Gene/Protein Disease Symptom Drug Enzyme Compound
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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anabolic-androgenic steroids (AAS) are used as ergogenic aids by athletes and non-athletes to enhance performance by augmenting muscular development and strength. AAS administration is often associated with various adverse effects that are generally dose related. High and multi-doses of AAS used for athletic enhancement can lead to serious and irreversible organ damage. Among the most common adverse effects of AAS are some degree of reduced fertility and gynecomastia in males and masculinization in women and children. Other adverse effects include hypertension and atherosclerosis, blood clotting, jaundice, hepatic neoplasms and carcinoma, tendon damage, psychiatric and behavioral disorders. More specifically, this article reviews the reproductive, hepatic, cardiovascular, hematological, cerebrovascular, musculoskeletal, endocrine, renal, immunologic and psychologic effects. Drug-prevention counseling to athletes is highlighted and the use of anabolic steroids is must be avoided, emphasizing that sports goals may be met within the framework of honest competition, free of doping substances.
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PMID:Adverse effects of anabolic steroids in athletes. A constant threat. 1600 68

The objective of this article is to relate the diagnostic and clinical evolution of a 15 year old patient with a congenital adrenal steroidogenesis dysfunction that can present as hypertension diagnosed later in life (adolescence), virilization or salt wasting (birth and childhood).
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PMID:[Congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency]. 1642 3

A 50-year-old woman, who presented with progressive androgenization, central obesity and severe hypertension, was initially suspected to have an adrenal virilizing tumor. Her serum testosterone level was in the male range (9.3-11.6 ng/ml) and was not suppressed with dexamethasone. Although no pathological abdominal or pelvic mass was detected, total hysterectomy and bilateral salpingo-oophorectomy was performed. Histopathological examination revealed a theca-cell tumor of the right ovary. Postoperatively the testosterone level returned to normal and the patient had regression of virilism. Our case illustrates that a virilizing ovarian tumor can be small and elude imaging studies, but may be detected by means of well-considered clinical management.
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PMID:Ovarian thecoma with androgenic manifestations in a postmenopausal woman. 1686 53

A retrospective study was performed on all patients with congenital adrenal hyperplasia (CAH) who were followed up at the King Hussein Medical Center (KHMC), Amman, Jordan, during the period from January 1996 to June 2006. The aim was to evaluate the clinical features, special problems, and corrective interventions for these patients. The records of 73 children (39 were genetic females and 34 were genetic males) with CAH were reviewed in the study. The age of the patients at last follow-up was between five months and 18 years. Diagnostic criteria for CAH were typical clinical features of the illness (salt loss, dehydration, virilization, macrogenitosomia, ambiguous genitalia, and accelerated growth) and typical hormonal abnormalities (decreased serum cortisol and elevated serum 17-hydroxyprogesterone). There were 62 patients with classical presentation; among them, salt-wasting (SW) form was seen in 41 patients (66%). There were 5 patients with the nonclassic form, while 6 others had cryptic presentation. Seven patients (9%) had hypertension, mostly due to salt-retaining CAH. Among the 39 females with CAH, 27 had developed mental anomalies of the external genitalia; 20 of them underwent surgical interventions of their external genitalia. Fourteen genetically female patients were wrongly diagnosed as 'male sex' at birth due to severe virilization. Seven of them were reassigned 'female sex' socially, legally, and surgically; the parents of one of them (a four-year-old girl) wanted the surgical intervention postponed for two to three years. Hysterectomy and gonadectomy were carried out for 6 of the other 7 patients who chose to keep the male gender. Our study indicates that newborns with developmental anomalies of the external genitalia should be diagnosed as early as possible so that medical, psychological, and social complications are minimized. A neonatal screening program for such a disorder can identify infants at risk for the development of life-threatening adrenal crisis and prevent incorrect sex assignment of affected female infants with intersex.
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PMID:Congenital adrenal hyperplasia: problems with developmental anomalies of the external genitalia and sex assignment. 1767 54

Steroid 11beta-hydroxylase deficiency is the second most common cause of congenital adrenal hyperplasia. 11beta-hydroxylase intervenes in cortisol synthesis and its deficiency leads to accumulation of adrenal androgens--producing prenatal virilization and, subsequently, hyperandrogenism--as well as 11-deoxycorticosterone, leading to the development of hypertension. We describe a 7-year-old girl who was referred for pubarche and accelerated skeletal maturation due to 11beta-hydroxylase deficiency. Because the patient's predicted height was below her target height, the combination of gonadotropin-releasing hormone analog and growth hormone was added to oral glucocorticoid therapy. With this therapeutic strategy, the patient's predicted height improved significantly and the girl reached a final height in agreement with her target height at the age of 13 years and 6 months.
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PMID:[11beta-hydroxylase deficiency: improvement of final height with growth hormone and gonadotropin-releasing hormone analog]. 1769 61

