Objective The sustained virological response (SVR) rate has improved to >70% for patients with hepatitis C virus genotype 1 treated with the triple therapy of telaprevir (TVR), pegylated interferon (PEG-IFN)-α, and ribavirin (RBV). However, this therapy has various adverse effects, although there have been no reports of it decreasing body weight.
Methods A total of 175 patients with chronic hepatitis C received one of three IFN-based regimens (35 received the PEG-IFN/RBV/TVR (PRT) regimen, 70 received the PEG-IFN/RBV (PR) regimen, and 70 received the IFN-β/RBV (FR) regimen) and body weight was followed for 12 weeks.
Resuts Decreases in body weight up to week 12 were significantly greater in the PRT group than in the PR or FR groups (p<0.001). The proportion of patients who experienced weight loss ≥5.0 kg by week 12 in the PRT group was significantly higher than in the PR or FR groups (p<0.001) regardless of baseline ghrelin level. The question 18 score (appetite) of the Beck Depression Inventory-II at week 12 was significantly higher in the PRT group than in the PR or FR groups (p<0.001). A multivariate analysis revealed PRT, the ghrelin level before treatment (<7.0 fmol/mL), and the question 18 score in week 12 (2 or 3) to be independent factors associated with a decrease in body weight ≥5.0 kg from week 0 to week 12.
Conclusion PEG-IFN/RBV/TVR therapy yielded high SVR rates, but it was associated with a decreased body weight due to TVR-induced appetite loss.

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Objective Clopidogrel is used to prevent the recurrence of non-cardiogenic ischemic stroke, but individual responsiveness to the drug varies. Moreover, it is known that smoking, which is a risk factor for ischemic stroke, affects the drug's pharmacokinetics. The objective of the present study was to investigate a possible relationship between smoking and responsiveness to clopidogrel in non-cardiogenic ischemic stroke patients.
Methods The study involved 209 non-cardiogenic ischemic stroke patients who were administered oral clopidogrel at a dosage of 75 mg/day for at least 1 week. Platelet aggregation in response to adenosine diphosphate (20 μM) was measured in each patient using the VerifyNow P2Y12 Assay. Platelet aggregation and the incidence of resistance to clopidogrel were compared between a smokers group (70 patients) and a non-smokers group (139 patients). Clopidogrel resistance was defined as a P2Y12 Reaction Units (PRU) value >230 and/or % inhibition <20%.
Results The mean PRU was 128.3±85.5 in the smokers group and 167.7±86.6 in the non-smokers group (p=0.002). The incidence of PRU >230 was 12.9% (9 patients) in the smokers group and 25.9% (36 patients) in the non-smokers group (p=0.033). The mean % inhibition was 48.6±30.7% in the smokers group and 36.9±27.6% in the non-smokers group (p=0.009). The incidence of patients with % inhibition <20% was 24.3% (17 patients) in the smokers group and 34.5% (48 patients) in the non-smokers group (p=0.155).
Conclusion The incidence of clopidogrel resistance was lower in the non-cardiogenic ischemic stroke patients who were smokers, thus indicating that these patients' responsiveness to this drug may be enhanced.

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A 29-year-old woman with ulcerative colitis underwent total colectomy with ileal-pouch-anal canal anastomosis in 1999. After the surgery, she developed refractory pouchitis. We administered metronidazole, mesalamine and ciprofloxacin; however, her clinical symptoms improved only very slightly. We initiated treatment with infliximab in June 2011 and discontinued the antibiotics. Thereafter, the patient's abdominal symptoms quickly improved. We discontinued the infliximab therapy in June 2012, after which time, the patient's abdominal symptoms remained in remission for 40 weeks, without the use of antibiotics. This report suggests that infliximab is useful not only for improving the clinical symptoms of refractory pouchitis, but also discontinuing antibiotic therapy in such patients.

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A flat, elevated lesion measuring 5 mm in diameter was found in the gastric body of an 80-year-old man. A biopsy showed moderately differentiated adenocarcinoma, and endoscopic ultrasonography revealed a hypoechoic mass located in the submucosa. Endoscopic submucosal dissection was subsequently performed, and a pathological examination revealed a tumor composed of adenocarcinoma and neuroendocrine carcinoma with submucosal infiltration. The pathological diagnosis was gastric mixed adenoneuroendocrine carcinoma (MANEC). An additional gastrectomy procedure was performed, and no recurrence was noted for at least three years. This case is interesting with respect to the carcinogenesis of endocrine cell carcinoma and MANEC.

