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11/487. Near-normal linear growth in the setting of markedly reduced growth hormone and IGF-1. A case report.

    A 14.2-year-old prepubertal boy diagnosed with complete-type growth hormone deficiency and tertiary hypothyroidism, keeps growing in the height range between -1 and -2 SD. He has been treated with levothyroxine only. To understand the growth mechanism of this boy, we analyzed the serum growth hormone (GH) with a radioimmunoassay (RIA), serum GH bioactivity with Nb2 and erythroid progenitor cell bioassays, and growth hormone-binding protein (GHBP) with a ligand-mediated immunofunctional assay (LIFA). In addition, IGF-1 and free IGF-1 were analyzed by immunoradiometric assay (IRMA) and insulin-like growth factor-binding protein-3 (IGFBP-3) by Western immunoblot. Peak GH-RIA responses to insulin, arginine and GH-releasing factor, and nocturnal GH secretion, were low (0.5-2.3 ng/ml); bioactive GH was low (0.313 ng/ml), and GHBP was elevated (84 ng/ml). The serum levels of IGF-1 and free IGF-1 were continuously low, 17.1-39.3 and 0.17-0.26 ng/ml, respectively. Moreover, serum IGFBP-3 levels were low (1.68- 1.39 mg/l) and IGFBP-3 protease activity was negative. prolactin and insulin were in the normal range. The result of the assay for growth-promoting activity showed that the patient's serum stimulated normal erythroid progenitor cells twice as potently as did healthy thin adult control serum. These results suggest that GH and IGF-1 are not indispensable for maintaining physical growth in this boy. Thus, it appears that circulating GH and IGF-1 are not mandatory requirements for maintaining normal physical growth, and other, as yet uncharacterized, pathways or growth factors might be sufficiently compensatory under certain conditions. ( info)

12/487. A previously unrecognised phenotype characterised by obesity, muscular hypotonia, and ability to speak in patients with angelman syndrome caused by an imprinting defect.

    The clinical features of angelman syndrome (AS) comprise severe mental retardation, postnatal microcephaly, macrostomia and prognathia, absence of speech, ataxia, and a happy disposition. We report on seven patients who lack most of these features, but presented with obesity, muscular hypotonia and mild mental retardation. Based on the latter findings, the patients were initially suspected of having prader-willi syndrome. dna methylation analysis of SNRPN and D15S63, however, revealed an AS pattern, ie the maternal band was faint or absent. Cytogenetic studies and microsatellite analysis demonstrated apparently normal chromosomes 15 of biparental inheritance. We conclude that these patients have an imprinting defect and a previously unrecognised form of AS. The mild phenotype may be explained by an incomplete imprinting defect or by cellular mosaicism. ( info)

13/487. The thyroid hormone receptor-beta gene mutation R383H is associated with isolated central resistance to thyroid hormone.

    Resistance to thyroid hormone (RTH) action is due to mutations in the beta-isoform of the thyroid hormone receptor (TR-beta). RTH patients display inappropriate central secretion of TRH from the hypothalamus and of TSH from the anterior pituitary despite elevated levels of thyroid hormone (T4 and T3). RTH mutations cluster in three hot spots in the C-terminal portion of the TR-beta. Most individuals with TR-beta mutations have generalized resistance to thyroid hormone, where most tissues in the body are hyporesponsive to thyroid hormone. The affected individuals are clinically euthyroid or even hypothyroid depending on the severity of the mutation. Whether TR-beta mutations cause a selective form of RTH that only leads to central thyroid hormone resistance is debated. Here, we describe an individual with striking peripheral sensitivity to graded T3 administration. The subject was enrolled in a protocol in which she received three escalating T3 doses over a 13-day period. indexes of central and peripheral thyroid hormone action were measured at baseline and at each T3 dose. Although the patient's resting pulse rose only 11% in response to T3, her serum ferritin, alanine aminotransferase, aspartate transaminase, and lactate dehydrogenase rose 320%, 117%, 121%, and 30%, respectively. In addition, her serum cholesterol, creatinine phosphokinase, and deep tendon reflex relaxation time fell (25%, 36%, and 36%, respectively). Centrally, the patient was sufficiently resistant to T3 that her serum TSH was not suppressed with 200 microg T3, orally, daily for 4 days. The patient's C-terminal TR exons were sequenced revealing the mutation R383H in a region not otherwise known to harbor TR-beta mutations. Our clinical evaluation presented here represents the most thorough documentation to date of the central thyroid hormone resistance phenotype in an individual with an identified TR-beta mutation. ( info)

