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PubMed1983

Biologic and clinical significance of red cell ferritin.

Red cell ferritin was measured in normal subjects and patients with disorders of iron metabolism, inflammation, liver dysfunction, impaired hemoglobin synthesis, and increased red cell turnover by means of radioimmunoassays with antibodies to liver (basic) and heart (acidic) ferritins. The normal mean values for basic and acidic ferritin were 8.9 and 22.7 altogram (ag)/cell, respectively. The red cell ferritin content reflected changes occurring in tissues both in iron deficiency and iron overload. Basic ferritin was more closely related to the body iron status than acidic ferritin, and the acidic/basic ferritin ratio was increased in iron deficiency and decreased in iron overload. The major factor determining the red cell ferritin content appeared to be the transferrin saturation, that is, the distribution of iron between monoferric and diferric transferrin. This is in keeping with recent data indicating a competitive advantage of diferric transferrin in delivering iron to erythroid cells. In addition, the red cell ferritin content was increased in thalassemic patients with normal iron status, appearing to be inversely related to the rate of hemoglobin synthesis. The determination of red cell ferritin, based on a commercially available basic ferritin assay, can have clinical application. It can be used for evaluating the adequacy of the iron supply to the erythroid marrow, particularly in patients with increased red cell turnover. Moreover, it may be useful in evaluating the body iron status in patients with hemochromatosis and liver disease.

Adolescent↗
PubMed2006

Sepsis-induced organ failure is mediated by different pathways in the kidney and liver: acute renal failure is dependent on MyD88 but not renal cell apoptosis.

Toll-like receptors (TLRs) are important in sepsis. Myeloid differentiation factor 88 (MyD88) is a key molecule involved in signal transduction by multiple TLRs. The objective of this study was to investigate the contribution of TLR4 and MyD88 to acute renal failure (ARF) induced by polymicrobial sepsis. Liver dysfunction and apoptosis in the spleen contribute to sepsis severity after cecal ligation and puncture (CLP). Therefore, we also investigated liver injury and splenic apoptosis. We used a mouse model of sepsis-induced ARF using CLP to generate polymicrobial sepsis. Despite fluid and antibiotic resuscitation the mice developed multi-organ failure, including ARF, which resembles human sepsis. We investigated the role of the TLR4 receptor by comparing C3H/HeJ mice (which lack TLR4) with C3H/He0UJ normal controls. The role of MyD88 was investigated by comparing MyD88 knockout mice (MyD88(-/-)) with wild-type controls. Following CLP, mice lacking TLR4 and wild-type mice both developed comparable ARF. However, MyD88(-/-) mice did not develop ARF compared to wild-type controls. In contrast, MyD88(-/-) mice developed liver injury comparable to wild type. After CLP, MyD88(-/-) mice had significantly reduced apoptosis in the spleen compared with wild type. Apoptosis was not detected in the kidney of wild-type or MyD88(-/-) mice after CLP. In summary, ARF induced by polymicrobial sepsis is dependent on MyD88, but not TLR4. The absence of MyD88 dissociates ARF from liver injury; liver injury is MyD88-independent. There was MyD88-dependent apoptosis in the spleen, but no apoptosis in the kidney. MyD88 may be a good drug target for some, but not all, organ dysfunctions following sepsis.

Acute Kidney Injury↗
PubMed1986

Reversible increase in serum alpha-fetoprotein content associated with hepatic dysfunction during chemotherapy for seminoma.

Serial monitoring of the serum content of the beta subunit of human chorionic gonadotropin (beta hCG) and alpha-fetoprotein (alpha FP) is useful in the initial staging of germ cell tumors and assessing the response to treatment. An increase in either marker during or following treatment almost always heralds disease progression and indicates the need for additional therapy. We report two patients in whom substantial increases in the serum content of AFP occurred during chemotherapy for advanced seminoma. Hepatic dysfunction was present in both patients; in one patient, a chronic carrier of hepatitis B virus, the liver dysfunction was associated with reactivation of hepatitis B manifested by anicteric hepatitis and hepatitis B e antigen positivity. Marked tumor regression had occurred in both patients, and chemotherapy was discontinued in spite of the elevated alpha FP level. The alpha FP content in the serum gradually returned to normal, and hepatic dysfunction resolved. Both patients remain free of disease 15 and 17 months following the last chemotherapy treatment. These cases illustrate that hepatic dysfunction and alpha FP production may occur during chemotherapy and that increases in serum alpha FP content must be interpreted with caution since the elevated alpha FP level does not always indicate progression of germ cell tumors.

