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develop in about 10% of patients with 45,XO/46,XY mosaicism; most such tumors are benign
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Bondy CA et al Care of girls and women with Turner syndrome: A guideline of the Turner Syndrome Study Group J Endocrinol Metab 2007 Jan:92(1):10 25 [PMID: 17047017] El-Mansoury M et al Hypothyroidism is common in Turner syndrome: results of a five-year follow-up J Clin Endocrinol Metab 2005 Apr;90(4):2131 5 [PMID: 15623818] Gravholt CH Epidemiological, endocrine and metabolic features of Turner syndrome Eur J Endocrinol 2004 Dec;151 (6):657 87 [PMID: 15588233] Hogler W et al Importance of estrogen on bone health in Turner syndrome: a cross-sectional and longitudinal study using dual-energy X-ray absorptiometry J Clin Endocrinol Metab 2004 Jan;89(1):193 9 [PMID: 14715849] Soriano-Guillen L et al Adult height and pubertal growth in Turner syndrome after treatment with recombinant growth hormone J Clin Endocrinol Metab 2005 Sep;90(9):5197 204 [PMID: 15998771] Sybert VP et al Turner s syndrome N Engl J Med 2004 Sep 16;351(12):1227 38 [PMID: 15371580]
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given on days 1 21 per month When growth stops, HRT is begun with estrogen and progestin; transdermal estrogen may be used to initiate pubertal development Girls and women with Turner syndrome have an increased risk of aortic coarctation (11%) and bicuspid aortic valves (16%); these cardiac abnormalities are more common in patients with webbed necks Bicuspid aortic valves are associated with an increased risk for infective endocarditis, aortic valvular stenosis or insufficiency, and ascending aortic aneurysm and dissection Partial anomolous pulmonary vein connections occur in 13% and can lead to left-to-right shunting of blood Adults with Turner syndrome have a high incidence of ECG abnormalities Women with Turner syndrome have a reduced life expectancy due in part to their increased risk for diabetes mellitus (types 1 and 2), hypertension, dyslipidemia, and osteoporosis Diagnostic vigilance and aggressive treatment of these conditions reduce the risk of aortic aneurysm dissection, ischemic heart disease, stroke, and fracture Patients are prone to keloid formation after surgery or ear piercing Yearly ocular examinations and periodic thyroid evaluations are recommended It is advisable to evaluate all patients with Turner syndrome with an ultrasound, along with MRI examination of the chest and abdomen, looking for cardiac, aortic, and renal abnormalities Patients with the classic 45,XO karyotype have a high risk of renal structural abnormalities, whereas those with 46 X/abnormal X are more prone to malformations of the urinary collecting system Patients with aortic root enlargement are usually treated with -blockade and serial imaging
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Syndromes of MEN are inherited as autosomal dominant traits and cause a predisposition to the development of tumors in different tissues, particularly involving endocrine glands (Table 26 17)
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1 MEN 1 (Wermer s Syndrome) 2 Turner Syndrome Variants
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Patients with small distal short arm deletions of the X chromosome (Xp-) that include the SHOX gene often have short stature and skeletal abnormalities but have a low risk of ovarian failure Transmission of Turner syndrome from mother to daughter can occur There may be an increased risk of trisomy 21 in the conceptuses of women with Turner syndrome Patients with deletions of the long arm of the X chromosome (distal to Xq24) often have amenorrhea without short stature or other features of Turner syndrome Abnormalities or deletions of other genes located on both the long and short arms of the X chromosome can produce gonadal dysgenesis with few other somatic features MEN 1 is a familial autosomal dominant multiglandular syndrome, with a prevalence of 2 10 per 100,000 people The presentation of MEN 1 is quite variable, even in the same kindred Parathyroid, enteropancreatic, and pituitary tumors can be present in one individual, though not necessarily at the same time Nonendocrine tumors also occur, such as subcutaneous lipomas, facial angiofibromas, and collagenomas In some affected individuals, tumors may start developing in childhood, whereas in others, tumors develop late in adult life About 90% of patients with MEN 1 gave germline mutations that are inherited as an autosomal dominant trait Patients with MEN 1 usually have detectable mutations in the 10 exons of the menin gene, located on the long arm of chromosome 11 (11q13) MEN 1 gene testing is available at a few centers and is able to detect the specific mutation in 60 95% of cases If no mutation is detected, genetic linkage analysis can be done if there are several affected members in the kindred Gene testing permits the rest of the kindred to be tested for the specific gene defect and allows informed genetic counseling With close endocrine surveillance of affected individuals, the initial biochemical manifestations (usually hypercalcemia) can often be detected as early as age 14 18 years in patients with a MEN 1 gene mutation, although clinical manifestations do not usually present until the third or fourth decade Hyperparathyroidism is the first clinical manifestation of MEN 1 in two-thirds of affected patients, but it may present at
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