ABSTRACT. Objective. To describe the results of a nationwide epidemiologic survey of Kawasaki disease for the 2-year period 1997 and 1998.Design. We sent a questionnaire to all hospitals with 100 beds or more throughout Japan (2663 hospitals) requesting data on patients with Kawasaki disease. Study items included name, sex, date of birth, date of initial hospital visit, diagnosis, address, recurrence, sibling cases, gammaglobulin treatment, and cardiac lesion in the acute stage or 1 month after onset.Results. Of the 2663 hospitals, 68.5% responded, reporting 12 966 patients-7489 males and 5477 females. Of the total patients reported, 6373 (incidence rate of 108.0 per 100 000 children <5 years old) occurred in 1997, and 6593 (111.7) in 1998. More than one half of the patients (54.9%) were <2 years old and 81.6% were <4 years old. In males, the incidence rates of cardiac lesions were 27.2 in the acute stage and 10.1 a month after onset. In females, the rates were 16.7 and 5.2, respectively. The incidence rates of cardiac lesions were highest in the youngest age group (<6 months old) both in the acute stage and 1 month after onset. The rates decreased with increasing ages. Although frequency of giant aneurysms was not high at the acute stage, it did not decrease 1 month after onset.Conclusion. The incidence rates have been steadily increasing for 11 years since 1987. The rate in 1998 was over 1.5 times higher than that in 1987. The age and sex distributions were identical in each survey. Although most of the cardiac lesions at the acute stage decreased to half or less 1 month after onset, giant aneurysms did not decrease and existed persistently after 1 month. Pediatrics 2001;107(3). URL: http://www.pediatrics.org/ cgi/content/full/107/3/e33; Kawasaki disease, epidemiology, incidence, nationwide survey.
To investigate the incidence of recurrent Kawasaki disease, and to discuss some of the potential risk factors, data of the 13th and 14th nationwide surveys of Kawasaki disease in Japan were analyzed. To calculate the rate of recurrence, 10 679 patients with 31 501.9 person‐years were observed. The mean observation period was 2.95 y. The rate of recurrence was 6.89 per 1000 person‐years, with a high incidence within the 12 mo following the first episode. Conclusion: The incidence was high among those under 3 y of age and those with cardiac sequelae during the first episode. None of the other factors affected the incidence.
Extramedullary plasmacytoma is a rare variant of plasma cell tumor involving organs outside the bone marrow. The vast majority of extramedullary plasmacytomas present as a secondary tumor of systemic myelomatosis of the bone marrow. We experienced a patient with extramedullary plasmacytomas of the head and tail of the pancreas presenting as secondary masses from extramedullary plasmacytoma of the maxillary sinus that had been treated 5 years previously. A 38-year-old Japanese man had undergone radiation therapy for an extramedullary plasmacytoma of the maxillary sinus 5 years before the current presentation. He experienced severe upper abdominal pain in November 1999, when laboratory data showed elevation of the serum amylase level. Computed tomography showed two isodensity masses, in the head and tail of the pancreas. Angiography showed two hypervascular masses, one in the head and the other in the tail of the pancreas, and encasement of the portal vein trunk junction. Laparotomy was performed, with the tentative diagnosis of extramedullary plasmacytoma of the pancreas, in order to obtain a definite diagnosis. Intraoperative biopsy revealed that the two pancreatic masses were extramedullary plasmacytomas. External radiation therapy was performed after the operation. When a pancreatic mass is noticed in patients with a history of plasmacytoma, secondary extramedullary plasmacytoma of the pancreas should be considered as a differential diagnosis.
Vascular factors have been shown to be highly involved in the deposition of the amyloid beta-protein (A beta) in the brain of Alzheimer's disease (AD). However, the detailed mechanism remains unknown. Here, we showed that more numerous deposits of A beta 40 and A beta 42 in the brain were found in AD patients than in controls. Together with evidence of no difference in the level of A beta 40 and A beta 42 in sera between sporadic AD and controls, a certain dysfunction of the blood-brain barrier could induce an abnormal transport of A beta from sera to the parenchyma in AD. In addition, vascular A beta deposits and mature A beta plaques stained by Congo red in AD brains contained more A beta 40 than A beta 42, whereas Congo red-negative immature plaques mainly consisted of A beta 42. Our confocal laser scanning microscopy demonstrated an intimate relationship between A beta 40 and the vascular network. The amount of mature plaques but not that of immature plaques was reportedly correlated with the severity of dementia in AD patients. These results suggest that serum-derived A beta 40 and/or A beta 42 cause A beta 40 deposition in and around blood vessels through unknown but possible mechanisms such as (1) endocytosis of A beta 40, (2) selective transport A beta 40 and A beta 42 into blood vessels and the parenchyma, respectively, and (3) proteolysis of A beta 42 into A beta 40 induced by a putative carboxyl dipeptidase in blood vessels including vascular feet, which is involved in A beta fibrillation and cognitive deterioration in the patients. Therefore, the accumulation of A beta 40 associated with blood vessels may play a critical role in the development of AD.
We have investigated the effects of isoflurane on receptor-operated Ca2+ channels (ROC) in vascular smooth muscle. In isolated rat thoracic aortic rings denuded of endothelium, the effects of isoflurane on phenylephrine-induced contraction and Ca2+ influx were evaluated in the presence of supramaximal doses of nifedipine or verapamil. Under isometric tension recording, the aortic rings were precontracted by phenylephrine 300 nmol litre-1 and exposed to 1.2%, 2.3% or 3.5% isoflurane. Phenylephrine-induced precontraction was enhanced with 2.3% isoflurane by mean 8.1 (SD 9.3)% (P < 0.05 vs 0% isoflurane). The constrictor effect of 2.3% isoflurane was not inhibited by depletion of intracellular Ca2+ stores with ryanodine 20 mumol litre-1, but was abolished in a Ca(2+)-free solution or by SK&F 96,365 30 mumol litre-1, an ROC blocker. Isoflurane-induced contraction was accompanied by increased intracellular free Ca2+ concentration, monitored using fura PE3. Unidirectional 45Ca2+ influx measurement in phenylephrine-stimulated aortic strips revealed that the mean amount of Ca2+ influx was significantly (P < 0.05) enhanced by 1.2% and 2.3% isoflurane, which were 117.1% and 119.7% of control values, respectively. Our results strongly suggest that isoflurane enhanced Ca2+ influx through ROC that had been submaximally activated by phenylephrine.
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