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Non-alcoholic fatty liver disease (NAFLD) represents one of the most common causes of chronic liver disease worldwide and is characterized by chronic liver inflammation and fibrosis leading to cirrhosis and increased risk of liver cancer in a proportion of patients. Effective anti-fibrotic agents have yet to be approved for the treatment of NAFLD. The present study aimed to evaluate the efficacy of dipeptidyl peptidase 4 inhibitors (DPP4-I) in the prevention of NAFLD progression in NAFLD patients with type 2 diabetes. The study was a single arm, multi-centre, non-randomised study of NAFLD patients with type 2 diabetes. NAFLD was diagnosed according to ultrasonographic findings. All the patients received 25 mg/day of alogliptin for 12 months. The efficacy of alogliptin in preventing NAFLD progression was assessed using overall NAFIC scores [non-alcoholic steatohepatitis (NASH), ferritin, insulin and type IV collagen 7S] and individual component scores according to baseline haemoglobin A1c (HbA1c) levels. Of the 39 patients enrolled in the study, 16 patients (40.3%) had NAFIC scores >2 points, indicating the presence of NASH. NAFIC scores markedly decreased following 12 months of alogliptin administration, but remained >2 points in 10 patients, indicating that NASH may have persisted in these patients. The relative risks for persistent NASH were 4.92 (95% confidence interval, 0.61-40.0) in the highest HbA1c tertile group compared with those in the lowest group. However, no statistically significant linear trend was observed across all HbA1c categories (P=0.145). DPP4-I may have efficacy against NAFLD progression in patients with type 2 diabetes with relatively lower HbA1c levels. DPP4-I may represent a potential new therapeutic strategy for the prevention of disease progression in NAFLD patients with type 2 diabetes.

Background: Unintended exposure to antitumor agents from an oral medicine may place healthcare workers and patients taking medicine at risk. In this study, the exposure to blister pack by CP (cyclophosphamide) and appropriate preventive procedures were examined., Findings: CP detected inside the blister pack of the tested seven lots by LC-MS/MS ranged from 8.2 to 199.6 ng. Raman imaging clearly showed that CP ingredient was completely covered by the tablet coating layer and had not leached out of the tablet. In addition, the amount of CP detected inside the vials was suppressed under the lower detection limit until day 28, and only 6.0 ng was detected only at day 56., Conclusions: Various amounts of CP were contaminated to not only the inside of the blister pack but also the outside. This contamination may be caused not only by the manufacturing environment but also by the CP oral tablets themselves through volatilization of CP. Refrigerated storage of CP oral tablets may protect healthcare workers and patients from contact with CP.

The link between changes in estimated glomerular filtration rate (eGFR) and cigarette smoking was evaluated in Japanese male workers with a 5-year follow-up. We examined the data of 456 Japanese male workers, aged 22-70 years, who were taking no medications, and from this group, 286 men (43.5±8.2 years) were followed for 5-years. Habits of cigarette smoking were obtained during interviews by well-trained staff. The influence of cigarette smoking on eGFR was evaluated. In the first analysis, there was no significant difference in eGFR between subjects with and without cigarette smoking. In the second analysis, eGFR was significantly reduced after 5 years in all subjects. Changes in eGFR in subjects with cigarette smoking (-1.90±12.31 ml/min/1.73 m²) were significantly smaller than those in subjects without cigarette smoking (-4.97±12.05 ml/min/1.73 m²). At follow-up, we found that eGFR was weakly and negatively correlated with the number of cigarettes smoked (/day). The present study indicated that cigarette smoking may be an important modifiable factor for eGFR in Japanese male workers who are not taking any medications.

A 81-year-old woman admitted with general fatigue was found to have a giant polyp in the gastric antrum by endoscopy. The polyp prolapsed into the duodenum through the pylorus. Angiographic examination of the abdomen revealed the polyp to be about 90×35 mm in size. Laparotomy was performed. It was finally diagnosed as heterotopic Brunner's gland adenoma which had a stalk on the antrum of the stomach. Heterotopic Brunner's gland adenoma is rare. Only 3 cases including the present case have been reported in Japan.

