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PubMed2002

Detection of posttrauma apoptosis and necrosis of hepatocytes and its significance.

OBJECTIVE: To study the role of apoptosis and necrosis of hepatocytes in the pathogenesis of acute liver dysfunction following severe trauma in rats. METHODS: Rat models of multiple fractures complicated by shock were established, in which apoptotic and necrotic hepatocytes were detected by flow cytometry (FCM) via double-staining technique of Annexin-V-flous and propidium iodide (PI). Observation of the pathological changes in the hepatocytes was also conducted by means of light and electron microscopy and electronphoresis respectively, and the correlation of these changes with liver function were evaluated. RESULTS: Hepatocytes underwent both apoptosis and necrosis in rat models of severe trauma. The quantities of necrotic hepatocytes increased progressively in positive correlation with the degree of hepatic injury, reaching the peak at 3 h post trauma. A proportion of the apoptotic cells underwent secondary necrosis, the number of the necrotic cells positively correlated with liver dysfunction deterioration. CONCLUSIONS: Both necrosis and apoptosis are important factors responsible for liver function damages following severe trauma. Necrosis of hepatic cells directly causes liver function damages that are further aggravated by secondary necrosis among apoptotic hepatocytes.

Animals↗
PubMed2003

Drug-induced hepatitis with autoimmune features during minocycline therapy.

A 25-year-old woman with no history of liver disease developed liver dysfunction associated with severe jaundice and general malaise following a prolonged therapy with minocycline for acne vulgaris. Serum anti-nuclear antibody was detected and immunoglobulin G level was elevated. Symptoms resolved and liver function normalized following minocycline discontinuation and corticosteroid administration. Our diagnosis was drug-induced hepatitis with autoimmune features, as liver histology revealed acute hepatitis. Drug-induced hepatitis should be considered when liver dysfunction or systemic symptoms develops during long-term minocycline therapy.

Acne Vulgaris↗
PubMed1998

Portal branch ligation with a continuous hepatocyte growth factor supply makes extensive hepatectomy possible in cirrhotic rats.

In a cirrhotic liver, the regenerative ability and specific functions are so impaired that excessive resection easily complicates postoperative liver dysfunction, which frequently leads to life-threatening multiple-organ failure. Hepatocyte growth factor (HGF), first identified as the most potent stimulator of DNA synthesis in primary hepatocytes, not only stimulates liver regeneration, but also accelerates hepatic function, improves fibrosis, and protects liver cells against injury. Therefore, we investigated the efficacy of preoperative portal branch ligation (PBL) (which can induce compensatory hypertrophy of the unaffected lobes) combined with a continuous HGF supply in the performance of extensive hepatectomy in cirrhotic rats. Cirrhosis was induced by intraperitoneal injections of dimethylnitrosamine (DMN) three times per week for 3 weeks. Five days after the last injection, when 70% hepatectomy is lethal, the rats underwent portal ligation of the left lateral and median branches (corresponding to approximately 70% of the total volume of the liver). Simultaneously, they were continuously treated with either recombinant human HGF (rhHGF) or vehicle from an intraperitoneally implanted osmotic pump. Four days after the portal ligation, the occluded lobes were resected. The HGF treatment rapidly increased both the wet weight of the unoccluded lobes and the hepatocellular DNA synthesis. The blood chemical analysis indicated that HGF significantly suppressed the posthepatectomy liver dysfunction. Most importantly, the HGF treatment markedly improved the survival rate of the rats at 48 hours after the major hepatectomy. In conclusion, PBL combined with a continuous HGF supply makes extensive hepatectomy possible in cirrhotic rats, mainly by promoting the hypertrophy of the unaffected lobes.

Animals↗
PubMed1982

Liver disease after bone marrow transplantation.

Liver dysfunction occurs after bone marrow transplantation but the relative importance of graft versus host disease and other factors, such as infection, radiation, and drugs, has not been clearly established. We have studied liver status before and after bone marrow transplantation in 43 consecutive patients and have related this to survival and factors that are recognised to cause liver injury. Minor abnormalities of liver tests occurred in 21% of patients before grafting but this did not influence survival or the development of liver disease after transplantation. During the first 50 days after grafting, 83% of patients had abnormal liver tests which were more severe in patients who subsequently died. Alanine transaminase was significantly higher in non-survivors and appeared to predict survival early after transplantation. Only non-survivors developed clinical signs of liver disease. Severe liver disease was always associated with graft versus host disease and atypia of the small bile ducts was the most useful histological marker of hepatic involvement with this disease. Two of the patients with hepatic graft versus host disease also has hepatic veno-occlusive disease and three fatalities had opportunistic infection of the liver, although, in the latter, death was not due primarily to liver dysfunction. Previous hepatitis and androgen therapy could not be implicated as important causes of hepatic damage but chemotherapy for acute leukaemia and conditioning regimens for bone marrow transplantation appear to be the most important factors in the development of hepatic veno-occlusive disease.

