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Desmopressin (DDAVP) stimulation test

Desmopressin (DDAVP) stimulation test
Literature review current through: Jan 2024.
This topic last updated: Mar 20, 2023.

INTRODUCTION — Arginine-vasopressin (AVP) is the natural human nonapeptide, which (in addition to its antidiuretic, vasoconstrictive, glycogenolytic, and platelet aggregation actions) plays an important role in the regulation of the corticotropin (ACTH)-adrenal axis. AVP and some of its analogs, such as porcine 8-lysine-vasopressin (LVP) and desmopressin (1-deamino, 8-D arginine-vasopressin), have been used in a number of clinical settings. Corticotropin-releasing hormone (CRH) has been widely utilized for the differential diagnosis of Cushing syndrome. However, desmopressin has been increasingly utilized in countries where CRH is not available for the differential diagnosis of ACTH-dependent hypercortisolism. It is also considered the vasopressin analog of choice to use for the postoperative surveillance of patients with ACTH-dependent Cushing syndrome and for the diagnosis of pseudo-Cushing syndrome [1-4].

This topic will review the various stimulation tests using the vasopressin analog desmopressin (DDAVP) in evaluating the pituitary-adrenal axis with a focus on pituitary disease. (See "Insulin-induced hypoglycemia test protocol" and "Diagnosis of adrenal insufficiency in adults".)

Desmopressin testing for bleeding disorders is reviewed elsewhere. (See "von Willebrand disease (VWD): Treatment of minor bleeding, use of DDAVP, and routine preventive care", section on 'DDAVP trial'.)

VASOPRESSIN PHYSIOLOGY — Arginine-vasopressin (AVP) is synthesized in the magnocellular neurons of the supraoptic and paraventricular nuclei and is stored in neurosecretory granules in the axons, which project to the posterior pituitary. In addition, AVP is co-secreted with corticotropin-releasing hormone (CRH) from smaller parvocellular neurons in a section of the paraventricular nuclei, which project their axons to the median eminence and portal system of the pituitary stalk [5]. At this site, AVP promotes the secretion of corticotropin (ACTH) via activation of arginine-vasopressin receptor 1B (AVPR1B, previously named V1B or V3 receptor) present in corticotropes [6].

Cortisol inhibits the secretion of both CRH and AVP from the paraventricular nuclei [7]. Cortisol deficiency decreases this inhibitory effect, leading to a persistent rise in vasopressin release, water retention, and hyponatremia [5,7,8]. The AVPR2 receptors on the cortical and medullary collecting kidney tubules mediate the antidiuretic response via the migration of aquaporin-2 water channels [9]. AVPR2 on vascular endothelium can modulate the release of factor VIII and von Willebrand factor [10]. Both AVPR1A and AVPR1B activate phospholipase C [6,11,12], while the AVPR2 is coupled to adenylyl cyclase [13,14].

AVP are expected to bind to all three receptors; desmopressin is a preferential AVPR2 receptor-selective agent and has only limited effects on AVPR1A and AVPR1B. (See "Hyponatremia and hyperkalemia in adrenal insufficiency".)

CLINICAL USES — Arginine-vasopressin (AVP), 8-lysine-vasopressin (LVP), and terlipressin have been used in a number of clinical settings [15]. In general, these have been abandoned in the differential diagnosis of ACTH-dependent hypercortisolism (due primarily to vasopressor actions and the availability of other tests). Desmopressin is the only vasopressin agonist that is currently used for this purpose. Other factors contributing to the increased use of desmopressin include the lack of commercially available ovine corticotropin-releasing hormone (CRH) for injection in many countries (including the United States and Canada) and the lower cost of desmopressin. Desmopressin has also been utilized more in countries where CRH is still available, as there is growing evidence that it may be equivalent or even superior to CRH [16]. Desmopressin stimulation tests have been used to:

Distinguish between the causes of ACTH-dependent Cushing syndrome (Cushing disease and ectopic ACTH syndrome).

Distinguish between Cushing syndrome and pseudo-Cushing syndrome (CRH after dexamethasone test) versus desmopressin tests. (See "Establishing the diagnosis of Cushing syndrome", section on 'CRH after dexamethasone test'.)