Background: Many studies have suggested that endoscopic obliteration using cyanoacrylate for bleeding gastric fundal varices is effective. However, serious complications by injection of cyanoacrylate into varices have also been reported., Methods: Thirty patients with bleeding gastric fundal varices underwent endoscopic injection sclerotherapy using 5% ethanolamine oleate under fluoroscopic guidance plus infusion of vasopressin and a transdermal nitroglycerin patch. The injection of 5% ethanolamine oleate was continued until it filled the varices and their feeder veins under fluoroscopic guidance. The injection needle was removed while thrombin glue was sprayed at the puncture site through the side hole of the injector needle to prevent bleeding from the puncture site., Results: Complete hemostasis was achieved in 28/30 patients (93.3%). The cumulative rebleeding rate after 1, 3 and 5 years was 13%, 19% and 19%, respectively. The 1-, 3-, and 5-year cumulative mortality rates were 31%, 54% and 59%, respectively. There was no complication related to infusion of vasopressin and sclerotherapy procedure., Conclusion: The sclerotherapy method carried out using 5% ethanolamine oleate combined with infusion of vasopressin under fluoroscopic guidance might be a feasible method for obliteration of gastric fundal varices as an alternative to cyanoacrylate.

In this study, we elucidated the efficacy of our prophylactic method for wound infection in pull-percutaneous endoscopic gastrostomy (PEG). The total 29 patients received the pull-PEG. The first 8 patients received the oral sterilization with povidone iodine and antibiotics at the time of pull-PEG (Group-I). The frequency of wound infection in this group was 50.0% (4/8). It was revealed that all infections were induced by methicillin resistant staphylococcus aureus (MRSA). 3 patients were MRSA positive in the throat. In Group-II, we eradicated MRSA in the throat before the pull-PEG by combination mupirocin calcium hydrate with the Group-I treatment. In contrast in Group-I, the frequency of wound infection was significantly reduced in Group-II (4.8%: 1/21). The results showed that our eradication method was very useful for prevention of the wound infection in pull-PEG treatment.

Transcranial Doppler sonography (TCD) has been increasingly used to detect embolic signals. A 49-year-old woman had repeated episodes of weakness and numbness of the right limbs. She was diagnosed as having transient ischemic attacks (TIAs). A cranial Gadolinium-enhanced MRI revealed multiple small lesions in the cortical-subcortical areas of the left middle cerebral artery territory. A TCD examination on admission detected 4 embolic signals on the left MCA trunk in a 30-minute examination period. TIAs completely ceased after the initiation of an antiplatelet therapy with aspirin. Embolic signals were not detected in later TCD studies. The embolic signals on the TCD strongly indicated that TIAs are caused by an embolic mechanism. TCD is potentially useful for assessing the efficacy of antiplatelet and anticoagulant therapies in patients with TIAs.

We report a 43-year-old woman who suffered from Listeria monocytogenes meningitis. She was admitted to our hospital because of headache, nausea, vomiting, and fever. On admission she had no abnormal neurological signs except for severe nuchal stiffness. Cerebrospinal fluid (CSF) examination on the day of admission revealed pleocytosis and increased total protein level. The CSF culture demonstrated Listeria monocytogenes. Because ampicillin therapy was not effective, erythromycin (8 g/day) was added. After 12 hours of erythromycin therapy, the patient complained of moderate hearing difficulty. Erythromycin was then stopped on the next day. Her hearing improved and became normal within 48 hours after discontinuation of erythromycin. Contrast MRI of the brain revealed enhancement of the ependyma of the lateral ventricle, suggesting the presence of ventriculitis. By parenteral administration of ampicillin and cephazolin, clinical symptoms improved quickly, and abnormal CSF and MRI findings were normalized. Listeria meningitis accompanied with ventriculitis has been reported in neonates and infants, but not in adults. In addition, this is the first case with erythromycin-induced hearing loss in the Japanese literature. Hearing should be regularly examined in patients who are treated with high-dose erythromycin (> or = 4 g/day), and the drug should be immediately discontinued when the patient develops hearing loss.