14/487. Access to TV contingent on physical activity: effects on reducing TV-viewing and body-weight.

    One child was recruited for a study assessing the effectiveness of a device aimed at reducing excessive television viewing and increasing exercising. The device was comprised of a control box which attaches to the electrical cord of a television set, and two sensors which attached to the wheel and corresponding wheel rim of a stationary bicycle. The child in this study was watching an excessive amount of TV (averaging over 4 hours per day), and she had a weight problem. An ABAB design was used in the study. After collecting baseline data, the child was required to ride a bicycle for 60 minutes to watch 60 minutes of TV, and this program successfully reduced TV viewing. Reductions in TV viewing and weight loss were found at a follow-up. ( info)

15/487. Short stature, myopia, severe developmental delay, and peculiar facial appearance in two brothers: a new syndrome?

    We report on 2 brothers with short stature, microcephaly, myopia, retarded osseous maturation, severe developmental delay, and minor anomalies including temporal narrowing, periorbital fullness, full cheeks in infancy, and protruding lower lip. Both brothers and their parents had normal chromosomes. fluorescence in situ hybridization with probes from all (sub-)telomeric chromosomal regions excluded a structural rearrangement involving telomeric segments. Because the pattern of congenital abnormalities is not like that of any well-known multiple congenital anomaly/mental retardation syndrome, we suggest a previously undescribed syndrome of autosomal recessive or X-linked inheritance. ( info)

16/487. Severe symptoms following a massive intentional L-thyroxine ingestion.

    L-thyroxine (T4) is commonly prescribed medication for hypothyroidism in humans and animals. Overdose has generally resulted in limited symptomatology managed with sedatives and beta-adrenergic receptor antagonists. We describe the largest acute T4 ingestion ever reported, which resulted in a profound thyrotoxicosis, resistant to treatment. A 34-y-old man ingested 900 (0.8 mg) tablets of veterinary T4 (720 mg) and was given 60 g of activated charcoal. He became lethargic on post-ingestion days 2 and 3; had vomiting, diaphoresis and insomnia on day 4; on day 5 he "looked like he had too much coffee", began "using a lot of words" and became agitated, assaultive and stopped speaking intelligibly; and on day 6 returned to the hospital combative and confused. He was diaphoretic, mydriatic, hyperreflexic, tremulous, with clear lungs and active bowel sounds, and received activated charcoal, haloperidol, diazepam, and phenobarbital, and was tracheally intubated. During hospitalization he was rehydrated, treated with propranolol and diazepam, but remained continuously tachycardic. On day 12 he became afebrile and his tachycardia resolved. Free T4 levels ranged from > 13 mcg/dL on day 6 to 1.2 mcg/dL on day 12. By discharge (day 15) he had lost 20 kilograms of body weight, but was clinically euthyroid 2 w later. This case suggests that large intentional T4 ingestions should be managed differently than current T4 overdose protocol. ( info)

17/487. A case of huge ovarian cyst of 21-year-old young woman.

    Huge ovarian tumors are rarely seen in modern surgical practice. As health care education and access to hospitals have improved over the past 30 years, the number of these reports have become almost negligible. However, these huge ovarian tumors still present many challenge, even life-threatening risks due to severe cardiovascular, pulmonary, and circulatory problems, including technical difficulties of surgery, massive hemorrhage, and postoperative complications. A knowledge of the deranged physiology and its management may avert these complications. We present the case of a 21-year-old woman with huge ovarian tumor. The total weight of the tumor was 136 pounds (62 kg). She was treated surgically with good results. ( info)

18/487. empty sella syndrome: does it exist in children?

