Cases reported "Obesity"

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1/26. 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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2/26. Bilateral giant adrenal myelolipoma and polycystic ovarian disease.

    We report a case of a nonfunctioning, synchronous, bilateral, very large adrenal myelolipoma in an obese woman. She had diabetes mellitus and oligomenorrhea due to polycystic ovarian disease, and for that, she was taking progesterone medication for over 12 years. The principal clinical findings, the etiology and pathogenesis, the diagnostic-tools including US-guided fine-needle biopsy to preoperative differential diagnosis, are discussed. copyright copyright 1999 S. Karger AG, Basel
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3/26. Corticotropin-independent Cushing's syndrome caused by an ectopic adrenal adenoma.

    Although nonsecreting suprarenal embryonic remnants are frequently found in the urogenital tract, adenomatous transformation resulting in glucocorticoid excess is a rare phenomenon. We report a case of a 63-yr-old woman that presented with new-onset hirsutism, facial plethora, hypertension, centripetal obesity, and a proximal myopathy. The 24-h urinary free cortisol excretion rate was elevated, and the serum ACTH level was suppressed. The patient failed an overnight and low dose dexamethasone suppression test and did not respond to CRH stimulation. In light of the undetectable baseline morning ACTH levels and the blunt response to CRH, the diagnosis of corticotropin-independent Cushing's syndrome was made. Imaging studies revealed normal adrenal glands and enlargement of a left pararenal nodule incidentally observed 4 yr before the onset of symptoms. Dramatic resolution of symptoms was observed after surgical removal of the 3.5-cm mass. Pathological exam confirmed adrenocortical adenoma in ectopic adrenal tissue. The case reported here represents the unusual circumstance in which the development of adenomatous transformation of ectopic adrenal tissue has been prospectively observed with imaging studies. It illustrates the importance of considering ectopic corticosteroid-secreting tumors in the context of corticotropin-independent Cushing's syndrome.
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4/26. bardet-biedl syndrome type 3 in an Iranian family: clinical study and confirmation of disease localization.

    bardet-biedl syndrome (BBS) is a group of autosomal recessive MCA/MR syndromes characterized by pigmentary retinopathy, postaxial polydactyly, hypogenitalism, obesity, and mental retardation. Five BBS loci have been identified; among them, BBS type 1 (BBS1) and type 3 (BBS3) are most common and most rare, respectively. We encountered an Iranian family that had seven affected members. All patients had a history of mild to severe obesity, but it was reversible in some patients by caloric restriction and exercise. All patients had pigmentary retinopathy, beginning as night blindness in early childhood and progressing toward severe impairment of vision by the end of the second decade. polydactyly varied in limb distribution, ranging from four-limb involvement to random involvement or even to nonaffectedness. Six of the seven patients were not mentally retarded. Although kidney anomaly or an adrenal mass was pres- ent in two patients, the fact that one patient had seven children rules out reproductive dysfunction. Linkage analysis with microsatellite markers showed that the disease in the family was assigned to a region around marker loci at 3p13-p12 (maximum lod score = 4.15 and recombination fraction straight theta = 0, at D3S1603 microsatellite marker), to which the BBS3 locus has been mapped. Haplotype analysis did not reduce the extent of the previously reported critical region of BBS3. A comparison of clinical manifestations of our patients with those of previously reported BBS3 patients did not support any type-specific phenotypes, though manifestations in our patients are similar to those in BBS3 patients of a family in Newfoundland.
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5/26. A case of severe hypertension caused by ACTH-independent macronodular adrenal hyperplasia.

    This report describes a rare case of ACTH-independent macronodular adrenal hyperplasia (AIMAH) arisen with symptomatic severe hypertension and hypokaliemia. A 55-year-old man was admitted to hospital with a clinical picture characterized by several episodes of transient ischemic attacks (TIA) and right hemiplegia, related to severe arterial hypertension. Laboratory tests showed urinary levels of catecholamines, metanephrines and vanillylmandelic acid (VMA) in normal range; high urinary free cortisol excretion, elevated serum cortisol with loss of the circadian rhythm and low ACTH plasma levels. ACTH failed to respond to CRH administration. serum cortisol levels were not modified after high doses of dexamethasone. MRI showed bilateral macronodular hyperplasia of adrenal glands, whereas pituitary-MRI did not show tumoral lesions. Therefore, ACTH-independent macronodular hyperplasia was suspected. Though obese, the patient had no typical Cushing habit, and symptomatic hypertension with hypokaliemia was the only clinical evidence for this rare kind of Cushing's syndrome. After obtaining a satisfactory control of blood pressure, the patient was successfully submitted to laparoscopic bilateral adrenalectomy and underwent complete clinical remission. The histology showed adrenal macronodular hyperplasia. During the twenty-four month follow-up, the patient had no further transient ischemic attacks or need of glucocorticoid replacement therapy and withdrew the antihypertensive drugs.
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6/26. Hypercortisolism in childhood: shortcomings of conventional diagnostic criteria.

    Two patients are described in whom hypercortisolism occurred prepubertally as a consequence of bilateral adrenocortical hyperplasia. In contrast with the manifestations of Cushing's syndrome in adults, these children presented with obesity and reduced stature and no other symptoms. Both patients excreted amounts of urinary 17-OHCS before and during a conventional suppression test with dexamethasone (0.5 mg every six hours) which were within the usual normal range. However, when urinary 17-OHCS excretion was expressed per gram of urinary creatinine or per square meter of surface area, and when the dose of dexamethasone was tailored to body mass (20mug/kg/day) the results were clearly abnormal, as were plasma corticoids and (in one patient) cortisol secretion rate. Resumption of linear growth occurred after bilateral adrenalectomy in both patients and was associated, in the one patient so studied, by a return of hypoglycemia-stimulated increases in plasma growth hormone levels from previously suppressed values to the normal range, and by a slight increase in the fasting plasma somatomedin concentration. The observations suggest that pediatric patients with hypercortisolism are likely to be overlooked when conventional criteria for laboratory diagnosis are used, but can be recognized by the simple diagnostic modifications used in these studies.
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7/26. obesity due to proopiomelanocortin deficiency: three new cases and treatment trials with thyroid hormone and ACTH4-10.