Adult↗
PubMed2001

Methotrexate poisoning with acute hepatorenal dysfunction.

A 17-year-old girl receiving high-dose methotrexate for the treatment of osteosarcoma developed complications of acute renal failure and liver dysfunction with a coagulation disorder. The methotrexate concentrations were quickly reduced from 600 micromol/L to 50 micromol/L by treatment with plasma exchange and hemodialysis at 72 hours after discontinuation of the drug. After this reduction, continuous hemodiafiltration was initiated to further lower the methotrexate concentrations because of the persistently high and then the actual rebound in the plasma concentrations after plasma exchange and hemodialysis treatment. Continuous hemodiafiltration was able to reduce the concentrations without any rebound, despite its low column clearance. The rebound in plasma methotrexate concentrations seems to be corrected by plasma methotrexate after plasma exchange and/or hemodialysis.

Acute Kidney Injury↗
PubMed2005

Hyperinsulinism in tyrosinaemia type I.

Tyrosinaemia type I (TT I) (McKusick 276700) is a heterogeneous disorder with a broad spectrum of clinical phenotypes. Although histological abnormalities of the pancreas are well recognized, there are only incidental reports of pancreatic dysfunction manifested as insulin-dependent diabetes mellitus. We report three subjects with TT I and acute liver dysfunction who had hyperinsulinism in early infancy. Hypoglycaemia persisted despite dietary treatment and one patient had inadequate lipolysis at the time of hypoglycaemia. All three patients were successfully treated with diazoxide (10 mg/kg per day) and chlorthiazide (35 mg/kg per day) and treatment was gradually withdrawn after 9, 13 and 34 months, respectively. The mechanism of pancreatic dysfunction in TT I is unknown but may be related to the toxic metabolites that accumulate in this condition. We conclude that hyperinsulinism is not a rare complication in TT I. In patients with persistent hypoglycaemia, C-peptide should always be measured. Treatment with diazoxide and chlorthiazide is highly effective, appears to be safe, and does not need to be continued lifelong.

Blood Glucose↗
PubMed2001

Splanchnic and systemic hemodynamic derangement in decompensated cirrhosis.

Patients with cirrhosis and portal hypertension exhibit characteristic hemodynamic changes with hyperkinetic systemic circulation, abnormal distribution of blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased. Splanchnic vasodilation is of pathogenic significance to the low systemic vascular resistance and abnormal volume distribution of blood, which are important elements in the development of the concomitant cardiac dysfunction, recently termed 'cirrhotic cardiomyopathy'. Systolic and diastolic functions are impaired with direct relation to the degree of liver dysfunction. Significant pathophysiological mechanisms are reduced beta-adrenergic receptor signal transduction, defective cardiac excitation-contraction coupling and conductance abnormalities. Vasodilators such as nitric oxide and calcitonin gene-related peptide are among the candidates in vasodilation and increased arterial compliance. Reflex-induced, enhanced sympathetic nervous system activity, activation of the renin-angiotensin aldosterone system, and elevated circulation vasopressin and endothelin-1 are implicated in hemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the hemodynamic and neurohumoral abnormalities in cirrhosis are part of a general cardiovascular dysfunction, influencing the course of the disease with the reduction of organ function, with sodium and water retention as the outcome. These aspects are relevant to therapy.

Coronary Circulation↗
PubMed1991

[Chemotherapeutic evaluation of pulmonary tuberculosis patients with a complication of hepatic dysfunction].

A retrospective study on the evaluation of antituberculous drugs for patients with hepatic dysfunction was undertaken to clarify treatment regimens. The values of GOT, GPT and T. Bil were used as indicators of liver function, and the "deterioration" in the liver function was defined as a level greater than 1.5 times the initial value. Of total 538 cases of active pulmonary tuberculosis, 103 cases (19.1%) had abnormalities in liver functions before chemotherapy, and 21 of 103 cases showed the deterioration in their liver functions during chemotherapy. There was little relationship between the initial status of liver functions and the incidence of their deteriorations after chemotherapy. Nine of 21 cases did not exceed the 3 times of normal ranges of liver functions. These nine cases could tolerate the same regimens of chemotherapy, and showed satisfactory clinical responses to chemotherapy with two exceptions: one died of tuberculosis and the other cerebrovascular disease. On the other hand, of 12 cases with elevated values of hepatic function greater than 3 times the normal limits, 6 cases discontinued chemotherapy. One case, however, died of hepatic failure related to chronic active hepatitis. Eight of 12 cases showed the rapid improvement of liver dysfunctions. These results suggest that antituberculous drugs are acceptable to patients with hepatic dysfunction as long as the elevations of GOT, GPT and T. Bil stay within 3 times of normal limits. Further chemotherapy could be continued under careful monitoring of liver functions even if the cases exhibit elevated levels of liver functions greater than 3 times the normal ranges.

