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PubMed1990

Clinical approach to inherited metabolic disorders in neonates.

Most inborn errors of intermediary metabolism presenting in the neonatal period fall schematically into three clinical categories: (1) those which lead to a neurological distress 'intoxication type' with a symptom-free interval, vomiting, comas, hypertonia, abnormal movements and frequent humoral disturbances (organic acidaemias, congenital urea cycle defects); (2) those which lead to a neurological distress 'energy deficiency' type. Frequent symptoms in this group include hyperlactacidaemia, severe hypotonia, cardiomyopathy, failure to thrive and malformations (congenital lactic acidaemias, fatty acid oxidation defects, peroxysomal disorders); (3) those which present evidence of liver dysfunction and hepatomegaly (glycogenesis, neoglucogenesis defects, galactosaemia, fructosaemia, tyrosinaemia type I). According to these three major clinical presentations and according to the proper use of few screening tests (blood gases, glucose, ammonia, lactic acid, electrolytes, acetest), we propose a method of diagnosis which groups these children into five schematical syndromes: type I MSUD; type II organic acidaemias; type III; congenital lactic acidosis; type IVa, urea cycle defects; type IVb, non-ketotic hyperglycinaemia, sulfite oxidase deficiency, peroxisomal disorders; type V liver dysfunctions. Once the above classification has been made, sophisticated and specific investigations can be planned (amino acid chromatography, organic acid chromatography, enzymatic studies, etc).

Acidosis, Lactic↗
PubMed1994

[Study of two cases of active pulmonary tuberculosis complicated by lung cancer].

In this study, we report on two patients diagnosed with active pulmonary tuberculosis who later developed complications of lung cancer. In both instances, lung cancer was not detected until after cessation of tuberculostatic drugs. Both patients were initially considered to be experiencing exacerbation of pulmonary tuberculosis. Patient 1 was a 77-year-old female. A roentgenogram of her chest revealed a cavitary lesion with infiltration into the right lung field. Her sputum tested positive for acid-fast bacilli. Although she was treated with isoniazid (INH), rifampicin (RFP) and streptomycin sulfate (SM), the RFP and INH treatments had to be discontinued due to liver dysfunction. Her general condition was deteriorated, and pleural effusion appeared on a subsequent chest roentgenogram. Primary squamous-cell lung cancer was confirmed by conducting a transbronchial biopsy. Patient 2 was a 59-year-old male. A roentgenogram of his chest revealed multiple cavitary lesions with infiltration into the bilateral lung field. His sputum also tested positive for acid-fast bacilli. Although he was treated with INH, RFP and SM, INH and RFP treatment had to be discontinued due to liver dysfunction and high fever. The shadow infiltrating the left lung field subsided, but a massive shadow appeared in the right lung field. Primary small-cell lung cancer was confirmed after conducting a sputum cytology. The patients was then administered cisplatin and etoposide. Patient 1 was diagnosed with lung cancer five months after being admitted to the hospital, and Patient 2 ten months after admission. Both patients succumbed due to lung cancer at seven and 26 months, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Elevated plasma ammonia level in hepatic cirrhosis: role of glucagon.

Elevated plasma ammonia level in hepatic cirrhosis has been attributed to a lack of conversion of enteric ammonia into urea or to its entry into systemic circulation via portasystemic shunting, or to both. It is exaggerated by excessive protein intake. Because hyperglucagonemia is well documented in cirrhosis and a protein meal is an effective glucagon secretagogue, plasma glucose, insulin, glucagon, and ammonia levels were determined in 50 cirrhotic patients after an overnight fast. Effects of a protein meal were also assessed in 20 of these patients. Plasma glucose was normal and remained unaltered after a protein meal. Insulin, glucagon, and ammonia levels were elevated, but only in patients with advanced liver dysfunction. Ammonia levels correlated significantly with glucagon (r = 0.61, p less than 0.001), but not with insulin or glucose levels. Insulin and glucagon levels rose after a protein meal in all patients and controls; whereas a significant rise in the ammonia level occurred only in decompensated cirrhotics. Elevation of the ammonia level was significantly correlated with fasting glucagon (r = 0.54, p less than 0.05), as well as with glucagon response (r = 0.65, p less than 0.01), but not with basal insulin or insulin response. Furthermore, the rise in ammonia level occurred too early to be accounted for by enteric generation. Finally, direct effects of glucagon administration on plasma glucose and serum ammonia were examined in 15 cirrhotic patients. Glucose response was significantly blunted in cirrhotic patients as compared with normal subjects, whereas serum ammonia rose promptly but only in cirrhotics, with maximum rise being noted in cirrhotic patients with advanced liver dysfunction. This study, therefore, suggests that hyperglucagonemia may contribute significantly to hyperammonemia in hepatic cirrhosis.

