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PubMed2003

Exposure of beef cattle to sub-clinical doses of Microcystis aeruginosa: toxin bioaccumulation, physiological effects and human health risk assessment.

Yearling beef cattle were fed 1 x 10(5) cells ml(-1) of toxic Microcystis aeruginosa in their drinking water for a period of 28 d. Feed and water intakes of four control and four treated animals remained unchanged following introduction of M. aeruginosa into the drinking water of the treatment animals, and there were no significant differences in feed and water intakes between control and treated animals. We tested the blood plasma of both control and treated animals twice each week for elevated concentrations of the liver enzymes gamma-glutamyl transferase (GGT), glyceraldehyde dehydrogenase (GADH), amino aspartate transferase (AST) and bilirubin. All tests were negative indicating no measurable liver dysfunction resulting from microcystin intoxication. We also tested for the presence of free microcystin in the liver and blood plasma by HPLC and ELISA and for total microcystin (free+bound) in the liver by GC-MS. If all the ingested microcystin was bioaccumulated within the liver, the concentration would have exceeded 3 microg MCYST-LR g(-1) fresh weight. HPLC and GC-MS analysis of the liver tissue and blood plasma from treated animals failed to detect any microcystins. ELISA analysis of liver tissue extracts from the treated animals indicated microcystin concentrations as high as 0.92 microg MCYST-LR equivalents g(-1) fresh weight although none was indicated in the blood plasma. The microcystin concentrations measured by ELISA in livers of treated animals were more than 1000 times higher than the limit of quantification by HPLC and GC-MS indicating the ELISA results were almost certainly due to cross reactivity with something other than intact MCYST-LR. Based on the detection limits of the HPLC and the per capita daily consumption of beef in Australia, it appears that consumption by beef cattle of water containing M. aeruginosa cell concentrations up to 1 x 10(5)cells ml(-1) for 4 weeks would not produce concentrations of microcystin within the liver or blood plasma that would present an unacceptable risk to human health based on World Health Organization protocols for determining such risks.

Animals↗
PubMed2000

Subclinical course of cholesteryl ester storage disease in an adult with hypercholesterolemia, accelerated atherosclerosis, and liver cancer.

Few cases of asymptomatic cholesteryl ester storage disease (CESD) due to low enzymatic activity of human lysosomal acid lipase/cholesteryl ester hydrolase (hLAL) have been reported thus far in adults Here, we describe a 51-year-old man with a long clinical history of mixed hyperlipoproteinemia and severe premature atherosclerosis, but with no signs of hepatomegaly, liver dysfunction, or splenomegaly. The disease was discovered by chance in a biopsy performed because of suspected liver cancer (proven to be a cholangiocarcinoma). Residual hLAL activity in peripheral leukocytes was determined to be 6% of control values. DNA sequence and restriction fragment length polymorphism analysis demonstrated that the patient was a compound heterozygote for the prevalent CESD exon 8 splice site mutation (G934A) and the deletion of a C (nucleotide 673, 674, or 675) in exon 6 of the hLAL gene, resulting in premature termination of protein translation at residue 195. The patient died of liver failure as a consequence of extensive tumor infiltration at age 52. Lipid analysis revealed moderate cholesteryl ester storage in the liver and in the suprarenal cortex, and massive accumulation in the testicular histiocytes and Leydig cells, resulting in a pronounced secondary atrophy of the seminiferous tubules. Our case study demonstrates that hepatomegaly is an inconstant feature, even in CESD patients compound heterozygous for a Wolman mutation which results in complete loss of hLAL enzymic activity. It also highlights the need to be aware of this condition as it may be underdiagnosed.

Adult↗
PubMed2001

Effect of interferon therapy on Japanese chronic hepatitis C virus patients with anti-liver/kidney microsome autoantibody type 1.