We studied the influence of EIS on the respiro-circulatory condition of patients with portal hypertension. Subjects were fifty patients with portal hypertension who were successfully injected more than 5.0 ml of sclerotant into varices. A prospective randomized controlled trial was proposed to elucidate the effect of prophylactic administration of pure oxygen. Twenty-five patients inhaled pure oxygen (O2), remaining twenty-five patients did not during EIS. Respiro-circulatory function of patients was evaluated by monitoring O2 saturation, pulse rate and blood pressure during EIS. PaO2 was measured before and after EIS in seven patients without O2. EIS by the 5% ethanolamine oleate with iopamidol (EOI) was performed under X-ray monitoring. O2 saturation in patients without O2 inhalation was lowered, whereas that in patients with O2 inhalation was stable during EIS. O2 saturation during injection of EOI and after EIS in patients without O2 inhalation was significantly lower than that in patients with O2 inhalation. Pulse rate was significantly lower and a rise in blood pressure was smaller in patients given O2. No significant differences of PaO2 was noted before and after EIS. In conclusion, the monitoring of O2 saturation, pulse rate and blood pressure is necessary during EIS. Prophylactic administration of pure oxygen may be useful for prevention of hypoxic state and respiro-circulatory stabilization during EIS.

In order to clarify the etiology of brain infarction in the posterior cerebral artery (PCA) territory, we investigated 85 patients (29 women and 56 men, mean age: 63.6 years old) with PCA territory infarction confirmed by computed tomography or magnetic resonance imaging. Patients with thalamic infarction alone were excluded from the present study. Cerebral angiography was performed in 72 subjects. The diagnosis of the mechanism of brain infarction was made on the basis of cerebral angiographic and echocardiographic (presence of cardiac disease as a potential embolic source) findings. Embolism was inferred when the presence of the patent PCA ipsilateral to the infarction, reopening of the occluded PCA or intraluminal filling defect was demonstrated by angiographic studies. In addition, we divided these patients into three groups according to potential source of emboli; cardiogenic, atherothrombotic (so-called artery-to-artery embolism) and embolism of undetermined origin. We diagnosed the patient to have thrombotic mechanism, when an occlusion of the PCA was demonstrated without presence of an embolic source (heart diseases or stenotic arterial lesions proximal to the occluded PCA). When the mechanism (embolic or thrombotic) could not be clearly distinguished, we categorized them "unclassified". When other apparent mechanisms such as arterial dissection, moyamoya disease etc, were demonstrated, we classified them in "miscellaneous". According to the above criteria, 50 patients (59%) were diagnosed as having embolism, only two patients (2%) had definite thrombosis, 28 patients (33%) "unclassified", and five patients (6%) "miscellaneous" (2 arterial dissection, 1 radiation vasculopathy, 1 migraine, 1 moyamoya disease).(ABSTRACT TRUNCATED AT 250 WORDS)

