Akira Hokama

Pili of an Aeromonas hydrophila Strain as a Possible Colonization Factor

Aeromonas hydrophila Ae6 had 2 morphologically distinctive kinds of pili. One appeared rigid and straight with a diameter of 9 nm (R‐pili). The other appeared wavy and flexible with a diameter of 7 nm (W‐pili). W‐pili were very few on the cell as compared with R‐pili. In this study, W‐pili were purified and characterized. The pili consisted of a subunit protein with a molecular weight of 21 kDa as estimated by SDS‐PAGE. There was no immunological cross‐reaction between W‐pili and other cellular components. The strain Ae6 and its purified W‐pili adhered to human and rabbit intestine and agglutinated human and rabbit erythrocytes. Organisms pretreated with the Fab fraction of anti‐pilus antibody failed to adhere to the intestine. Pretreatment of intestine with purified W‐pili blocked adherence of the organisms to the intestine. These results suggest that the W‐pili are the colonization factor of A. hydrophila Ae6.

Esophagitis dissecans superficialis and autoimmune bullous dermatoses: A review

Esophagitis dissecans superficialis (EDS) is a rare and severe endoscopic finding characterized by sloughing of large fragments of esophageal mucosal lining. Although EDS has been reported in association with serious illnesses and certain medications, the pathophysiological association of autoimmune bullous dermatoses with EDS has gained remarkable attention. Among these dermatoses, pemphigus vulgaris and pemphigoid frequently present with various types of esophageal involvement including EDS. We review the pathophysiology and clinical features of this involvement with the presentation of our experiences. The importance of endoscopic evaluation of this entity is discussed.

Alcoholic liver cirrhosis complicated with torsade de pointes during plasma exchange and hemodiafiltration

A 36-year-old man with severe alcoholic hepatitis was treated with plasma exchange combined with hemodiafiltration to remove endotoxins and inflammatory cytokines. During the treatment, he had critical arrhythmia (torsade de pointes [TdP]). His laboratory data showed hypomagnesemia, which was suspected to be responsible for the development of TdP. Patients with alcoholic liver disease tend to have hypomagnesemia and Q-T interval prolongation. Furthermore, hemodiafiltration may cause hypomagnesemia. Careful observation for electrolytic imbalance is necessary when clinicians treat patients with alcoholic liver failure with a liver support system.

Characterization of Aeromonas sobria TAP13 pili: A possible new colonization factor

Pili of Aeromonas sobria TAP13 were purified and characterized. The molecular mass of the pilin was estimated to be about 23 kDa by SDS-PAGE. The TAP13 pili were immunologically different from A. sobria Ae1 pili and A. hydrophila Ae6 W pili as previously reported, nevertheless all three had indistinguishable morphology and shared a high degree of homology in their N-terminal amino acid sequences. Strain TAP13 and its purified pili did not agglutinate human, rabbit or sheep erythrocytes. However, they adhered to rabbit intestine. Organisms pretreated with the Fab fraction of an antipilus antibody failed to adhere to rabbit intestine, and organisms did not adhere to intestine pretreated with purified pili. These results suggest that the pili are a colonization factor of A. sobria TAP13 for the rabbit intestine.

Endoscopic and radiographic features of gastrointestinal involvement in vasculitis

Vasculitis is an inflammation of vessel walls, followed by alteration of the blood flow and damage to the dependent organ. Vasculitis can cause local or diffuse pathologic changes in the gastrointestinal (GI) tract. The variety of GI lesions includes ulcer, submucosal edema, hemorrhage, paralytic ileus, mesenteric ischemia, bowel obstruction, and life-threatening perforation.The endoscopic and radiographic features of GI involvement in vasculitisare reviewed with the emphasis on small-vessel vasculitis by presenting our typical cases, including Churg-Strauss syndrome, Henoch-Schönlein purpura, systemic lupus erythematosus, and Behçets disease. Important endoscopic features are ischemic enterocolitis and ulcer. Characteristic computed tomographic findings include bowel wall thickening with the target sign and engorgement of mesenteric vessels with comb sign. Knowledge of endoscopic and radiographic GI manifestations can help make an early diagnosis and establish treatment strategy.