    OBJECT: The empty sella syndrome (ESS) is well documented in adults, and although the same phenomenon of herniation of the arachnoid space into the enlarged sella turcica has been noted in children, it is not widely known that children suffer from this syndrome. Therefore, the aims of this paper are to increase neurosurgeons' awareness of the existence of this phenomenon in children and to add to the scant body of literature on the subject. methods: The authors treated 12 children, ranging in age between 2 and 8 years, in whom neuroradiological studies demonstrated an enlarged sella turcica filled with cerebrospinal fluid and herniation of suprasellar and arachnoid spaces. The causes of ESS in these children were high intracranial pressure, neglected or improperly treated hydrocephalus, and suprasellar arachnoid cyst. Primary ESS was found as well. Most of the children presented with headache, abnormal body weight (the majority being underweight), and short stature. The results of hormone assays were normal in all children. CONCLUSIONS: If undiagnosed and untreated, ESS in children may lead to serious consequences, including impairment of pituitary and hypothalamic function and damage to the optic chiasm. It is important to raise awareness in the neurosurgical community about the existence of ESS in children so that it can be diagnosed and treated at an early stage. A classification system for the diaphragma sellae is recapitulated. ( info)

19/487. Endocrine effects of lithium carbonate in healthy premenopausal women: relationship with body weight regulation.

    The mechanisms involved in Li-induced weight gain remain unclear. The higher frequency of obesity in women than in men under Li treatment, suggests a role for reproductive hormones. The serum levels of the following hormones were evaluated in healthy young women at diverse stages of a control menstrual cycle, and during Li carbonate (900 mg/day) or placebo administration: prolactin, luteinizing hormone, follicle-stimulating hormone, 17-1 estradiol, progesterone, thyroxine, thyrotropin, cortisol, dehidroepiandrosterone sulfate, free testosterone, leptin and an oral glucose tolerance test, in order to measure the areas under the glucose and insulin curve. The body weight was assessed the day before and the last day of treatment. The Li serum levels 15 hours after the last dose were 0.31 /- 0.1 mEq/L. No significant changes in body weight and in the normal fluctuations of the reproductive hormones along the menstrual cycle were observed during Li administration. An increase in the serum levels of thyrotropic hormone ( p = 0.0001) was the only significant effect of Li, which may predispose to excessive weight gain after prolonged administration of the cation. The remarkable lack of effects of Li on these hormones, question the pertinence of studies conducted in healthy volunteers for the comprehension of the obesity observed in psychiatric patients who may be particularly prone to gain weight under prolonged treatment with high dose of Li. ( info)

20/487. A trial to determine the risk of decompression sickness after a 40 feet of sea water for 200 minute no-stop air dive.

    BACKGROUND: The USN93 probabilistic model of decompression sickness (DCS) predicts a DCS risk of 3.9% after a 40 ft of seawater (fsw) for 200 min no-stop air dive, although little data is available to evaluate the accuracy of this prediction. Based on an analysis of Navy safety Center data from diving on U.S. Navy standard air decompression tables, the observed incidence of DCS for this type of dive is 0.11%. Knowing the true incidence of the dive is important for deciding whether or not to adopt proposed probability based decompression procedures for U.S. Navy diving. HYPOTHESIS: The risk of DCS after a 40 fsw for 200 min no-stop air dive is 3.9%. methods: We conducted a closed sequential trial to determine the DCS incidence on this dive. RESULTS: Of 30 military divers who completed 91 dives, there were 2 cases of DCS (2.2%, 95% CI: 0.27 7.7%). The study was terminated early after the second DCS case because of the presence of neurological symptoms and signs. CONCLUSIONS: This study demonstrates that the incidence of DCS in a laboratory setting is higher than observed in fleet diving. Use of the 40 fsw for 200 min schedule in a decompression computer is likely to result in DCS incidence 2.5- to 70-fold greater than that observed in U.S. Navy diving using table-based procedures. ( info)
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