Adult↗
PubMed1987

Modification of lipid composition of erythrocyte membranes in chronic alcoholism.

The lipid composition and microviscosity of erythrocyte membranes have been studied in chronic alcoholics with macrocytosis and minimal liver dysfunction. The findings have been compared with those obtained in subjects with macrocytosis not related to ethanol abuse. In all instances, macrocytosis was accompanied by an increased microviscosity of erythrocyte membranes, together with an increase of the cholesterol/phospholipid and of saturated/unsaturated fatty acids ratio. Both microviscosity and saturated/unsaturated ratio were significantly higher in alcoholics compared to subjects with macrocytosis not related to ethanol abuse. These findings confirm that altered lipid composition and fluidity of erythrocyte membrane may be observed in chronic alcoholics with minimal liver dysfunction, possibly due to the "stabilising" properties of ethanol - among a number of drugs- on biological membranes.

Adult↗
PubMed1990

Alcohol and skeletal muscle disease.

Skeletal muscle myopathy is caused by prolonged ethanol misuse and affects between half and two-thirds of chronic alcohol misusers. This chronic myopathy is characterized by a selective reduction in Type II (fast twitch) fibre area; Type I (slow twitch) fibres are relatively unaffected. The myopathy is not mediated by the patients' corticosteroid and nutritional status, liver dysfunction or neurological changes, and there is little correlation between alcoholic myopathy and alcohol intake. However, plasma alpha-tocopherol and selenium levels in myopathic alcoholics are reduced. The myopathy may in some way be related to the reduced fractional rates of skeletal muscle protein synthesis that occur in alcohol misusers and implicates free radical reactions in the pathogenesis of the myopathy. We have established a rat model of chronic alcoholic myopathy. In this model anatomically distinct skeletal muscles were taken to represent Type I (i.e. soleus) or Type II (i.e. plantaris) fibres. There were selective losses of Type II muscle protein at the end of 6 weeks of ethanol feeding. These changes were also not apparently mediated by nutritional limitations, neurological changes or liver dysfunction. Skeletal muscle protein synthesis was also reduced, as was plasma alpha tocopherol and selenium levels. Thus the rat model is amendable for further work to elucidate the molecular mechanisms responsible for alcohol-induced muscle loss.

Alcoholism↗
PubMed2000

Chronic graft-versus-host disease of the liver: presentation as an acute hepatitis.

Chronic graft-versus-host disease (GVHD) of the liver usually presents as an indolent cholestatic disease in patients with skin, mouth, and eye involvement. We observed 14 patients in whom chronic GVHD of the liver presented with marked elevations of serum aminotransferases, clinically resembling acute viral hepatitis. Onset of liver dysfunction was at 294 days (range, 74-747 days) after allogeneic hematopoietic cell transplantation and coincided with a recent cessation or taper of immunosuppressive drugs. Median peak serum alanine transaminase (ALT) was 1,640 U/L (698-2,565 U/L), and median bilirubin was 12.3 mg/dL (0.9-55.9 mg/dL). All biopsies showed characteristic features of GVHD with damaged and degenerative small bile ducts. Other features included a marked lobular hepatitis, moderate to marked amounts of hepatocyte unrest, sinusoidal inflammation with perivenular necroinflammatory foci, and many acidophilic bodies scattered throughout the lobule. When high-dose immunosuppressive therapy was instituted soon after presentation, progressive improvement and eventual normalization of liver enzymes and bilirubin levels were observed. However, in cases in which the diagnosis was not made and therapy was delayed, a progressive cholestatic picture emerged with histologic evidence of loss of small bile ducts and portal fibrosis. We conclude that a distinct syndrome of chronic liver GVHD presenting as an acute hepatitis can be recognized in a patient at risk who is receiving no, or minimal, immunosuppressive medications. Liver biopsy is necessary to exclude viral causes of liver dysfunction and to confirm characteristic abnormalities of small bile ducts. Institution of high-dose immunosuppression can prevent progressive bile duct destruction and effect resolution of jaundice if given early.