Stimulate ACTH secretion from corticotroph tumors during petrosal sinus sampling. Most often, desmopressin is used as a substitute for CRH, but some studies have evaluated the combination [17].

During the follow-up of patients with Cushing disease to evaluate for possible recurrence of disease after surgical removal of their corticotrope tumor. (See "Primary therapy of Cushing disease: Transsphenoidal surgery and pituitary irradiation", section on 'Recurrence'.)

DESMOPRESSIN STIMULATION TEST PROCEDURE — The test is usually performed in the morning with the patient fasting. An intravenous (IV) line is established 30 minutes before the test is begun. Blood samples for measurement of plasma corticotropin (ACTH) and serum cortisol are obtained 15 minutes and immediately before and 15, 30, 45, 60, 90, and 120 minutes after the injection of desmopressin [18,19]. Shorter and longer versions of this test have been used [3,20-24]. In fact, sampling 15 minutes and immediately before, and at 15, 30, 45 and 60 minutes seems to perform as well as the 120-minute test [3,23].

The recommended dose of desmopressin is 10 mcg IV [18,19], although lower doses (5 to 8 mcg) have been used successfully [18,22,25].

Interpretation — Desmopressin, a selective AVPR2 receptor agonist, does not stimulate ACTH and cortisol levels in most healthy individuals who do not harbor ACTH-secreting corticotroph tumors. However, as many as 10 percent of healthy subjects do respond [18,21,22], presumably because of low-level pituitary expression of AVPR2 [26].

There are no accepted criteria to define a positive response to the desmopressin test [3]. Proposed criteria include the following:

A 33 percent increase in ACTH and an 18 percent increase in cortisol [27].

An increase in basal-to-peak cortisol greater than 20 percent or ACTH greater than 50 percent [28].

An ACTH peak >15.8 pmol/L or an absolute increase in ACTH >8.1 pmol/L [23].

Side effects — Desmopressin is an AVPR2 preferential agonist and lacks the vasoconstrictive, pallor, and abdominal discomfort mediated by the AVPR1A action of the natural vasopressins. However, it shares their effect on platelets. Symptomatic hyponatremia might occur after desmopressin injection; although uncommon patients should be advised to restrict fluid intake for 12 hours following its administration.

ACTH-DEPENDENT CUSHING SYNDROME — The desmopressin test is used in the evaluation of corticotropin (ACTH)-dependent Cushing syndrome [1,2,29,30].

Identifying the cause — Desmopressin can be used for the differential diagnosis of Cushing syndrome. At low doses (1 ng/kg/min), desmopressin fails to potentiate the effect of corticotropin-releasing hormone (CRH) on ACTH release in most normal subjects [31]. At a higher dose (10 mcg intravenous [IV]), it causes an increase in plasma ACTH and serum cortisol concentrations in most patients with Cushing disease [18,20,32-34], suggesting that the test could be used to diagnose this condition.

In patients with Cushing disease, using criteria of a 30 or 50 percent increase in plasma ACTH in response to desmopressin, 95 and 81 percent of patients respond, respectively; using the criterion of a greater than 20 percent increase in serum cortisol, 80 to 85 percent of patients respond [18,20,33-36]. However, in some reports, 8 of 25 (32 percent) of patients with ectopic ACTH syndrome, mostly benign carcinoid tumors, also responded [18,20,22,28,33,34,37-39].

Desmopressin has a relatively low affinity for the AVPR1B receptor [12,40] that is found on normal pituitary corticotrophs, on most adenomatous corticotrophs, and on some ACTH-secreting bronchial carcinoid adenomas [41]. It was unclear whether this response to desmopressin was mediated by abnormal expression of the AVPR2 on the cells of the corticotroph adenomas and ectopic ACTH-producing tumors [34] or by increased expression of the AVPR1B [38]. However, a study in patients with Cushing disease suggests that the ACTH response to desmopressin correlates better with AVPR2 expression levels than with AVPR1B [26]. A higher in vivo response to desmopressin than that observed in corticotroph adenoma cultures (compared with high in vitro CRH response) suggested that other unidentified mechanisms to stimulate ACTH release may also be implicated [42]. Responsiveness to desmopressin has been observed in a bronchial carcinoid tumor in vitro [39].

