Tricarboxylic acid (TCA) cycle, sphingolipid, and phosphatidylcholine metabolism are dysregulated in T. gondii infection-induced cachexia.

Cachexia is a life-threatening disease characterized by chronic, inflammatory muscle wasting and systemic metabolic impairment. Despite its high prevalence, there are no efficacious therapies for cachexia. Mice chronically infected with the protozoan parasite Toxoplasma gondii represent a novel animal model recapitulating the chronic kinetics of cachexia. To understand how perturbations to metabolic tissue homeostasis influence circulating metabolite availability we used mass spectrometry analysis. Despite the significant reduction in circulating triacylglycerides, non-esterified fatty acids, and glycerol, sphingolipid long-chain bases and a subset of phosphatidylcholines (PCs) were significantly increased in the sera of mice with T. gondii infection-induced cachexia. In addition, the TCA cycle intermediates α-ketoglutarate, 2-hydroxyglutarate, succinate, fumarate, and malate were highly depleted in cachectic mouse sera. Sphingolipids and their de novo synthesis precursors PCs are the major components of the mitochondrial membrane and regulate mitochondrial function consistent with a causal relationship in the energy imbalance driving T. gondii-induced chronic cachexia.

Case report: Significant liver atrophy due to giant cystic pheochromocytoma.

Introduction: Pheochromocytoma is a neuroendocrine tumor originating from chromaffin cells in the adrenal medulla. Giant pheochromocytomas with a maximum diameter of over 20 cm are particularly rare. Case presentation: We present a case of giant cystic pheochromocytoma in a 64-year-old woman who was found to have a right abdominal mass during an ultrasound examination, which is the largest pheochromocytoma ever documented in China. Meanwhile, obvious atrophy of the right lobe of the liver was found in preoperative CT and during the operation. Our literature review identified 20 cases with a diameter of over 20 cm. The average age at diagnosis was 51.7 (range 17-85), and 35% of cases did not exhibit classic symptoms. Conclusion: Giant pheochromocytoma is an uncommon neoplasm. It can be discovered late due to a lack of clinical manifestations. Diagnosis is dependent on imaging recognition together with catecholamine secretion. Surgical resection is the only curative treatment for such tumors.

The volumetric measurement of developing liver atrophy in patients with Chilaiditi's sign.

PURPOSE: The Chilaiditi's sign is a hepatodiaphragmatic interposition of the colon and is a rare diagnosed condition. This condition may cause a problem in liver transplantation applications which are progressively increasing in number. Although not reported in the literature, we observed that liver atrophy developed in the intestinal interposition region in patients with Chilaiditi's sign in computed tomography (CT) images. This study aimed to determine the amount of liver atrophy caused by the interposed colon, the factors that change the rate of atrophy, and the effects of this situation on the liver parenchyma. MATERIALS AND METHODS: A total of 30,000 patients who presented to radiology department with any reason between March 2012 and March 2013 and who underwent thoracoabdominal or abdominal CT imaging were retrospectively analyzed. The volumes of the liver right lobe and lateral/medial segments of the left lobe were estimated in cm3 using Volume Viewer application in 75 cases (20 females, 55 males) in which Chilaiditi's sign was observed in CT images. RESULTS: 17-27% of the lobes affected from the colon interposition were seen to develop atrophy. The ratio of right lobe volume to total liver volume was found to be higher in patients with left lobe atrophy (74%) than right lobe atrophy (55%) (p < 0.001). Similarly, the rate of the volume of the left lobe to the total liver volume was found to be higher in cases with right lobe atrophy (45%) compared to left lobe atrophy (26%) (p < 0.001). CONCLUSION: Hepatodiaphragmatic interposition of the colon can cause liver atrophy. This condition should especially be considered in the liver transplantation applications. Compensatory hypertrophy may develop in the unaffected liver lobe and CT is very useful for diagnostic imaging.

