• Journal of Veterinary Clinics
• /
• v.24 no.1
• /
• pp.73-75
• /
• 2007

Heat stroke can lead multi-organ damage with hemorrhage and necrosis in the lungs, heart, liver, kidneys, brain and Ut. Heat stroke occurs when the elevation of core body temperatures induce a failure of thermoregulatory mechanism. A four-year-old male African Lion(Panthera leo) showed clinical signs such as panting, tachycardia, hyperthermia, unconsciousness and mydriasis under He hish humidity and hot weather. Clinical treatment and pouring cool water was unsuccessful. Grossly, congestion of lungs and pleura was observed. Yellowish discoloration was observed in the renal cortex. Microscopically, the coagulative necrosis in kidney and congestion of lungs and spleen were observed. In our knowledge, this case was closely associated with acute heat stroke.

• YAKHAK HOEJI
• /
• v.54 no.3
• /
• pp.174-179
• /
• 2010

Acetaminophen is one of the most commonly used over-the-counter medication in Korea. It is a safe and effective medication for the treatment of mild to moderate pain or fever when used in therapeutic doses. However, acetaminophen overdose is a frequent cause of acute liver failure. The purpose of this study was to evaluate the acetaminophen use for adult patients at community pharmacies in Korea. This study was a 11-questionnaire survey conducted from December 15, 2009 to January 5, 2010. Of the 204 respondents, 117 (57.4%) had used acetaminophen products within 6 months. Only 20 (9.8%) reported having knowledge about the daily maximum doses of acetaminophen, and 3 out of 20 knew it correctly. Only 10 (4.9%) reported having knowledge about the potentialtoxicity of acetaminophen overdose, and 7 out of 10 knew that acetaminophen overdose could cause liver toxicity. The results of this study indicates a need for pharmacists to educate patients regarding the appropriate doses and potential toxicities of acetaminophen.

• Journal of Yeungnam Medical Science
• /
• v.33 no.1
• /
• pp.59-63
• /
• 2016

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and severe drug-induced hypersensitivity syndrome characterized by hematological abnormalities and multiorgan involvement. Liver involvement is the most common visceral manifestation. However, renal failure has been rarely described. The common culprit drugs are anticonvulsants and allopurinol. We experienced a patient with DRESS syndrome with acute interstitial nephritis caused by concomitant administration of quinolone and non-steroidal anti-inflammatory drugs (NSAIDs). A 41-year-old man presented with a diffuse erythematous rash and fever which developed after administration of quinolone and NSAIDs for a month due to prostatitis. He was diagnosed with DRESS syndrome. Skin rash, fever, eosinophilia, and elevations of liver enzymes improved with conservative treatment and discontinuation of the causative drugs. However, deterioration of his renal function occurred on day 8 of admission. The levels of blood urea nitrogen and serum creatinine increased and oliguria, proteinuria and urinary eosinophils were observed. Ultrasonography showed diffuse renal enlargement. The clinical features were compatible with acute interstitial nephritis. Despite intravenous rehydration and diuretics, renal function did not improve. After hemodialysis, his renal function recovered completely within 2 weeks without administration of systemic corticosteroid.

• Journal of Trauma and Injury
• /
• v.19 no.1
• /
• pp.59-66
• /
• 2006

Purpose: Acute liver failure after massive partial hepatectomy is critical condition with high mortality. To prevent postoperative liver failure from being induced by a massive partial hepatectomy, many doctors do a minimal resection on the single lobe of the liver that might cause postoperative bleeding from the remaining ruptured parenchyma. The objective of this study was to assess clinical experience with postoperative hepatic arterial embolization to control bleeding from the remaining ruptured liver during the postoperative period. Methods: This retrospective 4-year study was conducted from May 2002 to April 2006 and included consecutive patients who had sustained massive hepatic injuries and who had undergone a laparotomy, followed by postoperative hepatic arterial angiographic embolization to control bleeding. Data on the injury characteristics, the operative treatment and embolization, and the amount of transfused packed red cells (PRBC) were gathered and analyzed. In addition, data on the overall complications and survival rate were collected and analyzed. Results: Every case showed severe liver injury, higher liver injury scaling grade IV. Only ten cases involved a ruptured bilateral liver lobe. A lobectomy was done in 6 cases, a left lobectomy was done in 3 cases, and a primary suture closure of the liver was done in 2 cases. Suture closure was also done on the remaining ruptured liver parenchyma in cases of lobectomies. The postoperative hepatic arterial embolizations were done by using the super-selection technique. There were some cases of arterio-venous malformations and anomalous vessel branches. The average amount of transfused PRBC during 24 hours after embolization was $2.36{\pm}1.75$, which statistically significantly lower than that before embolization. Among the 11 cases, 9 patients survived, and 2 died. There was no specific complications induced by the embolization. Conclusion: In cases of postoperative bleeding in severe hepatic injury, if there is still a large amount of bleeding, postoperative hepatic arterial embolization might be a good therapeutic option.

