Efficacy of zinc administration in patients with hepatitis C virus-related chronic liver disease.

OBJECTIVE: Zinc supplementation has been shown to contribute to inhibition of liver fibrosis and improvement in hepatic encephalopathy. However, little is known about the anti-inflammatory effect of zinc on hepatitis C virus (HCV)-related chronic liver disease (CLD). We therefore examined the effects of zinc administration on inflammatory activity and fibrosis in the liver of patients with HCV-related CLD. MATERIAL AND METHODS: Polaprezinc, a complex of zinc and l-carnosine, was administrated at 225 mg/day for 6 months to 14 patients with HCV-related CLD, in addition to their ongoing prescriptions. Peripheral blood cell counts, liver-related biochemical parameters, serological markers for liver fibrosis, HCV-RNA loads, and serum levels of zinc and ferritin were evaluated before and after zinc administration. RESULTS: Serum zinc concentrations were positively correlated with hepatic reserve before zinc supplementation. A significant increase in serum zinc level was observed after zinc supplementation (64+/-15 versus 78+/-26 mg/dl, p=0.0156). Treatment with polaprezinc significantly decreased serum aminotransferase levels (aspartate aminotransferase (AST): 92+/-33 versus 63+/-23 IU/l, p=0.0004; alanine aminotransferase (ALT): 106+/-43 versus 65+/-32 IU/l, p=0.0002), whereas alkaline phosphatase levels were significantly increased (305+/-117 versus 337+/-118 U/l, p=0.0020). Serum ferritin levels were significantly decreased by treatment with polaprezinc (158+/-141 versus 101+/-80 ng/ml, p=0.0117). The reduction rate of ALT levels by polaprezinc was positively correlated with that of ferritin (r(2)=0.536, p=0.0389). There was a tendency toward a decrease in serum type IV collagen 7S levels after treatment with polaprezinc. However, administration of polaprezinc did not affect peripheral blood cell counts, other liver function tests, or HCV-RNA loads. CONCLUSIONS: These findings suggest that polaprezinc exerts an anti-inflammatory effect on the liver in patients with HCV-related CLD by reducing iron overload.

Adenocarcinoma arising from aberrant pancreas in the stomach.

We report herein a rare case of malignant transformation of aberrant pancreas in the stomach, associated with gastric outlet obstruction. A 58-year-old woman was admitted to our hospital, complaining of vomiting. Although barium meal examination and gastric endoscopy showed marked pyloric stenosis, the biopsy specimen obtained from the stenotic site revealed regenerative mucosa without malignancy. Abdominal computed tomography and endoscopic ultrasonography (EUS) also could not detect the cause of the obstruction. Histopathological examination of the surgically resected specimen showed the malignant transformation of aberrant pancreas in the stomach. It should be noted that one of the causes of gastric outlet obstruction may be aberrant pancreas or its malignant transformation.

[Sedation with intravenous midazolam during upper gastrointestinal endoscopy--changes in hemodynamics, oxygen saturation and memory].

BACKGROUND: Cardiorespiratory adverse effects are often observed in patients undergoing upper gastrointestinal endoscopy with sedation. In this study, we examined hemodynamics, oxygen saturation and memory during upper gastrointestinal endoscopy under sedation with intravenous midazolam. METHODS: Eight healthy outpatients without any obvious complications received intravenous midazolam 5 mg for sedation for upper gastrointestinal endoscopy. Blood pressure, heart rate and percutaneous arterial oxygen saturation (SpO2) were measured before, during and after endoscopy. After the arousal by intravenous flumazenil, we inquired the patients about the level of memory during the endoscopy. RESULTS: Blood pressure decreased significantly two minutes after midazolam administration, but increased significantly after the insertion of an endoscope which was not different from the control value. Heart rate increased significantly one and three minutes after the insertion of the endoscope. SpO2 decreased significantly after midazolam administration and stayed at around 95%. No patients remembered the procedure. CONCLUSIONS: Sedation with intravenous midazolam during upper gastrointestinal endoscopy is useful to control the cardiovascular responses, and to obtain amnesia. However, a decrease in SpO2 should be watched carefully.

[Bronchospasm during upper gastrointestinal endoscopy under sedation].

We experienced a case of bronchospasm during upper gastrointestinal endoscopy under sedation. An 80-year-old man came to our hospital with abdominal distension with pain, nausea and vomiting. He has the history of splenectomy, cholecystectomy for hemolytic anemia and thyroidectomy for thyroid cancer, surgery for bilateral shoulder joints and diabetes. Abdominal X-ray suggested obstruction of the small intestine. On the third hospital day, gastrointestinal endoscopy was scheduled for insertion of a long ileus tube. Under sedation with diazepam 10 mg and local anesthesia of the pharynx with lidocaine spray 24 mg, the endoscope was inserted and when it reached the esophageal-gastrojunction, respiratory rate increased to 30 breaths.min-1 with expiratory stridor. The endoscope was removed immediately. He was oro-tracheally intubated and artificially ventilated. On the fourth hospital day, he was extubated under bronchoscopy. No abnormalities were observed in the trachea, vocal cord, pharynx and larynx. Later, it was revealed that he had a history of hoarseness and dysphasia. His left recurrent nerve and cervical nerve had been resected with thyroid and right cervical nerve anastomosed to the rest of the left recurrent nerve. The insertion of upper gastrointestinal endoscope might have induced bronchospasm stimulating distal esophageal afferent vagal reflex partly by regurgitation of gastric acid under sedation.

[Septic shock associated with pyogenic liver abscess rescued with percutaneous transhepatic abscess drainage].

We report a case of septic shock associated with pyogenic liver abscess rescued with percutaneous transhepatic abscess drainage (PTAD). A 70-year-old male patient was admitted to our outpatient department of internal medicine with general fatigue, dullness of bilateral shoulders and extremities, appetite loss, weight loss, headache, and vertigo. Laboratory tests showed severe inflammatory indications, anemia, and high values of hepatobiliary enzymes and blood sugar. Abdominal ultrasonography and enhanced CT showed a pyogenic liver abscess of 10 cm in diameter at S 6-7 in the right hepatic lobe. The patient's condition deteriorated suddenly that night. From the results of abdominal ultrasonography and enhanced CT, we made diagnosis of septic shock associated with pyogenic liver abscess. Emergency abdominal ultrasound-guided PTAD was performed under local anesthetic. Postoperatively, the antibiotic was infused daily through a PTAD tube into the liver abscess space. He recovered and his laboratory tests improved gradually. On abdominal ultrasonography and enhanced CT, the liver abscess disappeared by 19th postoperative day, and PTAD tube was removed. There was no complication during PTAD treatment. We conclude that patients in septic shock should undergo further examinations immediately and treatment of the infected tissue should be started as soon as possible. PTAD may be an additional effective procedure for pyogenic liver abscess in septic shock. Furthermore, local antibiotic lavage through a PTAD tube into the liver abscess space may be an important supplementary method in the management of the illness.