Hiroyasu Yamada

Predicting the clinical response to cytapheresis in steroid-refractory or -dependent ulcerative colitis using contrast-enhanced ultrasonography

Objective. To evaluate the usefulness of transabominal ultrasound (US), including contrast-enhanced ultrasonography (CEUS), in predicting the response to cytapheresis therapy in patients with steroid-refractory or -dependent ulcerative colitis (UC). Material and methods. Between January 2005 and June 2008, 26 consecutive patients with steroid-refractory or -dependent UC were treated with granulocyte and monocyte adsorption apheresis (GCAP) or leukocytapheresis (LCAP) at our institute. The clinical activity of UC was evaluated by patients’ C-reactive protein (CRP) levels and clinical activity index (CAI) scores. All patients were evaluated by grey-scale US, power Doppler US (PDUS), and CEUS. In CEUS, the color signal patterns were classified as 1 of 2 patterns. In pattern 1, color signals were partially detected in the bowel wall (excluding muscularis propria, the outer thin layer of the bowel wall), whereas in pattern 2, color signals were detected in the entire bowel wall (excluding muscularis propria). Differences between remission or clinical response (group R) and no response (group N) were ascertained for clinical features, clinical activities, and US findings. Results. Differences between the two groups were not considered significant for the clinical features, clinical activities, and grey-scale US and PDUS findings. Using CEUS, 4 patients in group R showed pattern 2 (21%), while in group N, all patients showed this pattern, indicating a significant difference between the two groups (p<0.01). Conclusion. CEUS findings may be helpful in predicting the clinical response to cytapheresis for steroid-refractory or -dependent UC.

Magnifying colonoscopy used to predict disease relapse in patients with quiescent ulcerative colitis.

Background: Many patients with quiescent ulcerative colitis (UC) experience relapse. However, clinical and conventional colonoscopic signs are inadequate for predicting relapse. This studys aim was to investigate the effectiveness of magnifying colonoscopy in predicting relapse in patients with quiescent UC and to evaluate the association of the findings of magnifying colonoscopy with the histological findings. Methods: Magnifying colonoscopy was performed in 57 patients with clinical and endoscopic inactive UC. Patients were divided into 3 groups according to the findings of magnifying colonoscopy as MR (magnify‐regular), MI (magnify‐irregular), and MD (magnify‐defect). Their subsequent clinical course was compared to assess the clinical usefulness of magnifying observation in predicting relapse. We also compared histological findings according to Rileys criteria to each finding of magnifying colonoscopy. Results: Within 12 months, 1 of 18 patients (6.7%), 10 of 22 patients (45.5%), and 12 of 17 patients (70.6%) with findings of magnifying colonoscopy of MR, MI, and MD, respectively, experienced relapse. The MR group had a significantly low relapse rate compared with the MD and MI groups (P = 0.016, P = 0.002). When histological findings were compared with the findings of magnifying colonoscopy, the mean score of each variable, such as acute inflammatory cell infiltrate, chronic inflammatory cell infiltrate, and crypt architectural irregularities was significantly lower in the MR group than in the MD and MI groups. Conclusions: The findings of magnifying colonoscopy in patients with quiescent UC is useful for predicting relapse and is associated with histological grade of inflammation. Inflamm Bowel Dis 2009

Usefulness and limitations of transabdominal ultrasonography for detecting small-bowel tumors

Objective. New methods of examining the small bowel, e.g. capsule endoscopy (CE) and double-balloon endoscopy (DBE), have recently been developed. Transabdominal ultrasonography (TUS) is a conventional, non-invasive, and less-expensive modality. The aim of this study was to evaluate the usefulness and limitations of TUS for the detection of small-bowel tumors. Material and methods. A total of 371 patients who underwent CE and/or DBE were enrolled in the study. All patients underwent TUS prior to CE and DBE. We evaluated the sensitivity and specificity of TUS in detecting small-bowel tumors, diagnosis and size of tumors, overall detection rate of tumors by TUS, detection rate according to tumor size and shape, and the ultrasonographic features of the tumors. Results. The sensitivity and specificity rates of TUS were 26.4% and 98.6%, respectively. A total of 92 tumors detected by CE and/or DBE were analyzed. Mean size of small-bowel tumors was 20.0 mm. The detection rate of TUS was 25.0%; the detection rate for tumors smaller than 20 mm was only 1.8%, while that for tumors of 20 mm or larger was 59.5%. Despite the tumor size being 20 mm or larger, none of the granular lateral spreading lesions were detected by TUS, but all of the circumferential ulcerative lesions could be detected using this procedure. Conclusions. TUS is considered to be a useful modality for detecting small-bowel lesions of large volume. We consider that TUS is the first choice modality for examining small-bowel lesions because it is a non-invasive and non-expensive procedure that can detect large lesions.

Facial nerve palsy due to temporal bone metastasis from hepatocellular carcinoma.