Combined with CRH — When desmopressin is given in combination with corticotropin-releasing hormone (CRH), virtually all patients with Cushing disease have an increase in plasma ACTH concentrations, using the criterion of a 35 percent rise after CRH with desmopressin [37,43]. Some clinicians use the combined test routinely, but it is more expensive.

Some patients with ectopic ACTH secretion also respond [37,43,44]. Since obese subjects without Cushing syndrome may have a pronounced response to the combined CRH-AVP (arginine-vasopressin) stimulation test, it is important to use the test only in the setting of confirmed Cushing syndrome [45].

During petrosal sinus sampling — Desmopressin has been used in place of CRH to perform petrosal sinus sampling in small series [3,17,44,46-48]. There are differences of opinion about when to use this test clinically.

Many clinicians perform petrosal sinus sampling with CRH without first determining if the pituitary tumor responds to CRH. However, another approach is to perform a desmopressin test first (which is less expensive than CRH), and if the tumor is very responsive, then use desmopressin rather than CRH to stimulate ACTH during petrosal sinus sampling [49].

In a retrospective analysis of combined CRH and desmopressin testing during petrosal sinus sampling in 47 patients with proven Cushing disease and 7 with occult ectopic ACTH-secreting tumors, a post-stimulation gradient >2 was seen in 46 of 47 and 0 of 7 patients with Cushing disease and ectopic ACTH, respectively (diagnostic accuracy of 98.7 percent) [50]. However, desmopressin (alone or in combination with CRH) during inferior petrosal sinus sampling may, on occasion, yield a false-positive diagnosis of Cushing disease [51].

Some studies and meta-analyses have found that the ACTH response to desmopressin during inferior petrosal sinus sampling had a sensitivity of 95 to 99 percent for the diagnosis of Cushing disease and was equivalent or even superior to CRH [16,52-54]. Similar to CRH [55], its use to accurately lateralize the corticotroph tumor is of limited value [53]. Like with CRH [56-58], the measurement of prolactin as an index of the adequacy of inferior petrosal sinus sampling venous sampling is effective with desmopressin [59].

It has been suggested that desmopressin testing and the high-dose dexamethasone suppression test performed on separate occasions can reduce the need for petrosal sinus sampling [60]. A noninvasive algorithm to avoid petrosal sinus sampling has been proposed involving peripheral desmopressin and CRH testing in conjunction with pituitary and extensive whole-body imaging; this approach has the potential to avoid 47 percent of the current indications of bilateral inferior petrosal sinus sampling [27].

Cushing disease versus pseudo-Cushing syndrome — The desmopressin test may be useful to distinguish patients with Cushing disease from those with pseudo-Cushing syndrome [2]. Pseudo-Cushing syndrome is best defined as physiologic or non-neoplastic hypercortisolism and can occur in several disorders other than Cushing syndrome [1]. Examples include pregnancy, obesity, psychological or physical stress, depression, and chronic alcoholism.

Using a criterion for response of an ACTH increase of at least 4 pmol/L [61] or 6 pmol/L [36], patients with pseudo-Cushing syndrome are identified by a smaller increase [21,28,36,61,62]. However, the false-positive and false-negative rates are approximately 10 percent. Furthermore, 13 to 60 percent of healthy subjects respond to desmopressin (although less frequently than patients with Cushing disease). A subsequent study suggested that use of an absolute increase in ACTH of 37 pg/mL (8.1 pmol/L) has a better sensitivity (88 percent) and specificity (96 percent) [23], but this criterion has not been tested widely. Thus, caution must be used as desmopressin alone is not sufficiently specific to establish a diagnosis of Cushing syndrome [3,18,19,21,32]. (See "Causes and pathophysiology of Cushing syndrome", section on 'Pseudo-Cushing syndrome'.)