Adolescent↗
PubMed2005

[Case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment].

A 92-year-old man with a history of bronchial asthma and allergic rhinitis received antibiotics for sepsis by methicillin-resistant Staphylococcus aureus and multidrug-resistant Enterococcus gallinarum. During the antibiotics treatment, skin eruptions, liver dysfunction, and hypereosinophilia developed, followed by dyspnea, congestive heart failure, electrocardiographic abnormalities, and diffuse mild myocardial hypokinesis. After the discontinuation of the antibiotics and the administration of steroid, skin eruptions, liver dysfunction, and hypereosinophilia improved parallel with the improvement of the congestive heart failure. Vancomycin hydrochloride and teicoplanin were suspected as the causative drugs on the basis of the treatment course. Although congestive heart failure is rare in the case of drug-induced hypereosinophilia, it is one of life-threatening complications. We describe herein a case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment, successfully treated with steroid after the discontinuation of the causative drug.

Aged, 80 and over↗
PubMed1991

[Bone marrow transplantation in a pediatric case of acute nonlymphocytic leukemia with hepatitis C].

An allogenic bone marrow transplantation (BMT) in an acute nonlymphocytic leukemia (ANLL) patient with post-transfusion hepatitis C is presented. A 13-year-old girl was admitted to our hospital on May 1988, and diagnosed as having ANLL M2 according to the FAB classification. During the induction and post-induction chemotherapy, 116 units of blood products were transfused to her as the supportive therapy until October 1988, when non-A non-B hepatitis developed. As the persistent liver dysfunction interfered with anti-leukemic chemotherapy on the protocol, allogeneic BMT from her HLA identical MLR nonreactive brother was done on July 1989. Preconditioning regimen consisted of busulfan and cyclophosphamide. GVHD prophylaxis consisted of cyclosporine A and short term methotrexate. After the BMT, her liver dysfunction once improved; her serum amino-transferase levels were normal for about 3 months. Soon after discontinuation of cyclosporine A, however, her liver function deteriorated again. The examination of hepatitis C virus antibody in her sera, which had been harvested sequentially and stored at -40 degrees C, on November 1989 revealed that she had been already seropositive at the time of BMT. The BMT-induced immunologic changes may have influenced the natural course of hepatitis C virus infection in the patient.

Adolescent↗
PubMed1999

Elevated carboxy terminal cross linked telopeptide of type I collagen in alcoholic cirrhosis: relation to liver and kidney function and bone metabolism.

BACKGROUND: The carboxy terminal cross linked telopeptide of type I collagen (ICTP) has been put forward as a marker of bone resorption. Patients with alcoholic liver disease may have osteodystrophy. AIMS: To assess circulating and regional concentrations of ICTP in relation to liver dysfunction, bone metabolism, and fibrosis. METHODS: In 15 patients with alcoholic cirrhosis and 20 controls, hepatic venous, renal venous, and femoral arterial concentrations of ICTP, and bone mass and metabolism were measured. RESULTS: Circulating ICTP was higher in patients with cirrhosis than in controls. No overall significant hepatic disposal or production was found in the patient or control groups but slightly increased production was found in a subset of patients with advanced disease. Significant renal extraction was observed in the controls, whereas only a borderline significant extraction was observed in the patients. Measurements of bone mass and metabolism indicated only a mild degree of osteodystrophy in the patients with cirrhosis. ICTP correlated significantly in the cirrhotic patients with hepatic and renal dysfunction and fibrosis, but not with measurements of bone mass or metabolism. CONCLUSIONS: ICTP is highly elevated in patients with cirrhosis, with no detectable hepatic net production or disposal. No relation between ICTP and markers of bone metabolism was identified, but there was a relation to indicators of liver dysfunction and fibrosis. As the cirrhotic patients conceivably only had mild osteopenia, the elevated ICTP in cirrhosis may therefore primarily reflect liver failure and hepatic fibrosis.

