Activation-recovery intervals of 12-lead electrocardiograms before and after catheter ablation in patients with Wolff-Parkinson-White syndrome

Preexcitation in Wolff-Parkinson-White syndrome (WPW) has been reported to induce long-lasting changes in ventricular recovery properties. However, there has not been a report concerning changes in the activation-recovery interval (ARI) in 12-lead ECGs before and after catheter ablation (CA) in patients with WPW syndrome. The present study compared changes in ARIs from 12-lead ECGs with those from body surface unipolar leads before and after CA to examine whether ARIs from limb leads of 12-lead ECGs provide useful information on changes in recovery properties in addition to the ARIs from precordial leads. The study population consisted of 27 manifest WPW patients with a left- (n=18, group A) or right-sided accessory pathway (n=9, group B). ARIs in leads I, II, and III were strongly correlated with those in unipolar leads over the left lateral, left lower, and right lower chest, respectively. ARIs in leads aVR, aVL, and aVF showed a significant correlation with those in unipolar leads over the right upper, left upper, and lower anterior chest, respectively. These correlations were maintained before and after CA. Furthermore, in group A, ARIs in lead V1 tended to increase on day 7 post CA compared with before CA and on day 1. In group B, ARIs in lead III significantly decreased on day 7 compared with before CA and on day 1. These findings suggest that ARIs from the limb leads of 12-lead ECGs may represent those from unipolar leads of a particular area over the body surface, and that ARIs from 12-lead ECGs may provide useful quantitative information on changes in recovery properties before and after CA in patients with manifest WPW syndrome.     

Portal-systemic encephalopathy due to a congenital extrahepatic portosystemic shunt: three cases and literature review

Extrahepatic portal-systemic encephalopathy due to congenital extrahepatic portosystemic shunt has so far been rarely reported in the literature. We herein report 3 such cases without liver cirrhosis or portal hypertension which were presented with the chief complaint being disturbance of consciousness and abnormal behavior. In all cases the brain computed tomography scan revealed no pathological findings, while electroencephalogram showed a diffuse slow activity with triphasic waves. The laboratory data revealed a high serum ammonia level. Percutaneous transhepatic portography demonstrated portosystemic shunts. After these shunts were surgically occluded, the serum ammonia level reached a normal range and encephalopathy disappeared. A liver biopsy also revealed neither fibrosis nor cirrhosis in any of the cases. The 23 previously reported cases are also discussed.     

A case of leukemia of the appendix presenting as acute appendicitis

A 71-year-old man was admitted to our hospital because of right lower abdominal pain. He was suspected of having acute appendicitis and soon after admission, appendectomy was performed. Macroscopically, the appendix was greatly swollen and reddened, but had no abscess. Microscopically, polymorphonuclear leukocytes were not found, but diffuse infiltration of atypical cells was observed. Examination of a bone marrow aspirate revealed 74% blasts that were peroxidase stain positive. We diagnosed acute myelogenous leukemia (FAB classification, M2). He received induction chemotherapy, but died 49 days after admission. Leukemic cell infiltration of the appendix is rare and acute appendicitis as the initial manifestation of leukemia is even rarer.     

Desensitization for sulfasalazine-induced skin rash in a patient with ulcerative colitis

A patient with ulcerative colitis developed a sulfasalazine-induced skin allergy manifested by a urticaria rash. The patient underwent drug desensitization. The first desensitization, done according to Holdsworth's protocol, resulted in eruption with itching at a dose of 800 mg. The second desensitization, with Das's protocol, failed to reintroduce the drug because of urticarial eruptions. The third challenge, with a more gradual increase in sulfasalazine dose than that use in Holdsworth's protocol, successfully desensitized the patient. The relationship between the drug and various adverse reactions is reviewed and the desensitization to sulfasalazine is discussed.     

A case of sarcoidosis manifesting as annular opacities after multiple nodular shadows]

A 40-year old man was admitted to our hospital because nodular shadows in the right upper lung field had shown deterioration on chest radiographs during a regular check-up (Sep. 28, 2000). Transbronchial lung biopsy specimens showed findings compatible with sarcoidosis. During follow-up, the nodular shadows became bigger, spread in both lung fields and turned into multiple annular opacities. In December, lung biopsy specimens obtained by VATS showed central areas of ground-glass attenuation corresponding to areas of alveolar septal inflammation, in contrast to the denser periphery, where polypoid organized granulation tissue in peripheral air spaces predominated. After 2 months, the opacities disappeared without treatment. In our case, the annular opacities on CT corresponded histologically to BOOP. It is interesting to note the relationship between sarcoidosis and BOOP.     