In one head-to-head comparison, desmopressin testing had better specificity (90 percent) but less sensitivity (82 percent) [61] or perhaps better [63] than the dexamethasone suppressed-ovine CRH test (63 percent specificity; 100 percent sensitivity) for distinguishing Cushing disease from pseudo-Cushing syndrome. Another study suggested that the combination of dexamethasone (given in the evening) and desmopressin (8 mcg, IV), may improve performance in differentiating Cushing disease and pseudo-Cushing syndrome, but only nine subjects with pseudo-Cushing syndrome were studied [25]. (See "Establishing the diagnosis of Cushing syndrome", section on 'CRH after dexamethasone test'.)

Evaluating for remission of Cushing disease — Postoperative desmopressin testing may be useful in individuals who had a strong response preoperatively. In a study of 14 patients in remission of their Cushing disease by transsphenoidal microadenomectomy, none responded to CRH or desmopressin immediately after surgery, but five patients who were not cured did respond to CRH, desmopressin, or both [64]. Responsiveness to CRH returned over a period of several months as normal hypothalamic-pituitary-adrenal function was restored, but the response to desmopressin did not return. A useful approach has been suggested in which preoperative desmopressin be performed to inform the use of desmopressin to monitor patients long term for recurrence [3,64].

Some studies suggest that in patients who have achieved initial remission after pituitary surgery, those who have a cortisol response to follow-up desmopressin testing (>193 nmol/L [7 mcg/dL] in one report [65] or >14 percent in another [66]) are more likely to have a recurrence [65-67]. In one report, there was no concordance between the clinical response to surgery and the postoperative response to desmopressin [35]. Some studies have demonstrated that some patients who lacked a response to desmopressin after successful adenomectomy did subsequently respond, even years before frank hypercortisolism reappeared [68].

A combined dexamethasone-desmopressin test (CDDT) may also be a predictor of recurrence after pituitary surgery. Dexamethasone is added to decrease the nonspecific response of normal corticotrophs to desmopressin. In one report of 38 patients following successful pituitary surgery for Cushing disease, 1 mg of dexamethasone was administered overnight, and 10 mcg desmopressin was injected intravenously on the following morning. An increase of serum plasma cortisol and ACTH of more than 50 percent was an early predictor of recurrence (100 percent sensitivity, 89 percent specificity) [69]. Rather than use percent changes, another study found that an increase of cortisol of 7.4 micrograms/dL (204 nmol/L) in response to desmopressin within six months of surgery was a useful cutoff to predict continued remission versus subsequent recurrence. While late-night salivary cortisol may best discriminate recurrence [70], desmopressin testing may be useful when salivary cortisol results are inconsistent or not available [71].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diagnosis and treatment of Cushing syndrome".)

SUMMARY

Vasopressin physiology Arginine-vasopressin (AVP) is synthesized in the magnocellular neurons of the supraoptic and paraventricular nuclei, which project to the neurohypophysis; it is also co-secreted with corticotropin-releasing hormone (CRH) from single parvocellular neurons in the paraventricular nuclei, which project their axons to the median eminence and portal system. AVP has three distinct receptors, which mediate a number of physiologic effects, including its antidiuretic effect and regulation of corticotropin (ACTH). (See 'Vasopressin physiology' above.)

Desmopressin stimulation tests The desmopressin test is used most commonly in countries where CRH is not currently available or too costly; desmopressin testing is now more widely utilized and shown to be equivalent or even superior to CRH. Desmopressin stimulation tests are used for several indications:

Cushing disease versus ectopic ACTH Distinguish between the causes of ACTH-dependent Cushing syndrome (Cushing disease and ectopic ACTH syndrome). (See 'Clinical uses' above and 'Identifying the cause' above.)

Cushing disease versus pseudo-Cushing – Distinguish between Cushing disease and pseudo-Cushing syndrome. (See 'Cushing disease versus pseudo-Cushing syndrome' above.)

Combined dexamethasone-desmopressin test Combined low-dose, overnight dexamethasone followed by desmopressin test on the following morning appears promising as an early predictor of recurrence of Cushing disease following corticotroph tumor resection; long-term assessment of larger number of patients will be necessary to determine the usefulness of this test. (See 'Evaluating for remission of Cushing disease' above.)

ACKNOWLEDGMENT — The views expressed in this topic are those of the author(s) and do not reflect the official views or policy of the United States Government or its components.