A 66-year-old male experienced the sudden onset of amnesia and generalized convulsions, and during the subsequent month developed consciousness disturbance, disorientation, memory disturbance, abnormal speech and behavior, pseudobulbar palsy, unsteadiness and urinary/fecal incontinence. The initial brain CT scan was unremarkable, and the MRI findings were also unremarkable, except for evidence of several scattered lacunar strokes in the cerebral white matter. 99mTc-HM-PAO-SPECT, however, revealed multifocal large hypoperfused lesions in the cerebrum. The erythrocyte sedimentation rate and serum CRP, LDH and gamma-globulin levels were elevated. CSF studies showed mild pleocytosis and increased protein levels. The patient's subsequent course was marked by fever, SIADH, adrenal enlargement, splenomegaly, pulmonary infiltration and pancytopenia. The neurological signs progressively worsened, until the patient lapsed into an apallic state and died 3 months after the onset of symptoms. Autopsy disclosed diffuse intravascular B lymphomatous proliferation in the brain, lungs, kidneys, adrenals, spleen and pancreas. Until now, the brain SPECT findings of IL were not very well known, but in our patient, SPECT was capable of demonstrating the pathophysiologic changes very precisely. SPECT was able to provide valuable information on the pathophysiology of IL and may therefore become another powerful tool in the diagnosis of IL.

We report an 82-year-old retired man who developed syndrome of inappropriate secretion of ADH (SIADH) caused by sodium valproate (VPA). He had been taking VPA for treatment of symptomatic epilepsy due to cardioembolic stroke. Although he was clinically asymptomatic, he was found to have decreased level of serum sodium concentration (128 mEq/l). Association of hyponatremia, normal urinary sodium concentration, high urine osmolality and increased concentration of serum ADH strongly suggested the presence of SIADH. There were no underlying disorders which can cause SIADH, such as malignant neoplasm with autonomous ADH release, non-malignant pulmonary diseases and active disorders of the central nervous system. Eight days after discontinuation of VPA administration serum sodium level increased (142 mEq/l) to the normal level. Then, we started the administration of VPA again to confirm that VPA was responsible for developing hyponatremia. As a result, he developed SIADH with hyponatremia (128 mEq/l) again, which improved after discontinuation of the administration. Therefore, we concluded that the SIADH might have been caused by administration of VPA. This is the first report on adverse effect of VPA causing SIADH.

Treatment with recombinant tissue plasminogen activator (rt-PA) has been applied in acute cardioembolic stroke to reopen the occluded vessel and improve the patient's neurologic deficit. However, the effect of this therapy on intracardiac thrombus has not been documented previously. A forty-five-year-old man with dilated cardiomyopathy developed acute cardioembolic stroke with disturbance of consciousness, right hemianopia, right hemiplegia, and global aphasia. Cerebral angiography demonstrated occlusion of the left middle cerebral artery trunk. Intravenous administration of 30 megaunits (MU) of recombinant tissue plasminogen activator was commenced two hours after the ictus and completed within sixty minutes. Cerebral angiography was repeated just after this treatment and demonstrated a new occlusion of the left intracranial internal carotid artery along with occlusion of a branch of the left external artery. The authors subsequently performed two-dimensional echocardiography and found a mobile thrombus in the left ventricle. In patients with intracardiac mobile thrombi, recombinant tissue plasminogen activator seems to accelerate breakup or detachment of the thrombi and subsequent recurrent embolization. Therefore, it seems better to pay attention to the presence of mobile intracardiac thrombus before commencing intravenous infusion of rt-PA.

A patient with ataxic hemiparesis and ipsilateral cheiro-oral dysesthesia (tingling) due to a single lacunar infarct at the border between the posterior limb of the internal capsule and the corona radiata is described. A 47-year-old hypertensive man was admitted because of weakness of the right upper and lower limbs with ipsilateral peri-oral and palmar dysesthesia, which developed during bathing in the morning. Upon admission, neurological examination revealed right hemiparesis with ipsilateral limb ataxia and ipsilateral peri-oral and palmar dysesthesia. Based on neurological finding, he was diagnosed as having ataxic hemiparesis with ipsilateral cheiro-oral syndrome. Brain computed tomography and magnetic resonance imaging demonstrated a small lesion at the border between the posterior limb of the left internal capsule and the corona radiata, which was enhanced with gadolinium-DTPA administration. It has been reported that the disturbance of the cortico-pontine tract causes ataxic hemiparesis and that of the thalamo-cortical projection causes cheiro-oral syndrome. These findings of the present case, therefore, suggest that both of these pathways run closely together at the border between the posterior limb of the internal capsule and the corona radiata.

