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Clinical and Pathological Findings on Intoxication by Yellow Phosphorus After Ingesting Firework Cracker: A Rare Case of Autopsy

Abstract

Yellow phosphorus is a toxic substance used in the production of firework cracker, fireworks, ammunition and agricultural dung. When ingested, it shows its effects mainly in the liver, the kidneys, and the brain. A four-year-old girl had died as a result of acute hepatic failure caused by ingesting a firework cracker. The case showed high levels of hepatic enzymes, along with non-specific signs such as nausea, vomiting and diarrhea. Autopsy revealed diffuse microvesicular steatosis in the liver and disseminated degeneration in the proximal tubules of the kidneys. In cases with concomitant hepatorenal failure and cardiovascular collapse, death is inevitable. However, when only hepatic failure develops, hepatic transplantation may be lifesaving. Although intoxication from ingesting yellow phosphorus has a very high rate of mortality, forensic cases are extremely rare in the literature.

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Histopathology of Hepatic Sinusoidal Obstruction Syndrome After Neoadjuvant Oxaliplatin-Based Chemotherapy

Abstract

Sinusoidal obstruction syndrome („blue liver syndrome“) has been frequently associated with oxaliplatin-based neoadjuvant chemotherapy in patients with colorectal liver metastasis. Hepatotoxic vascular lesions in the nontumourous liver parenchyma result in hypoperfusion and tissue hypoxia leading to lower tumour response to oncologic treatment and to increase the risk of liver metastasectomies. Furthermore, hepatic parenchyma injuries could be aggravated by hepatic resection itself. Contrary to standard surgical techniques, radiofrequency assisted liver resection significantly reduce harmful intraoperative blood loss and perfusion-reperfusion effects. We compared histological alterations in 59 specimens of bloodless radiofrequency-assisted liver recetions made for colorectal metastases to those in 38 specimens of standard liver resections. In general, the main histologic alterations in both examined groups related to oxaliplatin include SOS lesions (69.35%), fibrosis (50.95%) and steatosis (38%). After scoring of histopathological parameters based on modified criteria according to Rubbia-Brandt et al., they were statistically insignificant between both groups for portal and/or porto-portal fibrosis (59.3% vs 47.4%, respectively) and moderate/severe macrovacuolar steatosis (10.2% vs 26.3%). Similar distribution between groups was shown for surgical hepatitis with „borderline“ statistical significance (23,7% vs 42,1%, p= 0.05). However, there were significant differencies in vascular lesions, particularly for hemorrhagic centrilobular necrosis (10,2% vs 31,5%, p= 0.01) and peliosis (15,2% vs 36,8%, p= 0.04), but were not significant for sinusoidal dilatation and congestion as well as surgical necrosis. Highgrade vascular lesions such as hemorrhagic centrilobular necrosis and peliosis are less frequent in cases of radiofrequency-assisted liver recetions and might be associated with better clinical outcome in these patients.

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Imatinib-induced subclinical liver injury: histological changes of non-tumorous hepatic parenchyma

Abstract

Background: Severe clinical hepatitis after imatinib treatment has been reported anecdotally. Hepatic tissue of patients with liver matastasis is often fragile and difficult to handle during liver resection from gastrointestinal stromal tumor (GIST).

Objective: Observe hepatic tissue of these patients and examine the detailed histopathology underlying the change in the texture of non-tumorous hepatic parenchyma of these patients.

Materials and methods:We reviewed six GIST patients with liver metastases who underwent hepatic resection at King Chulalongkorn Memorial Hospital between July 2004 and November 2005. Four patients did not have imatinib and two patients received imatinib for four and eight months before liver resection. Preoperative hepatic biochemistry profiles of all patients were unremarkable. We examined histopathology of non-tumorous hepatic parenchyma of these patients using H-E staining, and additional histochemistry for vascular endothelial growth factor and epidermal growth factor receptor using immunohistochemistry staining.

Results: In all patients, common histopathological changes were swelling of hepatocytes, diffuse parenchymal congestion, dilatation of central vein, and infiltration of portal tract by mononuclear cells. However, there was significant zone 3 hepatocytolysis only in patients who received imatinib treatment. Additionally, moderate degree of hepatic steatosis correlated well with the duration of imatinib exposure. Immunohistochemical study could not demonstrate any difference between these two groups.

