Inner ear function following underlay myringoplasty.

INTRODUCTION: Inner ear function can be modified by middle ear surgery. OBJECTIVES: This study aimed to describe bone threshold conduction changes after myringoplasty. DESIGN: Prospective study. MATERIALS AND METHODS: Determination of preoperative and 6- to 12-month postoperative bone conduction thresholds for patients consecutively treated by primary underlay myringoplasty. RESULTS: The mean bone conduction threshold improvement was 1 +/- 6 dB (p = 0.006). There were significant differences in bone conduction threshold changes by surgical approach and for patients with tympanosclerosis. There were no 'dead ears' following intervention, and only a 1% risk of impairment. CONCLUSIONS: Anatomically successful myringoplasty can partially improve bone conduction with minimal risk of impairment.

[Insulin edema in patients with diabetes mellitus and recent diabetic ketoacidosis (epidemiology and case reports)]. / Insulinovyi otek u bol'nykh sakharnym diabetom, nedavno perenesshikh diabeticheskii ketoatsidoz (épidemiologicheskie dannye i klinicheskie varianty).

Insulin edema (IE) has been known for a long time as one of complications caused by insulin therapy, but even today its pathogenesis stays unclear, and epidemiology unknown. IE incidence in patients over 15 years of age receiving treatment in the year 2003 for diabetic ketoacidosis (DKA) in the city of Donetsk (adult population 858200) has been retrospectively studied according to clinical archives and national diabetics register data. Presented are three own observations on the development of IE after DKA treatment. 13 (17%) out of 76 DKA patients had IE. Keeping in mind reoccurring DKA incidents--16%. During IE the known duration of Diabetes Mellitus came out to be 5 years on average, and did not differ from insulin therapy duration, whereas the Diabetes Mellitus duration in non DKA group without edemas exceeded the continuance of insulin treatment by over two years (P < 0.05).

Adult-onset nesidioblastosis causing hypoglycemia: an important clinical entity and continuing treatment dilemma.

HYPOTHESIS: Nesidioblastosis is an important cause of adult hyperinsulinemic hypoglycemia, and control of this disorder can often be obtained with a 70% distal pancreatectomy. DESIGN: The records of all adult patients operated on for hypoglycemia between 1974 and 1999 were reviewed retrospectively. Patients with the pathologic diagnosis of nesidioblastosis were contacted for follow-up (1.5-21 years) and are presented. Patients' results were compared with those of 36 other individuals with this disorder who were previously reported in the literature. SETTING: The University of Chicago Medical Center (Chicago, Ill), a tertiary care facility. PATIENTS: A consecutive sample of all patients operated on for hypoglycemia. INTERVENTIONS: Seventy percent distal pancreatectomy for all patients with nesidioblastosis, and maintenance therapy with verapamil hydrochloride for 2 patients. MAIN OUTCOME MEASURES: Achievement of normoglycemia with and without medication, development of insulin-dependent diabetes mellitus, pancreatic exocrine insufficiency, and need for reoperation. RESULTS: Of 32 adult patients who underwent surgical exploration for hyperinsulinemic hypoglycemia at our institution, 27 (84%) were found to have 1 or more insulinomas, and 5 (16%) were diagnosed with nesidioblastosis. Each patient with nesidioblastosis underwent a 70% distal pancreatectomy. Follow-up duration for the 5 patients ranged from 1.5 to 21 years, with 3 patients (60%) asymptomatic and taking no medications, and 2 patients (40%) experiencing some recurrences of hypoglycemia. The 2 patients with recurrences are now successfully treated with a calcium channel blocker, an approach, to our knowledge, never before reported for adult-onset nesidioblastosis. CONCLUSIONS: Nesidioblastosis is an uncommon but clinically important cause of hypoglycemia in the adult population, and must always be considered in a patient with a presumptive preoperative diagnosis of insulinoma. This study indicates that a 70% distal pancreatectomy is often successful in controlling hypoglycemia, and rarely results in diabetes mellitus. However, the optimal treatment of this disorder remains to be determined.

Carcinogenicity of diethylnitrosamine in newborn, infant, and adult mice.

Modifying effects of age, sex, and mouse strain on diethylnitrosamine (DEN) carcinogenesis have been investigated in C57BL/6Jx C3HeB/FeJ F1 (B6C3F1) and C3HeB/FeJxA/J F1 (C3AF1) hybrid mice. Animals each received four IP injections of 1.5 or 3.0 micrograms DEN/g body weight. The first injections were administered on days 1, 15, or 42 of life. Subsequent treatments were delivered at 3-, 6-, and 6-day intervals, respectively. Mice were kept under observation for the remaining life-span. DEN treatment induced tumors in liver, lungs, and forestomach in descending order of frequency. The majority of the induced liver tumors were hepatocellular carcinomas. Animals treated as newborns and infants developed significantly more liver tumors than animals that were treated as young adults. Newborn and infant females developed liver tumors at a later age (B6C3F1) and with a lower incidence (C3AF1) than similarly treated males. The B6C3F1 mice developed more hepatocellular carcinomas and a higher rate of pulmonary metastases than the C3AF1 mice. In contrast, C3AF1 mice developed lung tumors with a higher incidence and multiplicity than B6C3F1 hybrids. Forestomach tumors were observed also with a slightly but significantly higher incidence in C3AF1 mice.

Prenatal multicarcinogenesis by ethylnitrosourea in mice.

The Role of prenatal age, sex, and the maternal background upon the incidence, multiplicity, and spectrum of tumors induced by ethylnitrosourea has been studied in the offspring of reciprocal hybrids of the same genotype. The first generation (F1) offspring of C57BL/6J X C3HeB/FeJ and the reciprocal hybrids were observed throughout their life-span for tumor development following single i.p. injections of ethylnitrosourea (60 microng/g) given to pregnant mothers at 12, 14, 16, or 18 days of gestation. Animals exposed to ethylnitrosourea survived on the average for only 90 weeks. They developed by that age tumors in lungs, livers, ovaries, nervous system, and forestomach. Control mice killed at 90 weeks were essentially free of tumors. The fetal age at the time of administration of the carcinogen was one of the most significant modulators of tumor development in lung, liver, ovaries, and nervous system. The sex of the animals influenced the rate of development of liver tumors, whereas maternal background affected the multiplicity of lung tumors.