11 beta-Hydroxylase deficiency is a rare form of congenital adrenal hyperplasia, resulting in virilization, glucocorticoid deficiency and hypertension. There have been no previous reports in the literature of a successful pregnancy in a severely affected female. We report the first successful pregnancy resulting in a live birth for a female with 11 beta-hydroxylase deficiency and outline management issues from preconception to successful birth. We also report 2 novel mutations in the CYP11B1 gene leading to 11 beta-hydroxylase deficiency.
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PMID:Successful pregnancy in a patient with severe 11-beta-hydroxylase deficiency and novel mutations in CYP11B1 gene. 1772 34

Adrenocortical carcinoma is a rare disease. A 32 years old lady presented with complaints of hypertension, abdominal swelling, weight gain, hirsutism and bone pains. She was found to have a large adrenocortical carcinoma with associated Cushing's and virilization syndromes. Radical adrenalectomy was done with subsequent plan for Mitotane and radio frequency ablation for hepatic metastasis. However, she succumbed to respiratory failure due to ARDS, a month after operation.
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PMID:Adrenocortical carcinoma with endocrine syndromes. 1807 May 81

Prenatal treatment of congenital adrenal hyperplasia (CAH) with dexamethasone to minimize the genital virilization of external genitalia of affected girls has been in use since the mid-1980s. The positive effect of reducing virilization is now established. However, experimental data from animal studies and observations on adverse medical events in human newborns have raised concerns about the long-term safety of the treatment. Most animal studies on prenatal treatment with synthetic glucocorticoids have been designed to mimic treatment for lung maturation in preterm infants. The primary focus has been on a possible impact on fetal programming and the development of the metabolic syndrome with insulin resistance, type 2 diabetes, and high blood pressure. Altered reactivity to stress as a function of differences in reactivity of the HPA axis and glucocorticoid receptor function have been assayed. Effects on cognition, especially memory, have been observed. In children at risk for CAH and treated prenatally with dexamethasone, no overall effects on full-scale IQ have been observed, but a negative effect on verbal working memory has been reported. Contradictory effects on social behavior with respect to shyness and inhibition have been discussed. There is an urgent need for in-depth studies of long-term outcome in prenatal treatment of CAH regarding both maternal side effects and possible negative metabolic as well as cognitive and behavioral effects in the growing fetus and the child in her development into adulthood.
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PMID:Long-term outcome of prenatal treatment of congenital adrenal hyperplasia. 1849 35

Patients with congenital adrenal hyperplasia arising from mutations of 11beta-hydroxylase, the final enzyme in the glucocorticoid biosynthetic pathway, exhibit glucocorticoid deficiency, adrenal hyperplasia driven by unsuppressed hypothalamo-pituitary-adrenal activity, and excess mineralocorticoid activity caused by the accumulation of deoxycorticosterone. A mouse model, in which exons 3-7 of Cyp11b1 (the gene encoding 11beta-hydroxylase) were replaced with cDNA encoding enhanced cyan fluorescent protein, was generated to investigate the underlying disease mechanisms. Enhanced cyan fluorescent protein was expressed appropriately in the zona fasciculata of the adrenal gland, and targeted knock-out was confirmed by urinary steroid profiles and, immunocytochemically, by the absence of 11beta-hydroxylase. The null mice exhibited glucocorticoid deficiency, mineralocorticoid excess, adrenal hyperplasia, mild hypertension, and hypokalemia. They also displayed glucose intolerance. Because rodents do not synthesize adrenal androgens, changes in reproductive function such as genital virilization of females were not anticipated. However, adult homozygote females were infertile, their ovaries showing an absence of corpora lutea and a central proliferation of disorganized steroidogenic tissue. Null females responded normally to superovulation, suggesting that raised systemic progesterone levels also contribute to infertility problems. The model reveals previously unrecognized phenotypic subtleties of congenital adrenal hyperplasia.
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PMID:Cyp11b1 null mouse, a model of congenital adrenal hyperplasia. 1902 89

The authors describe a case of an adult woman with congenital adrenal hyperplasia caused by 11beta-hydroxylase deficiency. The patient presented not only typical features of this disease such as virilization and hypokaliemic hypertension but also rare pathologies, such as ectopic adrenal tissues, salt loss during infancy, and functional adrenomedullary hyperactivity. In spite of the severe disease and delays in its diagnosis and adequate treatment, significant improvement in appearance and normalization of blood pressure as well as the birth of a healthy child were achieved. The paper also discusses current opinions concerning the pathogenesis and treatment in CAH with 11beta-hydroxylase deficiency as well as difficulties in diagnostic and therapeutic management.
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PMID:[Congenital adrenal hyperplasia caused by 11beta-hydroxylase deficiency. A case report]. 1934 18


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