Acute Disease↗
PubMedDate not supplied

Nitric oxide in hepatic encephalopathy and hyperammonemia.

Chronic alcoholism, viral hepatitis or hepatotoxic drug overdose result in liver dysfunction which may lead to a neuropsychiatric disorder termed hepatic encephalopathy (HE). Although, the exact molecular mechanisms underlying the pathophysiology of HE are not known, excitatory/inhibitory neurotransmitter imbalance leading to dysfunction of the glutamate-nitric oxide (NO) system is thought to play a major role. Activation of the NMDA subtype of glutamate receptors leads to increase in intracellular calcium, which initiates several calcium-dependent processes including NO formation. NO is a gaseous, highly reactive, freely diffusible molecule with a short half-life. Recent studies demonstrate increased expression of the neuronal isoform of NO synthase (NOS) and the uptake of L-arginine (the obligate precursor of NO) in both chronic and acute HE. Hyperammonemia associated with liver dysfunction results in increased NO, which may lead to learning and memory impairments and cerebral edema commonly seen, particularly in acute hyperammonemia.

Animals↗
PubMed1981

Hyperalimentation-induced cholestasis. Increased incidence and severity in premature infants.

Two hundren sixty-seven neonates who received parenteral nutrition were monitored for signs of liver dysfunction. Cholestatic jaundice occurred in we infants, with a higher incidence in the more immature infants. There was an inverse correlation between severity of jaundice and the degree of prematurity. Infants with cholestasis remained without gastrointestinal feedings and received parenteral nutrition for periods of time significantly higher than infants without cholestasis. The incidence of this complication did not seem to correlate with the amount of protein infusate (amino acid solution). A higher incidence of sepsis was noted in infants who were affected by cholestasis. Close monitoring for signs of liver dysfunction in all neonates receiving parenteral nutrition is strongly recommended.

Bilirubin↗
PubMed2006

The use of prostaglandins in the immediate postsurgical liver transplant period.

INTRODUCTION: Experimental evidence has suggested that prostaglandins have positive effects on hepatic perfusion after transplantation. However, randomized clinical trials have failed to show their usefulness to decrease the incidence of primary nonfunction. In order to demonstrate its therapeutic role, we performed a clinical study in which PGE1 was administered only after the appearance of posttransplant liver dysfunction. MATERIALS AND METHODS: Forty patients with macroscopic signs of hypoperfusion or lacking bile production at the end of the operation (n = 24) or with an increase in transaminases and fall in biliary production in the first 24 hours postsurgery (n = 16) were administered alprostadil (PGE1; 0.01 mug/kg/min to the maximum plateau of 0.06 mug/kg/min). We measured the mean values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), activated thromboplastin time-ratio (aPTT-r), international normalized ratio (INR), bilirubin, creatinine and plasma nitrogen, PaO(2)/FiO(2) at the start of the treatment and every 6 hours for 48 hours, and daily diuresis. RESULTS: There appeared to be a significant decrease in AST, INR, aPTT-r, and creatinine clearance (P < .05), while there was a significant rise in the blood urea nitrogen (P < .001). ALT and bilirubin did not show significant variations. The PaO(2)/FiO(2) ratio showed a significant decrease (P < .001) in pulmonary vasodilatation. CONCLUSIONS: Prostaglandins used in the manner in our study showed a significant efficiency to improve liver dysfunction after transplantation.

Alprostadil↗
PubMedDate not supplied

Prevalence of serum HGV-RNA among hemodialysis patients in Turkey.

A possible agent for human non-A-E hepatitis has been identified and named hepatitis G virus (HGV). The aim of this study is to evaluate the prevalence of serum HGV-RNA among hemodialysis patients in our country and the possible correlations of serum HGV-RNA with antibody to hepatitis C virus (anti-HCV), chronic liver dysfunction, number of blood transfusions, serum hepatitis B surface antigen (HBs Ag), duration of hemodialysis therapy, history of renal transplantation and patients' age and sex. Seventy-eight hemodialysis patients and 59 healthy controls were included in the study. Twenty-seven of 78 hemodialysis patients (34.6%) and two of the 59 healthy controls were serum HGV-RNA positive (p < 0.01, x2 = 17.8). There was no significant difference between the HGV-RNA positive and HGV-RNA negative groups regarding mean duration of dialysis therapy, anti-HCV, chronic liver dysfunction, number of blood transfusions, serum HBs Ag, duration of hemodialysis therapy, history of renal transplantation and patients' age and sex. In conclusion, hemodialysis patients carry the risk for HGV infection and transmission routes and clinical significance of HGV infection in these patients remain to be defined.

