• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.9 no.1
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• pp.108-113
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• 2006

In case of Wilson's disease complicated with hemolytic anemia and fulminant hepatic failure; plasma exchange or liver transplantation should be considered. We report an 11 year-old male with fulminant Wilson's disease who developed hemolytic crisis. He was recovered by exchange transfusion after 6 times of plasma exchange.

• Archives of Plastic Surgery
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• v.33 no.4
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• pp.454-457
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• 2006

Purpose: The anastomosis of hepatic artery to recipient vessel has a major role in a liver transplantation, so its occlusion is the most important cause of failure of liver transplantations. We made the study to reveal the peculiarities in pediatric liver transplantations compared with adult cases. Methods: From January 1999 to September 2005, we performed 99 cases of pediatric liver transplantation. The mean age at operation was 4.17 years of age. The hepatic vein and portal vein are anastomosed by the general surgeons and then the hepatic artery is anastomosed by the plastic surgeons. The Doppler ultrasonography and computed tomography were used for postoperative checkup for hepatic artery patency. Results: There were no immediate complications, but hepatic arterial occlusion was developed in 3 cases (2.8%). In pediatric patients, the anastomosis of hepatic artery is more difficult than adults because of the rapid respiratory and pulse rate, the small vascular diameter, and the large gap of diameter difference between the recipient and the donor vessels. Conclusion: We could confirm that pediatric liver transplantations are relatively safe but long learning curve was needed.

• Journal of Yeungnam Medical Science
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• v.40 no.2
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• pp.136-145
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• 2023

Hepatic encephalopathy (HE) is a severe neuropsychiatric abnormality in patients with either acute or chronic liver failure. Typical brain magnetic resonance imaging findings of HE are bilateral basal ganglia high signal intensities due to manganese deposition in chronic liver disease and hyperintensity in T2, fluid-attenuated inversion recovery, or diffusion-weighted imaging (DWI) with hemispheric white matter changes including the corticospinal tract. Low values on apparent diffusion coefficient mapping of the affected area on DWI, indicating cytotoxic edema, can be observed in acute HE. However, neuropsychological impairment in HE ranges from mild deficits in psychomotor abilities affecting quality of life to stupor or coma with higher grades of hepatic dysfunction. In particular, the long-lasting compensatory mechanisms for the altered metabolism in chronic liver disease make HE imaging results variable. Therefore, the clinical relevance of imaging findings is uncertain and differentiating HE from other metabolic diseases can be difficult. The recent introduction of concepts such as "acute-on-chronic liver failure (ACLF)," a new clinical entity, has led to a change in the clinical view of HE. Accordingly, there is a need to establish a corresponding concept in the field of neuroimaging diagnosis. Herein, we review HE from a historical and etiological perspective to increase understanding of brain imaging and help establish an imaging approach for advanced new concepts such as ACLF. The purpose of this manuscript is to provide an understanding of HE by reviewing neuroimaging findings based on pathological and clinical concepts of HE, thereby assisting in neuroimaging interpretation.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.62-67
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• 2004

Trauma remains one of the important sources leading to systemic inflammatory response anti sub-sequent multiple organ failure. Although hepatic microvascular dysfunction occurs during trauma, the mechanism responsible remains unclear. The aim of this study was to investigate the effect of trauma on hepatic vascular stress gene expression. Femur fracture (EFx) was induced by torsion to the femur at midshaft. Liver samples were taken for RT-PCR analysis of mRNA for gtenes of interest: endothelin-1 (ET-1), its receptors $ET_A$ and $ET_B$, nitric oxide synthases (iNOS and eNOS), cyclooxygenase-2 (COX-2), heme oxygenase-1 (HO-1), and tumor necrosis tactor-${\alpha}$ (TNF-${\alpha}$). The expression of ET-1 mRNA was significantly increased by FFx. Expression of mRNA in FFx group showed no change in $ET_A$, $ET_B$, iNOS and HO-1 and showed a slight increase of 2.2-fold and 2.7-fold for eNOS tll1d COX-2, respectively. The level of TNF-${\alpha}$ mRNA significantly increased in FFx group. In conclusion, mild trauma alone causes little change in expression of vasoactive mediators.

• Toxicological Research
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• v.12 no.2
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• pp.265-270
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• 1996

Effects of a single administration of dichloromethane (DCM) on the hepatic drug metabollzing activity were determined using adult female rats. Rats were treated with DCM (3 mmol/kg, ip) and the disappearance of antipyrine (100 mg/kg, iv) or ethanol (2 g/kg, ip) from blood was measured. The blood concentration and half-life of antipyrine was not influenced by DCM administration. And DCM did not alter the blood concentration of ethanol measured for 240 min after the treatment. The effect of DCM treatment on in vitro cytochrome P-450-dependent enzyme activities was examined as well. No significant difference in either aniline hydroxylase or aminopyrine N-demethylase was observed in hepatic microsomal fractiorts of rats treated with DCM 24 hr prior to sacrifice. The present study indicates that acutely given DCM does not alter the metabolism of xenobiotics in vivo. The failure of DCM to alter the in vitro hepatic microsomal drug metabolizing activity was also noted.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.276-285
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• 2000