Lesión quirúrgica de vía biliar compleja. Manejo conservador / Complex bile duct injury. Conservative management

RESUMEN La colecistectomía laparoscópica es el tratamiento de elección para la litiasis vesicular sintomática. Aunque la tasa de complicaciones es baja, las lesiones de la vía biliar representan un grave problema. La asociación con una lesión vascular (lesión compleja) genera un impacto adicional, disminuyendo la calidad de vida y la sobrevida a largo plazo. Presentamos el caso de una paciente con lesión compleja por compromiso vascular del pedículo hepático derecho que desarrolló una atrofia del parénquima correspondiente. Ante la ausencia de complicaciones sépticas, el tratamiento no operatorio pudo realizarse en forma exitosa.

ABSTRACT Laparoscopic cholecystectomy is considered the standard of care for symptomatic cholelithiasis. Although the rate of complications is low, bile duct injuries represent a serious problem. The association with vascular injury (complex injury) poses an additional impact by reducing the quality of life and long-term survival. We report the case of a female patient with complex injury due to vascular involvement of the right hepatic pedicle who developed right liver atrophy. Non-operative management was successful due to the absence of septic complications.

Increased Hepatic Microvascular Density, Oxygenation, and VEGF in the Hypertrophic Lobe following Portal Vein Embolization in Rabbits.

INTRODUCTION: The microvascular events following portal vein embolization (PVE) are poorly understood despite the pivotal role of the microcirculation in liver regeneration and tumor progression. We aimed to assess the changes in hepatic microvascular perfusion and neo-angiogenesis after experimental PVE. METHODS: PVE of the cranial liver lobes was performed in 12 New Zealand White rabbits divided into 2 groups of permanent (P-PVE) and reversible PVE (R-PVE), respectively. Hepatobiliary scintigraphy and CT were used to evaluate hepatic function and volume. Hepatic microcirculation was assessed using a handheld vital microscope (Cytocam) to measure microvascular density (total vessel density; TVD) before PVE, right after PVE, and 20 min after PVE, as well as at 14 days (D14 post-PVE) and 35 days (D35 post-PVE). Additionally, on D35, microvascular PO2 and liver parenchymal VEGF were assessed. RESULTS: Eleven rabbits were included after PVE (R-PVE, n = 5; P-PVE, n = 6). TVD in the nonembo-lized (hypertrophic) lobes was higher than in the embolized (atrophic) lobes of the P-PVE group at D35 post-PVE (36.7 ± 7.2 vs. 23.4 ± 4.9 mm/mm2; p < 0.05). In the R-PVE group, TVD in the nonembolized lobes was not increased at D35. Function and volume were increased in the nonembolized lobes of the P-PVE group compared to the embolized lobes, but not in the R-PVE group. Likewise, the mmicrovascular PO2 and VEGF staining rate were higher in the nonembolized lobes of the P-PVE group at D35 post-PVE. DISCUSSION/CONCLUSION: Successful volumetric and functional hypertrophy of the nonembolized lobe was accompanied by microvascular alterations featuring increased neo-angiogenesis, microvascular density, and microvascular oxygen pressure following P-PVE.

Significant Liver Atrophy Due to Vascular Compromise Associated With Adult Congenital Diaphragmatic Hernia.

Diaphragmatic hernia in adults is mostly post-traumatic in origin, and rarely congenital. In both situations, the right side is less commonly involved due to the protection offered by the liver and earlier closure of the right pleuroperitoneal canal. A congenital diaphragmatic hernia may present in adulthood with multi-visceral contents, of which the liver is an extremely rare content, mentioned only in a few previous reports. A herniated liver may mimic a pulmonary tumor and may be completely atrophic due to sustained compression of the venous outflow. Careful operative planning is essential to identify and reduce the liver, along with other contents. We are reporting two adults with a congenital diaphragmatic hernia, with multi-visceral contents and an atrophied liver. The first patient was a 28-year-old man with a remote history of trauma found to have a large right diaphragmatic hernia on imaging. The right liver was completely atrophied due to right hepatic venous compression, while the left liver underwent massive hypertrophy and rotation of the left portal axis. Exploratory laparotomy and reduction of contents, along with mesh repair, were accomplished with satisfactory results. The second patient was a 26-year-old man with Down's syndrome detected to have multiple bowel loops in the right thorax on imaging. At laparoscopy, a Larrey's type of Morgagni hernia with a right paramedian defect was found. The left liver was atrophied into a leaf-like appendage due to possible portal obliteration and was dissected away from the diaphragm edge. Appropriate mesh repair was completed by a minimally invasive technique.

