RE) cells until the later stages of the disease. As iron absorption is inversely related to RE cells stores, a failure of RE to retain iron has been proposed as the basic defect in GH. In RE cells of GH subjects, we examined the activity of iron regulatory protein (IRP), a reliable indicator of the elusive regulatory labile iron pool, which modulates cellular iron homeostasis through control of ferritin (Ft) and transferrin receptor gene expression. RNA-bandshift assays showed a significant increase in IRP activity in monocytes from 16 patients with untreated GH compared with 28 control subjects (1.5-fold) and five patients with secondary hemochromatosis (SH) with similar iron burden (fourfold). In 17 phlebotomy-treated GH patients, IRP activity did not differ from that of control subjects. In both GH and SH monocyte-macrophages, Ft content increased by twofold and the L subunit-rich isoferritin profile was unchanged as compared with controls. IRP activity was still upregulated in vitro in monocyte-derived macrophages of GH subjects but, following manipulations of iron levels, was modulated normally. Therefore, the sustained activity of monocyte IRP found in vivo in monocytes of GH patients is not due to an inherent defect of its control, but is rather the expression of a critical abnormality of iron metabolism, eg, a paradoxical contraction of the regulatory iron pool. By preventing Ft mRNA translation, high IRP activity in monocytes may represent a molecular mechanism contributing to the inadequate Ft accumulation and insufficient RE iron storage in GH.

Adult↗
PubMed1997

Stimulatory action of endothelin-1 on rat Leydig cells: involvement of endothelin-A subtype receptor and phospholipase A2-arachidonate metabolism system.

In a previous report we have observed that endothelin-1 (ET-1) is able to stimulate testosterone (T) production by rat Leydig cells revealing an interaction with human chorionic gonadotropin (hCG). The present study was designed to further characterize the stimulatory action of ET on testicular steroidogenesis, to evaluate which subtype of ET receptors is involved in this activity and to examine the role of phospholipase A2 (PLA2)-arachidonate metabolism system in ET-1 transduction mechanism. To this purpose we investigated: i) the interaction of ET-1 with another secretagogue of T, like luteinizing hormone releasing hormone (LHRH); ii) the interference of ET(A) and ET(B) receptor antagonists (BQ-123 and BQ-788, respectively) and of inhibitors of PLA2 (quinacrine) and arachidonate lipoxygenase pathway (nordihydroguaiaretic acid:NDGA) on ET-1-induced T and PGE2 secretion from purified rat Leydig cells. Data obtained indicate that ET-1 amplified T and PGE2 response to LHRH and this secretagogue in turn potentiated testicular steroidogenesis stimulated by endothelin. The ET(A) antagonist, BQ-123, inhibited in a dose-related fashion ET-1-induced T production whereas ET(B) antagonist, BQ-788, failed to affect T response to the peptide. Furthermore, ET(A) antagonist inhibited the stimulatory effect of ET-1 on hCG- or LHRH-induced T secretion and it was able to exert a dose-dependent inhibition of ET-1-stimulated PGE2 output. Moreover, a PLA2 inhibitor quinacrine inhibited the stimulatory action of ET-1 on T production and suppressed basal and ET-1-induced PGE2 release whilst a lipoxygenase blocker NDGA did not modify T response to the peptide. Taken together these findings i) indicate additivity of effects between ET-1 and LHRH in stimulating T and PGE2 production; ii) confirm that ET(A) subtype receptors mediate the stimulatory action of ET-1 on rat Leydig cells; iii) strongly suggest that PLA2-arachidonate metabolism system is involved in endothelin transduction mechanism.

Animals↗
PubMed1997

Pituitary adenylate cyclase-activating polypeptide regulates rat Leydig cell function in vitro.