AIM: The aim of this study was to determine the prevalence of anti-liver/kidney microsome autoantibody type 1 (anti-LKM-1) among hepatitis C virus (HCV)-infected Japanese patients at various stages (chronic hepatitis, liver cirrhosis and hepatocellular carcinoma), and to assess the influence of anti-LKM-1 on interferon therapy. METHODS: A total of 390 serum samples from 215 HCV-infected patients with chronic hepatitis (HCV-CH), 81 HCV-infected patients with liver cirrhosis (HCV-LC), and 94 HCV-HCC infected patients were subjected to examination. Ninety-one HBsAg-positive patients and 137 healthy subjects served as controls. Anti-liver/kidney microsome autoantibody type 1 was determined by using a newly developed ELISA using recombinant cytochrome P450 IID6 as the antigen. RESULTS: Anti-liver/kidney microsome autoantibody type 1 was detected in six of the 390 (1.5%) chronic HCV-infected patients (four were HCV-CH and two were HCV-LC); in contrast, it was not detected in control groups. Among the 110 HCV-CH patients treated with interferon (IFN), four were positive for anti-LKM-1. No change in anti-LKM-1 immunoreactivity from negative to positive during interferon therapy was observed. Moreover, no increase in the serum alanine aminotransferase level was observed in these four patients with anti-LKM-1. CONCLUSION: Our study indicates that: (i) anti-LKM-1 does not aggravate the liver disease associated with HCV infection; and (ii) no change in anti-LKM-1 immunoreactivity from negative to positive or no aggravations of liver dysfunction were observed among HCV-CH patients during the IFN therapy for Japanese patients with liver disease.

Autoantibodies↗
PubMed2000

Tissue inhibitor of metalloproteinases-1 promotes liver fibrosis development in a transgenic mouse model.

Tissue inhibitor of metalloproteinases-1 (TIMP-1) has been shown to be increased in liver fibrosis development both in murine experimental models and human samples. However, the direct role of TIMP-1 during liver fibrosis development has not been defined. To address this issue, we developed transgenic mice overexpressing human TIMP-1 (hTIMP-1) in the liver under control of the albumin promoter/ enhancer. A model of CCl(4)-induced hepatic fibrosis was used to assess the extent of fibrosis development in TIMP-1 transgenic (TIMP-Tg) mice and control hybrid (Cont) mice. Without any treatment, overexpression of TIMP-1 itself did not induce liver fibrosis. There were no significant differences of pro-(alpha1)-collagen-I, (alpha2)-collagen-IV, and alpha-smooth muscle actin (alpha-SMA) mRNA expression in the liver between TIMP-Tg and Cont-mice, suggesting that overexpression of TIMP-1 itself did not cause hepatic stellate cell (HSC) activation. After 4-week treatment with CCl(4), however, densitometric analysis revealed that TIMP-Tg-mice had a seven-fold increase in liver fibrosis compared with the Cont-mice. The hepatic hydroxyproline content and serum hyaluronic acid were also significantly increased in TIMP-Tg-mice, whereas CCl(4)-induced liver dysfunction was not altered. An active form of matrix metalloproteinases-2 (MMP-2) level in the liver of TIMP-Tg-mice was decreased relative to that in Cont-mice because of the transgenic TIMP-1. Immunohistochemical analysis revealed that collagen-I and collagen-IV accumulation was markedly increased in the liver of CCl(4)-treated TIMP-Tg-mice with a pattern similar to that of alpha-SMA positive cells. These results suggest that TIMP-1 does not by itself result in liver fibrosis, but strongly promotes liver fibrosis development.

Actins↗
PubMed2001

[Hypertransaminasaemia and impaired liver function in a patient with oligosymptomatic celiac disease].

Hypertransaminasaemia and impaired liver function in a patient with oligosymptomatic celiac disease. We describe the case of a 45-year-old man who was referred for evaluation of elevated aminotransferases. One year before referral the patient developed an ischemic stroke followed by a subdural hematoma three months later. In our outpatient clinic the patient presented with a malabsorption syndrome including diminished vitamin-K-dependent clotting factors. Serologic testing was positive for IgA antigliadin antibodies and IgA antiendomysial antibodies. Celiac disease was confirmed by an upper endoscopy examination and biopsies obtained from the distal duodenum. Histological examination showed villous atrophy, crypt hyperplasia and an increase in intraepithelial lymphocyte count consistent with celiac disease. After initiation of a gluten-free diet the malabsorption syndrome as well as liver dysfunction improved. Serum aminotransferase levels normalized within 6 months. The clinical course demonstrates involvement of the liver in patients with celiac disease.

Alanine Transaminase↗
PubMed1992

Choline: an important nutrient in brain development, liver function and carcinogenesis.

Choline is required to make certain phospholipids which are essential components of all membranes. It is a precursor for biosynthesis of the neurotransmitter acetylcholine and also is an important source of labile methyl groups. Much attention has been given to the effect of supplemental choline upon brain function, i.e., enhancement of acetylcholine synthesis and release. In addition, choline supplements administered to rats in utero or shortly after birth permanently after brain function. The mechanisms for this effect is unknown and under investigation at this time. Healthy humans fed diets deficient in choline, and humans fed parenterally have decreased plasma choline concentrations and develop liver dysfunction that is similar to that seen in choline-deficient animals. In experimental animals, fatty liver occurs in choline deficiency because phosphatidylcholine synthesis is required for very low-density lipoprotein secretion. This accumulation of lipids in liver may explain why choline-deficient rats spontaneously develop hepatocarcinoma. We found that choline deficiency was associated with the accumulation of 1,2-diacylglycerol, an activator of protein kinase C. Several lines of evidence indicate that cancers might develop secondary to abnormalities in protein kinase C-mediated signal transduction.

