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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corticosteroids represent the most important and frequently used class of anti-inflammatory drugs and are the reference therapy for numerous neoplastic, immunological and allergic diseases. However, their substantial efficacy is often counter-balanced by multiple adverse events. These corticosteroid-induced adverse events represent a broad clinical and biological spectrum from mild irritability to severe and life-threatening adrenal insufficiency or cardiovascular events. The purpose of this article is to provide an overview of the available data regarding the frequency, screening and prevention of the adverse events observed in adults during systemic corticosteroid therapy (topically administered corticosteroids are outside the remit of this review). These include clinical (i.e. adipose tissue redistribution, hypertension, cardiovascular risk, osteoporosis, myopathy, peptic ulcer, adrenal insufficiency, infections, mood disorders, ophthalmological disorders, skin disorders, menstrual disorders, aseptic necrosis, pancreatitis) and biological (i.e. electrolytes homeostasis, diabetogenesis, dyslipidaemia) events. Lastly, data about the prescription of corticosteroids during pregnancy are provided. This review underscores the absence of data on many of these adverse events (e.g. lipodystrophy, dyslipidaemia). Our intent is to present to practitioners data that can be used in a practical way to both screen and prevent most of the adverse events observed during systemic corticosteroid therapy.
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PMID:Corticosteroid-induced adverse events in adults: frequency, screening and prevention. 1786 24

Two months after monolateral adrenalectomy, a 47-year-old woman stopped taking corticosteroid replacement therapy in the first 15 days of therapy. She was admitted to the Department of Internal Medicine because of hypertension, severe hypercalcemia, uncompensated metabolic alkalosis and clinical symptoms of acute adrenal insufficiency. The presence of hypokalemia and hypernatremia precluded a diagnosis of hypocortisolism, therefore no corticosteroids were given during the time required to investigate the cause of hypercalcemia, which resulted negative. Administration of intravenous saline infusion produced no improvement in her clinical condition. Despite electrolyte alterations, hydrocortison (100 mg i.v.) and zoledronate (4 mg i.v.) were also administered, leading to a rapid and marked improvement in her clinical picture within a few hours, with normalization of the calcemia and the other electrolytic disturbances. After her neurological condition had fully normalized, the patient admitted she had been assuming large amounts of liquorice as a laxative for many years; this compound very likely compensated the adrenal insufficiency by inhibiting 11 b steroid-dehydrogenase and disguised the clinical presentation at the time of admission. This case report confirms that, though rare, hypercalcemia may be a finding in acute adrenal insufficiency and can be rapidly corrected by corticosteroid administration. Furthermore, excessive liquorice intake can induce a clinical picture resembling that of primary hyperaldosteronism. In patients with adrenal insufficiency, it can, at least in part, disguise its metabolic effects and delay diagnosis and treatment.
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PMID:Acute adrenal crisis and hypercalcemia in a patient assuming high liquorice doses. 1829 99

This report concerns a case of cortisol-producing adrenocortical adenoma without the phenotype of Cushing's syndrome. A left adrenal tumor was incidentally detected in this patient. A diagnosis of adrenal Cushing's syndrome was based on the results of endocrinological and radiological examinations, although she showed none of the physical signs of Cushing's syndrome, glucose intolerance, hypertension or dyslipidermia. After a successful laparoscopic left adrenalectomy, the pathological diagnosis was adrenocortical adenoma. Slow tapering of glucocorticoids was needed to prevent adrenal insufficiency after surgery, and the plasma ACTH level remained high even though the serum cortisol level had reached the upper limit of the normal range. Further examination showed a urinary THF + allo-THF/THE ratio of 0.63, which was lower than that of control (0.90 +/- 0.13, mean +/- SD). Serum cortisol/cortisone ratios after the cortisone acetate administration were also decreased, and the serum half-life of cortisol was shorter than the normal range which has been reported. These findings indicated a partial defect in 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) activity, which converts cortisone to cortisol. Our case suggests that a change in 11beta-HSD1 activity results in inter-individual differences in glucocorticoid efficacy.
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PMID:A case of cortisol producing adrenal adenoma without phenotype of Cushing's syndrome due to impaired 11beta-hydroxysteroid dehydrogenase 1 activity. 1849 11

Antiphospholipid syndrome (APS) is an acquired thrombotic disorder. It mainly occurs with systemic disease or as a primary disorder. All organs may be involved by thrombosis, but to date the most common endocrine manifestation is chronic adrenal insufficiency. Very few cases of hypopituitarism with primary APS have been reported. We report the case of a 27-year-old woman, victim of a stroke leading to double vision and intracranial hypertension. Magnetic resonance imaging showed a macro-adenoma with hemorrhage of a suprasellar lesion. Hormone assessment showed hyper prolactinemia with positive anticardiolipin antibody. Our case is the second reported associating APS with apoplexy. We discuss the clinical, biological and radiological features observed in our case. We conclude that APS should be searched for whenever a history of adenoma with apoplexy is found associated with recurrent thrombosis.
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PMID:[Pituitary necrosis and antiphospholipid syndrome]. 1893 32

A patient was presented with four days of vomiting, abdominal pain and sweating. At presentation the Capillary Blood Glucose (CBG) was 1.7 mmol/L, the Blood Pressure (BP) was 182/102 mmHg, and the pulse 100 bpm. On examination, he was sweaty, pale and cold. The initial differential diagnosis was hypoglycaemia secondary to insulin abuse, hypoadrenalism or insulinoma, the transient hypertension being considered a consequence of sympathetic stimulation. He remained clinically well overnight with a CBG of 10-14 mmol/L following intravenous glucose. The next morning he complained of nausea and abdominal pain. The BP had risen to 203/127 mmHg when he was later reviewed, having been given 10mg intramuscular metoclopramide. Shortly afterwards, he developed acute pulmonary oedema and had become hypoglycaemic again; a phaeochromocytoma crisis was suspected. Treatment with alpha-adrenoceptor blockade with intravenous phenoxybenzamine was advised. However, the patient deteriorated and died in the Intensive Care Unit within two hours. Autopsy examination confirmed a phaeochromocytoma in the left adrenal, with haemorrhage within the head of pancreas, but no evidence of a pancreatic tumour.
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PMID:Phaeochromocytoma crisis presenting with profound hypoglycaemia and subsequent hypertension. 1926 23

Hyponatremic hypertensive syndrome (HHS) is rare and is characterized with hypertension together with hyponatremia, hypokalemia and low plasma osmolarity and considered to be based on renal ischemia. It can rarely develop due to antiphospholipid syndrome (APS). We reported a case of 43-year-old man with unilateral renal artery stenosis due to primary APS. He presented with a hypertensive hyponatremic episode. First, he was treated with antihypertensive drugs. Further, radiological imaging showed enlargement of bilaterally adrenal glands that mimic adrenal masses. Unilateral nephrectomy and adrenalectomy were performed. Pathological examination revealed necrosis in the adrenal tissue and thrombosis in its artery. After operation, acute adrenal insufficiency developed in the patient because of hemorrhagic infarction of bilaterally adrenal glands. He improved after intravenous hydrocortisone treatment. His therapy was maintained with oral prednisolone and fludrocortisone. This patient with HHS, due to primary APS, is the first case in literature and acute adrenal insufficiency is a rare complication of APS.
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PMID:Primary antiphospholipid syndrome presenting as hyponatremic hypertensive syndrome and acute adrenal insufficiency following it: a rare case. 1936 33

The deficiency of 17 alpha-hydroxylase/17,20-lyase causes a rare autosomal recessive disorder presenting with congenital adrenal insufficiency (CAH) and sexual infantilism. Both 17 alpha-hydroxylase and 17,20-lyase reactions are catalyzed by a single polypeptide, cytochrome P450c17 (CYP17), which is encoded by the CYP17A1 gene. We describe the clinical, hormonal, and molecular findings of a 33-yr-old patient presenting with primary amenorrhea, late onset hypertension, and hypokalemic myopathy. The molecular analysis of CYP17A1 revealed a novel homozygous missense mutation resulting in the substitution of arginine to lysine at the amino acid position 21 (p.R21L).
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PMID:A novel mutation in the N-terminal region of the CYP17A1 gene in a patient with 17 alpha-hydroxylase/17,20-lyase deficiency. 1963 99

Brown widow spider (BrWS) (Latrodectus geometricus) venom produces intense systemic reactions such as cramps, harsh muscle nociceptive, nauseas, vomiting and hypertension. The proposed pathogenic mechanisms resulting in these accidents have principally been damages occurring at the nervous system. However, it is suspected that there is also damage of the adrenal glands, as a result of the experimental animal's clinical manifestations, which developed symptoms compatible with acute adrenal insufficiency. We have currently found that the adrenal gland is damaged by this venom gland homogenates (VGH) producing severe alterations on cortex cells resulting in death by acute adrenal insufficiency. In general, the ultrastructural study on the glands of mice under transmission electronic microscopy observations showed alterations in the majority of the intracellular membranes within 3 to 24h. BrWSVGH also showed specific actions on extracellular matrix proteins such as fibronectin, laminin and fibrinogen. In addition, zymogram experiments using gelatin as substrates detected gelatinolytic activity. The molecular exclusion fractionation of crude BrWSVGH resulted in 15 fractions, of which F1 and F2 presented alpha/beta-fibrinogenase and fibronectinolytic activities. Fractions F6, F14 and F15 showed only alpha-fibrinogenase activity; in contrast, the gelatinolytic action was only observed in fraction F11. Only metalloproteinase inhibitors abolished all these proteolytic activities. Our results suggest that adrenal cortex lesions may be relevant in the etiopathogenesis of severe brown widow spider envenoming. To our knowledge, this is the first report on adrenal gland damages, fibrinogenolytic activity and interrelations with cell-matrix adhesion proteins caused by L.geometricus VGH. The venom of this spider could be inducing hemostatic system damages on envenomed patients.
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PMID:Activities against hemostatic proteins and adrenal gland ultrastructural changes caused by the brown widow spider Latrodectus geometricus (Araneae: Theridiidae) venom. 1975 72

A 34-year-old woman presented with weight gain, hirsutism, recent hypertension and secondary amenorrhea. Laboratory findings showed hypokalemia, elevated cortisol and androgen levels with normal urine metanephrines and normal aldosteronemia. Abdominal magnetic resonance imaging showed a right heterogeneous adrenal mass measuring 4 x 6 cm with mixed component of fat and adrenal tissue suggesting corticosurrenaloma. After right adrenalectomy, blood pressure normalized and hypokalemia resolved. In the postoperative course, the patient presented adrenal insufficiency treated with hydrocortisone hemisuccinate. Histological examination showed a single tumor mass composed of an admixed population of adrenal cortical and medullary cells. Immunohistochemical evaluation was positive for chromogranin A.
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PMID:Corticomedullary mixed tumor of the adrenal gland. 1987 23

A 41-year-old female was admitted to our clinic due to weight gain and facial edema. The patient also reported hair loss, amenorrhea and the formation of striae. The laboratory diagnostics ensured the diagnosis of Cushing's syndrome. Unfortunately, the patient was among the 5-10% of patients in whom neither laboratory testing nor imaging revealed the source of the cortisol excess. Due to the dramatic decrease of her general condition, and the appearance of hypertension and diabetes mellitus we chose to refer the patient to bilateral minimally invasive adrenalectomy. The advantage of this therapeutic approach is, that it is a definitive treatment that provides immediate control of hypercortisolism. As disadvantage, the resultant permanent hypoadrenalism requires a lifelong glucocorticoid and mineralocorticoid replacement therapy. Furthermore, given that the problem was caused by occult pituitary microadenoma, Nelson's syndrome has to be considered. As only one adrenal could be excised due to technical reasons, the underlying pathology is thus not solved. In spite of this, the patient's general condition improved dramatically without need for replacement therapy. As the mortality of patients with persistent moderate hypercortisolism is increased 3,8- to 5 fold, mainly due to cardiovascular reasons, thorough surveillance for signs of recurrence is mandatory to be ready for quick intervention.
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PMID:[Unexplained weight gain in a 41-year-old woman]. 1990 56


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