Precancerous Lesions and Liver Atrophy as Risk Factors for Hepatolithiasis-Related Death after Liver Resection for Hepatolithiasis.

BACKGROUND: Cholangiocarcinoma and secondary biliary cirrhosis can develop after liver resection for hepatolithiasis and are causes of hepatolithiasis-related death. We determined potential risk factors for hepatolithiasis-related death and subsequent cholangiocarcinoma, including precancerous lesions such as biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of the bile duct, in patients undergoing liver resection for hepatolithiasis. METHODS: The study cohort included 62 patients who underwent liver resection for hepatolithiasis without concomitant cholangiocarcinoma and had surgical specimens available for pathological examination. Univariate and multivariate analyses were conducted to examine risk factors associated with subsequent cholangiocarcinoma after hepatolithiasis and hepatolithiasis-related death. In 28 patients with BilIN lesions, the specimens were immunohistochemically stained for γ-H2AX and S100P. RESULTS: In the study cohort, the causes of death were subsequent cholangiocarcinoma, biliary cirrhosis, and other diseases in 5, 3, and 7 patients, respectively. Liver atrophy, precancerous lesions, postoperative repeated cholangitis, and jaundice for ≥1 week during the follow-up period were risk factors for hepatolithiasis-related death. Multivariate analysis showed that liver atrophy and precancerous lesions were independent risk factors for hepatolithiasis-related death. Liver atrophy or precancerous lesions were also risk factors for subsequent cholangiocarcinoma by univariate analysis. The positive expression of γ-H2AX and S100P was observed in 18 and 14 of the 28 BilIN lesions, respectively. CONCLUSIONS: Liver atrophy and precancerous lesions with malignant transformation were risk factors not only for subsequent cholangiocarcinoma but also hepatolithiasis-related death after liver resection for hepatolithiasis, indicating that long-term follow-up is necessary even after liver resection in patients harboring these risk factors.
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Hepatic atrophy treatment with portal vein embolization to control intrahepatic duct stenosis-associated cholangitis.

We present two cases of hepatic atrophy treatment with portal vein embolization (PVE) to control intractable cholangitis. The first case was a 60-year-old male who was admitted for repeated episodes of cholangitis. He had undergone cholecystectomy and Roux-en-Y choledochojejunostomy 2 years earlier. Imaging studies showed left intrahepatic duct dilatation and anastomotic site stricture. The patient was reluctant to undergo another surgery. Thus, we decided to perform left PVE to induce atrophy of the left liver. The left liver shrank and stayed silent for 5 years, but a radiological intervention was necessary to treat symptomatic anastomotic stenosis. The patient has done well for 12 years after PVE. The second case was a 51-year-old female who was also admitted for repeated episodes of cholangitis. She had undergone excision of type I choledochal cyst 2 years earlier. Imaging studies showed right hepatic duct stenosis. Cholangitis developed repeatedly. Thus, radiologic interventions were performed 8 times over 9 years. Finally, she was referred for surgery, but she was very reluctant to undergo another surgery. We planned a wait-and-see strategy following right PVE. After PVE, the right liver progressively shrank. Three months after PVE, we decided to wait for a longer period until further atrophy of the right liver. The patient has been doing well for 14 months after PVE without any episode of cholangitis. In conclusion, experience from our two cases suggests that hepatic parenchymal induction therapy through percutaneous PVE can be a therapeutic option for patients with perihilar biliary stenosis-associated cholangitis.

Progressive atrophy in a deformed liver as a contributor to sigmoid volvulus.