    The symptoms of severe early-onset obesity, adrenal insufficiency, and red hair define the proopiomelanocortin (POMC) deficiency syndrome as described so far in two children with complete loss-of-function mutations of the human POMC gene. In POMC deficiency, obesity reflects the lack of POMC-derived peptides as ligands at the melanocortin (MC) MC4 and MC3 receptors, which are expressed in the hypothalamic leptin-melanocortin pathway of body weight regulation. Hypocortisolism and alteration of pigmentation are caused by the lack of POMC-derived peptides at the adrenal MC2 receptor and the skin MC1 receptor, respectively. Here we describe three new cases of complete loss-of-function mutations of the POMC gene. patients were diagnosed based on the clinical trials of red hair, adrenal insufficiency, and early-onset severe obesity. One previously described translation initiation mutation (C3804A) as well as one new nonsense (A6851T) and two new frame-shift mutations (6996del and 7100 2G) were found in homozygosity or compound heterozygosity. The heterozygous parents were found to have high normal or mildly elevated body weight, suggesting a dosage effect of the POMC gene product on weight regulation. To compensate for the lack of hypothalamic melanocortin function, we initiated a trial in the two previously published patients with intranasal ACTH4-10, a melanocortin fragment for which an anorexic effect has been described recently. During 3 months with increasing doses of ACTH4-10, no change of body weight or metabolic rate was observed, suggesting that at least in these two POMC-deficient patients ACTH4-10 is without any compensatory effect. In the same two patients, further investigation revealed a mildly elevated TSH. However, a 1-yr treatment with thyroid hormone did not result in a significant reduction of body weight.
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8/26. Resistant hypertension, obesity, sleep apnea, and aldosterone: theory and therapy.

    hypertension resistant to 2 antihypertensive drugs is more common among obese patients than among lean patients. The case we describe and the observations we report suggest that refractoriness among obese hypertensives is frequently caused by obstructive sleep apnea and/or inappropriately high plasma aldosterone levels. In other words, obese hypertensives may have sleep apnea, obese hypertensives without sleep apnea may have inappropriately elevated levels of plasma aldosterone, and a surprising number of obese patients with sleep apnea also have elevated levels of aldosterone. The mechanisms by which obesity and obstructive sleep apnea increase aldosterone levels and raise blood pressure are not understood, but sympathetic nervous system activation and production of nonclassical adrenal stimuli are two possibilities. Obstructive sleep apnea can be detected with a careful history and various sleep studies. Inappropriately elevated aldosterone levels can be detected by measuring the ratio of plasma aldosterone concentration to plasma renin activity. Successful treatment of these resistant hypertensives often can be achieved by devices that provide positive pressure to the upper airway to correct obstructive sleep apnea and by incorporating an aldosterone antagonist in the therapeutic regimen.
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9/26. Bilateral carcinoma in situ of the testis and cystic fibrosis transmembrane conductance regulator (CFTR) mutation in an azoospermic patient with late-onset 21beta-hydroxylase deficiency.

    Testicular cancer can impair spermatogenesis. In addition, chemotherapy or radiotherapy used for its treatment further damage testicular function mainly affecting highly proliferating germ cells. The multifaceted etiology of male infertility includes, among others, alterations of male reproductive tract differentiation such as monolateral or bilateral congenital absence of vas deferens and perturbations in adrenal steroid synthesis on a genetic basis such as 21beta-hydroxylase deficiency. Herein, we report the case of a male patient with primary infertility, probably related to a combination of genetic and acquired factors with different expressions over time.
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10/26. Bilateral adrenocortical adenomas causing ACTH-independent Cushing's syndrome at different periods: a case report and discussion of corticosteroid replacement therapy following bilateral adrenalectomy.

    We report a rare case of bilateral adrenocortical adenomas causing ACTH-independent Cushing's syndrome at different periods 9 yr apart. The subject, a 24-yr-old woman, in June 1989 had a typical Cushingoid appearance. Her baseline plasma cortisol levels did not show a diurnal rhythm and she had a very low baseline plasma ACTH level. plasma cortisol levels could not be suppressed by overnight low-dose or two-day high-dose dexamethasone suppression test. Marked uptake of 131I-6beta-iodomethyl-19-norcholesterol (NP-59) was observed in the right adrenal gland. Abdominal computed tomography (CT) showed a right adrenal tumor. The right adrenal gland with adenoma was removed. The non-tumorous part of the adrenal cortex was atrophic. By April 1998, she had experienced a weight gain of more than 20 kg over a two-yr period. The baseline plasma cortisol levels were at the lower limit of the normal range with loss of diurnal rhythmicity. The baseline plasma ACTH levels were very low. Neither a two-day low-dose nor a two-day high-dose dexamethasone suppression test could suppress serum cortisol or urinary free cortisol levels. NP-59 adrenal scan revealed increased uptake of the left adrenal gland at 72 h after intravenous injection of the tracer. Abdominal CT and magnetic resonance imaging (MRI) all demonstrated a left adrenal mass. Left adrenalectomy was performed in June 1998; histological features showed a cortical adenoma and atrophic change in the non-tumorous part of the adrenal cortex. Elevated plasma ACTH levels after bilateral adrenalectomy could be suppressed with conventional corticosteroid replacement therapy and overnight low-dose dexamethasone suppression test.
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