Adult↗
PubMed1999

Portal vein thrombosis in paroxysmal nocturnal haemoglobinuria.

A 28-year-old man was hospitalized with nausea, vomiting, abdominal pain and low-grade fever. He had a 6-month history of paroxysmal nocturnal haemoglobinuria (PNH), and laboratory data showed anaemia and liver dysfunction. An abdominal ultrasonography showed ascites and portal vein thrombosis. After receiving antithrombotic treatment, the portal vein thrombosis did not extend. Portal vein thrombosis is very rare but should be considered when we encounter liver dysfunction associated with PNH as well as hepatic vein thrombosis. Ultrasonography is very useful in detecting portal vein thrombosis and facilitating early diagnosis. Warfarin is very effective in preventing exacerbation of portal vein thrombosis in PNH.

Adult↗
PubMed1982

Can severe vincristine neurotoxicity be prevented?

Neurotoxicity in vincristine treatment has generally been considered a consequence of the cumulative dose of the drug, and liver dysfunction had been recognised as an indication to reduce the dosage. We demonstrate that neurotoxicity is also related to individual doses and that even when there is no other evidence of liver dysfunction, a raised level of serum alkaline phosphatase may predict severe neurotoxicity. Exposure to vincristine following IV injection of the drug was studied in 27 subjects by measuring the area under the vincristine plasma concentration time curve (AUC 0-infinity). A statistically significant relationship was found between the AUC0-infinity and the degree of neurotoxicity. The AUC0-infinity was related both to dose and to elevation of serum alkaline phosphatase, suggesting that elimination of the drug is impaired when serum alkaline phosphatase is raised. Among patients with elevated serum alkaline phosphatase, a small reduction in the dose of the drug resulted in lower vincristine plasma AUC0-infinity and less neurotoxicity.

Adolescent↗
PubMed2001

Analysis of patients with longitudinal intestinal lengthening procedure referred for intestinal transplantation.

BACKGROUND/PURPOSE: Longitudinal intestinal lengthening procedures (LILP) in patients with short gut syndrome (SGS) enhances small intestinal peristalsis and decreases bacterial overgrowth without reducing absorptive surface. Therefore, patients theoretically may be easily weaned off TPN. The aim of this study was to evaluate the impact of failed LILP in SGS patients referred for intestinal transplantation. METHODS: Twenty-seven (11%) of 230 children with SGS and total parenteral nutrition (TPN) dependency evaluated for intestinal transplantation at our institution had undergone LILP. This was performed at a mean age of 1.7 years (range, 1 day to 14.7 years); the mean age at the time of evaluation was 3.3 years (range, 0.4 to 17 years). Two patients underwent LILP immediately after birth. The principle diagnoses producing SGS were gastroschisis (n = 8), intestinal atresia (n = 11), neonatal volvulus (n = 7) and necrotizing enterocolitis (n = 1). Before LILP, the mean length of intestine was 32 cm (range, 8 to 70 cm). Fifteen (56%) patients had jaundice at the time of evaluation. RESULTS: All but one child were considered candidates for intestinal transplantation. The mean intestinal length achieved after LILP was 48 cm (range, 16 to 100). The mean follow-up from the date of LILP was 876 days (range, 109 to 4,109 days). After LILP, only 9 (33%) patients increased their caloric intake through the enteral route by > or =50%, and only 1 patient could be weaned off TPN. In the patients with liver dysfunction at the time of LILP, none recovered. Most of the patients had multiple episodes of sepsis after LILP. Fourteen (52%) of 27 patients underwent intestinal transplantation, 7 combined with a liver allograft because of TPN-induced end-stage liver disease. Six of the transplanted patients are alive and TPN free. Of the remaining 13 (48%) nontransplanted patients, 9 patients died. The main cause of death was TPN-induced liver failure. Three patients are on partial TPN, and only 1 patient was weaned off TPN. The presence of an ileocecal valve did not impact on outcome. Surprisingly, patients with > or =50% of colon at the time of LILP had poorer survival than those with less. Twelve (44%) of 27 patients had surgical complications, and in both patients with LILP performed in the neonatal period it failed immediately with acute complications. There were no differences in patient survival rate for patients with SGS without LILP (n = 203) and those with LILP (n = 27). CONCLUSION: Based on patients with unsuccessful LILP referred for intestinal transplantation, we believe this procedure should be avoided in the neonatal period, in those patients with liver dysfunction, and when intestinal length is <50 cm.

