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Background: Deafness is a rare but important complication of mumps virus infection. Its incidence has been estimated at 0.5 to 5.0 per 100,000 cases of mumps, but recent reports from Japan, where mumps is endemic, suggest that the incidence might be higher., Objective: Prospective office-based study to determine the incidence of hearing loss in children with mumps., Methods: Forty pediatric practices participated in this survey. The study population consisted of patients < or =20 years old with mumps seen between January 2004 and December 2006. Clinical diagnosis of mumps was made by experienced pediatricians. Among those from whom written consent was obtained, parents were asked to conduct hearing screening tests by rubbing fingers near the ears twice daily for 2 weeks. Patients suspected with hearing loss were further examined by an otolaryngologist., Results: Among 7400 children who underwent hearing ability assessment after clinical onset of mumps, 7 had confirmed hearing loss; none had been previously vaccinated against mumps. In all cases, hearing loss was unilateral but severe and did not improve over time., Conclusions: The incidence of hearing loss in children due to mumps was 7/7400 (approximately 1/1000 cases), which is higher than previously suggested. Prevention of deafness is another important reason for assuring universal immunization against mumps.

A case of cerebral aspergillosis during induction chemotherapy for acute lymphoblastic leukemia was described. A 5-year-old boy complained of headache and left homonymous hemianopsia during induction chemotherapy for acute lymphoblastic leukemia. CT scan and MR imaging survey demonstrated cerebral fungal lesion as well as multifocal lung lesions. A cerebral lesion appeared as a low density mass in right occipital lobe with marginal enhancement on CT scan, and iso- and high-signal intensity appeared with marginal gadolinium enhancement on T1- and T2-weighted MR imaging. Although fungus balls in the lung responded well to daily intravenous administration of amphotericin-B for 2 months, the cerebral lesion showed a rather expansive character as invading into neighbouring falx, opposite occipital lobe, meninges, and occipital bone. Extensive removal of the brain lesion from the parenchyma, falx, invaded dura, and skull was surgically performed. The lesion was confirmed as aspergillosis by Grocott's methenamine histological stain. Surgical intervention and concomitant use of amphotericin-B for a month resulted in complete remission of the aspergillosis. After 6 years, a cranioplasty was successfully completed for the occipital bone defect.

We investigated liver function in 27 children with acute lymphocytic leukemia (ALL) after cessation of therapy. Induction therapy consisted of prednisolone+vincristine (VP regimen) alone (16 patients) or with addition of daunorubicin (4 patients) or L-asparaginase (7 patients). Patients treated with VP regimen received short courses of VP regimen every 12 weeks for the first year of maintenance. Twenty-five patients remained in first complete remission and had completed 3-year maintenance therapy with methotrexate (MTX) and 6-mercaptopurine (6-MP) 1-7 years prior to this study. Twenty-three patients had received transfusions of packed red blood cells or fresh whole blood (1-11 units; median: 2 units) but none had evidence of either hepatitis B or hepatitis C. Alanine aminotransferase (ALT), which was measured every 3 months during maintenance therapy, had values more than three times the upper limit of the normal range in 25% of the measurements in more than half of the patients. However, by 3 months after the completion of maintenance therapy, ALT had normalized in all patients and remained normal in all but two patients until the time of this study. Serum bilirubin, serum albumin, and prothrombin time were all within normal limits. Fasting and 2-hour postprandial total serum bile acids were high in 5 of 13 patients and in 6 of 13 patients, respectively. The ratio of cholic acids+deoxycholic acids to chenodeoxycholic acids+lithocholic acids was below 1 in all but two patients, whereas this ratio was above 1 in all controls. Our bile acid profile results indicate the necessity of careful long-term follow-up of survivors of ALL treated with hepatotoxic chemotherapy during childhood.

An ultrastructural study of four cases of acute nonlymphocytic leukemia with abnormal nuclear lobulation was done. These cases were classified as M3 (Case 1), M3 variant (Cases 2 and 3), and M5, differentiated type (Case 4), on the basis of light microscopy according to the FAB classification. Ultrastructural observation of the leukemic cells of Cases 2 and 3 showed large bundles of fibrils in addition to abnormalities in the endoplasmic reticulum and granules, as had been reported in cases of acute promyelocytic leukemia. Large bundles of fibrils and abnormal nuclear lobulation also seemed to be characteristic of the M3 variant. However, the relationship between these structures was not identified. The exact nature of nuclear lobulation is not known, but seems to be related to some kind of intrinsic force and may be a presentation of the premature occurrence of lobulation intrinsic to the granulocyte or monocyte nucleus.

Cytological examination of the cerebrospinal fluid (CSF) was performed in 88 children with acute lymphocytic leukemia at the time of initial diagnosis (54 cases), during (day 1-15, 17 cases) or after (day 37-58, 17 cases) the remission induction chemotherapy. Leukemic cells were found on cytological examination in 23 cases (42.6%), 5 cases (29.4%) and 2 cases (11.8%), respectively, and the incidence of central nervous system (CNS) leukemia had a tendency to decrease during the induction chemotherapy. The follow-up study of 15 cases of CNS leukemia at diagnosis revealed that the leukemic cells in CSF had decreased within 2 weeks and then disappeared after the induction chemotherapy. These findings indicate the therapeutic effect of induction chemotherapy including prednisolone on subclinical CNS leukemia at diagnosis.

Six children with refractory acute lymphocytic leukemia were treated with vincristine combined with diltiazem. In four of five children who took the drug as scheduled, a cytolytic effect was observed. One child showed massive cell destruction which caused hyperuricemic nephropathy. The only adverse effect was atrioventricular block in two children, which was completely reversible. Increased neurotoxicity was not observed in any child.

Ten children with advanced neuroblastoma were treated with regimens containing cis-dichlorodiammineplatinum (CDDP-regimens). Six cases had been refractory or had evidenced inadequate response to previous chemotherapy consisting of cyclophosphamide and adriamycin or vincristine, and radiotherapy. Clinical response was evaluable for 9 cases. Complete response was obtained in 2 cases, partial response in 2 cases, minor response in 2 cases, no change in 1 case and progressive disease in 2 cases. Six of these 9 cases had 2nd look surgery after several CDDP-regimens. Complete resection of tumor was possible in 1 case, subtotal resection in 4 cases and partial resection in 1 case. In an additional case whose clinical response was impossible because of absence of palpable tumor, the tumor had completely disappeared by the time of surgery. Three cases have survived for 5 months, 5 months and 28 months respectively without clinical evidence of tumor, 2 cases for 9 months and 12 months, respectively, with tumor. Four cases died of progressive tumor growth at 9 months, 10 months, 10 months, and 59 months, respectively. One case died of pneumonia at 10 months without clinical evidence of tumor. These results are far better than in our previous experience. Nephrotoxicity was observed in all cases, but it was tolerable in all cases including 3 heminephrectomized children. Hypomagnesemic, hypocalemic tetany was observed in 1 case. This complication was ameliorated by administration of magnesium gluconate. Mean +/- standard deviation of the lowest serum concentration of calcium and magnesium during this medication was 9.75 +/- 0.76 mg/dl and 1.39 +/- 0.44 mg/dl, respectively, against 7.56 +/- 1.64 mg/dl and 0.90 +/- 0.29 mg/dl without the medication, respectively. CDDP is concluded to be against neuroblastoma and its toxicity is tolerable. Magnesium gluconate administration is essential for prevention of tetany.