Adult↗
PubMed2007

Characterization of liver disease and lipid metabolism in the Niemann-Pick C1 mouse.

Niemann-Pick type C1 (NPC1) disease is an autosomal-recessive cholesterol-storage disorder characterized by liver dysfunction, hepatosplenomegaly, and progressive neurodegeneration. The NPC1 gene is expressed in every tissue of the body, with liver expressing the highest amounts of NPC1 mRNA and protein. A number of studies have now indicated that the NPC1 protein regulates the transport of cholesterol from late endosomes/lysosomes to other cellular compartments involved in maintaining intracellular cholesterol homeostasis. The present study characterizes liver disease and lipid metabolism in NPC1 mice at 35 days of age before the development of weight loss and neurological symptoms. At this age, homozygous affected (NPC1(-/-)) mice were characterized with mild hepatomegaly, an elevation of liver enzymes, and an accumulation of liver cholesterol approximately four times that measured in normal (NPC1(+/+)) mice. In contrast, heterozygous (NPC1(+/-)) mice were without hepatomegaly and an elevation of liver enzymes, but the livers had a significant accumulation of triacylglycerol. With respect to apolipoprotein and lipoprotein metabolism, the results indicated only minor alterations in NPC1(-/-) mouse serum. Finally, compared to NPC1(+/+) mouse livers, the amount and processing of SREBP-1 and -2 proteins were significantly increased in NPC1(-/-) mouse livers, suggesting a relative deficiency of cholesterol at the metabolically active pool of cholesterol located at the endoplasmic reticulum. The results from this study further support the hypothesis that an accumulation of lipoprotein-derived cholesterol within late endosomes/lysosomes, in addition to altered intracellular cholesterol homeostasis, has a key role in the biochemical and cellular pathophysiology associated with NPC1 liver disease.

ATP Binding Cassette Transporter 1↗
PubMed2001

Role of platelet-activating factor in hepatectomy with Pringle's maneuver.

BACKGROUND: Interruption of hepatic inflow is commonly used to reduce blood loss during extensive liver resection, but may cause liver dysfunction. The present study investigated the effects of platelet-activating factor (PAF) antagonist E5880 on total liver warm ischemia and 70% hepatectomy. METHODS: Rabbits were used in this study and were divided into four groups: group 1, those treated with only 70% hepatectomy; group 2, those treated with only 20 min Pringle's maneuver; group 3, those treated with both Pringle's maneuver and 70% hepatectomy without pretreatment; and group 4, those pretreated with PAF antagonist E5880 (0.3 mg/kg) followed by Pringle's maneuver and 70% hepatectomy. The remnant liver function was then evaluated after reperfusion. RESULTS: Seven-day survival rates in both groups 1 and 2 were 100%. E5880 treatment significantly increased 7-day survival rate (group 4: 38% vs group 3: 0%, P < 0.05) after a combination of Pringle's maneuver and 70% hepatectomy. The elevations of serum liver enzymes (GOT, GPT, mGOT, and LDH) were significantly inhibited in group 4 at 1 and 4 h after reperfusion. Portal venous pressure and the energy charge of liver were also significantly improved in group 4, compared with those in group 3. Endothelin-1 levels of arterial and portal venous blood progressively increased after reperfusion; however, there were no significant differences between the two groups. Leukocyte infiltration into the liver was significantly inhibited in group 4. CONCLUSION: E5880 pretreatment has protective effects on liver function after 70% hepatectomy with Pringle's maneuver in rabbits.

Adenine Nucleotides↗
PubMed1993

Outcome of 21 patients with biliary atresia living more than 10 years.

The outcome of 21 survivors (8 males, 13 females; age range, 11 to 29 years) followed for > 10 years after surgery for biliary atresia are discussed. Of the 21 patients, 18 with type III disease had hepatic portoenterostomy (Kasai operation), and 3 with type I disease had hepaticoenterostomy. Twenty patients are alive leading almost normal lives; however, 13 (61.9%) patients did have a history of complications, including hemorrhage from esophageal varices in 10, from a gastric ulcer or erosion in 3, and from a duodenal ulcer in 2; biliary reobstruction in 3; and multiple pulmonary arteriovenous fistulae in 2. Of those with complications, 7 required surgery. One died suddenly at the age of 19 years of a bleeding gastric ulcer. Liver function is normal in 9 (45.0%) of the 20 alive patients, 2 (10.0%) have slight hepatic dysfunction, and 9 (45.0%) have mild-to-moderate hepatic dysfunction. Liver function is almost normal in 3 patients who had a history of variceal hemorrhage.