The effect of a prior defect on secondary liver atrophy is unknown. We describe a case of sigmoid volvulus that was facilitated by progressive atrophy in a deformed liver. A 75-year-old man with abdominal pain and fullness was referred to our hospital. Computed tomography (CT) revealed reduced left hepatic lobe volume and a whirl sign, characteristic of sigmoid volvulus. The sigmoid volvulus was successfully detorted with endoscopy. Retrospective evaluation of liver morphology on CT and magnetic resonance imaging showed that the portal vein at the liver hilum was denuded due to a parenchymal defect of the medial segment, with compression by the crossing artery. As pulse Doppler ultrasonography demonstrated reduced portal blood flow in the region where liver atrophy developed, compression of the denuded portal vein presumably facilitated secondary atrophy and contributed to sigmoid volvulus. The present case shows that a deformed liver itself can be a cause of secondary atrophy. Therefore, continued monitoring of liver morphology and evaluation of portal blood flow to predict liver atrophy may be required, when an individual with a partial liver defect is encountered.

Decreased mitochondrial metabolic requirements in fasting animals carry an oxidative cost.

Many animals experience periods of food shortage in their natural environment. It has been hypothesised that the metabolic responses of animals to naturally-occurring periods of food deprivation may have long-term negative impacts on their subsequent life-history.In particular, reductions in energy requirements in response to fasting may help preserve limited resources but potentially come at a cost of increased oxidative stress. However, little is known about this trade-off since studies of energy metabolism are generally conducted separately from those of oxidative stress.Using a novel approach that combines measurements of mitochondrial function with in vivo levels of hydrogen peroxide (H2O2) in brown trout (Salmo trutta), we show here that fasting induces energy savings in a highly metabolically active organ (the liver) but at the cost of a significant increase in H2O2, an important form of reactive oxygen species (ROS).After a 2-week period of fasting, brown trout reduced their whole-liver mitochondrial respiratory capacities (state 3, state 4 and cytochrome c oxidase activity), mainly due to reductions in liver size (and hence the total mitochondrial content). This was compensated for at the level of the mitochondrion, with an increase in state 3 respiration combined with a decrease in state 4 respiration, suggesting a selective increase in the capacity to produce ATP without a concomitant increase in energy dissipated through proton leakage. However, the reduction in total hepatic metabolic capacity in fasted fish was associated with an almost two-fold increase in in vivo mitochondrial H2O2 levels (as measured by the MitoB probe).The resulting increase in mitochondrial ROS, and hence potential risk of oxidative damage, provides mechanistic insight into the trade-off between the short-term energetic benefits of reducing metabolism in response to fasting and the potential long-term costs to subsequent life-history traits.

Les restrictions alimentaires sont courantes dans le milieu naturel et peuvent impacter de nombreux animaux. Il a été émis l'hypothèse que les animaux, face à ces épisodes de restriction alimentaire, mettaient en place des réponses métaboliques pouvant affecter leurs histoires de vie future.En particulier, si une diminution des besoins énergétiques lors du jeûne peut contribuer à préserver les réserves de l'animal cela peut néanmoins entraîner une augmentation du stress oxydant. Ce type de compromis n'a toutefois pas encore été démontré car l'étude du métabolisme énergétique est généralement réalisée séparément de celle du stress oxydant.Par une nouvelle approche combinant des mesures du fonctionnement mitochondrial et des niveaux in vivo de peroxyde d'hydrogène (H2O2) chez la truite commune (Salmo trutta), nous montrons ici que le jeûne entraîne une économie d'énergie dans un tissu métaboliquement très actif tel que le foie, mais au coût d'une augmentation significative en H2O2, une forme majeure des espèces réactives de l'oxygène.Après deux semaines de jeûne, les truites communes ont réduit leurs capacités respiratoires mitochondriales (état 3, état 4 et l'activité de la cytochrome c oxydase) principalement du fait d'une réduction de la taille du foie (et donc du nombre total de mitochondries). Une compensation a été observée au niveau de la mitochondrie. Cela se traduit par une augmentation de la respiration en état 3 et une diminution concomitante de celle en état 4, suggérant une augmentation sélective des capacités de production de l'ATP sans augmentation parallèle de l'énergie dissipée par la fuite de protons. La diminution des capacités métaboliques du foie chez les poissons à jeun était associée in vivo à des niveaux quasiment doubles de H2O2 mitochondriaux (mesurés par la sonde MitoB).Cette augmentation en espèces réactives de l'oxygène dans les mitochondries, avec son risque inhérent de dommages oxydatifs, apporte une vision mécanistique du compromis entre les bénéfices énergétiques à court terme d'une réduction métabolique en réponse au jeûne et les possibles coûts à long terme sur leurs traits histoires de vie futurs. A http://onlinelibrary.wiley.com/doi/10.1111/1365-2435.13125/suppinfo is available for this article.