The present study was designed to evaluate the effects of both pituitary adenylate cyclase-activating polypeptide (PACAP)-27 and PACAP-38 on testosterone, cAMP and prostaglandin E2 (PGE2) production by purified rat Leyding cells. Because PACAP-38 shares homology with vasoactive intestinal peptide (VIP), the effects of VIP and both PACAP and VIP receptor antagonists on testicular steroidogenesis were also examined. PACAP-38 potentiated testosterone response to a low effective dose of human chorionic gonadotropin (hCG), while PACAP-27 was without effect. Furthermore, PACAP-38 amplified testosterone response to a wide concentration range of hCG until the submaximal dose. VIP evoked a dose-dependent increase of both basal and hCG-induced testosterone production. PACAP potentiation of steroidogenesis was nullified in the presence of a PACAP antagonist, but was not modified by a VIP antagonist. Moreover, while VIP antagonist blunted testosterone response to VIP, PACAP antagonist was without effect. Increasing concentrations of PACAP-38 evoked a dose-response enhancement of both cAMP and PGE2 production. However, this fatty acid is not involved in PACAP activity, as a prostaglandin blocker indomethacin did not modify the effect of PACAP on steroidogenesis. Taken together these findings: (i) demonstrate that PACAP-38 is able to activate both cAMP- and phosphatidylinositol-dependent mechanisms in Leydig cells; (ii) indicate that the peptide exerts an amplificatory action on testicular steroidogenesis stimulated by hCG and that this activity is receptor-mediated, as it is prevented by a PACAP receptor antagonist; (iii) predict the existence of specific PACAP receptors (type 1 binding sites) on Leydig cells.

Animals↗
PubMed1997

Assessment of antihypertensive effect by blood pressure monitoring: applications to bisoprolol and lisinopril in a double-blind study.

The aim of this study was to evaluate the antihypertensive effect of drugs according to the initial ambulatory blood pressure (BP) level. After a 15-day placebo run-in period, 105 patients with moderate essential hypertension (mean age, 52 years) underwent 24-h BP monitoring (spacelabs: 1 measure/15 min). Patients were subdivided into two groups: the "High" group, with 24-h mean values of systolic BP (SBP) > 137 or diastolic BP (DBP) > 87 mm Hg, and the "Low" group, with SBP < or = 137 and DBP < or = 87 mm Hg. All patients received, in a random and double-blind design, either bisoprolol (10 mg q.d.) or lisinopril (20 mg q.d.) for 8 weeks. At the end of this active treatment period, office and ambulatory BP measurements were performed. Casual measurements revealed similar BP decreases in all subgroups receiving bisoprolol and lisinopril; BP monitoring showed that the antihypertensive effect depended on the baseline mean 24-h value; -15/-12 mm Hg for bisoprolol and -18/-13 mm Hg for lisinopril in the High group; -7/-6 mm Hg for bisoprolol and -6/-6 mm Hg for lisinopril in the Low group. This study shows that the antihypertensive effect depended on initial ambulatory BP values, with a lower BP decrease in the Low group. Assessment of the antihypertensive effect on ambulatory BP is useful in clinical trials.

Adrenergic beta-Antagonists↗
PubMed1997

Screening patients with celiac disease for primary biliary cirrhosis and vice versa.

BACKGROUND: An association between celiac disease and primary biliary cirrhosis has been reported in a few cases, mainly as individual case reports. OBJECTIVES: To screen adult patients with celiac disease for primary biliary cirrhosis and patients with primary biliary cirrhosis for intestinal celiac involvement. METHODS: The celiac group consisted of 336 adults (218 women and 118 men; mean age, 36 yr; range 18-74 yr) with celiac disease diagnosed by serological and histological tests, 38 with newly diagnosed celiac disease and 298 with previously diagnosed celiac disease who were consuming a gluten-free diet. The mean follow-up period was 6 yr (range, 1-16 yr). Liver function parameters and autoantibody levels were determined, and, when indicated, histological tests were performed. The biliary cirrhosis group consisted of 65 subjects (58 women and seven men) (mean age, 59 yr; range, 35-67 yr) with primary biliary cirrhosis diagnosed 1-17 years previously (mean, 7 yr) on the basis of the usual biochemical, serological, and histological criteria. Antigliadin and antiendomysium antibody levels were determined, and two biopsy specimens from the distal duodenum obtained during endoscopy were evaluated. RESULTS: In patients with celiac disease, impairment of liver function was frequently found at diagnosis (16 of 38, or 44%), but primary biliary cirrhosis was diagnosed in only one case. In patients with primary biliary cirrhosis, no cases of celiac disease, as currently defined, were found. CONCLUSIONS: Our findings indicate that celiac disease and primary biliary cirrhosis are rarely associated and support the hypothesis that the intestinal lesions per se are not responsible for the liver disease.