Conclusion: In two cases of subclinical hepatotoxicity from exposure to imatinib, histopathologic findings were consistent with drug induced liver injury. Imatinib induced liver injury may be more common than obvious clinical hepatitis.

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Pharmacological Approaches for Nonalcoholic Fatty Liver Disease

Abstract

Background and aims: Nonalcoholic fatty liver disease (NAFDL) is a multifactorial condition with a wide spectrum of histological severities, from asymptomatic hepatic steatosis to nonalcoholic steatohepatitis (NASH) with or without fibrosis. NAFLD is highly common and potentially serious in children and adolescents and affects approximately one third of the general population. It is closely associated with obesity, insulin resistance and dyslipidemia. NASH is a histological diagnosis and has a great significance because it can progress to cirrhosis, liver failure, and hepatocellular carcinoma (HCC), and is associated with both increased cardiovascular and liver related mortality. The purpose of this review is to summarize the evidence for current potential therapies of NAFLD.

Material and Methods: We searched MEDLINE from 2010 to the present to identify the pharmacological approaches for NAFLD.

Results and conclusions: NAFLD may be a new risk factor for extrahepatic diseases such as cardiovascular disease (CVD), chronic kidney disease (CKD), colorectal cancer, type 2 diabetes mellitus (T2DM) and osteoporosis. Currently there is no specific targeted treatment for NAFLD/NASH.

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Non-invasive quantification of liver fibrosis regression following successful treatment of chronic hepatitis C with direct acting antivirals

Abstract

Introduction. The past years have revolutionized the treatment of hepatitis C virus (HCV) infection, with high rates of sustained virologic response (SVR). Furthermore, liver fibrosis has recently been redefined as a dynamic, reversible process. Methods. We performed a prospective cohort study to assess the role of laboratory evaluations and non-invasive measurement of liver stiffness in establishing the right time for starting treatment and in assessing the regression of liver fibrosis in Romanian patients treated with direct acting antivirals (DAA) for genotype 1b chronic hepatitis C. Results. We present the results for 102 patients, with a mean age of 58.5 years, and a rate of SVR of 100%. Our study has ruled out older age (p=0.628), IL28B non-CC genotype (p=0.693), baseline viral load above the cutoff of 600,000 IU/mL (p=0.353), and the presence of diabetes mellitus (p=0.272) or baseline steatosis (p=0.706) as factors potentially influencing the regression of liver fibrosis following DAA treatment of HCV infection with the 3D regimen. The quantitative regression of liver stiffness was inversely correlated with the duration of HCV infection (p=0.017), suggesting that timely treatment might associate better outcomes in terms of liver fibrosis. Conclusion. Our study’s results point towards the need to start DAA treatment earlier in patients with HCV infection.

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Diabetes Mellitus, Obesity and Underlying Non Alcoholic Fatty Liver Disease - Independent Risk Factors for Hepatocellular Carcinoma

Abstract

Background and Aims. Hepatocellular carcinoma (HCC) is one of the most common malignancies. Obesity, together with the underlying liver steatosis, has received increased attention as a risk factor for HCC. Diabetes Mellitus (DM) is also reported to be associated with HCC. We aimed to estimate the risk of HCC in obese and diabetic patients. Material and method. We prospectively analyzed 414 obese and diabetic patients, over a period of 5 years. We evaluated all patients using screening methods such as abdominal ultrasound and serum alpha-fetoprotein every 6 month, in order to detect HCC occurrence. Kaplan-Meier analysis estimated the cumulative incidence of HCC. Univariate and multivariate Cox regression analysis assessed the association between HCC and obesity. Results. Median follow-up was 4.3 years. 11 from 77 cirrhotic obese patients, and 18 from 150 non-cirrhotic obese patients developed HCC (p=ns). 7 from 51 patients with DM and cirrhosis, and 14 from 136 non-cirrhotic patients with DM developed HCC (p=ns). The cumulative incidence of HCC was 2.8%, respectively 2.6%, in cirrhotic patients with obesity or DM, compared with 2.2%, respectively 2.0%, in non-cirrhotic patients with obesity or DM (p=ns). Conclusion. Obesity and DM, along with nonalcoholic fatty liver disease (NAFLD), seems to be independent risk factors for HCC occurrence.