Alanine Transaminase↗
PubMed1998

Fibrosing cholestatic hepatitis after living related-donor renal transplantation.

A 43-year-old man underwent living related-donor renal transplantation because of chronic renal failure in 1991. During the transplant period, both donor and recipient were seronegative for hepatitis B surface antigen (HBsAg). The donor was seropositive for antibody to hepatitis B surface antigen (anti-HBs) due to hepatitis B virus (HBV) vaccination. After transplantation, FK506 and methylprednisolone had been administered to the patient as immunosuppressants. In 1993, HBsAg appeared in his serum. His alanine aminotransferase level elevated gradually during 1995 and then in 1996, general fatigue, ascites and jaundice developed. At this time his serum was positive for hepatitis B e antibody, contained more than 100000 Meq/mL HBV-DNA and 100% precore mutant. Despite subsequent intensive therapy, liver dysfunction progressed and this patient died of hepatic failure 2 months following admission. At autopsy, the liver exhibited cholestasis, fibrosis extending from the portal tracts, mild inflammation and hepatocytes with a ground-glass appearance. In addition, HBsAg and hepatitis B core antigens had accumulated in the hepatocytes. Consequently, the final diagnosis was fibrosing cholestatic hepatitis (FCH) due to precore mutant HBV infection contracted after renal transplantation. It is unclear when and where the recipient liver became HBV infected. Nevertheless, after renal transplantation, while receiving immunosuppressive drugs, HBV appeared to have the potential to cause hepatic failure and FCH may have been a fatal complication for the recipient.

Adult↗
PubMed1995

Quantifying oxidative injury in the liver.

Oxidative injury is a mechanism common to both ischemia-reperfusion (IR) and leukocyte-mediated injury. Reperfused tissue beds and elaborated mediators can activate a cascade of intercellular and interorgan injuries that often precipitates multiple organ failure. Initiation of lung injury by gut IR is a case in point, but concomitant liver injury may have been overlooked because of the absence of comparably sensitive physiological markers. In this study, we explore the hypothesis that occurrence of portally derived oxidant-induced liver dysfunction may be detected with both sensitivity and specificity. We simulated pure oxidative injury to the liver and separated the contributions from secondary systemic oxidation. Both tissue and plasma indicators were evaluated, each reflecting aspects of oxidation, membrane integrity, and metabolic function. Tissue markers readily detect oxidative liver injury, but systemic 3-hydroxybutyrate (3-OHB) concentration and ketone body ratio (KBR) are the most sensitive. Comparison of 3-OHB concentrations against the corresponding KBR can be used to distinguish adjustments within a physiological range from the transition into injury.

3-Hydroxybutyric Acid↗
PubMed1992

Idiopathic pulmonary fibrosis and high prevalence of serum antibodies to hepatitis C virus.

The prevalence of serum antibodies to hepatitis C virus (HCV) was assessed by an enzyme-linked immunosorbent assay (ELISA) in 66 patients (46 male and 20 female; mean age +/- SEM, 61.5 +/- 10.1 yr) with idiopathic pulmonary fibrosis (IPF). Nineteen (28.8%) were positive for this test. The frequency of HCV positiveness was significantly higher in the patients with IPF than in the 9,464 control subjects, whose ages were comparable with those of the patients (3.66%, p less than 0.05). Importantly, 12 of the 19 patients with IPF and positive ELISA results (63.2%) had positive results on the Chiron recombinant immunoblotting assay (RIBA), which is known to be more specific for HCV. We judged the 12 perceptible reactions as eight reactive and four indeterminate. When we examined liver function retrospectively, only two of eight patients who tested positive for the HCV had liver dysfunction, suggesting that anti-HCV positivity in IPF was not observed as a result of liver disease. These results lead us to speculate that HCV infection may play an important role in the pathogenesis of IPF, or that the sera of patients with IPF may contain some antibody against an unknown epitope and cross-react with the anti-HCV assay.

Aged↗
PubMed1986

Feminization in a galactosemic girl in the presence of hypergonadotropic hypogonadism.