Adolescent↗
PubMed1996

In vivo and in vitro iron-replaced zinc finger generates free radicals and causes DNA damage.

The estrogen receptor (ER) is a ligand-activated transcription factor whose DNA-binding domain (ERDBD) has eight cysteines, which coordinate two zinc atoms, forming two zinc finger-like structures. We demonstrate the capability of iron to replace zinc in zinc finger (hereby referred to as iron finger) both in vivo (using Escherichia coli BL21 (DE3)) and in vitro. Iron has the ability to substitute for zinc in the ERDBD as demonstrated by mobility shift and methylation interference assays of iron finger, which show specific recognition of the estrogen response element. The DNA binding constants for both in vivo and in vitro iron-replaced zinc fingers were similar to that of the native finger. Atomic absorption analysis revealed a ratio of 2:1 iron atoms/mol of ERDBD protein, as found for zinc in the crystal structure of native ERDBD. More importantly, we demonstrate that iron finger in the presence of H2O2 and ascorbate generates highly reactive free radicals, causing a reproducible cleavage pattern to the proximate DNA, the estrogen response element. The deoxyribose method, used to detect free radical species generated, and the resultant cleaved DNA ends, caused by iron finger, suggest that the free radicals generated are hydroxyl radicals. Due to the close proximity of the zinc finger to DNA, we postulate that iron-substituted zinc finger may generate free radicals while bound to genetic regulatory response elements, leading to adverse consequences such as iron-induced toxicity and/or carcinogenesis.

Base Sequence↗
PubMed1996

Aspirin inhibition of naloxone-induced luteinizing hormone secretion in man.

It is well known that endogenous opioid peptides exert a tonic inhibitory control on GnRH release, leading to the inhibition of LH secretion, whereas eicosanoids, particularly prostaglandin E2(PGE2), stimulate GnRH output. Furthermore, in vitro studies suggest the existence of an interaction between these two regulatory systems in animals. The present work was designed to evaluate the acute effect of the prostaglandin blocker aspirin on plasma LH response to the opiate antagonist naloxone or GnRH in normal volunteers in a placebo-controlled, single-blind study. To exclude a hypothetical action of aspirin directly at the testis level, plasma testosterone concentrations were monitored during basal sampling after acetylsalicylic acid ingestion, whereas the efficacy of the drug as a prostaglandin blocker was tested by the determination of seminal PGE2 levels. Aspirin pretreatment significantly lowered seminal PGE2 levels (from 86 +/- 5 before to 11 +/- 2 micrograms/mL [corrected] after drug administration; P < 0.001) without affecting testosterone concentrations. Moreover, the drug induced a significant reduction of LH response to naloxone, assessed as the mean integrated area under the curve, from 1666.5 +/- 116 to 1197.5 +/- 98 mUI/mL per min (P < 0.05), whereas it did not influence GnRH-induced LH release. We conclude that the effective cycloxygenase blockade inhibits the stimulatory activity of naloxone on LH release, suggesting that the inhibitory tone of opioids on GnRH secretion may be caused by the block of hypothalamic prostaglandin biosynthesis with consequent inhibition of PGE2-induced GnRH secretion.

Adult↗
PubMed1995

Deregulation of cyclin E in breast cancer.

