Cases reported "Adrenal Insufficiency"

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1/337. Adrenal suppression in children with the human immunodeficiency virus treated with megestrol acetate.

    Symptoms and laboratory evidence of adrenal suppression developed in 2 children with the human immunodeficiency virus after megestrol acetate (MA) therapy was discontinued; both required transient glucocorticoid replacement therapy. High-dose corticotropin stimulation testing performed on children with the human immunodeficiency virus treated or not treated with MA showed that baseline and post-corticotropin cortisol levels were extremely low in 7 of 10 treated patients and normal in 10 of 10 members of a control group (P <.01). MA may suppress adrenal function, and replacement glucocorticoids may prevent or relieve associated symptoms at times of severe stress or on discontinuation of MA therapy.
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2/337. adrenal insufficiency in smith-lemli-opitz syndrome.

    We describe three unrelated patients with adrenal insufficiency and RSH or smith-lemli-opitz syndrome (SLOS), a disorder due to deficient synthesis of cholesterol. These patients presented with hyponatremia, hyperkalemia, and decreased aldosterone-to-renin ratio, which is a sensitive measure of the renin-aldosterone axis. All patients had profound serum total cholesterol deficiency (14-31 mg/dl) and marked elevation of 7-dehydrocholesterol (10-45 mg/ dl). Two patients were newborn infants with 46, XY karyotypes and complete failure to masculinize; one of these patients also had cortisol deficiency. Both patients died within 10 days of birth of cardiopulmonary complications while on adrenal replacement therapy. The third patient diagnosed with SLOS at birth presented at age 7months with fever and diarrhea and was noted to have profound hyponatremia. This patient is maintaining normal serum electrolytes on mineralocorticoid replacement. We conclude that adrenal insufficiency may be a previously undetected and treatable manifestation in SLOS. We hypothesize that deficiency of cholesterol, an adrenal hormone precursor, may lead to insufficient synthesis of adrenal steroid hormones.
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3/337. Coexistence of primary endocrine deficiencies: a unique case of male hypergonadism associated with hypoparathyroidism, hypoadrenocorticism, and hypothyroidism.

    The unique combination of male hypogonadism with hypoparathyroidism, hypoadrenalism, hypothyroidism, diabetes mellitus, and alopecia totalis has been documented in a male patient who has been followed over the past 28 years. In this patient, first seen at the age of six for hypoparathyroidism alone, repeated clinical and laboratory endocrine evaluation detected the sequential development of the additional endocrine deficiencies. The presence of abnormal serum antibodies is consistent with an atuoimmune pathogenesis of this syndrome.
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4/337. adrenal insufficiency caused by primary aggressive non-Hodgkin's lymphoma of bilateral adrenal glands: report of a case and literature review.

    A 64-year-old woman was hospitalized because of poor general condition, gastrointestinal upset, unexplained fever, electrolyte imbalances, and an incidental finding of bilateral huge adrenal masses on computerized tomography (CT) of the abdomen. Non-Hodgkin's lymphoma (NHL) of B-cell origin was proven by ultrasound-guided aspiration biopsy of the left adrenal gland. Meanwhile, primary adrenal insufficiency was confirmed by her low serum cortisol level, high ACTH level, and inadequate adrenal response to the rapid ACTH stimulation test. The diagnosis of primary adrenal NHL was supported by detailed physical examinations, bone marrow examination, and such imaging studies as CT scan and sonography. She received three courses of chemotherapy with cyclophosphamide, vincristine, and prednisolone and there was an initial transient response, but she died of sepsis and progression of NHL three and a half months later.
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ranking = 4.5
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5/337. Novel missense mutation (Leu466Arg) of the DAX1 gene in a patient with X-linked congenital adrenal hypoplasia.

    We identified a DAX1 missense mutation, a substitution of arginine for leucine at codon 466 (Leu466Arg), in an infant with X-linked congenital adrenal hypoplasia (AHC). A heterozygous substitution, Leu466Arg, was also identified in his mother and sister. Since leucine at position 466 is well conserved among other orphan nuclear hormone receptor superfamilies and Leu466Arg was not detected among 50 normal Japanese control individuals, the mutation is most likely responsible for X-linked AHC. It is interesting to note that Leu466Arg among all mutations ever reported is located at the most C-terminal region of the DAX-1 protein. Most mutations identified previously were located in the C-terminal presumptive ligand binding domain. Hence, the C-terminal end of the DAX-1 protein may play an important role in the biological function, such as in normal adrenal embryogenesis.
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6/337. hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor.

    A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin d (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure.
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7/337. Severe hyponatremia caused by hypothalamic adrenal insufficiency.

    A 60-year-old woman was admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values of ACTH and cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia.
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ranking = 3.5
keywords = adrenal
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8/337. A case of primary bilateral adrenal lymphoma with partial adrenal insufficiency.

    Unilateral or bilateral non-Hodgkin's lymphomas arising primarily in the adrenal glands are extremely rare. These lymphomas are usually present with large, bilateral adrenal masses with or without lymphadenopathy, and may be accompanied by adrenal insufficiency in some cases. A review of the literature indicates that patients with primary lymphoma of the adrenal glands usually do not have disease elsewhere, and if present, it is frequently extranodal. We report here an unusual case of primary bilateral adrenal lymphoma with partial adrenal insufficiency.
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9/337. Adrenal suppression secondary to inhaled fluticasone propionate.

    BACKGROUND: Inhaled glucocorticoids are the medical treatment of choice in many of patients with asthma. Fluticasone propionate is an inhaled glucocorticoid with little systemic bioavailability via the oral route and infrequent association with systemic adverse effects at the recommended dosage. OBJECTIVE: To report a case of adrenal suppression and exogenous glucocorticoid excess from inhaled fluticasone propionate. methods: A 9-year-old girl with a previous history of episodic asthma was placed on 550 microg of fluticasone propionate daily for severe labile asthma diagnosed by history and methacholine challenge. The patient returned 6 months later with complaints of increased appetite, nausea, and feeling "hot and flushed." On physical exam she had stigmata of Cushing's syndrome. The patient subsequently developed orthostatic hypotension and moderate dehydration following a viral illness. After a long taper of fluticasone propionate the patient' s adrenal function returned to normal and she had no acute or chronic exacerbations of her asthma. RESULTS: Her 8 AM cortisol was undetectable with an ACTH of 21 pg/mL. The serum prolactin, TSH, free thyroxine, insulin-like growth factor i, and renin activity were all normal. An MRI study of her head was also normal. Repeat methacholine challenges while receiving a much smaller dose fluticasone propionate showed a significant decrease in airway reactivity. CONCLUSION: Adrenal suppression can occur from inhaled fluticasone propionate at a dosage less than has been previously reported.
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ranking = 1
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10/337. Combined hypothalamic hypothyroidism and secondary adrenal insufficiency. Misdiagnosed as primary hypothyroidism.

    A case of combined, selective, hypothalamic hypothyroidism and secondary adrenal insufficiency is described. serum levels of thyroid-stimulating hormone (TSH), before and after thyrotropin-releasing factor (TRF) administration, were in the range generally considered to be indicative of primary, rather than secondary, hypothyroidism. Hence, the clinical usefulness of serum TSH levels to unequivocally provide an accurate distinction between primary and secondary hypothyroidism must be questioned. The paucity of clinical findings suggestive of adrenal insufficiency in this case is emphasized, and the usefulness of adrenal screening tests in hypothyroid subjects seems clear.
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ranking = 3.5
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