Adolescent↗
PubMed2001

Endothelial-derived nitric oxide and angiotensinogen: blood pressure and metabolism during mouse pregnancy.

The regulation of blood pressure during pregnancy involves several biological pathways. Candidate genes implicated in hypertensive diseases during pregnancy include those of the renin-angiotensin system and nitric oxide synthase (NOS). We evaluated blood pressure and metabolic characteristics during pregnancy in mutant mice. These included mice with a null mutation in the endothelial NOS (eNOS) gene (Nos3(-/-)), four copies of the angiotensinogen gene (Agt(2/2)), and mutations in both genes [four copies of Agt and heterozygous deficient for eNOS (Agt(2/2)Nos3(+/-)), four copies of Agt and homozygous deficient for eNOS (Agt(2/2)Nos3(-/-))]. Blood pressure measurements of nulliparous females from mutant strains were compared with two common laboratory strains C57Bl6/J and SV129 throughout their first pregnancy. Serum and urine analysis for the evaluation of renal and liver physiology were measured in the prepregnant state and during the third trimester of pregnancy. Throughout pregnancy blood pressures in all mutant strains were higher compared with controls. Agt(2/2)Nos3(-/-) showed the highest blood pressures and C57Bl6/J the lowest. Control mice, but not mutant mice, showed a second trimester decline in blood pressure. No immediate differences were noted regarding behavioral characteristics, renal or liver function parameters. Mice deficient for eNOS, mice with overexpression of Agt, and mice with mutations in both genes demonstrated higher blood pressure throughout pregnancy. There was no evidence of renal dysfunction, liver dysfunction, or hemolysis among any of the strains studied. We conclude that Nos3 and Agt are important genes in the regulation of blood pressure during pregnancy.

Angiotensinogen↗
PubMed2000

Strongyloidiasis--progress in diagnosis and treatment.

Strongyloidiasis is an intestinal parasitic disease caused by Strongyloides stercoralis. Basically, detecting larvae of S. stercoralis in feces makes definitive diagnosis. The ordinary agar plate culture method developed at our department is much simpler to handle and much more sensitive than the conventional filter paper culture method. It is considered to be the most useful method in the diagnosis of strongyloidiasis and in evaluation of the eradicating effect. Among chemotherapeutic agents, thiabendazole representing the benzimidazole compounds is most effective. However, it has a problem in safety, since its adverse effects and liver dysfunction occur with a high incidence, and it can be severe. Regarding the effects of mebendazole, albendazole and ivermectin, a study was conducted which included many patients. A high incidence of liver dysfunction was observed with mebendazole, and eradicating effect was not sufficient with albendazole. Ivermectin is different from benzimidazole compounds in a pharmacokinetic profile. However, ivermectin showed a strong anthelmintic effect with the least toxicity. We therefore consider ivermectin is the most useful drug for the treatment of strongyloidiasis.

Antiprotozoal Agents↗
PubMed2006

Short-term effects of di-(2-ethylhexyl) phthalate on testes, liver, kidneys and pancreas in mice.

AIM: To determine the biochemical effect of di-(2-ethylhexyl) phthalate (DEHP) on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium. METHODS: Diets containing 2% DEHP were given to male Crlj:CD1(ICR) mice for 10 days. The dose of DEHP was 0.90 +/- 0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-(2-ethylhexyl) phthalate (MEHP), nitrogen oxides (NOx) produced by peroxidation of nitric oxide (NO) with free radicals, and lipid peroxidation induced by the chain reaction of free radicals. RESULTS: Histological observation and serum analysis showed the presence of severe spermatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver. CONCLUSION: The results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.

Animals↗
PubMed1992

Hyperammoniemic coma in a patient with ureterosigmoidostomy and normal liver function.

Hyperammoniemic encephalopathy has been reported after ureterosigmoidostomy. Its development is related to a problem of bacterial overgrowth and, most often, is favored by the presence of an underlying liver dysfunction. We report the case of a 43-year-old woman with a ureterosigmoidostomy done 28 years earlier who developed hyperammoniemic coma induced by an acute rectocolitis and in the absence of any detectable liver dysfunction. Neither administration of Lactilol and neomycin nor rectal tube drainage were effective; systemic antimicrobial therapy effective against the urease-producing gram-negative bacilli was required and led to a decrease in serum ammonia levels and a dramatic clinical improvement.