Cyclin E, a regulatory subunit of cyclin dependent kinase-2, is thought to be rate limiting for the G1/S transition during the mammalian cell cycle. Previously, we showed severe alterations in cyclin E protein expression in human mammary epithelial cell lines and in surgical material obtained from patients with various malignancies. To understand the functional basis of these alterations we analyse here the regulation of cyclin E in breast cancer cells. We find that while cyclin E protein and its associated kinase activity in normal cells are cell cycle regulated, in tumor cells it remains in an active complex throughout the cell cycle. We also analysed cyclin E for possible deletions which could result in its constitutive function and found two novel truncated variants in its coding region. These variant forms of cyclin E were detected in several normal and tumor cell lines and tissue specimens. However, Western blot analysis indicated that only the multiple isoforms of cyclin E protein were expressed in tumor but not the normal tissue specimen, suggesting post transcriptional regulation of cyclin E. Lastly, in vitro analyses indicated that these truncated variant forms of cyclin E are biochemically active in their ability to phosphorylate histone H1. Collectively these observations suggest the presence of more than one form of cyclin E mRNA in all cells, normal and tumor. Once translated in tumor cells, the protein products of these truncated forms could give rise to a constitutively active form of cyclin E containing complexes.

Base Sequence↗
PubMed1995

Portal hypertension and iron depletion in patients with genetic hemochromatosis.

Clinically, portal hypertension has been considered to be less common and less severe in patients with cirrhosis resulting from iron overload in homozygotes for genetic hemochromatosis than in patients with cirrhosis of other causes. To characterize the prevalence and progression of portal hypertension in genetic hemochromatosis (GH), 120 cirrhosis and iron-overloaded patients were compared with a control group of 120 patients with postnecrotic cirrhosis (PNC) who were matched for gender, age, Child's class, and alcohol abuse. Gastroesophageal endoscopy and abdominal ultrasonography were performed at diagnosis and repeated every 12 months and every 6 months, respectively, to evaluate the presence and severity of varices, the caliber of the portal vein and its collaterals, and splenic size. At diagnosis a similar frequency of varices was observed in patients with GH (25%) and in PNC (24%), as well as of portal vein abnormalities and spleen enlargement. During the follow-up period, all but two of the patients with GH were treated by phlebotomy and depleted of excess iron. After a mean of 6 +/- 4.3 (SD) years of observations (range, 2 to 10 years), varices were improved or completely reversed in 26% of patients with cirrhosis and GH but in only 5% of those with PNC (P < .01). Bleeding from varices was observed in only one patient with GH but in five patients with PNC. Of 22 patients with GH in whom portal hypertension was unmodified or worsened, 16 had coexistent hepatic viral infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Arachidonic acid and its metabolites effects on testosterone production by rat Leydig cells.

Arachidonic acid (AA) seems to play an important role in testicular steroidogenesis, although controversial data exist in the literature. In the present study AA induced a dose related increase of testosterone (T) formation and, at the highest dose, stimulated the production of prostaglandin E2 (PGE2), leukotrienes B4 (LTB4) and C4 (LTC4) by purified rat Leydig cells. The contemporary addition of the prostaglandin synthesis blocker, indomethacin (IND), and AA further increased T formation, decreased PGE2 levels and did not modify LTB4 and LTC4 concentrations. The addition of a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA, 5 microM), did not influence the stimulatory effect of AA on T and PGE2 formation while it decreased the output of LTB4 and LTC4. When 20 microM NDGA was used in addition to AA the expected reduction of leukotrienes release was observed together with a surprising impairment of T and PGE2 secretion. PGE2 and PGF2 alpha did not modify basal T production but reduced HCG-stimulated T secretion at the 10 nM dose. When 5-12- and 15-HETE were tested an enhancement of basal T formation was observed at the 10nM dose. 5-HETE (10nM) stimulated HCG-induced T production. LTA4, LTB4 and LTE4 did not influence basal T output while LTC4 and LTD4 inhibited it. LTC4 (10nM) induced a decrease of HCG-stimulated T production. These findings suggest that: 1) exogenous AA stimulates T secretion; 2) conversion of AA to cycloxygenated and lipoxygenated metabolites is not required for its steroidogenic effect; 3) cycloxygenated and lipoxygenated compounds play a diverse modulatory role on testicular steroidogenesis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1995

Duodenal ferritin synthesis in genetic hemochromatosis.