Endoscopic and histopathological features of gastrointestinal amyloidosis

Amyloidosis is a rare disorder, characterized by the extracellular deposition of an abnormal fibrillar protein, which disrupts tissue structure and function. Amyloidosis can be acquired or hereditary, and systemic or localized to a single organ, such as the gastrointestinal (GI) tract. Clinical manifestations may vary from asymptomatic to fatal forms. Primary amyloidosis (monoclonal immunoglobulin light chains, AL) is the most common form of amyloidosis. AL amyloidosis has been associated with plasma cell dyscrasias, such as, multiple myeloma. Secondary amyloidosis is caused by the deposition of fragments of the circulating acute-phase reactant, serum amyloid A protein (SAA). Common causes of AA amyloidosis are chronic inflammatory disorders. Although GI symptoms are usually nonspecific, histopathological patterns of amyloid deposition are associated with clinical and endoscopic features. Amyloid deposition in the muscularis mucosae, submucosa, and muscularis propria has been dominant in AL amyloidosis, leading to polypoid protrusions and thickening of the valvulae conniventes, whereas granular amyloid deposition mainly in the propria mucosae has been related to AA amyloidosis, resulting in the fine granular appearance, mucosal friability, and erosions. As a result, AL amyloidosis usually presents with constipation, mechanical obstruction, or chronic intestinal pseudo-obstruction while AA amyloidosis presents with diarrhea and malabsorption Amyloidotic GI symptoms are mostly refractory and have a negative impact on quality of life and survival. Diagnosing GI amyloidosis requires high suspicion of evaluating endoscopists. Because of the absence of specific treatments for reducing the abundance of the amyloidogenic precursor protein, we should be aware of certain associations between patterns of amyloid deposition and clinical and endoscopic features.

Tissue necrosis caused by extravasated propofol.

To the editor: Clinical reports and animal studies have shown that extravasated propofol causes no serious sequelae [1–3]. However, we experienced a case in which accidentally extravasated propofol is likely to have caused necrosis of the forearm skin and muscle. A 37-year-old undernourished man with a history of alcohol abuse underwent an emergency operation (resection of the stomach and drainage of the abdominal cavity) for panperitonitis due to perforation of a gastric ulcer. Eleven days later, a reoperation was performed to stop the leakage in a lesion at the anastomosis of the stomach to the small intestine. After reoperation, the patient fell into septic shock, and continuous arteriovenous hemodialysis was instituted for acute renal failure. The patient was managed with a ventilator in the intensive care unit, and, for sedation, propofol (Diprivan) was administered continuously into the superficial vein on the palmar side of the right forearm through a 22-gauge cannula with 5% glucose solution. The amount of propofol administered ranged from 100 to 200 mg·h 1 (1.8–3.6mg·kg 1·h 1). No other medication was administered into this line. After 8 days of continuous infusion of propofol, phlebitis and swelling of the forearm were observed in the vein where propofol was administered. Because an extravasation of propofol was suspected, the venous line was removed. Propofol had been infused for approximately 12h at a rate of 150mg·h 1 (2.7 mg·kg 1·h 1) until the accidental extravasation of propofol became evident. Necrosis developed in the skin and muscle of the forearm (Fig. 1). The necrotic lesion was limited to the perivascular area. Although granulation at the margin of the necrotic lesion had been recognized 2 weeks later, the tissue under the necrosis had not recovered, and a skin defect ultimately remained. Three months after the onset of septic shock, the patient died from multiple organ failure. Although there have been several reports of extravasated propofol, this is the first report of a case in which extravasated propofol caused tissue necrosis. Propofol has been recognized to be a less invasive drug, because of its chemical properties, isotonicity, and neutral pH [4]. In previous reports of accidental extravasation [1,2] and intra-arterial injection [5–7] of propofol, propofol was harmless and did not induce any serious tissue damage. In this case, however, we could not find any cause of the tissue necrosis other than extravasated propofol. Although the general condition of this patient, including undernutrition and septic shock, was an important factor for skin necrosis by extravasation of propofol, we should be aware that extravasation of propofol can cause tissue necrosis.