• Toxicological Research
• /
• v.24 no.4
• /
• pp.281-287
• /
• 2008

Impairment of hepatic metabolism of sulfur-containing amino acids has been known to be linked with induction of liver injury. We determined the early changes in the transsulfuration reactions in liver of rats challenged with a toxic dose of $CCl_4$ (2 mmol/kg, ip). Both hepatic methionine concentration and methionine adenosyltransferase activity were increased, but S-adenosylmethionine level did not change. Hepatic cysteine was increased significantly from 4 h after $CCl_4$ treatment. Glutathione (GSH) concentration in liver was elevated in $4{\sim}8$ h and then returned to normal in accordance with the changes in glutamate cysteine ligase activity. Cysteine dioxygenase activity and hypotaurine concentration were also elevated from 4 h after the treatment. However, plasma GSH concentration was increased progressively, reaching a level at least several fold greater than normal in 24 h. ${\gamma}$-Glutamyltransferase activity in kidney or liver was not altered by $CCl_4$, suggesting that the increase in plasma GSH could not be attributed to a failure of GSH cycling. The results indicate that acute liver injury induced by $CCl_4$ is accompanied with extensive alterations in the metabolomics of sulfurcontaining amino acids and related substances. The major metabolites and products of the transsulfuration pathway, including methionine, cysteine, hypotaurine, and GSH, are all increased in liver and plasma. The physiological significance of the change in the metabolomics of sulfur-containing substances and its role in the induction of liver injury need to be explored in future studies.

• Herbal Formula Science
• /
• v.17 no.2
• /
• pp.123-132
• /
• 2009

Acetaminophen (AP) is widely used as an over-the-counter analgesic and antipyretic drug. AP-induced hepatotoxicity is a common consequence of AP overdose and may lead to acute liver failure. In this study, we investigated the liver damage in mice using single dose (300 mg/kg) of AP and the possible protective effects of administration (50-200 mg/kg body weight) of Joo-Juk on acetaminophen-induced liver damage in mice. The alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activities were determined in the plasma of mice. The effect of Joo-Juk on lipid peroxidation product thiobarbituric reacting substances (TBARS) and some antioxidant enzymes superoxide dismutase (SOD), catalase, d-aminolevulinate dehydratase ($\sigma$-ALA-D) activities, and gluthathione peroxidase (GPx), were also evaluated in the mouse liver homogenate. AP caused liver damage as evident by statistically significant increased in plasma activities of AST and ALT. There were statistically significant losses in the activities of SOD, catalase, $\sigma$-ALA-D, and GPx and an increase in TBARS in the liver of AP-treated group compared with the control group. However, Joo-Juk was able to counteract these effects. These results suggest that Joo-juk can act as hepato-protectant against AP toxicity and is a good candidate for further evaluation as an effective chemotherapeutic agent.

• Annals of Hepato-Biliary-Pancreatic Surgery
• /
• v.28 no.2
• /
• pp.238-247
• /
• 2024

Backgrounds/Aims: Prolonged use of steroids after liver transplantation (LT) significantly increases the risk of diabetes or cardiovascular disease, which can adversely affect patient outcomes. Our study evaluated the effectiveness and safety of early steroid withdrawal within the first year following LT. Methods: This study was conducted as an open-label, multicenter, randomized controlled trial. Liver transplant recipients were randomly assigned to one of the following two groups: Group 1, in which steroids were withdrawn two weeks posttransplantation, and Group 2, in which steroids were withdrawn three months posttransplantation. This study included participants aged 20 to 70 years who were scheduled to undergo a single-organ liver transplant from a living or deceased donor at one of the four participating centers. Results: Between November 2012 and August 2020, 115 patients were selected and randomized into two groups, with 60 in Group 1 and 55 in Group 2. The incidence of new-onset diabetes after transplantation (NODAT) was notably higher in Group 1 (32.4%) than in Group 2 (10.0%) in the per-protocol set. Although biopsy-proven acute rejection, graft failure, and mortality did not occur, the median tacrolimus trough level/dose/weight in Group 1 exceeded that in Group 2. No significant differences in safety parameters, such as infection and recurrence of hepatocellular carcinoma, were observed between the two groups. Conclusions: The present study did not find a significant reduction in the incidence of NODAT in the early steroid withdrawal group. Our study suggests that steroid withdrawal three months posttransplantation is a standard and safe immunosuppressive strategy for LT patients.