  1. Findling JW, Raff H. DIAGNOSIS OF ENDOCRINE DISEASE: Differentiation of pathologic/neoplastic hypercortisolism (Cushing's syndrome) from physiologic/non-neoplastic hypercortisolism (formerly known as pseudo-Cushing's syndrome). Eur J Endocrinol 2017; 176:R205.
  2. Vassiliadi DA, Tsagarakis S. DIAGNOSIS OF ENDOCRINE DISEASE: The role of the desmopressin test in the diagnosis and follow-up of Cushing's syndrome. Eur J Endocrinol 2018; 178:R201.
  3. Castinetti F, Lacroix A. Is Desmopressin Useful in the Evaluation of Cushing Syndrome? J Clin Endocrinol Metab 2022; 107:e4295.
  4. Fleseriu M, Auchus R, Bancos I, et al. Consensus on diagnosis and management of Cushing's disease: a guideline update. Lancet Diabetes Endocrinol 2021; 9:847.
  5. Zimmerman EA, Nilaver G, Hou-Yu A, Silverman AJ. Vasopressinergic and oxytocinergic pathways in the central nervous system. Fed Proc 1984; 43:91.
  6. Sugimoto T, Saito M, Mochizuki S, et al. Molecular cloning and functional expression of a cDNA encoding the human V1b vasopressin receptor. J Biol Chem 1994; 269:27088.
  7. Raff H. Glucocorticoid inhibition of neurohypophysial vasopressin secretion. Am J Physiol 1987; 252:R635.
  8. Zimmerman EA, Ma LY, Nilaver G. Anatomical basis of thirst and vasopressin secretion. Kidney Int Suppl 1987; 21:S14.
  9. Deen PM, Verdijk MA, Knoers NV, et al. Requirement of human renal water channel aquaporin-2 for vasopressin-dependent concentration of urine. Science 1994; 264:92.
  10. Bichet DG, Razi M, Lonergan M, et al. Hemodynamic and coagulation responses to 1-desamino[8-D-arginine] vasopressin in patients with congenital nephrogenic diabetes insipidus. N Engl J Med 1988; 318:881.
  11. Thibonnier M, Auzan C, Madhun Z, et al. Molecular cloning, sequencing, and functional expression of a cDNA encoding the human V1a vasopressin receptor. J Biol Chem 1994; 269:3304.
  12. de Keyzer Y, Auzan C, Lenne F, et al. Cloning and characterization of the human V3 pituitary vasopressin receptor. FEBS Lett 1994; 356:215.
  13. Birnbaumer M, Seibold A, Gilbert S, et al. Molecular cloning of the receptor for human antidiuretic hormone. Nature 1992; 357:333.
  14. Lolait SJ, O'Carroll AM, McBride OW, et al. Cloning and characterization of a vasopressin V2 receptor and possible link to nephrogenic diabetes insipidus. Nature 1992; 357:336.
  15. Ferrante E, Barbot M, Serban AL, et al. Indication to dynamic and invasive testing in Cushing's disease according to different neuroradiological findings. J Endocrinol Invest 2022; 45:629.
  16. Govindarajan V, Lu VM, Clarke JE, et al. Positive predictive value and trends of inferior petrosal sinus sampling (IPSS) in diagnosing cushing disease and ectopic ACTH secretion: A systematic review and meta-analysis. Clin Neurol Neurosurg 2022; 220:107350.
  17. Machado MC, de Sa SV, Domenice S, et al. The role of desmopressin in bilateral and simultaneous inferior petrosal sinus sampling for differential diagnosis of ACTH-dependent Cushing's syndrome. Clin Endocrinol (Oxf) 2007; 66:136.
  18. Malerbi DA, Mendonça BB, Liberman B, et al. The desmopressin stimulation test in the differential diagnosis of Cushing's syndrome. Clin Endocrinol (Oxf) 1993; 38:463.
  19. Scott LV, Medbak S, Dinan TG. ACTH and cortisol release following intravenous desmopressin: a dose-response study. Clin Endocrinol (Oxf) 1999; 51:653.
  20. Terzolo M, Reimondo G, Alì A, et al. The limited value of the desmopressin test in the diagnostic approach to Cushing's syndrome. Clin Endocrinol (Oxf) 2001; 54:609.