Adolescent↗
PubMed2005

[Congenital galactosaemia: an unusual presentation].

Congenital galactosaemia reveals usually in the second and third weeks of life with a severe liver dysfunction. We report on a case of congenital galactosaemia with, on the one hand, an early onset liver failure, without any free interval, and on the other hand, an hemophagocytic syndrome as a severe secondary outbreak with pulmonary haemorrhage. Appropriate diet led to normalisation of liver function. Hemophagocytosis, probably linked to an associated Klebsiella Pneumoniae sepsis, had a favourable outcome after antibiotic and corticosteroid therapy.

Galactosemias↗
PubMed1999

Factors impacting the survival of children with intestinal failure referred for intestinal transplantation.

PURPOSE: The aim of this study was to analyze factors impacting on the survival of pediatric patients with intestinal failure referred for intestinal transplantation (ITx). METHODS: Two hundred fifty-seven children (mean age, 3.4+/-0.26 years) with intestinal failure were evaluated for ITx between 1990 and 1998. All patients were dependent on total parenteral nutrition (TPN) for a mean of 31+/-2.7 months. The mean follow-up time from the date of evaluation was 9.2+/-0.9 months. RESULTS: Eighty-two (32%) children underwent ITx with a mean waiting time of 10.1+/-1.3 months (simultaneous liver-intestinal allograft in 68% instances). Of the 175 patients who did not undergo transplantation, 120 died, 23 were lost to follow-up, and 32 are alive. Younger patients (< or =1 year) had poorer survival rates than patients older than 1 year (P<.0001). The patients with the worse prognosis were those with necrotizing enterocolitis, and those with the best prognosis were those with Hirschsprung's disease. Patients with "surgical" causes had poorer survival rates than those with "nonsurgical" causes (P<.04). Patients with bridging fibrosis or established cirrhosis had an earlier mortality than patients with portal fibrosis (P<.003). The worst survival rate was found for patients with bilirubin levels of greater than 3 mg/dL (P<.0001), plateletcounts less than 100.000/mL (P<.0001), prothrombin time greater than 15 seconds (P = .03) or partial thromboplastin time greater than 40 seconds (P<.04). Children who at the time of evaluation needed only an isolated intestinal allograft had a better prognosis than those who required a combined liver-intestine allograft (P<.00001). With multivariate analysis independent prognosis risk factors of poor outcome were hyperbilirubinemia and severity of histopathologic damage. CONCLUSIONS: Early referral for ITx should occur before the development of liver dysfunction, taking into consideration the aforementioned risk factors that would facilitate the development and ominous evolution to liver failure.

Child, Preschool↗
PubMed2001

Massive intravenous immunoglobulin treatment in pregnancy complicated by Guillain-Barré Syndrome.

A pregnant woman developed acute demyelinating poly-neuropathy (Guillain-Barré syndrome (GBS)) in the 28th week of gestation (GW) after flu-like infection. Hypertension, liver dysfunction, and a decrease in consciousness level developed at 29GW. Blood chemical analysis revealed increased levels of liver enzymes GOT 247 IU/l and GPT 624 IU/l. Viral serological study showed a positive test for Epstein-Barr virus IgM. Weakness of bilateral facial muscles and limbs, a loss of tendon reflexes, and generalized paresthesia were detected by neurologic examinations. Over the course of 5 days, a massive dose (100g) of intravenous immunoglobulin (MIVIg) was infused in 30GW. An average manual muscle testing score by the Medical Research Council method and peak flow value began to be significantly restored during and after MIVIg infusions. Values of the liver enzymes gradually decreased, and improvement of the muscle weakness and dysbasia was observed. Her pregnancy normally ended in spontaneous vaginal delivery of a healthy infant in 37GW. This is the first report confirming the efficacy of MIVIg, without plasmapheresis, in GBS-complicated pregnancy.

Adult↗
PubMed1988

Hepatic changes in rats following subchronic administration of FYROL 6, an organophosphorus ester flame retardant.