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Can examination of tissue stained with Oil red O be postponed up to three months?

References [1] Levene AP, Kudo H, Thursz MR, Anstee QM, Goldin RD. Is Oil Red-O Staining and Digital Image Analysis the Gold Standard for Quantifying Steatosis in the Liver? Hepatology. 2010;51(5):1859-. [2] Thomsen JL, Hansen TP. Lipids in the proximal tubules of the kidney in diabetic coma. The American journal of forensic medicine and pathology. 2000;21(4):416-8. [3] Parai JL, Kodikara S, Milroy CM, Pollanen MS. Alcoholism and the Armanni-Ebstein lesion. Forensic science, medicine, and pathology. 2012

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Severe hepatocytolisis syndrome - a challenge in medical therapy of Cushing’s disease

. 3,31-38. 4. Rockall, A. G., Sohaib, S. A., Evans, D., Kaltsas, G., Isidori, A. M., Monson, J. P., Besser, G.M., Grossman, A.B. & Reznek, R. H. (2003). Hepatic steatosis in Cushing’s syndrome: a radiological assessment using computed tomography. Eur J Endocrinol. 149(6), 543-548. 5. Biller, B. M., Grossman, A. B., Stewart, P. M., Melmed, S., Bertagna, X., Bertherat, J., Buchfelder, M.,Colao, A.,Hermus, A. R.,Hofland, L.J., Klibanski, A., Lacroix, A., Lindsay, J.R., Newell-Price, J., Nieman, L.K., Petersenn, S., Sonino, N., Stalla, G

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Epidemiology and Natural History of Nafld/Epidemiologija I Prirodna Istorija Nealkoholne Masne Jetre

adults: A systematic review. J Hepatol 2011; 56: 255-66. 7. Socha P, Horvath A, Vajro P, Dziechciarz P, Dhawan A, Szajewska H. Pharmacological interventions for nonalcoholic fatty liver disease in adults and in children: a systematic review. J Pediatr Gastroenterol Nutr 2009; 48: 587-96. 8. Bellentani S, Scaglioni F, Marino M, Bedogni G. Epide - miology of Fatty Liver Disease. Dig Dis 2010; 28: 155-61. 9. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, et al. Prevalence of hepatic steatosis in

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Hepatic stellate cells activation and liver fibrosis after chronic administration of ethanol

Abstract

Hepatic stellate cells (HSC) are a nonparenchymal population of liver cells. In normal conditions, they store vitamin A, control the turnover of the extracellular matrix, and regulate the contractility of the sinusoids. Acute and chronic damage such as that brought about by alcohol activates the stellate cells and they are then responsible for the liver's inflammatory fibrotic response. Hence, alcohol consumption leads to hepatitis, steatosis, fibrosis and cirrhosis of liver by way of different mechanisms depending on effect upon the nonparenchymal cells of the liver.

The aim of our study was to assess the histological changes in the liver of rats after chronic alcohol consumption. In our work, we evaluated the intensity of liver fibrosis and the number of Kupffer cells and active hepatic stellate cells present within a test population. In the experiment, we used 10 Wistar rats of 250 gram weight. The animals were placed within one of two groups: A (experimental) and C (control). Group A received alcohol for 4 weeks, while group C received just water. The rats of both groups were decapitated 24 hours after the end of the experiment. The samples of liver were then evaluated after H&E, Masson’s trichrome staining and an immunohistochemical reaction to desmin (a marker of quiescent HSC) and α-smooth muscle actin (marker of active HSC) antibody. In our work, we observed intensive fibrosis in the portal spaces and perivenular areas in group A samples. Moreover, Kupffer cells and stellate cells with positive α-SMA expression were more numerous in group A than in the group C, and these correlate with the area of intensive fibrosis. The expression of desmin in the HSC was seen in both groups to a similar level.

Conclusion: Chronic alcohol consumption activates the transdifferentiation of hepatic stellate cells into the positive α-SMA myofibroblast-like cells which are responsible for fibrogenesis.

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