Acute Disease↗
PubMed1987

Halothane metabolism in cirrhotic rats.

A rat model was used to determine whether the metabolism of halothane is changed in the presence of cirrhosis and whether exacerbation of liver dysfunction is correlated with such a change. Cirrhosis was produced by gavaging enzyme-induced male Wistar rats with carbon tetrachloride in corn oil once weekly for 12 weeks. Control rats received corn oil only. After a 3-week period without treatment, blood and urine were collected from each rat for determination of background levels of inorganic fluoride, bromide, and trifluoroacetic acid (halothane metabolites) and for assessment of liver function. Rats were then anesthetized with 1.05% halothane in 50% oxygen for 3 h. Following anesthesia, serial blood and urine samples were taken to monitor halothane metabolism and liver function. No differences were observed between cirrhotic and non-cirrhotic rats in serum levels and urinary excretion of halothane metabolites. However, serum levels of SGOT and SGPT were significantly increased about 1.5-fold in the noncirrhotic group and about 2.5-fold in the cirrhotic group after anesthesia. The increased levels observed in the cirrhotic group were significantly greater than in the noncirrhotic group. The results imply that the exacerbation of liver dysfunction after halothane anesthesia is most likely related to an indirect effect, such as change in liver blood flow, rather than to toxic metabolites.

Animals↗
PubMed2005

Serum molybdenum concentration in healthy Japanese adults determined by inductively coupled plasma-mass spectrometry.

The serum molybdenum (Mo) concentrations in 70 Japanese adults (35 males and 35 females) not receiving any medical care or treatment were determined by inductively coupled plasma-mass spectrometry. Serum Mo concentration in the subjects ranged from <0.1 to 9.11 ng/mL. More than half (55.7%) of the subjects showed values of less than 1 ng/mL and only 6 (8.6%) subjects showed more than 2 ng/mL. The mean+/-SD, geometrical mean (GM), range of GM+/-geometrical SD (GSD) and median value were 1.21+/-1.34, 0.81, 0.30 to 2.16, and 0.90 ng/mL, respectively. Among age, body mass index and several serum biochemical values, activities of aspartate aminotransferase and alanine aminotransferase showed significant associations with serum Mo; 15 subjects suspected of having liver dysfunction showed significantly higher serum Mo than others. We propose a range of 0.10-4.73 ng/mL, estimated as a range of GM+/-2GSD of serum Mo in the remaining 55 subjects without liver dysfunction, as a reference range of serum Mo in Japanese healthy adults.

Adult↗
PubMed1989

[The present status in prophylaxis and treatment of HIV infected patients with hemophilia in Japan].

Thirty six hemophiliacs with HIV infection were treated with high-dose glycyrrhizin, Stronger Neo-Minophagen C (SNMC). The dose was 100-200 ml of SNMC in eighteen patients and 400-800 ml in the other 18. The patients were divided into an asymptomatic carrier (AC) group and AIDS related complex (ARC)/AIDS group. SNMC was administered intravenously daily for the first 3 weeks, every second day for the following 8 weeks to 36 HIV positive hemophilia patients in accordance with the protocol proposed by the Japanese National Research Committee. The CD 4/CD 8 ratio and CD 4 positive lymphocyte counts did not change during the treatment period. However, significant improvement was noted in some cases. A slight increase in mitogenic responsiveness to phytohemagglutinin, Concanavalin A and pokeweed mitogen was noted in most patients of both groups, especially in the AC group administered over 400 ml of SNMC. Furthermore, complete improvement was noted in liver dysfunction, which has been thought to be a major problem in hemophiliacs treated with blood products. Thus prophylactic administration of high-dose SNMC to HIV positive hemophiliacs having impaired immunological ability and liver dysfunction was considered to be effective to prevent the development from AC/ARC to AIDS.

AIDS-Related Complex↗
PubMed1984

Halothane hepatitis and the anaesthesiologist.

There is no longer any doubt that liver dysfunction following surgery and anaesthesia may sometimes be attributable to the inhalational anaesthetic agent halothane. Much controversy still surrounds the entity of halothane hepatitis, which continues to vex the practising anaesthesiologist. The incidence, causation, pathogenesis and diagnosis of halothane hepatitis are presented, and the safety and practicality of halothane administration in the presence of liver dysfunction are discussed.

Anesthesia, Inhalation↗