This study conducted to evaluate the subchronic toxicity of FYROL 6 [diethyl N,N-bis-(2-hydroxyethyl)aminomethylphosphonate] in rats demonstrated an hepatic effect not commonly reported for related compounds. Sprague-Dawley rats of both sexes were gavaged daily with 0, 10, 100, or 500 mg/kg FYROL 6 in corn oil for 13 wk. No treatment-related mortality and few signs of toxicity were noted during the study. Fyrol 6 did not inhibit plasma, erythrocyte, or brain cholinesterase activities. Treatment-related necropsy and microscopic alterations were restricted to the liver. Increased liver weights, hepatocellular hypertrophy, and eosinophilia of centrilobular hepatocytes were evident in 100-mg/kg females and in both sexes at 500 mg/kg. Morphometric analysis revealed a 40% increase in cross-sectional area of individual hepatocytes in 500-mg/kg males, compared to controls. There was no morphologic evidence of hepatic necrosis or clinical evidence of liver dysfunction. This study demonstrated low toxicity for FYROL 6 and treatment-related changes restricted to the liver suggestive of an adaptive response to FYROL 6.

Animals↗
PubMed2005

Successful liver transplantation for giant cell hepatitis and Coombs-positive hemolytic anemia: a case report.

Giant cell hepatitis (GCH) with autoimmune hemolytic anemia (AHA) is a distinct entity with an aggressive course. Drugs, autoimmunity, and viruses have been implicated in its etiology. Without treatment, liver dysfunction is progressive and fatal. Although successful immunosuppressive treatment has been reported, a few patients have undergone liver transplantation with recurrence of the primary disease in the allograft. We report, an 18-year-old boy with progressive GCH with AHA without recurrence in the allograft following deceased donor (DD) liver transplantation.

Adolescent↗
PubMed2005

Elevated plasma adiponectin concentrations in patients with liver cirrhosis correlate with plasma insulin levels.

BACKGROUND: Adiponectin is a hormone secreted by adipocytes and has anti-diabetic and anti-atherogenic properties. Hypoadiponectinemia is associated with insulin-resistant diabetes and liver dysfunction. The aim of this study was to determine plasma adiponectin and insulin levels in patients with liver cirrhosis. METHODS: Adiponectin and insulin levels were determined in 38 patients with cirrhosis and 30 healthy controls, and were correlated with various clinical and biochemical parameters. Patients included 21 with Child A, eight Child B, and nine with Child C liver cirrhosis. RESULTS: Log adiponectin and insulin levels were significantly elevated in patients with cirrhosis compared with the control. In liver cirrhosis, the level of adiponectin increased proportionately with the Child's classification score. In control subjects, plasma adiponectin correlated inversely with insulin levels. In contrast, plasma adiponectin correlated positively with insulin levels in patients with liver cirrhosis. Plasma adiponectin levels did not correlate with age, sex, body mass index, total bilirubin, aspartate aminotransferase, and fasting blood sugar levels in both groups, while alanine aminotransferase correlated negatively with adiponectin in control subjects as reported previously. CONCLUSION: Our results of high plasma adiponectin in patients with liver cirrhosis could reflect an imbalance between its production by adipocytes and metabolism in the liver.

Adiponectin↗
PubMed2006

Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia.

A 47-year-old Japanese woman was diagnosed as having acute biphenotypic leukemia with association of t(9;22)(q34;q11). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immunohistochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-beta1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult acute biphenotypic leukemia may cause the unusual "disorganized" hepatic fibrosis.

Becaplermin↗
PubMed1997

Transjugular liver biopsy with an automated device.

PURPOSE: To determine the potential for use of an automated device for transjugular liver biopsy. MATERIALS AND METHODS: In 29 consecutive patients with liver dysfunction in whom percutaneous transperitoneal biopsy was contraindicated because of thrombocytopenia, severe coagulopathy, or marked ascites, transjugular liver biopsy was performed with an 18-gauge automated device. Histopathologic specimens were quantitatively and qualitatively analyzed. Complications related to the biopsy procedure were noted. RESULTS: In all patients, an adequate biopsy specimen (mean length, 12.0 mm +/- 5.5; range, 5.0-20.0 mm) was obtained during a single pass. In all tissue samples, a confident histopathologic diagnosis was made. Additional information was obtained in 15 patients with cirrhosis who had coexisting diffuse hepatic disease. No complications related to the procedure were noted. CONCLUSION: Use of an automated biopsy device is recommended for transjugular liver biopsy, as it enables safe acquisition of high-quality hepatic tissue samples.

Biopsy, Needle↗