Effects of cholecystokinin and carbachol on membrane fluidity in pancreatic acini

The effects of pancreatic secretagogues on the membrane fluidity of pancreatic acini were investigated using 1-[4-(trimethylammonium)phenyl]-6-phenyl-1,3,5-hexatriene iodide as a probe. Two kinds of pancreatic secretagogues, one category of which induces acute pancreatitis (cholecystokinin and carbachol) and another which does not induce acute pancreatitis (bombesin, CCK-JMV-180, and secretin), as well as lecithin were used to investigate the effect of changes in membrane fluidity of acini. Our study revealed that the membrane fluidity of the pancreatic acini was unaffected by a physiological dose (10^–11 M) of cholecystokinin. However, stimulation with a supramaximal dose of cholecystokinin (10^–8 M) increased membrane fluidity markedly within 20 min. Membrane fluidity increased dose-dependently with increasing CCK stimulation. A supramaximal dose of cholecystokinin also induced bleb formation and increased LDH release. These phenomena were blocked by simultaneous incubation with CR1505 (Loxiglumide), a potent antagonist of peripheral cholecystokinin receptors. A supramaximal dose of carbachol (10^–3 M) also induced increases in the membrane fluidity. Pancreatic secretagogues that do not induce acute pancreatitis did not induce alterations in membrane fluidity. Lecithin increased both membrane fluidity and LDH release. These observations suggest that this increase in membrane fluidity of the pancreatic acini may be related to membrane alteration and to functional damage of the acini. These observation can serve as a window to detect the development of acute pancreatitis at an early stage.This study was supported by Scientific Research grant C-06671267 from the Ministry of Education, Science and Culture, and by a grant from the Ministry of Health and Welfare of Japan.     

Survivin: a novel target for indomethacin-induced gastric injury

BACKGROUND & AIMS: Nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal erosions and ulcers. Apoptosis is one of the mechanisms. The role of survivin, an antiapoptosis protein, in NSAID-induced gastric injury is unknown. We examined the role of survivin in NSAID-induced gastric mucosal and gastric cell injury. METHODS: We examined: (1) the effects of indomethacin (nonselective NSAID), celecoxib and NS-398 (cyclooxygenase [COX]-2-selective NSAIDs), SC-560 (a COX-1-selective NSAID), and SC-560 plus celecoxib on survivin expression and extent of injury in rat gastric mucosa; (2) the effects of indomethacin, NS-398, SC-560, and SC-560 plus NS-398 on survivin expression and injury in gastric epithelial (RGM-1) cells; and (3) the effects of survivin suppression with small interfering RNA (siRNA) on RGM-1 cell integrity at baseline and following indomethacin injury. RESULTS: Indomethacin treatment dose-dependently reduced survivin protein levels and caused severe injury of gastric mucosa and RGM-1 cells. Suppression of survivin expression with siRNA in RGM-1 cells caused cell damage and increased susceptibility to injury by indomethacin. Celecoxib treatment caused exfoliation of the mucosal surface epithelium, but neither caused deep erosions or altered survivin expression. Neither NS-398 nor SC-560 treatment altered survivin levels or produced injury in vivo or in vitro. COX-1 and COX-2 inhibitor combination caused injury in vivo and in vitro but did not decrease survivin expression. CONCLUSIONS: (1) Indomethacin, but not selective COX-1 or COX-2 inhibitors alone or in combination, reduces survivin expression in gastric mucosal cells and (2) significant reduction of survivin precedes greater severity of gastric injury.     

A case report of plasmapheresis in the treatment of acute disseminated encephalomyelitis

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease of the central nervous system associated with significant morbidity and mortality. High-dose corticosteroid administration has been considered the mainstay of treatment for ADEM; however, some patients with ADEM are refractory to steroid therapy. We report a case of a 17-year-old man suffering from ADEM who did not respond to corticosteroid therapy, but who exhibited a dramatic recovery with plasmapheresis. He became comatose, requiring ventilatory support, and exhibited abnormalities of some brainstem reflexes prior to treatment. He underwent sequential courses of plasma exchange therapy for three days. Plasma exchanges were carried out with concomitant continuous hemodiafiltration (CHDF) to control intracranial pressure by stabilizing pH, plasma Na+ concentration, and colloid osmotic pressure. After plasma exchanges, his reflexes and level of consciousness gradually improved. Eleven months after this treatment, he had only minimal neurological deficit that did not interfere with any of his activities of daily living. The efficacy of plasmapheresis for ADEM has not yet been established. Plasmapheresis may be indicated for ADEM, not only for patients with severe disease in whom high-dose corticosteroid treatment has failed, but also as first-line treatment for ADEM. Early initiation of plasmapheresis appears to be associated with moderate to marked improvement. Early recognition and early treatment of ADEM are thus of paramount importance.