Adolescent↗
PubMed1999

Bilirubin pigmentation of human teeth caused by hyperbilirubinemia.

This study was conducted to identify bilirubin in deciduous teeth obtained from two patients with a history of severe liver dysfunction. Teeth were histologically analyzed and bilirubin was extracted and quantified spectrophotometrically. Histological analysis revealed a green line in the dentine running parallel to the incremental lines. A chloroform/methanol/acetic acid (30:10:0.5, v/v) extract of the teeth was evaporated and the residue dissolved in chloroform. Absorption spectra were prepared before and after the diazo reaction. The absorption maximum shifted from 450 nm before to 540 nm after the diazo reaction and was higher than that of normal deciduous teeth. These results indicate that the discolouration of teeth in patients with severe liver dysfunction is due to bilirubin deposition.

Bilirubin↗
PubMed2002

Pharmacokinetics of ciprofloxacin in patients with acute renal failure undergoing continuous venovenous haemofiltration: influence of concomitant liver cirrhosis.

To determine an adequate dosage of ciprofloxacin in critically ill medical patients on continuous venovenous haemofiltration, we studied the pharmacokinetics of ciprofloxacin in eight critically ill medical patients with renal failure treated with continuous venovenous haemofiltration using polysulfone membranes. Three of those patients also presented with severe liver dysfunction. For comparison, three patients with approximately normal renal function and two patients with impaired renal function were included. During haemofiltration, plasma concentrations of ciprofloxacin were variable. In all critically ill patients ciprofloxacin elimination was significantly slowed; the mean half-life was similarly prolonged to about 14 h in patients on haemofiltration and those with approximately normal renal function. In critically ill patients with impaired renal function not on haemofiltration, the mean half-life was longest. Ciprofloxacin clearance by haemofiltration was a quarter of the total clearance. Although a unique dose recommendation can hardly be made because of the high variability of pharmacokinetics during haemofiltration, a daily dose of 800 mg (400 mg b.i.d.) in average can be regarded as appropriated for reaching a target plasma concentration of 2 to 3 micrograms/mL (mean concentration). Because the half-life of ciprofloxacin was further prolonged by the presence of liver cirrhosis, the dose should be reduced to 600 mg in patients on haemofiltration with concomitant severe liver dysfunction.

Acute Kidney Injury↗
PubMed2001

[Clinical efficacy of treatment with low-dose flutamide in maximum androgen blockade therapy].

To prevent treatment withdrawal due to flutamide-induced liver dysfunction, we performed maximum androgen blockade (MAB) therapy by combining a luteinizing hormone-releasing hormone agonist or orchiectomy with low-dose flutamide (125 mg x 2/day) in patients with prostate cancer. In this study, the efficacy, adverse effects such as hepatotoxicity, and compliance were compared retrospectively between 35 patients who received low-dose flutamide therapy (1995-1999) and 27 patients who received flutamide at its ordinary dose (125 mg x 3/day). No significant difference was observed in the response rate (> or = PR) as determined from the prostate-specific antigen parameter (p = 0.6211) or the incidence of hepatotoxicity based on the aspartate aminotransferase and alanine aminotransferase levels. However, flutamide withdrawal due to liver dysfunction was less frequent in the low-dose group (2.9%) than in the ordinary dose group (18.5%) (p = 0.0386). MAB therapy using low-dose flutamide is expected to prevent the reduction in the compliance due to side effects and to improve the long-term prognosis in patients with prostate cancer, who are mostly elderly individuals.

Aged↗
PubMed2003

Effect of the CYP3A4 inhibitor erythromycin on the pharmacokinetics of lignocaine and its pharmacologically active metabolites in subjects with normal and impaired liver function.