Paraquat is a very potent herbicide which causes fatal toxicity when ingested, and there is no specific antidote against it. Human ingestion induces acute renal failure, hepatic dysfunction and progressive respiratory failure with high mortality rate. Clinical investigation and medical treatment were done on two cases of acute renal failure caused by paraquat poisoning admitted to the Department of Internal Medicine, Wonkwang University Oriental Chonju Medical Hospital. We report two cases of patients who survived after acute paraquat intoxication, by means of oriental medicine such as Gamdutang, a typical antidote of toxins, chinese ink as an absorbent and burned powder of Rhei Radix et Rhizoma for laxative and so on, western medicine such as gastric lavage, diuretics and fluid therapy. We suggest more experiments and studies related to such treatment for paraquat poisoning be conducted.

• Journal of Veterinary Clinics
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• v.28 no.6
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• pp.617-620
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• 2011

A 6-month-old orange winged Amazon parrot (Amazona amazonica) was presented for evaluation of weight loss, anorexia, and abdominal distension for two months. Clinical and laboratory examinations revealed evidence of hepatic failure, including transudative ascites, increased serum serum aspartate aminotransferase and bile acids, and decreased albumin-to-globulin ratio. Hepatic fibrosis with bile duct hyperplasia and chronic hepatitis was diagnosed by liver biopsy. The cause of this condition remained unclear, but exposure to hepatotoxins was suggested.

• Neonatal Medicine
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• v.15 no.2
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• pp.183-189
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• 2008

Infantile hepatic hemangioendotheliomas (IHHEs) are benign vascular tumors, but can be associated with the life-threatening complications, such as congestive heart failure, disseminated intravascular coagulation, and massive bleeding. Various therapeutic options have been developed and the treatment response depends on the patient's clinical status and the nature of the lesion. In the case of a symptomatic IHHE, a non-invasive and precise diagnosis should be performed promptly before the therapeutic method is chosen. Additionally, it should be kept in mind that the residual lesions have malignant potential. We report a case of a congenital giant IHHE that was successfully reduced in size by interferon-$\alpha$ and completely removed by surgical tumor resection with a hepatic lobectomy.

• Clinical Nutrition Research
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• v.12 no.2
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• pp.154-167
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• 2023

Hepatic encephalopathy (HE) associated with liver failure is accompanied by hyperammonemia, severe inflammation, depression, anxiety, and memory deficits as well as liver injury. Recent studies have focused on the liver-brain-inflammation axis to identify a therapeutic solution for patients with HE. Lipocalin-2 is an inflammation-related glycoprotein that is secreted by various organs and is involved in cellular mechanisms including iron homeostasis, glucose metabolism, cell death, neurite outgrowth, and neurogenesis. In this study, we investigated that the roles of lipocalin-2 both in the brain cortex of mice with HE and in Neuro-2a (N2A) cells. We detected elevated levels of lipocalin-2 both in the plasma and liver in a bile duct ligation mouse model of HE. We confirmed changes in cytokine expression, such as interleukin-1β, cyclooxygenase 2 expression, and iron metabolism related to gene expression through AKT-mediated signaling both in the brain cortex of mice with HE and N2A cells. Our data showed negative effects of hepatic lipocalin-2 on cell survival, iron homeostasis, and neurite outgrowth in N2A cells. Thus, we suggest that regulation of lipocalin-2 in the brain in HE may be a critical therapeutic approach to alleviate neuropathological problems focused on the liver-brain axis.

• Archives of Pharmacal Research
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• v.24 no.4
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• pp.333-337
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• 2001

The pharmacokinetic changes of diltiazem (DTZ) and its main metabolite, deacetyldiltiazem (DAD) were studied after oral administration of DTZ to normal rabbits and mild and medium folate-induced renal failure rabbits. DTZ 10 mg/kg was given to the rabbits either orally (n=6). Plasma concentrations of DTZ and DAD were determined by a high performance liquid chromatography assay. The area under the plasma concentration-time curves (AUC) and maximum plasma concentration ($C_{max}$) of DTZ were significantly increased in mild and medium folate-induced renal failure rabbits. The metabolite ratio of the DTZ to DAD were significantly decreased in mild and medium folate-induced renal failure rabbits. The volume of distribution ($V_{d}$) and total body clearance ($CL_{t}$) of DTZ were significantly decreased in mild and medium folate-induced renal failure rabbits. The elimination rate constant ($\beta$) of DTZ was significantly decreased in folate-induced renal failure rabbits, but that of DAD was significantly increased. These findings suggest that the hepatic metabolism of DTZ was inhibited and the $V_{d}$, $CL_{t}$ and $\beta$ of DTZ were significantly decreased in mild and medium folate-induced renal failure rabbits.