Liver atrophy after percutaneous transhepatic portal embolization occurs in two histological phases: Hepatocellular atrophy followed by apoptosis.

AIM: To clarify the histological changes associated with liver atrophy after percutaneous transhepatic portal embolization (PTPE) in pigs and humans. METHODS: As a preliminary study, we performed pathological examinations of liver specimens from five pigs that had undergone PTPE in a time-dependent model of liver atrophy. In specimens from embolized lobes (EMB) and nonembolized lobes (controls), we measured the portal vein to central vein distance (PV-CV), the area and number of hepatocytes per lobule, and apoptotic activity using the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. Immunohistochemical reactivities were evaluated for light chain 3 (LC3) and lysosomal-associated membrane protein 2 (LAMP2) as autophagy markers and for glutamine synthetase and cytochrome P450 2E1 (CYP2E1) as metabolic zonation markers. Samples from ten human livers taken 20-36 d after PTPE were similarly examined. RESULTS: PV-CVs and lobule areas did not differ between EMB and controls at day 0, but were lower in EMB than in controls at weeks 2, 4, and 6 (P ≤ 0.001). Hepatocyte numbers were not significantly reduced in EMB at day 0 and week 2 but were reduced at weeks 4 and 6 (P ≤ 0.05). Apoptotic activity was higher in EMB than in controls at day 0 and week 4. LC3 and LAMP2 staining peaked in EMB at week 2, with no significant difference between EMB and controls at weeks 4 and 6. Glutamine synthetase and CYP2E1 zonation in EMB at weeks 2, 4, and 6 were narrower than those in controls. Human results were consistent with those of porcine specimens. CONCLUSION: The mechanism of liver atrophy after PTPE has two histological phases: Hepatocellular atrophy is likely caused by autophagy in the first 2 wk and apoptosis thereafter.

Chronic liver disease in cattle associated with ingestion of Brachiaria spp. / Doença hepática crônica em bovinos associada com ingestão de Brachiaria spp.

ABSTRACT: One hundred and ninety livers condemned due to chronic disease (fibrosis) were evaluated in a bovine slaughterhouse over 12 months. Hepatic lymph nodes were also examined while still attached to livers. The major macroscopic lesion observed in the livers was moderate to severe atrophy of the left lobe associated with compensatory hypertrophy of the right lobe. Histologically, the main changes corresponded to sites of macroscopic lesions, and fibrosis was observed in all livers, along with bile duct hyperplasia and neovascularization. Masson's trichrome stain highlighted the fibrous connective tissue. Most of the livers analyzed had macrophages with foamy cytoplasm and a peripheral nucleus that infiltrated fibrotic areas. Immunohistochemistry (IHC) for macrophages with monoclonal antibody clone MAC 387 revealed that the cytoplasm of the foamy macrophages of the liver and of the hepatic lymph nodes were positively immunostained. These cells are frequently associated to the consumption of grasses of the genus Brachiaria. Although the liver gross lesions described in this study have not been previously reported in animals consuming Brachiaria , the associated changes observed histologically, such as fibrosis and infiltration of foamy macrophages, showed a new form of chronic liver disease probably associated with the consumption of this forage. The IHC technique was important to prove that the foam cells observed are macrophages.

