Cases reported "Hirsutism"

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1/20. Unilateral macronodular adrenal hyperplasia as an unusual cause of Cushing's syndrome--a case study.

    To appraise clinicians of the problems that may be encountered in the diagnosis and management of Cushing's syndrome, we present a case report of a 20-year old female, who was admitted with a recently developed central obesity, ammenorrhea hirsuitism, proximal myopathy and depression. She was found to have multiple striae, thin skin, elevated blood pressure glycosuria and hyperglycaemia. Morning and mid-night plasma cortisol concentrations revealed elevated levels, with a loss of diurnal variation. There was a failure of the normal suppressibility of cortisol secretion by low doses of dexamethasone, while a significant suppression of plasma cortisol concentration was observed with high doses of dexamethasone. There were no significant abnormalities observed in the pituitary fossa on skull radiograph and on the cranial computerised tomographic scan. After a period of stabilisation, she had a bilateral adrenalectomy done, with a histopathological finding of a left adrenal macronodular hyperplasia, while the right adrenal gland was small and friable. There was an uneventful post-operative period, with a gradual return to normality of most of the presenting complaints. The hyperglycaemia and hypertension got controlled without medications, while her menstrual cycles resumed within three months of bilateral adrenalectomy. This case report illustrates that an adrenal-dependent Cushing's syndrome may mimic a pituitary-dependent one, especially as regards the suppressibility of plasma cortisol secretion by high doses of dexamethasone.
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2/20. A patient with congenital hypertrichosis, gum hyperplasia and macromastia.

    A syndrome of congenital hypertrichosis, hirsutism, gum hyperplasia and macromastia is described. The patient was demonstrated to have mild hyperinsulinemia with normal oral glucose tolerance test. This is the second such patient reported in the literature.
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3/20. Congenital adrenal hyperplasia - how to improve the transition from adolescence to adult life.

    Congenital adrenal hyperplasia (CAH) is caused by a defect in the biosynthesis of cortisol that results in maximal activity of the hypothalamic-pituitary adrenal axis with hyperplasia of the adrenals and hyperandrogenism due to the accumulation of androgen precursors. In the salt-wasting subtype of the disorder, which accounts for appr. 75 % of patients with classical CAH, patients are unable to synthesise sufficient amounts of aldosterone and are prone to life-threatening salt-losing crises, whereas the simple virilising form is predominantly characterized by clitoris hypertrophy and posterior labial fusion. In addition, a non-classical variant can be discerned which in most cases is diagnosed at the time of puberty or early adolescence when hirsutism and menstrual irregularities may occur. The vast majority of CAH patients have 21-hydroxylase deficiency (90 - 95 %). Less common forms, such as 11beta-hydroxylase deficiency, will not be discussed in this review. Unfortunately, a considerable number of CAH patients is lost to regular and competent follow-up once they move out of paediatric care. This is most probably the result of insufficient co-operation between paediatric and adult endocrinologists at the time of transition from adolescence to adulthood. Furthermore, there is a lack of clinical guidance regarding psychosexual development in these patients. In this overview we will focus on special aspects of CAH treatment in adolescence and adulthood, and report on our 10-year experience with a transfer system for endocrine patients from paediatric to internal medical care, known as the "Kieler Modell". For practical purposes, we here provide charts for follow-up of CAH patients that can be adapted for use in any endocrine outpatient clinic.
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ranking = 1.2
keywords = hyperplasia
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4/20. The case of the elusive androgen.

    OBJECTIVE: To describe a case of androgen excess and discuss the important factors in diagnosis and management. methods: A case report is presented of a postmenopausal woman who had had severe hirsutism for 18 months. Her history, clinical and laboratory findings, treatment, and outcome are chronicled. The pertinent literature--especially that related to the differential diagnosis of hyperandrogenism--is also reviewed. RESULTS: A 62-year-old woman had progressive hirsutism of the face, back, and abdomen as well as alopecia of the scalp, for which spironolactone therapy had proved ineffective. Laboratory studies showed a testosterone level of 644 ng/dL. Preoperative evaluation pointed to an ovarian source of testosterone. After total abdominal hysterectomy and bilateral oophorectomy, histologic examination of the ovaries showed bilateral hilar cell hyperplasia. Three months later, the serum testosterone level remained high (556 ng/dL), and repeated computed tomography of the abdomen disclosed a previously unseen 9-mm adenoma of the left adrenal gland, which was removed laparoscopically. Because of a persistently high testosterone value (546 ng/dL), the patient underwent dexamethasone suppression studies, followed by adrenal stimulation with corticotropin; no pathologic findings were demonstrated. Finally, gonadotropin suppression with nafarelin, 200 mg intranasally daily for 6 weeks, yielded a prompt and sustainable decrease in the testosterone level. This result was associated with dramatic clinical improvement. CONCLUSION: It is speculated that the patient had residual testosterone-producing tissue originating from primitive mesenchymal cells from the urogenital ridge, which was responsive to gonadotropins, in an unidentified abdominal or pelvic site.
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keywords = hyperplasia
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5/20. Rabson-Mendenhall syndrome.