BACKGROUND/AIMS: The molecular defect of genetic hemochromatosis (GH) is unknown. It is believed that low expression of duodenal ferritin in GH is caused by tissue or cell specific defect of ferritin synthesis. Our study was designed to ascertain whether the control of duodenal ferritin synthesis in GH was defective. METHODS: Expression at the single cell level of H and L ferritin messenger RNAs and protein and activity of the iron regulatory factor, which controls the translation of ferritin messenger RNA, were assessed in 43 duodenal biopsy specimens from individuals with GH, secondary hemochromatosis (SH), anemia, or normal iron balance. RESULTS: Signal for ferritin H and L subunit messenger RNAs was detected in both absorptive and nonabsorptive cells by in situ hybridization, but in 10 of 14 patients with untreated GH, the signal was lower than in patients with SH or normal subjects. However, immunostaining for ferritin protein documented a diffuse/cytoplasmic pattern, whereas a supranuclear/granular staining was found in normal subjects or patients with SH. The spontaneous activity of duodenal iron regulatory factor was consistently higher in patients with GH than in normal subjects or subjects with anemia or SH. CONCLUSIONS: In patients with GH, ferritin gene transcription is preserved in both absorptive and nonabsorptive intestinal cells. Low accumulation of ferritin is not caused by a defective control of ferritin synthesis but by low expression of ferritin messenger RNA and sustained activity of iron regulatory factor.

Adolescent↗
PubMed1995

Hepatitis C virus RNA and liver histology in blood donors reactive to a single antigen by second-generation recombinant immunoblot assay.

The clinical significance of single band reactivity (indeterminate pattern) at anti-hepatitis C virus (HCV) second-generation recombinant immunoblot assay (RIBA-2) was investigated in symptomless subjects with normal liver function tests to obtain data for their counseling and clinical management. Serum and hepatic HCV RNA were determined by the nested polymerase chain reaction, and liver histology was evaluated in 40 symptomless blood donors with stable indeterminate RIBA-2 pattern, including 38 reactive to c22-3. All but one had normal alanine aminotransferase (ALT) levels. Two new immunoblot tests, RIBA-3 and INNO-LIA HCV Ab III (LIA-III), which incorporate additional HCV antigens, were also done to assess whether they could identify the viremic subjects. Ten cases (25%, confidence interval 12 to 38) were HCV RNA positive. Three of the HCV RNA-positive and none of the HCV RNA-negative subjects had chronic hepatitis. RIBA-2 strong intensity of reaction (score > 2+) was observed in all the HCV RNA-positive and in 12 HCV RNA-negative subjects. RIBA-3 and LIA-III gave positive results in 9 of 10 and 10 of 10 HCV RNA-positive, but also in 8 of 30 and 24 of 30 HCV RNA-negative subjects. A c-22-3 reactivity score of 4+ by RIBA-3 and E2/NS1 reactivity by LIA-III were both strongly associated with HCV RNA (P < .001). Based on relatively high prevalence of chronic hepatitis in our series (30%), apparently healthy subjects with stable indeterminate RIBA-2 pattern and HCV RNA positivity should be considered for liver biopsy independently of ALT profile.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet.

The prevalence of hypertransaminasemia and the effect of gluten-free diet (GFD) were evaluated in 158 consecutive adult celiac patients, 127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67 patients (42%) had raised aspartate and/or alanine transaminase levels (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25 to 470, respectively), whereas 91 patients had normal liver function tests (LFT). Patients with and without hypertransaminasemia were comparable for epidemiological data, body mass index (18.5 vs. 19.6), and severity of intestinal histological involvement. All patients were given a strict GFD and were followed for 1 to 10 years (median, 4). At 1 year, a highly significant improvement in intestinal histology was observed in both groups (P < .0001). In the 67 patients with raised transaminase levels body mass index (BMI) also increased significantly (from 18.5 to 21.0, P < .001), and transaminase levels normalized in 60 (95%). In the other seven cases liver biopsy showed fatty infiltration in two and chronic active hepatitis (CAH) in the other five, related to chronic infection with hepatitis B virus in three and hepatitis C virus in one, and to autoimmune type in the fifth. We conclude that in adult celiac patients elevated serum transaminases are a frequent finding and normalize in most cases after GFD. When they persist, liver biopsy is mandatory to further investigate hepatic involvement, which is our series was mainly attributable to CAH.

Adolescent↗