RESUMO: Cento e noventa e dois fígados condenados devido à doença crônica (fibrose) foram avaliados em um abatedouro de bovinos durante 12 meses. Os linfonodos hepáticos, quando ainda estavam ligados aos fígados, também foram examinados. A principal lesão macroscópica observada no fígado foi moderada a acentuada atrofia do lobo esquerdo associada à hipertrofia compensatória do lobo direito. Histologicamente, as principais alterações correspondiam aos locais das lesões macroscópicas, e fibrose foi observada em todos os fígados, juntamente com a hiperplasia de ductos biliares e neovascularização. A coloração de Tricrômico de Masson destacou o tecido conjuntivo fibroso. A maioria dos fígados analisados apresentavam macrófagos com citoplasma espumoso e um núcleo periférico que infiltravam as áreas de fibrose. A imuno-histoquímica (IHQ) para macrófagos realizada com o anticorpo monoclonl clone MAC 387 revelou imunomarcação positiva no citoplasma dos macrófagos espumosos do fígado e dos linfonodos hepáticos. Essas células estão frequentemente associadas ao consumo de gramíneas do gênero Brachiaria . Apesar das lesões hepáticas macroscópicas descritas neste trabalho não terem sido previamente relatadas em animais que consomem Brachiaria , as alterações histológicas associadas, como fibrose e infiltração de macrófagos espumosos, mostram uma nova forma crônica de doença hepática provavelmente associada à ingestão desta forragem. A técnica de IHQ foi importante para provar que as células espumosas observadas são macrófagos.

Abnormal right hepatic artery injury resulting in right hepatic atrophy: diagnosed by laparoscopic cholecystectomy.

An intact hepatic artery is the gateway to successful hepato-biliary surgery. Introduction of laproscopic cholecystectomy (LC) has stimulated a renewed interest in the anatomy of hepatic artery. In this case report we have highlighted importance of variations of right hepatic artery in terms of origin and course We present a rare asymptomatic case of liver atrophy due to an intraoperative lesion of right hepatic artery. We also performed a literature review about surgical vascular lesions and tried to confirm the right concept behind "non trivial procedure" of the LC.

Comparison of percutaneous transhepatic portal vein embolization and unilateral portal vein ligation.

AIM: To compare the effect of percutaneous transhepatic portal vein embolization (PTPE) and unilateral portal vein ligation (PVL) on hepatic hemodynamics and right hepatic lobe (RHL) atrophy. METHODS: Between March 2005 and March 2009, 13 cases were selected for PTPE (n = 9) and PVL (n = 4) in the RHL. The PTPE group included hilar bile duct carcinoma (n = 2), intrahepatic cholangiocarcinoma (n = 2), hepatocellular carcinoma (n = 2) and liver metastasis (n = 3). The PVL group included hepatocellular carcinoma (n = 2) and liver metastasis (n = 2). In addition, observation of postoperative hepatic hemodynamics obtained from computed tomography and Doppler ultrasonography was compared between the two groups. RESULTS: Mean ages in the two groups were 58.9 ± 2.9 years (PVL group) vs 69.7 ± 3.2 years (PTPE group), which was a significant difference (P = 0.0002). Among the indicators of liver function, including serum albumin, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, platelets and indocyanine green retention rate at 15 min, no significant differences were observed between the two groups. Preoperative RHL volumes in the PTPE and PVL groups were estimated to be 804.9 ± 181.1 mL and 813.3 ± 129.7 mL, respectively, with volume rates of 68.9% ± 2.8% and 69.2% ± 4.2%, respectively. There were no significant differences in RHL volumes (P = 0.83) and RHL volume rates (P = 0.94), respectively. At 1 mo after PTPE or PVL, postoperative RHL volumes in the PTPE and PVL groups were estimated to be 638.4 ± 153.6 mL and 749.8 ± 121.9 mL, respectively, with no significant difference (P = 0.14). Postoperative RHL volume rates in the PTPE and PVL groups were estimated to be 54.6% ± 4.2% and 63.7% ± 3.9%, respectively, which was a significant difference (P = 0.0056). At 1 mo after the operation, the liver volume atrophy rate was 14.3% ± 2.3% in the PTPE group and 5.4% ± 1.6% in the PVL group, which was a significant difference (P = 0.0061). CONCLUSION: PTPE is a more effective procedure than PVL because PTPE is able to occlude completely the portal branch throughout the right peripheral vein.

Therapeutic induction of hepatic atrophy for isolated injury of the right posterior sectoral duct following laparoscopic cholecystectomy.