AIMS: The objectives of this study were: (i) to evaluate the effect of a cytochrome P450 (CYP) 3A4 inhibitor, erythromycin, on the pharmacokinetics of intravenous lignocaine and its two pharmacologically active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX); (ii) to assess whether the effects of the erythromycin inhibitory action on lignocaine clearance and the results of the MEGX liver function test depend on liver functional status; and (iii) to determine the effects of both moderate and severe liver dysfunction on the disposition kinetics of lignocaine. METHODS: The study was carried out on 10 healthy volunteers, and 10 Child's class A and 10 class C cirrhotic patients, according to a double-blind, randomized, two-way crossover design. On day 1 of the investigation, all subjects received three oral doses of erythromycin (600 mg of the ethylsuccinate ester) or placebo, and two further doses on day 2. One hour after the fourth dose, subjects were given 1 mg kg-1 lignocaine intravenously. Timed plasma samples were then obtained until 12 h for determination of the concentrations of lignocaine, MEGX and GX. RESULTS: Erythromycin caused statistically significant, although limited, modifications of lignocaine and MEGX pharmacokinetic parameters. In healthy volunteers, lignocaine clearance was decreased from 9.93 to 8.15 ml kg-1 min-1[mean percentage ratio (95% CI), 82 (65-98)] and the half-life was prolonged from 2.23 to 02.80 h [mean percentage ratio (95% CI), 130 (109-151)]; MEGX area under the concentration-time curve from 0 h to 12 h was increased from 665 to 886 ng ml-1 h [mean percentage ratio (95% CI), 129 (102-156)]. Quantitatively similar modifications were observed in the two cirrhotic groups. GX concentrations were lowered in all study groups, although not to statistically significant extents. Erythromycin coadministration caused no appreciable interference with the results of the MEGX test. Only in patients with Child's grade C liver cirrhosis were lignocaine kinetic parameters significantly altered with respect to healthy volunteers. Thus, clearance was approximately halved, steady-state volume of distribution was increased, and terminal half-life was more than doubled. CONCLUSIONS: Although erythromycin only modestly decreases lignocaine clearance, it causes a concomitant elevation of the concentrations of its pharmacologically active metabolite MEGX. A pharmacodynamic study following lignocaine infusion to steady state appears necessary to assess the actual clinical relevance of these combined effects. The degree of liver dysfunction has no influence on the extent of the erythromycin-lignocaine interaction, whereas it markedly influences the extent of the changes in lignocaine pharmacokinetics. These findings indicate that no dose adjustment is needed in patients with moderate liver cirrhosis, whereas the lignocaine dose should be halved in patients with severe cirrhosis.

Adult↗
PubMed1994

The Taipan snake venom time: a new test for lupus anticoagulant.

AIMS: To develop a specific test for lupus anticoagulant activity with reduced sensitivity to coagulation factor deficiency that would be suitable for analysis of plasmas from patients receiving oral anticoagulants. METHODS: A coagulation test based on the Taipan snake venom time (TSVT) with a platelet neutralisation procedure (PNP) was developed and compared with dilute Russell's viper venom time (DRVVT). The TSVT was used to test plasmas from patients receiving oral anticoagulant or heparin with mild liver dysfunction and with documented lupus anticoagulant. RESULTS: The optimised conditions for the TSVT were established and a reference range was determined in normal healthy subjects. Results were considered positive for lupus anticoagulant if the ratio was > or = 1.1 and was reduced by > or = 10% or to < 1.1 in the PNP. In 43 samples from patients receiving oral anticoagulants there was no correlation between level of anticoagulation and TSVT, and only seven samples had increased TSVTs. Of these, five corrected on mixing with normal plasma and two gave equivocal results. The patients with mild liver dysfunction all had normal TSVTs. The TSVT in plasmas from patients receiving heparin correlated with the heparin concentrations (as measured by the APTT, r2 = 0.81). Some anticoagulated plasmas showed correction in the PNP and were regarded as false positive. Fourteen of 17 patients known to have lupus anticoagulant (on the basis of DRVVT results) were also positive by the TSVT; two of the remaining three were borderline and one was negative. CONCLUSIONS: The TSVT showed satisfactory intra-assay precision and reasonable sensitivity to lupus anticoagulant, compared with the DRVVT. The TSVT was influenced by the presence of heparin but was not sensitive to the effects of oral anticoagulant. Like other lupus anticoagulant tests, it does not seem to have a 100% detection rate, but this may be due to the presence of lupus anticoagulant subtypes with distinct activities or the requirement of cofactors other than prothrombin or beta 2 glycoprotein-I.

