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Introduction: The use of technetium 99m diethylenetriaminepentaacetic acid-galactosyl human serum albumin (99mTc-GSA) scintigraphy parameters, HH15 and LHL15, in assessing the future liver remnant function is not expedient because of their nonlinear behaviour against liver volume. Uptake rate constant for the binding of 99mTc-GSA to asialoglycoprotein receptors is probably more favourable, but the reported calculation methods are complex. We devised a simple method to calculate the uptake rate constant, KrGSA. Methods: Radioactivity counts for the entire liver and heart regions were extracted at 10, 20, and 30 min. Using whole liver and heart volumes measured from single-photon emission computed tomography images, free radioactivity corresponding to the liver blood pool was subtracted. The time activity curve was fitted to the equation L(t) = L(∞) × [1 − Exp (−kt)] using Microsoft Office Excel (add-in free programme Solver)®, where L(∞) is the count at plateau level and k denotes KrGSA. Results: KrGSA values accurately identified liver cirrhosis and were similar to the KICG. The areas under the curve for KrGSA and KICG in the receiver operating characteristic analysis were 0.808 and 0.795, respectively, and a good correlation was seen between KrGSA and KICG. Discussion/Conclusion: KrGSA can be utilized as an alternative to KICG in assessing the future liver remnant function.

A 40-year-old man suffered from short bowel syndrome. Since a large amount of intestinal output and watery diarrhea hampered his quality of life, we tried to control the intestinal output by reducing the secretion of gastric acid with lansoprazole. Because the small intestine was only 10 cm in length and effective absorption of oral lansoprazole was doubtful, we monitored his intragastric pH for 24 hours and confirmed that the holding time above pH 3.0 was 14.5 hours (60.4%). He spent his home life eating porridge during the day, and receiving total parenteral nutrition of 1,100 mL/day at night while taking lansoprazole as an oral tablet (30 mg) once a day.

To explore the underlying mechanism of rapid liver hypertrophy by liver partition in associating liver partition and portal vein ligation for staged hepatectomy (ALPPS), liver partition at different sites was investigated. Increased inflammatory cytokines owing to the liver partition have been reportedly responsible. If this were true, rapid liver hypertrophy should be achieved regardless of where the liver was split. A male Sprague-Dawley rat model was created, in which a liver split was placed inside the portal vein ligated lobe (PiLL), in addition to the ALPPS and portal vein ligation (PVL) models. Liver regeneration rate, inflammatory cytokine levels, activation status of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway and expressions of regenerating islet-derived (Reg)3&alpha, and Reg3&beta, were investigated. The liver regeneration rate was significantly higher in the ALPPS group than in the PiLL group, whereas inflammatory cytokine levels were nearly equal. Additional volume increase in ALPPS group over PVL and PiLL groups was JAK2/STAT3-dependent. Reg3&alpha, expressions were observed only in the ALPPS group. An increase in inflammatory cytokines was not enough to describe the mechanism of rapid liver hypertrophy in ALPPS. Expressions of Reg3&alpha, could play an important role in conjunction with an activation of the JAK2/STAT3 pathway.

Purpose: The involvement of hepatic stellate cells (HSCs) with ischemia-reperfusion (I/R) injury in rat liver was examined using gliotoxin, which is known to induce HSC apoptosis. Methods: Male Sprague-Dawley rats were used. HSC was represented by a glial fibrillary acidic protein (GFAP)-positive cell. Liver ischemia was produced by cross-clamping the hepatoduodenal ligament. The degree of I/R injury was evaluated by a release of aminotransferases. Sinusoidal diameter and sinusoidal perfusion rates were examined using intravital fluorescence microscopy. Results: Gliotoxin significantly decreased the number of GFAP-positive cells 48 h after dosing (2.50 ± 0.19% [mean ± SD] in the nontreated group vs. 1.91 ± 0.46% in the gliotoxin-treated group). Liver damage was significantly suppressed by the pretreatment with gliotoxin. Sinusoidal diameters in zone 3 were wider in the gliotoxin group (10.25 ± 0.35 µm) than in the nontreated group (8.21 ± 0.50 µm). The sinusoidal perfusion rate was maintained as well in the gliotoxin group as in normal livers, even after I/R. Conclusions: Pretreatment with gliotoxin significantly reduced the number of HSCs in the liver and further suppressed liver injury following I/R. It is strongly suggested that HSCs play a functional role in exacerbating the degree of I/R injury of the liver.

In the portal vein resection of long distance, an interposition by autologous vein is mandatory. External iliac vein (EIV) has been used, but harvesting the EIV is associated with severe venous congestion of the affected lower extremity. We have reconstructed the EIV using a ringed expanded polytetrafluoroethylene (ePTFE) graft. Thirteen patients underwent this surgery. The right EIV was used for reconstructing the portal vein, and the retrieved portion of EIV was interposed by the ePTFE graft. We evaluated size and length of the graft, graft patency, girth of thigh, time for reconstruction of EIV, and graft infection. ePTFE grafts of 8 or 10 mm in diameter were used. The length of ePTFE graft used was 4.4 ± 0.5 cm. Graft patency was kept in 76.9% patients. Graft obstruction was encountered in three patients, and the girth of right thigh increased by about 10 cm. Time for reconstruction of EIV was 29.5 ± 6.8 min. Graft infection did not occur in any patients. Reconstruction of the EIV using a ringed ePTFE graft seems to be a feasible option for preventing the swelling of the affected lower extremity after procurement of EIV for repairing the portal vein.