    Rabson-Mendenhall syndrome is characterized by growth retardation, dysmorphisms, lack of subcutaneous fat, acanthosis nigricans, enlarged genitalia, hirsutism, premature and dysplastic dentition, coarse facial features, paradoxical fasting hypoglycemia and post-prandial hyperglycemia, extreme hyperinsulinemia and pineal hyperplasia. We describe a six-month-old female child with physical features suggestive of the Rabson-Mendenhall syndrome. The child also had medullary nephrocalcinosis.
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ranking = 0.2
keywords = hyperplasia
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6/20. Drug-induced hirsutism.

    hirsutism is a symptom or sign, which may have more serious associations than cosmetic and psychological concern alone, such as adrenal hyperplasia and ovarian tumor, particularly if it develops well after puberty. Some medicines having androgenic activity may also cause this problem. Here, we present a case of a young unmarried girl who was given anabolic steroid for the treatment of dysmenorrhoea which resulted in hirsutism.
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ranking = 0.2
keywords = hyperplasia
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7/20. Hilus cell pathology and hirsutism.

    Hilus cell abnormalities are uncommon causes of hirsutism with virilization. Although hilus cell tumours have been well described, hilus cell hyperplasia is rare and is poorly defined clinically. We describe three cases of hilus cell hyperplasia and compare them with a case of hilus cell tumour. Both pathologies were associated with increased testosterone and oestradiol secretion. Suppression of testosterone to the 'normal range' in response to exogenous oestrogen was seen only in the cases with hyperplasia; only partial responsiveness was seen in the case with hilus cell tumour. Bilateral oophorectomy offers the potential for cure for both hilus cell hyperplasia and tumour.
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keywords = hyperplasia
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8/20. Isolated dehydroepiandrosterone sulphate hypersecretion: a case report.

    The case of a 17-year-old male with isolated hypersecretion of dehydroepiandrosterone sulphate (DHEAS) is described. cushing syndrome, congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency, an androgen producing adrenal tumour, and elevated plasma DHEAS due to an increased renal threshold were excluded. Selective renal vein catheterization confirmed bilateral, isolated adrenal DHEAS hypersecretion. The dexamethasone suppression suggests a functional nature of this alteration. This condition has to be considered in the differential diagnosis of excessive adrenal androgen production in males, or of hirsutism in females.
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ranking = 0.2
keywords = hyperplasia
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9/20. Macromastia in a woman treated with penicillamine and oral contraceptives. A case report.

    A patient with Wilson's disease treated with penicillamine developed severe hirsutism. After treatment with oral contraceptives, her breasts enlarged rapidly, and she experienced cyclic mastodynia. Around the time of her breast enlargement she also developed gingival hyperplasia.
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ranking = 0.2
keywords = hyperplasia
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10/20. Familial hypersecretion of adrenal androgens transmitted as a dominant, non-HLA linked trait.

    Clinical evidence of adrenal androgen hyperfunction (premature pubarche, hirsutism, amenorrhea) occurred in the studied proband, her mother, maternal aunt (twin sisters), and maternal great-grandmother. The basal levels of androgen in the first three were variably elevated. In all the members of this family who were tested, the response of 17-hydroxyprogesterone and progesterone to adrenocorticotropic hormone stimulation was either normal or of the type seen in heterozygotes for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Of particular importance is the fact that neither the proband nor her mother or maternal aunt had the type of response seen in homozygotes presenting the attenuated form of congenital adrenal hyperplasia. The disorder appears to be a familial condition resulting in excessive levels of adrenal androgens beginning during childhood years, causing hirsutism and amenorrhea and interfering with normal pubertal and adult ovarian function. Glucocorticoid therapy suppresses adrenal androgen levels; in two individuals, conception occurred twice in each during such treatment in otherwise amenorrheic individuals. The pattern of transmission of the disorder appears to be either autosomal or X-linked dominant, and not linked to the homologous leucocytic antibodies (HLA) region of the sixth chromosome.
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ranking = 0.4
keywords = hyperplasia
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