Adult↗
PubMed2003

[Significance of intracellular cytokines levels in peripheral lymphocytes for evaluation of surgical stress after hepatectomy in patients with hepatocellular carcinoma].

It is difficult to evaluate surgical stress of patients with hepatocellular carcinoma (HCC). Cytokine production from the liver is decreased due to the liver dysfunction that is usually associated with HCCs. Therefore, we evaluated surgical stress after hepatectomy by measuring intracellular cytokines of lymphocytes in peripheral blood. We examined 22 patients with digestive cancers (8 with HCC, 10 with gastric cancer, and 4 with esophageal cancer). The concentrations of serum IL-6 levels 6 h after hepatectomy, gastrectomy, and esophagectomy were 268 +/- 84, 309 +/- 93, and 1,323 +/- 364 pg/ml, respectively. There was no significant difference between hepatectomy and gastrectomy, though based on clinical observations, it is estimated the surgical stress of hepatectomy was greater than that of gastrectomy. Conversely, the percentage of CD4+IL-6+ cells 6 h after surgery was 8.5 +/- 2.8, 3.3 +/- 0.6, and 7.8 +/- 3.4%, respectively. The percentage of CD4+IL-6+ cells after hepatectomy was significantly higher than that after gastrectomy. We estimated that the percentage of CD4+IL-6+ cells was an appropriate indicator of surgical stress on HCC, because the percentage of CD4+IL-6+ cells correlated well with the duration of surgery more than did the serum IL-6 levels. These results suggest that the percentage of CD4+IL-6+ cells may help in accurately evaluating surgical stress in patients with liver dysfunctions such as HCC.

CD4-Positive T-Lymphocytes↗
PubMed1990

Endocarditis in the 80s in a general hospital in Auckland, New Zealand.

The clinical and investigative features of 102 episodes of infective endocarditis were analysed retrospectively. The most frequent presenting symptoms (malaise, fever, sweats, myalgia, weight loss) were non-specific. Fever, cardiac murmur, tachycardia, vascular phenomena and a change in mental state were the most common physical signs at admission. Anaemia was present in half the episodes and renal and liver dysfunction in about one-third. Streptococci (61) and staphylococci (31) were the causative organisms in all but 10 episodes. The commonest predisposing factors were underlying cardiac disease (52 per cent) and a preceding focus of infection (14.6 per cent). Left ventricular failure (33 per cent) and focal neurological disease (29 per cent) occurred frequently. Valvular surgery was performed in 20 episodes, with two in-hospital deaths. Overall hospital mortality was 27.5 per cent and death was most commonly neurological (11/28). A higher mortality was associated with elevated total white blood count, microscopic haematuria, renal or liver dysfunction at admission, S. aureus endocarditis, the development of left ventricular failure or focal neurological disease, age greater than or equal to 60 years and persistence of fever after one week of antibiotic therapy. The absence of both renal dysfunction at admission and subsequent microscopic haematuria identified a group with a very low hospital mortality (4.7 per cent). The three-year mortality of the entire group was 43.5 per cent.

Adult↗
PubMed1996

Small bowel bacterial overgrowth in patients with alcoholic cirrhosis.

A total of 89 patients with alcoholic cirrhosis and 40 healthy subjects were included in a study to assess the prevalence of intestinal bacterial overgrowth and to analyze its relationship with the severity of liver dysfunction, presence of ascites, and development of spontaneous bacterial peritonitis (SBP). Bacterial overgrowth was measured by means of a breath test after ingestion of glucose. Intestinal bacterial overgrowth was documented in 27 (30.3%) of the 89 patients with alcoholic cirrhosis and in none of the healthy subjects. The prevalence of intestinal bacterial overgrowth was significantly higher in cirrhotics with ascites (37.1%) than in those with no evidence of ascites (5.3%) and among patients with Pugh-Child class C (48.3%) than in patients with a class A (13.1%) or B (27%). Twelve (17.1%) of the 70 patients with ascites developed an episode of SBP. The prevalence of spontaneous bacterial peritonitis was significantly higher in patients who had intestinal bacterial overgrowth (30.7%) than in patients who did not (9.09%). We conclude that intestinal bacterial overgrowth occurs in approximately one third of patients with cirrhosis secondary to alcohol, particularly in patients with ascites and advanced liver dysfunction. Moreover, bacterial overgrowth may be a condition favoring infection of the ascitic fluid.

Adult↗