In order to evaluate the efficacy of warfarin for the secondary prevention of cardioembolic stroke due to nonvalvular atrial fibrillation (NVAF), we retrospectively investigated the frequencies of recurrent brain embolism and hemorrhagic complications in 68 subjects (62 +/- 9 years old, 54 men and 14 women), who had experienced at least one cardioembolic stroke prior to the study period. The follow-up period was 39 +/- 27 months. Paroxysmal and persistent atrial fibrillation were seen in 37 and 31 subjects, respectively. We assigned the subjects to three subgroups according to types of the events during the follow-up; recurrence group, hemorrhage group, and non-accident group. Prothrombin time (international normalized ratio, INR) was assessed as mean value during the follow-up period. The prothrombin time at the time of recurrence and hemorrhagic complication was also taken into consideration for data analysis. Recurrent brain embolism was observed in three patients (1.4%/yr). Major bleeding occurred in 12 patients (5.5%/yr) and three of them were fatal (subarachnoid hemorrhage, brain hemorrhage, and acute subdural hematoma). The mean value of INR in the hemorrhage group (3.0) was higher than that in the recurrence group (2.2) and in the non-accident group (2.3) (p < 0.001, vs. non-accident group). The lowest mean value of INR in the hemorrhage group was 2.5. The prothrombin time in the recurrence group did not differ from that in the non-accident group. The death rate in the hemorrhage group (4/12, 33.3%) was higher than those in the recurrence group (0) and in the non-accident group (4/53, 7.5%) (p < 0.01, vs. non-accident group).(ABSTRACT TRUNCATED AT 250 WORDS)

We report a case showing supranuclear vertical gaze palsy and convergence nystagmus caused by a unilateral lesion of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). The patient was a 54-year-old female with mitral stenosis and regurgitation and atrial fibrillation, who suddenly developed vertigo and double vision. She was admitted to our hospital because of persisting diplopia 4 days after onset, although vertigo had resolved within 1 hour. On admission she was alert, but presented with supranuclear vertical gaze palsy and convergence nystagmus. Other cranial nerves were intact and motor strength, deep tendon reflexes, sensations were also normal. There were no cerebellar signs. Cranial MRI demonstrated a unilateral ischemic lesion at the left thalamo-mesencephalic junction that involved the unilateral riMLF. Cerebral angiography revealed no abnormalities. Vertical gaze palsy has been reported to be caused by a lesion involving bilateral riMLF or unilateral posterior commissure, and convergence nystagmus usually by a lesion near or within the dorsal mesencephalon. However, recent reports have demonstrated a histopathologic evidence that vertical gaze palsy was caused by unilateral riMLF lesion. The present case confirms clinically that both vertical gaze palsy and convergence nystagmus can be developed by a lesion of unilateral riMLF.

We reported a case with the superior vena cava syndrome and compression neuropathy of the right brachial plexus after pacemaker implantation. A 27-year-old man with the second degree atrio-ventricular block had underwent pacemaker implantation via the right subclavian vein at the age of 19. Since the age of 25, he occasionally experienced paresthesia and swelling in his right arm after excessive work. These symptoms gradually resolved within a few days by rest. On June 2, 1990, he noticed swelling and paresthesia of his right face, arm and upper trunk after excessive labor. A few days later, weakness of right hand developed. On examination on June 8, the right arm was edematous, but not cyanotic. There were weakness and hypoactive muscle stretch responses in the right upper extremity with hypesthesia of all modalities in the neck, arm and upper trunk of the right side. Venous angiography showed total occlusion of the right brachiocephalic vein and superior vena cava and well-developed collateral channels. We speculate that swelling of the right upper extremity, which became overt when arterial blood supply to that limb outbalanced impaired venous drainage, finally compressed the right brachial plexus.