To the Editor, Temporal bone metastasis would be rare. Although the occurrence of facial nerve palsy is frequently a result of cranial bone metastasis in a patient with cancer, the incidence of facial nerve palsy as a consequence of temporal bone metastasis is rare. When facial nerve palsy is accompanied by other cranial nerve palsies, especially of the neighboring cranial nerves V and VIII, temporal bone metastasis should be suspected. We report here a rare patient with facial nerve palsy due to temporal bone metastasis from hepatocellular carcinoma (HCC). A 49-year-old man, with hepatitis B virus-related liver cirrhosis, had suffered from ascites for several years. He was admitted to our unit in February 2003 because of upper gastrointestinal bleeding secondary to esophageal varices. Hemostasis was achieved by endoscopic ligation of the varices. The liver disease based on routine liver function tests was classified as Child-Pugh Grade C. Abdominal computed tomography (CT) showed a small low-density area in the medial part of the liver, but no enhancement throughout dynamic study (Fig. 1a). Alpha-fetoprotein (AFP) was 39 ng/ mL, and protein induced by vitamin K deficiency and antagonist-II (PIVKA-II) was 118 mAU/mL. At that time, no further examination was performed. One to 3 days later, the patient presented with rightsided facial weakness with pain, showing peripheral paresis of the right facial nerve. There was no history of previous neurological deficit, and laboratory tests showed no evidence of viral infection such as cytomegalovirus or herpes virus. One month later, the symptoms and pain progressively worsened with trachyphonia and dysphagia. Neurological examination revealed right V, VII, VIII, IX, XI and XII cranial nerve palsies. Non-contrast CT of the brain showed a large lesion in the pyramidal part of the right temporal bone as an expansile osteolytic mass. Cranial magnetic resonance imaging (MRI) revealed that the lesion was isointense on T1 and T2-weighted images compared with the brain parenchyma. In addition, the lesion was markedly enhanced with gadopentatate dimeglumine, suggesting malignancy of unknown origin (Fig. 1b). Because of poor hepatic reserve, it was difficult to perform surgery. Instead, the right temporal bone was irradiated with a total dose of 50 Gy. Although little improvement in facial paresis was noted, the patient reported marked pain relief. Three months later, the patient developed refractory ascites with poor general condition. Surprisingly, CT showed a well-enhanced large tumor around the medial part of the liver, suggesting a large HCC (Fig. 1c). Tumor markers were elevated with AFP of 580 ng/mL and PIVKA-II of 287 mAU/mL. Hepatectomy was ruled out because of poor hepatic reserve and rapid tumor progression. Two weeks later, the patient died due to deterioration of his general condition. Autopsy showed massive HCC with tumor thrombosis in the right portal trunk and small metastatic nodules throughout the liver. A tumor in the pyramidal part of the right temporal bone was identified, which invaded the cochlea. Histopathologically, the liver tumors were poorly differentiated HCC. The temporal bone tumor was diagnosed as a metastasis of HCC with histopathological features similar to the primary lesion (Fig. 1d). Other metastatic lesions were found in the lungs, peritoneum, sternum, mediastinal lymph nodes and hepatic hilar lymph nodes. Common primary cancers that metastasize to the temporal bone are breast and lung. Among bone metastases from HCC, the frequency of cranial bone metastasis is only approximately 1%, while the vertebrae, ribs, sternum, long bones and pelvis are frequent metastatic sites. A careful search of the Medline database showed only five patients of temporal bone metastasis from HCC. They showed advanced stage inevitably. The last patient had only a small focus of HCC exceptionally: temporal bone metastasis from HCC was presenting in a living post-transplanted liver. The incidence of HCC is increasing worldwide. Early detection by imaging procedures and curative treatment has improved survival. Improvement in cancer therapy, including liver transplantation, is associated with prolonged survival, and presentation at late age with metastases including bone metastases from HCC becomes more common. Thus, temporal bone metastasis from HCC would increase. Indeed, the largest autopsy study performed by Gloria-Cruz et al. demonstrated that temporal bone metastasis is not as uncommon as previously reported. Temporal bone metastasis should be included in the differential diagnosis of cirrhotic patients who present with facial nerve palsy, especially accompanied by other cranial nerve palsies, although the situation might be very rare.

Neurotensin-like immunoreactivity (NTLI) concentration in the cerebrospinal fluid of children and its alteration in a febrile aseptic meningitis

Neurotensin-like immunoreactivity (NTLI) concentrations in the cerebrospinal fluid (CSF) of normal children and patients with febrile aseptic meningitis, aged 7 months to 15 years, were studied. The NTLI concentrations in CSF of 27 children with normal CSF findings were 160.1 +/- 54.6 pg/ml (mean +/- S.D.). The NTLI concentration in CSF of 26 patients in an acute phase of aseptic meningitis was 110.6 +/- 51.1 pg/ml which was significantly (P less than 0.01) lower than the controls. These patients had a mean temperature of 101.4 +/- 1.5 degrees F which remained elevated for an average of 3.5 days. The NTLI concentrations in CSF of 23 patients in a recovery phase (after blood and CSF findings became normal with no fever) were 166.5 +/- 57.8 pg/ml, which did not differ significantly from the normal. There were no statistical correlations between the NTLI concentration in CSF and the protein concentration or total cell count in CSF. These results suggest that NTLI concentration changes during a febrile aseptic meningitis and that it may be associated with thermoregulation.

Ontogenic development of neurotensin-like immunoreactivity in the gastrointestinal tract and the influence of dietary changes in rats.

The ontogenic development of neurotensinlike immunoreactivity (NTLI) in the gastrointestinal tract was studied in three groups of male rats on different diets. Group I rats were weaned physiologically. Group II rats received only mothers milk until 25 days of age. Group III rats were fed mothers milk alone for 20 days and then switched abruptly to laboratory chow. The NTLI concentration in the gastrointestinal tract from the esophagus to the small intestine was almost the same as that in adult rats before weaning. It increased after weaning to a peak on day 20 or 25, and then decreased to the adult level. The NTLI concentration in the cecum and large intestine, however, decreased from high neonatal level, reaching the adult level on day 20 or 25, and it remained constant thereafter. Prolonged mothers milk feeding alone enhanced neurotensin production in the esophagus and postponed the physiological decrement of NTLI concentrations in the duodenum and small intestine. The sudden change from mothers milk to laboratory chow accelerated the decrement of intestinal NTLI concentrations.