Purification and characterization of Aeromonas sobria Ae24 pili: a possible new colonization factor

Pili of Aeromonas sobria Ae24 were purified and characterized. The molecular mass of the pilin was estimated to be about 19 kDa by SDS-PAGE. The Ae24 pili were electrophoretically distinguishable from previously reported Aeromonas hydrophila Ae6 W pili and A. sobria Ae1 pili, although all three had indistinguishable morphology and shared a high degree of homology in the N-terminal amino acid sequences. Strain Ae24 and its purified pili adhered to rabbit intestine and agglutinated human and rabbit erythrocytes. Hemagglutination was inhibited by D-galactose and D-mannose, but not by L-fucose. Organisms pretreated with Fab fraction of the antipilus antibody failed to adhere to the intestine. Organisms did not adhere to intestine pretreated with the purified pili. These findings suggest that the pili are a colonization factor of A. sobria Ae24 for the rabbit intestine, and that the receptor is galactose- and mannose-containing structure.

Fucoidan enhances intestinal barrier function by upregulating the expression of claudin-1

AIM To evaluate the protective effects of fucoidan on oxidative stress-induced barrier disruption in human intestinal epithelial cells. METHODS In Caco-2 cell monolayer models, the disruption of barrier function by oxidative stress is mediated by H₂O₂. The integrity of polarized Caco-2 cell monolayers was determined by measuring the transepithelial resistance (TER) and permeability was estimated by measuring the paracellular transport of FITC-labeled 4-kDa dextran (FD4). The protective effects of fucoidan on epithelial barrier functions on polarized Caco-2 cell monolayers were evaluated by TER and FD4 flux. The expression of tight junction (TJ) proteins was assessed using reverse-transcription polymerase chain reaction (RT-PCR) and immunofluorescence staining. RESULTS Without H₂O₂ treatment, fucoidan significantly increased the TER compared to control (P < 0.05), indicating a direct enhancement of intestinal epithelial barrier function. Next, H₂O₂ disrupted the epithelial barrier function in a time-dependent manner. Fucoidan prevented the H₂O₂-induced destruction in a dose-dependent manner. Fucoidan significantly decreased H₂O₂-induced FD4 flux (P < 0.01), indicating the prevention of disruption in paracellular permeability. RT-PCR showed that Caco-2 cells endogenously expressed claudin-1 and -2, and occludin and that H₂O₂ reduced the mRNA expression of these TJ proteins. Treatment with fucoidan attenuated the reduction in the expressions of claudin-1 and claudin-2 but not occludin. Immunofluorescence staining revealed that the expression of claudin-1 was intact and high on the cell surface. H₂O₂ disrupted the integrity of claudin-1. Treatment with fucoidan dramatically attenuated the expression of claudin-1. CONCLUSION Fucoidan enhanced intestinal epithelial barrier function by upregulating the expression of claudin-1. Thus, fucoidan may be an appropriate therapy for the treatment of inflammatory bowel diseases.

A patient with primary biliary cirrhosis associated with autoimmune hemolytic anemia.

Abstract: Primary biliary cirrhosis is often associated with autoimmune conditions, such as thyroid disease, sicca complex, and rheumatoid arthritis. However, an association with autoimmune hemolytic anemia has rarely been reported. We present a case of primary biliary cirrhosis associated with warm type autoimmune hemolytic anemia, and we review prior reports.