A galactosemic girl has been followed in our clinic since her 8th day of life when the diagnosis of transferase-deficiency galactosemia was made until her present age of 21 years. Although she presented with direct hyperbilirubinemia and severe liver dysfunction, her subsequent somatic and intellectual development under a strict galactose-free diet was normal. Liver function normalized. Her pubertal stage was Tanner B II and PH II at age 11.7 years and progressed normally to B V and PH V, but menarche did not occur. At age 16.8 years, low estradiol (51 pmol/L) and high gonadotropin levels (LH 44 U/L; FSH 43 U/L) were measured. Severely hypoplastic ovaries with a streak-like aspect were seen on laparoscopy. Sex chromatin was positive. Follow-up studies over the next 4 years confirmed elevated LH and FSH levels with an excessive response to stimulation with LHRH and persistently low estradiol levels (41 to 117 pmol/L). After an intravenous load of 200 mg DHEA-S, plasma estrone levels rose 1.8-fold and estradiol 11.4-fold above basal, demonstrating prompt conversion of androgens to estrogens. For over one year, the patient has been treated with the synthetic progestin norethisterone (15 mg per day for 10 days in a row every month) which has resulted in regular menstrual bleedings.

Adult↗
PubMed1992

Disseminated intravascular coagulation in lupus erythematosus with acute liver damage.

A case of disseminated intravascular coagulation (DIC) in a patient with systemic lupus erythematosus (SLE) with acute liver dysfunction is described. A 37-year-old man with SLE developed acute DIC and marked liver damage after fracture of the right clavicle and pharyngitis. Treatment with high-dose steroids, heparin, antithrombin III, gabexate mesilate, and antibiotics resulted in prompt improvement. The recovery of an SLE patient after acute DIC and marked liver damage is considered very rare. We report here such a case and discuss the previous reports.

Adult↗
PubMed1995

Reproductive function and outcome of pregnancy after liver transplantation in women.

OBJECTIVE: To discuss menstrual function before and after liver transplantation, immunosuppression during pregnancy, outcome and management of pregnancy, and use of contraception in women after liver transplantation. MATERIAL AND METHODS: We review the relevant medical literature and describe our clinical experience in the management of gynecologic and obstetric issues in recipients of liver transplants. RESULTS: Menstrual abnormalities, such as amenorrhea, oligomenorrhea, irregular bleeding, and metrorrhagia, are common in women with liver disease and may often be the first clinical indication of liver dysfunction. Normal menstrual function is frequently restored after transplantation. Successful pregnancies have occurred in recipients of liver transplants, but such pregnancies are often complicated by preterm delivery, preeclampsia, and infection. Use of immunosuppressive medications should be maintained during pregnancy, and drug concentrations should be carefully monitored; none has been found to be teratogenic. Pregnancy does not seem to accelerate graft rejection. Barrier contraception or sterilization, if appropriate, seems to be the safest option for these patients. CONCLUSION: Because liver transplantation leads to restoration of normal menstruation, female patients of reproductive age must be counseled about the possibility of pregnancy and the use of contraception. Pregnancy should be avoided for at least the first 6 months after transplantation. With specialized care and attention, pregnancies are generally associated with good outcomes.

Chronic Disease↗
PubMed1992

Cognitive patterns in school-age children with end-stage liver disease.

Although children with end-stage liver disease (ESLD) have been found to have cognitive delays, the relationship between patterns of cognitive function and diagnostic category, age of onset, duration and severity of disease has not been assessed before transplantation. Verbal and performance IQ (VIQ, PIQ) scores and scores on Bannatyne's cognitive factors for 43 children with ESLD were compared with those of 15 control children with cystic fibrosis (CF) and with existing normative data. Children with biliary atresia had deficits in PIQ, spatial and sequential scores. Children with alpha-1 antitrypsin deficiency did not differ significantly from CF controls but did show deficits compared with normative data. Children with onset of disease in the first year of life had deficits on all cognitive measures compared with both control groups. In contrast, children with later onset differed from the normative population only on VIQ and the acquired knowledge factor. In multiple regression analyses, duration of disease and indexes of liver dysfunction combine to predict cognitive scores. These preliminary findings suggest that children with early onset of liver disease are at high risk for cognitive impairment.

Biliary Atresia↗
PubMed1991

[Effects of intraarterial infusion chemotherapy on liver function in patients with hepatocellular carcinoma].

Periodic infusion chemotherapy from the reservoir implanted by direct arterial puncture (Seldinger method) was performed in 21 cases of hepatocellular carcinoma. The effectiveness of treatment in terms of efficacy and liver function in about 12 patients who survived more than 6 months was investigated. Owing to the progressive liver atrophy and liver dysfunction with ascites, some cases had to delay infusion treatment. Thus, it is necessary to check liver function regularly.