Laparoscopic cholecystectomy has resulted in various bile duct injuries. Treatment of these injuries is usually difficult and often leads to an intractable clinical course. We herein present a case of isolated right anterior sector (RAS) duct injury induced by laparoscopic cholecystectomy. The bile duct injury was successfully treated by hepatic atrophy induction. Imaging studies revealed that the RAS duct was severed, probably due to rare anatomical variations. Considering the difficulty in surgical reconstruction, atrophy induction of the involved hepatic parenchyma was attempted. This treatment consisted of embolization of the RAS portal branch to inhibit bile production, induction of heavy adhesion at the bile leak site to ensure percutaneous pigtail clamping, and sequential clamping and removal of pigtail catheters. This procedure took 3 months prior to pigtail catheter removal. She was free from other complications during the first 12 months and to date. She will be followed up for 5 years overall including surveillance for hepatobiliary complications. Although this therapeutic induction of atrophy approach is not universally applicable, it can be considered to be a feasible option in unique situations such as this one.

Therapeutic induction of hepatic atrophy for isolated injury of the right posterior sectoral duct following laparoscopic cholecystectomy

Laparoscopic cholecystectomy has resulted in various bile duct injuries. Treatment of these injuries is usually difficult and often leads to an intractable clinical course. We herein present a case of isolated right anterior sector (RAS) duct injury induced by laparoscopic cholecystectomy. The bile duct injury was successfully treated by hepatic atrophy induction. Imaging studies revealed that the RAS duct was severed, probably due to rare anatomical variations. Considering the difficulty in surgical reconstruction, atrophy induction of the involved hepatic parenchyma was attempted. This treatment consisted of embolization of the RAS portal branch to inhibit bile production, induction of heavy adhesion at the bile leak site to ensure percutaneous pigtail clamping, and sequential clamping and removal of pigtail catheters. This procedure took 3 months prior to pigtail catheter removal. She was free from other complications during the first 12 months and to date. She will be followed up for 5 years overall including surveillance for hepatobiliary complications. Although this therapeutic induction of atrophy approach is not universally applicable, it can be considered to be a feasible option in unique situations such as this one.

Surgical management of patients with post-cholecystectomy benign biliary stricture complicated by atrophy-hypertrophy complex of the liver.

BACKGROUND: Atrophy-hypertrophy complex (AHC) of the liver rarely complicates post-cholecystectomy benign biliary strictures (BBS). This study aimed to analyse the effect of AHC on the surgical management of patients with BBS. METHODS: Between 1989 and 2005, 362 patients underwent surgical repair for BBS at a tertiary referral centre in northern India. A total of 36 (10%) patients had AHC. Patients with AHC (n= 36) were compared with those without (n= 336) to define the factors associated with the development of AHC. RESULTS: Overall, 35 patients with AHC underwent Roux-en-Y hepaticojejunostomy; right hepatectomy was performed in one patient. The interval between bile duct injury and stricture repair did not influence the development of AHC (mean 24 months in AHC patients vs. 19 months in non-AHC patients; P= 0.522). Of the 36 patients with AHC, 26 (72%) had hilar strictures (Bismuth's types III, IV, V), as did 163 of the 326 (50%) patients without AHC (P= 0.012). Patients with AHC had more blood loss at surgery (mean blood loss 340 ml in the AHC group vs. 190 ml in the non-AHC group; P= 0.004) and required more blood transfusion (mean blood transfused 300 ml vs. 120 ml; P= 0.001). Surgery was prolonged in AHC patients (mean duration of operation 4.2 hours in the AHC group vs. 2.8 hours in the non-AHC group; P= 0.001). Over a mean follow-up of 43 months (range 6-163 months), three of 36 (8%) AHC patients required re-intervention for recurrent strictures, compared with nine of 326 (3%) non-AHC patients (P= 0.006). CONCLUSIONS: Iatrogenic injury at the hepatic hilum predisposes for the development of AHC. Surgery is more difficult and blood transfusion requirements are higher in patients with AHC during surgical repair of BBS. Atrophy-hypertrophy complex is a risk factor for recurrent stricture formation after hepaticojejunostomy.