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A 55-year-old man was referred to our hospital for a further examination of a pancreatic cystic tumor with a solid component exhibiting vascularity. A few days later, the patient was admitted with a complaint of sudden severe epigastric pain. Enhanced CT showed the loss of vascularity in the tumor. In particular, contrast-enhanced endoscopic ultrasonography (EUS) clearly demonstrated the disappearance of the blood flow, and a histological examination revealed acinar cell carcinoma with central necrosis. To our knowledge, this is the first case in the literature of acinar cell carcinoma associated with the sudden disappearance of vascularity. In this case, contrast-enhanced harmonic EUS was especially useful for assessing the degree of vascularity.

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Pulmonary tumor thrombotic microangiopathy (PTTM) is a fatal cancer-related complication with rapid progression. Although the underlying molecular mechanisms of PTTM remain unclear, platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) may play important roles in the pathogenesis of PTTM. We herein report a case of PTTM that was diagnosed antemortem by pathology using pulmonary wedge aspiration. The patient was treated with a combination therapy of imatinib (PDGF receptor antagonist), bevacizumab (VEGF receptor inhibitor), S-1, and cisplatin. These findings suggest that molecular-target drugs are effective for the treatment of PTTM.

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A 13-year-old boy was brought to our hospital after recovering from ventricular fibrillation that occurred after an episode of chest pain during training with his soccer team. Subsequent 64-slice multidetector computed tomography revealed the left coronary artery arising from the right sinus of Valsalva, which coursed between the ascending aorta and root of the main pulmonary artery. Surgical correction including unroofing of the left coronary ostium and pulmonary artery translocation was performed successfully. One year later, he remained asymptomatic and was back on his soccer team.

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A 17-year-old boy with homocystinuria was found to have a systolic murmur during a routine examination. Echocardiography demonstrated pulmonary hypertension (PH), and computer tomography angiography showed pulmonary thrombi. Although 12-month anticoagulation treatment reduced the thrombotic material within the main branch, it failed to clear thrombotic materials in the left and right lobar branches. Two years later, the patient was admitted to our hospital due to a worsening of PH. Treatment with bosentan, sildenafil and beraprost, in addition to anti-coagulant therapy, did not improve his PH. Balloon pulmonary angioplasty (BPA) was performed to remove the pulmonary thrombi. BPA markedly improved the patient's hemodynamics and exercise capacity. Close follow-up is scheduled to prevent any potential future thrombotic complications.

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We herein present a case of bilateral serous retinal detachment (SRD) as a presenting sign of nephrotic syndrome (NS). A 48-year-old man complained of decreased vision related to bilateral SRD. Laboratory tests revealed NS (serum albumin, 17 g/L: proteinuria, 15.40 g over 24 hours). Following treatment for edema with a diuretic, the bilateral SRD resolved completely, with a full recovery of the patient's vision. A kidney biopsy disclosed glomerular and vascular amyloid deposits; the amyloid stained strongly with anti-λ antiserum. Therefore, a diagnosis of AL amyloidosis was made. The sudden appearance of SRD should raise suspicion of a diagnosis of NS. Prompt recognition of this symptom is important for early treatment and restoration of the visual function.

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Heavy chain deposition disease (HCDD) is a rare entity. γ-HCDD is the predominant subtype and is characterized by glomerular and tubular deposition of a single γ-heavy chain subclass. To our knowledge, γ-HCDD with simultaneous deposition of two subclasses has not yet been described. A 39-year-old woman presented with hypertension, nephrotic syndrome, anemia, microscopic hematuria and progressive renal dysfunction. A light microscopic examination of renal biopsy specimens showed nodular glomerulosclerosis. Electron microscopy revealed electron-dense deposits along the glomerular and tubular basement membranes. Immunofluorescence microscopy showed positive glomerular and tubular staining for immunoglobulin G (IgG) and negative staining for κ and λ light chains. An analysis of the IgG subclass showed positive staining for both IgG2 and IgG4. We herein describe a unique case of γ-HCDD with concurrent deposition of two subclasses, presenting a new subtype to the disease spectrum.