Adult↗
PubMed1991

[A case of lymphoma which developed bone, liver, and skin lesions two years after the diagnosis of lymphoid interstitial pneumonia].

We reported a case of lymphoid interstitial pneumonia (LIP) in 1985. The patient, a 37-year-old housewife, had suffered from cough and dyspnea. Her chest roentgenograms revealed bilateral diffuse micronodular shadows. After open lung biopsy in 1983, the lesion was interpreted as LIP in the premalignant state. After pulse therapy her condition remarkably improved. She was readmitted because of fever and shoulder pain in 1985. X-ray films revealed punched out lesions on the extremities. As liver dysfunction and skin eruptions had been recognized to wax and wane since the first admission, transcutaneous liver biopsy and skin biopsy was done. The diagnosis was middle- to large-sized T cell lymphoma. CHOP therapy seemed effective. However there appeared dyspnea and cotton-like patchy shadows in both lung fields. Despite chemotherapy, she died of pulmonary fungal and cytomegaloviral infection in 1986. As a result of the reevaluation of the open lung biopsy specimen, we concluded that this case should have been considered as lymphoma at onset.

Adult↗
PubMed1988

[A case of polycystic kidney with bilateral nephrectomy].

A 56-year-old woman in chronic hemodialysis had been suffering from uncontrollable fever for the past 7 months. Her original disease was diagnosed as familial polycystic kidney and three of her five brothers were found to have the same disease. Her chromosome was 46,XX,21P+ and laboratory examination revealed severe anemia, malnutrition, liver dysfunction, pyuria and candidiasis of urine. Abdominal echogram and CT scan revealed polycystic kidneys and multiple liver cysts. She was admitted to our hospital and was diagnosed as having pyelonephritis of the right kidney. As her condition was not improved by conservative therapy right nephrectomy was performed. One month later, spiking fever and left tenderness reappeared. Those symptoms could not be controlled by conservative therapy and left nephrectomy was performed again. Pathological examination on nephrectomized kidneys showed interstitial nephritis, hyaline degeneration and proliferative change of glomeruli, microabscess, colloid of tubules and calcification of parts of Henle's loops. Nephrectomy has been performed in 1.6 to 10.0% of polycystic kidneys due to references since 1952. Eight of the 22 polycystic kidneys (36.3%) seen at our hospital during the past 10 years have been removed.

Female↗
PubMed1986

[Dynamics of biochemical and hematological indicators in calves from cows receiving different diets during the weaning period].

Studies were carried out in 2 groups of calves from cows fed a hay-free keto- and acidosis-producing diet (group I) and a diet containing an excess of protein and starch (group II). The laboratory studies were conducted: in cows ante partum, and in calves prior to and 3 hours after drinking colostrum, and on the 1st, 3rd, 14th and 30th day of life. The determined parameters were: hematologic, acid alkaline balance and metabolism of protein, saccharide and fat. The calves from the cows of both groups were born underweight with metabolic acidosis in group I and compensated acid-alkaline balance in group II. Changes in proteins, lipids, i.e. compounds produced by the liver were found to be the most dynamic and the most pronounced in calves from group I. The calves from this group were also much slower to reach the physiological norms of adult cows. The conclusions drawn are as follows: 1. Systemic acidosis distinctly inhibits the concentration of the compounds produced by the liver; 2. The diet containing an excess of and starch, though it does not affect the acid-alkaline balance, does lead to liver dysfunction; 3. Within one month the calves failed to reach the normal functional performance of the liver of adult cows.

Acid-Base Equilibrium↗
PubMed1984

The function and morphology of the liver in porphyria cutanea tarda.

The aminopyrine breath test, postprandial serum bile acids, and routine liver tests were assessed as indicators of liver dysfunction in 38 patients with porphyria cutanea tarda. In 17 patients needle biopsy specimens of the liver were obtained. Bile acids were increased in almost all the patients studied (97%) but impairment of aminopyrine demethylation was found in only 45%. More than 50% of cases had elevated activities of serum alanine aminopeptidase, leucine aminopeptidase, gammaglutamyl transpeptidase (GGTP), and alanine aminotransferase (ALAT). All liver biopsy specimens showed fluorescence characteristic of porphyrins. Histologic examination of biopsy material revealed cellular lesions in all cases, the most common pathological findings being fatty degeneration of varying degree and iron accumulation. The most frequent electronmicroscopic changes in the liver were fat droplets, granules containing bile material, and siderosomes in the cytoplasm of hepatocytes. However, there was no evident relationship between morphological and functional liver changes.

Adult↗