• Journal of Digestive Cancer Research
• /
• v.2 no.1
• /
• pp.28-31
• /
• 2014

Pancreatic cancer is a highly aggressive cancer with poor prognosis. Although, gemcitabine is the current standard regimen as first-line chemotherapy for advanced pancreatic cancer, effective regimens of second-line chemotherapy after gemcitabine failure have not been established yet. We report a case of gemcitabine refractory pancreatic cancer treated with second-line chemotherapy with FOLFIRINOX regimen. A 57-year-old-woman visited our hospital for pancreatic body mass detected by computed tomography (CT). The patient underwent distal pancreatectomy and splenectomy and the pathologic results after surgery demonstrated adenocarcinoma. Follow-up was performed after surgery and CT and positron emission tomography (PET) 4 months after surgery revealed multiple hepatic metastases. The patient underwent first-line chemotherapy with gemcitabine and erlotinib for recurred pancreatic cancer. However, CT after 7 cycles of the chemotherapy showed the progression of multiple hepatic metastases and switch to second-line chemotherapy with FOLFIRINOX was initiated. CT after 16 cycles of the FOLFIRINOX showed the complete remission of multiple hepatic metastases. The patient was admitted for infective endocarditis with septic pneumonia 17 months after the initiation of FOLFIRINOX. However, the patients died from the progression of septic embolism and acute respiratory distress syndrome.

• Journal of Chest Surgery
• /
• v.24 no.2
• /
• pp.190-196
• /
• 1991

Clinical experience of 48 acute pericarditis with effusion was reviewed and presented. There were 28 male and 20 female patients ranging from 3 years to 77 years old. Malignant effusion; Twenty patients had underlying malignancy. These etiologies were lung ca[8 patients, 40%], breast ca[7 patients 35%], lymphoma[2 patients, 10%], esophageal ca[1 patients, 5%], stomach ca[1 patient, 5%], ovarian ca[1 patient, 5%]. Uremic effusion; 15 patients with renal failure required surgical intervention. Traumatic effusion; 7 patients had traumatic pericarditis. These etiologies were stab wound [5 patients, 71.4%] and aspiration[2 patients, 28.6%]. Pyogenic effusion: 6 patients had pyogenic pericarditis. These etiologies were empyema thoracis[3 patients, 50%], liver abscess[2 patients, 33.3%], pneumonia[1 patient, 16.7%]. The patients were treated by pericardiocentesis, subxiphoid tube drainage, pericardiectomy: 4 of them underwent pericardiocentesis; 37, subxiphoid tube drainage; 5, pericardiectomy. We conclude that subxiphoid tube pericardial drainage was effective for treatment of pericardial effusion.

• The Korean Journal of Physiology and Pharmacology
• /
• v.20 no.1
• /
• pp.15-23
• /
• 2016

Acetaminophen (APAP) overdose is one of the most common causes of acute liver failure. The study aimed to investigate the protective effect of carnosic acid (CA) on APAP-induced acute hepatotoxicity and its underlying mechanism in mice. To induce hepatotoxicity, APAP solution (400 mg/kg) was administered into mice by intraperitoneal injection. Histological analysis revealed that CA treatment significantly ameliorated APAP-induced hepatic necrosis. The levels of both alanine aminotransferase (ALT) and aspartate transaminase (AST) in serum were reduced by CA treatment. Moreover, CA treatment significantly inhibited APAP-induced hepatocytes necrosis and lactate dehydrogenase (LDH) releasing. Western blot analysis showed that CA abrogated APAP-induced cleaved caspase-3, Bax and phosphorylated JNK protein expression. Further results showed that CA treatment markedly inhibited APAP-induced pro-inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and MCP-1 mRNA expression and the levels of phosphorylated $I{\kappa}B{\alpha}$ and p65 protein in the liver. In addition, CA treatment reduced APAP- induced hepatic malondialdehyde (MDA) contents and reactive oxygen species (ROS) accumulation. Conversely, hepatic glutathione (GSH) level was increased by administration of CA in APAP-treated mice. Mechanistically, CA facilitated Nrf2 translocation into nuclear through blocking the interaction between Nrf2 and Keap1, which, in turn, upregulated anti-oxidant genes mRNA expression. Taken together, our results indicate that CA facilitates Nrf2 nuclear translocation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity.