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Dexamethasone Suppression Test (dexamethasone + suppression_test)
Kinds of Dexamethasone Suppression Test Selected AbstractsShould the dexamethasone suppression test be resurrected?ACTA PSYCHIATRICA SCANDINAVICA, Issue 4 2005Acta Psychiatrica Scandinavica First page of article [source] Personality pathology, depression and HPA axis functioningHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 4 2001I. Schweitzer Abstract Hypothalamic pituitary adrenal (HPA) axis functioning, as measured by the dexamethasone suppression test (DST), has been extensively investigated in major depressive disorder (MDD). Evaluating DST response in MDD patients while simultaneously considering clinically relevant personality disorders may further clarify the contribution of both personality pathology and HPA axis function to depressive symptoms. The present study measured personality pathology by administering the revised version of the Millon Clinical Multiaxial Inventory (MCMI-II) in a sample of 25 patients diagnosed with MDD. Analyses revealed that suppressors (n,=,19) scored significantly higher than non-suppressors (n,=,6) on six of the 13 MCMI-II personality disorder scales: Avoidant, Schizoid, Self-Defeating, Passive-Aggressive, Schizotypal and Borderline. Increased personality pathology was associated with normal suppression of cortisol following the DST. This suggests that suppression of the DST may be associated with depressive states linked with personality pathology while the more biologically based depression is associated with abnormal HPA pathophysiology. Copyright © 2001 John Wiley & Sons, Ltd. [source] Use of aminoglutethimide in the treatment of pituitary-dependent hyperadrenocorticism in the dogJOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2002M. D. Pérez Alenza The aim of this study was to evaluate the efficacy and safety of aminoglutethimide in the treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). Ten dogs were diagnosed with PDH based on clinical and laboratory data, adrenal function tests (adrenocorticotropic hormone [ACTH] stimulation test and urinary cortisol/creatinine ratio [UCCR] combined with a high dose oral dexamethasone suppression test) and ultrasonographic evaluation of the adrenal glands. Aminoglutethimide was administered daily at a dose of 15 mg/kg bodyweight for one month. Median basal cortisol concentration and post-ACTH cortisol concentration one month after treatment were significantly lower than pretreatment values. Complete response was achieved in one dog, and partial response was obtained in three dogs. Severe side effects of anorexia, vomiting and weakness occurred in one dog and medication was withdrawn. Two further dogs developed decompensations of concurrent diseases and medication was stopped in these animals as well. Mild toxicity occurred in four dogs. Moderate to severe elevations in liver enzymes occurred in all dogs. The efficacy of this drug is lower than that observed using mitotane and ketoconazole, and adverse effects limit its use. Aminoglutethimide, using the protocol described, cannot be recommended for long-term management of PDH in the dog. [source] A case of fatal anaphylaxis in a dog associated with a dexamethasone suppression testJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2005DACVECC, DACVIM, Michael Schaer DVM Abstract Objective: To describe a case of fatal anaphylaxis in a dog associated with a ,routine' dexamethasone suppression test. Case summary: An 8-year-old, spayed female dog, was treated with parenteral dexamethasone for a diagnosis of immune-mediated thrombocytopenia. The dog had responded to treatment, but 9 months later was evaluated for endogenous hyperadrenocorticism, prior to surgery for a ruptured anterior cruciate ligament. A normal ACTH stimulation test was followed by a high-dose dexamethasone suppression test. Immediately following the intravenous injection of dexamethasone, the dog developed severe anaphylactic shock and died. The postmortem examination findings supported the diagnosis of anaphylaxis. New information provided: The anaphylaxis in this dog was fulminating and by-passed the usual early signs of drug hypersensitivity. This is the first case in the veterinary literature reporting on dexamethasone as the cause of this dog's catastrophic event. [source] The Use of 17-Hydroxyprogesterone in the Diagnosis of Canine HyperadrenocorticismJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2002J.M.E. Ristic A number of dogs are seen with clinical signs consistent with hyperadrenocorticism (HAC), supporting CBC and biochemical findings, but the disease cannot be confirmed with either the ACTH stimulation test or the low-dose dexamethasone suppression test (LDDST). Therefore, another screening test is required to aid diagnosis in these atypical cases of HAC. The aim of this study was to investigate whether measuring 17-hydroxyprogesterone (OHP) concentrations could be used in this role. Plasma cortisol and OHP concentrations were measured in dogs with clinical signs suggestive of HAC before and after administration of exogenous ACTH. In dogs with HAC, plasma OHP showed an exaggerated response to ACTH stimulation. This was seen in both typical cases of HAC with a positive cortisol response to ACTH administration and in atypical cases with negative screening test results. The test can be performed on plasma already taken for a conventional ACTH stimulation test. Post-ACTH OHP concentrations decreased after treatment with mitotane or adrenalectomy. These results suggest that OHP measurements can be used as an aid to diagnose and manage canine HAC. [source] The 4-mg intravenous dexamethasone suppression test in the diagnosis of Cushing's syndromeCLINICAL ENDOCRINOLOGY, Issue 1 2010Caroline Jung Summary Objective, Optimal diagnostic criteria for the 4-mg intravenous dexamethasone suppression test (IVDST) in patients with Cushing's syndrome (CS), compared with normal subjects, have not been established. We evaluated the performance of the 4-mg IVDST for differentiating CS from normal subjects and to define the responses in CS of various aetiologies. Design, subjects, measurements, Thirty-two control subjects [normal and overweight/obese participants with or without type 2 diabetes) were prospectively studied, and data from 66 patients with Cushing's disease (CD), three with ectopic ACTH syndrome (EAS), 14 with adrenal Cushing's (AC)] and 15 with low probability of CS (LPC) from three tertiary hospitals were retrospectively evaluated. Dexamethasone was infused at 1 mg/h for 4 h. Plasma cortisol and ACTH were measured at ,60 min (baseline), ,5 min, +3 h, +4 h, +5 h and at +23 and +23·5 h on Day 2. Results, Control subjects (including those with type 2 diabetes) exhibited a marked suppression of cortisol which was maintained until Day 2. Two of 15 patients with LPC had Day 2 cortisol results that overlapped with CS. Patients with CD demonstrated partial suppression, with rebound hypercortisolism on Day 2. Patients with AC and EAS did not suppress cortisol levels. Day 2 cortisol level of >130 nmol/l (or >20% of the baseline) diagnosed CS with 100% sensitivity and 96% specificity. Conclusion, While the IVDST allowed complete discrimination between control subjects and CS, 13% of LPC overlapped with CS. Given the small number of EAS, no conclusion can be drawn regarding the utility of this test in the differential diagnosis of CS. [source] Screening of Cushing's syndrome in adult patients with newly diagnosed diabetes mellitusCLINICAL ENDOCRINOLOGY, Issue 2 2007Giuseppe Reimondo Summary Objective Recent studies have shown that a relatively high number of diabetic patients may have unsuspected Cushing's syndrome (CS). The aim of the present study was to screen for CS in adult patients with newly diagnosed diabetes mellitus who were not selected for clinical characteristics, such as poor control and obesity, which may increase the pre-test probability of CS. Design, patients and measurement We prospectively evaluated 100 consecutive diabetic patients at diagnosis from 2003 to 2004. No patient had clear Cushingoid features. Screening was performed by using the overnight 1-mg dexamethasone suppression test (DST) after complete recovery from acute concomitant illnesses and attainment of satisfactory glycaemic control. The threshold of adequate suppression after DST was set at 110 nmol/l. Results Five patients failed to suppress cortisol after DST and underwent a repeated DST and a confirmatory standard 2-day, 2-mg DST after 3,6 months from the baseline evaluation. In one woman, a definitive diagnosis of CS was made by a surgically proven pituitary adenoma, and glycaemic control improved after cure of CS. Conclusions The results of the present study support the view that unknown CS is not rare among patients with diabetes mellitus. This is the first demonstration that screening for CS may be feasible at the clinical onset of diabetes in an unselected cohort of patients. Therefore, early diagnosis and treatment of CS may provide the opportunity to improve the prognosis of diabetes. [source] Long-term remission rates after pituitary surgery for Cushing's disease: the need for long-term surveillanceCLINICAL ENDOCRINOLOGY, Issue 5 2005A. Brew Atkinson Summary Objective, There have been a few reports on long-term remission rates after apparent early remission following pituitary surgery in the management of Cushing's disease. An undetectable postoperative serum cortisol has been regarded as the result most likely to predict long-term remission. Our objective was to assess the relapse rates in patients who underwent transsphenoidal surgery in order to determine whether undetectable cortisol following surgery was predictive of long-term remission and whether it was possible to have long-term remission when early morning cortisol was measurable but not grossly elevated. Endocrinological factors associated with late relapse were also studied. Patients, We reviewed the long-term outcome in 63 patients who had pituitary surgery for the treatment of Cushing's disease between 1979 and 2000. Measurements, Case notes were reviewed and the current clinical and biochemical status assessed. Our usual practice was that early after the operation, an 08:00 h serum cortisol was measured 24 h after the last dose of hydrocortisone. This was followed by a formal low-dose dexamethasone suppression test. Current clinical status and recent 24-h urinary free cortisol values were used as an index of activity of the Cushing's disease. If there was evidence suggesting relapse, a low-dose dexamethasone suppression test was performed. In many patients, sequential collections of early morning urine specimens for urinary cortisol to creatinine ratio were also performed in an attempt to diagnose cyclical and intermittent forms of recurrent hypercortisolism. We did this if there was conflicting endocrine data, or if patients were slow to lose abnormal clinical features. Results, Mean age at diagnosis was 40·3 years (range 14,70 years). Mean follow-up up time was 9·6 years (range 1,21 years). Forty-five patients (9 males/36 females) achieved apparent remission immediately after surgery and were subsequently studied long term. Of these 45 patients, four have subsequently died while in remission from hypercortisolism. Ten of the remaining 41 patients have relapsed. Of those 10, six demonstrated definite cyclical cortisol secretion. Two of the 10 had undetectable basal serum cortisol levels in the immediate postoperative period. Thirty-one patients are still alive and in remission. Fourteen (45%) of the 31 who remained in remission had detectable serum cortisol levels (> 50 nmol/l) immediately postoperatively, and remain in remission after a mean of 8·8 years. Our relapse rate was therefore 10/45 (22%), after a mean follow-up time of 9·6 years, with mean time to relapse 5·3 years. Conclusions, The overall remission rate of 56% (35/63) at 9·6 years follow-up is disappointing and merits some re-appraisal of the widely accepted principle that pituitary surgery must be the initial treatment of choice in pituitary-dependent Cushing's syndrome. Following pituitary surgery, careful ongoing expert endocrine assessment is mandatory as the incidence of relapse increases with time and also with increasing rigour of the endocrine evaluation. A significant number of our patients were shown to have relapsed with a cyclical form of hypercortisolism. [source] A dose,response study of salivary cortisol after dexamethasone suppression test in Cushing's disease and its potential use in the differential diagnosis of Cushing's syndromeCLINICAL ENDOCRINOLOGY, Issue 6 2003Margaret Castro Summary objective, A dose,response study with different doses of dexamethasone (dex) to assess the corticotrophic resistance in Cushing's disease (CD) using salivary cortisol as an end point has not yet been evaluated. We also reported our experience with salivary cortisol compared to plasma cortisol determination during dex suppression test (DST) and after ovine corticotrophin release hormone (oCRH) test in the differential diagnosis of Cushing's syndrome (CS). design, We studied 46 patients with CS, including 28 patients with CD, 16 with adrenal disease and two with occult ectopic adrenocorticotropic hormone (ACTH) tumours. Salivary cortisol was compared to plasma cortisol and ACTH during a DST 2 mg for 2 days, 8 mg for 2 days and 24 mg for 1 day, and after oCRH test. results, We observed a dose-dependent suppression of salivary cortisol, plasma cortisol and ACTH in CD patients. Salivary cortisol presented a higher percentage of suppression than plasma cortisol: 42%vs. 15% (P < 0·002), 82%vs. 67% (P < 0·002) and 90%vs. 83% (P < 0·03) after 2, 8 and 24 mg/day dex, respectively. The lowest percentage of suppression was observed for plasma ACTH. The parallelism of these lines identified that the criterion of 65% suppression of salivary cortisol corresponding to 50% suppression of plasma cortisol after 8 mg/day for 2 days is consistent with CD. The sensitivity and specificity using 50% suppression for plasma cortisol were 81% and 83%, respectively, for 8 mg DST. Using the criterion of 65% suppression of salivary cortisol, the sensitivity and specificity were 86% and 100%, respectively, for 8 mg DST. After oCRH test the sensitivity and specificity were 86% and 91%, respectively, for ACTH, 100% and 64%, respectively, for plasma cortisol and 93% and 91%, respectively, (20% of increment) or 86% and 100%, respectively, (35% increment) for salivary cortisol. conclusion, In conclusion, salivary cortisol presents more profound suppression than plasma cortisol or ACTH in a dose,response pattern after different doses of dex in patients with CD. In addition, our data suggest that measurement of salivary cortisol might improve the DST as compared to plasma cortisol in the differential diagnosis of CS. [source] Does subclinical hypercortisolism adversely affect the bone mineral density of patients with adrenal incidentalomas?CLINICAL ENDOCRINOLOGY, Issue 1 2003D. Hadjidakis Summary objective Subclinical hypercortisolism (SH) is detected increasingly in a substantial proportion of patients with incidentally discovered adrenal adenomas. The clinical implications of SH are currently unclear. Osteoporosis is a well-known complication of glucocorticoid excess. So far, the impact of SH on bone mineral density (BMD) has been studied in a limited number of reports with discordant results. In the present study we evaluated the BMD in a large cohort of post-menopausal women with adrenal incidentalomas. patients and measurements,Forty-two post-menopausal women with incidentally discovered adrenal masses and radiological features highly suggestive of benign adrenal adenomas were investigated. All patients underwent a standard low-dose dexamethasone suppression test (LDDST; 0·5 mg 6-hourly for 2 days). The diagnosis of subclinical hypercortisolism (SH) was based on post-LDDST cortisol concentrations of > 70 nmol/l. According to this criterion patients were subdivided into two groups: with (n = 18; group A) or without (n = 24; group B) SH. There was no significant difference in age, years since menopause and body mass index between these groups. BMD was measured at L2,L4 vertebrae and three sites of the proximal femur by the dual energy X-ray absorptiometry (DEXA) method. results Post-menopausal women with SH (group A) exhibited slightly but significantly lower absolute and age-adjusted BMD values compared to group B patients in the femoral neck (BMD g/cm2: 0·72 ± 0·08 vs. 0·79 ± 0·09; Z -score: ,0·20 ± 0·82 vs. +0·43 ± 0·94, P < 0·05) and trochanter (BMD g/cm2: 0·60 ± 0·09 vs. 0·69 ± 0·10; Z -score: ,0·32 ± 1·0 vs. +0·30 ± 1·05, P < 0·01). BMD measurements of the Ward's triangle were also lower in group A patients but the difference did not reach statistical significance (BMD g/cm2: 0·60 ± 0·10 vs. 0·68 ± 0·13, P = 0·06). There was no difference in the lumbar vertebrae between the two groups (BMD g/cm2: 0·888 ± 0·13 vs. 0·90 ± 0·16, P = 0·78; z-score: +0·50 ± 1·16 vs. +0·11 ± 1·5, P = 0·36). The number of patients in the osteoporotic range was minimal with no significant difference between the two groups. However, the frequency of osteopenia in group A was significantly greater than in group B patients in the trochanter and Ward's triangle areas. Serum osteocalcin (BGP) levels were significantly lower in group A compared to group B patients (18·6 ± 8·6 vs. 26·2 ± 8·1 ng/ml, P < 0·01); no difference existed regarding parathyroid hormone (PTH) concentrations (43 ± 15·6 vs. 41·2 ± 14·8 pg/ml, P = 0·72). conclusions In this series, post-menopausal women with subclinical hypercortisolism had lower absolute and age-adjusted BMD values and a higher rate of osteopaenia in the trabecular loaded and mixed cortical,trabecular bone of proximal femur. These data demonstrate that the subtle hypercortisolism of patients with adrenal incidentalomas may have an adverse effect on the bone mass of these patients. [source] CLINICAL AND IMAGING STUDY: Glucocorticoid negative feedback in methadone-maintained former heroin addicts with ongoing cocaine dependence: dose,response to dexamethasone suppressionADDICTION BIOLOGY, Issue 1 2006Bruno Aouizerate ABSTRACT Combined cocaine and illicit opiate use is common. This study aimed to test the hypothesis that cocaine dependence in former heroin-addicted patients maintained on methadone treatment is associated with enhanced glucocorticoid negative feedback. Multiple dose dexamethasone suppression tests, using a conventional 2.0 mg dose, and two lower doses, 0.5 mg and 0.125 mg, were performed in 10 methadone-maintained former heroin addicts with ongoing cocaine dependence (C-MM), 10 stabilized methadone-maintained former heroin addicts with no ongoing drug or alcohol use (MM), and 22 normal volunteers (NV). At 9 hours, there was no difference in plasma adrenocorticotropin hormone (ACTH) and/or cortisol levels among groups on the baseline day, as well as after the two lower doses of dexamethasone. At 17 hours, C-MM and MM had significantly lower plasma ACTH and/or cortisol levels than NV. However, C-MM did not significantly differ from MM in their hormonal levels. When the hormonal responses to dexamethasone are expressed as magnitude of lowering from baseline, there was no significant difference at any dose among groups. Therefore, C-MM exhibited a normal glucocorticoid negative feedback in the morning. Using the standard interpretation of dexamethasone suppression testing based on the examination of the actual hormonal levels rather than the difference from baseline condition, C-MM appear to have glucocorticoid effects similar to MM, yet were both greater than NV in the late afternoon. Thus, further studies are needed to know whether altered glucocorticoid negative feedback is related to chronic cocaine exposure, or is the result of former heroin addiction and/or its long-term treatment with methadone. [source] | ||||||||||||||||||||||