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A 76-year-old man with a history of type 2 diabetes mellitus was admitted with cholangitis caused by cholangiocarcinoma. Cholangitis with Escherichia coli (E. coli) bacteremia recurred due to the unstable bile drainage. At 1 month after recurrence, rapidly progressive glomerulonephritis with nephrotic syndrome was manifested. Renal biopsy findings were consistent with immunoglobulin A (IgA)-dominant postinfectious glomerulonephritis (PIGN). After ensuring that the recurrent cholangitis was controlled by drainage and antibiotic therapy, oral prednisolone was initiated, and the patient's renal function and proteinuria subsequently gradually improved. This is the first case report of IgA-dominant PIGN associated with cholangitis caused by E. coli infection.

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A 47-year-old man was referred to our department due to multiple metastases in the lungs and liver with pleural dissemination six weeks after undergoing curative surgery for lung pleomorphic carcinoma. He received two regimens of chemotherapy, both of which resulted in disease progression. Considering his good general condition, he was treated with cisplatin plus gemcitabine (GP). The metastatic lesions exhibited a complete response after six courses of GP, and the patient has remained free from recurrence for over six years. An immunohistochemical analysis revealed that the tumor was highly expressive of gemcitabine transporter human equilibrative nucleoside transporter 1, thus suggesting a high sensitivity to gemcitabine.

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A 52-year-old Japanese man with congenital amblyopia and oculocutaneous albinism was admitted to our hospital. Chest CT showed reticular opacities and traction bronchiectasis without honeycombing. Specimens obtained by a video-assisted thoracoscopic surgery showed patchy chronic fibrotic lesions. We diagnosed him with Hermansky-Pudlak syndrome (HPS). A mutation in the HPS1 gene was detected, and the diagnosis was confirmed. The patient was treated with prednisolone, pirfenidone, and azathioprine, but he nevertheless died within four months. Autopsy lung specimens showed diffuse alveolar damage suggesting comparatively rapid deterioration, although this presentation was not typical of an acute exacerbation. These pathological changes may be a possible progression pattern in HPS patients.

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We herein describe the case of a 60-year-old man with a history of Behçet's disease and myelodysplastic syndrome who received cord blood transplantation (CBT). The patient was given anti-thymocyte globulin conditioning and tacrolimus to prevent graft-versus-host disease. Two months after CBT, his blood Tac concentration measured by an antibody-conjugated magnetic immunoassay (ACMIA) was found to have increased >4-fold, even after the Tac treatment was stopped. This false response was caused by the interference of endogenous heterophilic antibodies with ACMIA. Therefore, physicians must be aware of possible false ACMIA results for patients with a history of autoimmune disease and/or treated by xenogeneic antibody therapy.

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Phlegmonous gastritis (PG) is a rare, acute, severe infectious disease of the gastric wall that is often fatal due to Streptococcus spp. A 77-year-old man with diabetes and a gastric ulcer was urgently admitted due to prolonged nausea and vomiting. Computed tomography revealed widespread diffuse thickening of the gastric wall, and PG was suspected. The patient expired less than 9 hours after admission despite intensive treatments. Later, an analysis of the blood and gastric juice revealed group A streptococcus (GAS) and virulence factors associated with toxic shock syndrome (TSS). We herein diagnosed a patient with an extremely aggressive course of PG caused by GAS TSS.

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A 69-year-old man with diabetes mellitus was diagnosed with a prostate abscess. Although the pathogen was fluoroquinolone-resistant Escherichia coli and the oral administration of trimethoprim-sulfamethoxazole was initiated, the infection recurred after three months. The antibiotic therapy was subsequently changed to intravenous fosfomycin, and the patient's condition promptly improved. Four weeks of fosfomycin therapy was successfully continued without any adverse events. In the era of antibiotic resistance, revival of forgotten drugs is an important issue for clinicians. Fosfomycin can be applied as an alternative option for prostate infections, considering the remaining susceptibility of multidrug-resistant pathogens to fosfomycin and the good pharmacokinetics of this drug in prostatic tissue.

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