  21. Malerbi DA, Fragoso MC, Vieira Filho AH, et al. Cortisol and adrenocorticotropin response to desmopressin in women with Cushing's disease compared with depressive illness. J Clin Endocrinol Metab 1996; 81:2233.
  22. Sakai Y, Horiba N, Tozawa F, et al. Desmopressin stimulation test for diagnosis of ACTH-dependent Cushing's syndrome. Endocr J 1997; 44:687.
  23. Rollin GA, Costenaro F, Gerchman F, et al. Evaluation of the DDAVP test in the diagnosis of Cushing's Disease. Clin Endocrinol (Oxf) 2015; 82:793.
  24. Le Marc'hadour P, Muller M, Albarel F, et al. Postoperative follow-up of Cushing's disease using cortisol, desmopressin and coupled dexamethasone-desmopressin tests: a head-to-head comparison. Clin Endocrinol (Oxf) 2015; 83:216.
  25. Araya AV, Romero C, Lemp M. Combined dexamethasone and desmopressin test in the differential diagnosis of ACTH-dependent Cushing's syndrome and pseudo-cushing's states. Pituitary 2017; 20:602.
  26. Wang FF, Tang KT, Yen YS, et al. Plasma corticotrophin response to desmopressin in patients with Cushing's disease correlates with the expression of vasopressin receptor 2, but not with that of vasopressin receptor 1 or 3, in their pituitary tumours. Clin Endocrinol (Oxf) 2012; 76:253.
  27. Frete C, Corcuff JB, Kuhn E, et al. Non-invasive Diagnostic Strategy in ACTH-dependent Cushing's Syndrome. J Clin Endocrinol Metab 2020; 105.
  28. Tsagarakis S, Vasiliou V, Kokkoris P, et al. Assessment of cortisol and ACTH responses to the desmopressin test in patients with Cushing's syndrome and simple obesity. Clin Endocrinol (Oxf) 1999; 51:473.
  29. Nieman LK. Recent Updates on the Diagnosis and Management of Cushing's Syndrome. Endocrinol Metab (Seoul) 2018; 33:139.
  30. Nieman LK. Diagnosis of Cushing's Syndrome in the Modern Era. Endocrinol Metab Clin North Am 2018; 47:259.
  31. Gaillard RC, Riondel AM, Ling N, Muller AF. Corticotropin releasing factor activity of CRF 41 in normal man is potentiated by angiotensin II and vasopressin but not by desmopressin. Life Sci 1988; 43:1935.
  32. Scott LV, Medbak S, Dinan TG. Desmopressin augments pituitary-adrenal responsivity to corticotropin-releasing hormone in subjects with chronic fatigue syndrome and in healthy volunteers. Biol Psychiatry 1999; 45:1447.
  33. Colombo P, Passini E, Re T, et al. Effect of desmopressin on ACTH and cortisol secretion in states of ACTH excess. Clin Endocrinol (Oxf) 1997; 46:661.
  34. Tsagarakis S, Tsigos C, Vasiliou V, et al. The desmopressin and combined CRH-desmopressin tests in the differential diagnosis of ACTH-dependent Cushing's syndrome: constraints imposed by the expression of V2 vasopressin receptors in tumors with ectopic ACTH secretion. J Clin Endocrinol Metab 2002; 87:1646.
  35. Losa M, Mortini P, Dylgjeri S, et al. Desmopressin stimulation test before and after pituitary surgery in patients with Cushing's disease. Clin Endocrinol (Oxf) 2001; 55:61.
  36. Moro M, Putignano P, Losa M, et al. The desmopressin test in the differential diagnosis between Cushing's disease and pseudo-Cushing states. J Clin Endocrinol Metab 2000; 85:3569.
  37. Newell-Price J, Perry L, Medbak S, et al. A combined test using desmopressin and corticotropin-releasing hormone in the differential diagnosis of Cushing's syndrome. J Clin Endocrinol Metab 1997; 82:176.
  38. Dahia PL, Ahmed-Shuaib A, Jacobs RA, et al. Vasopressin receptor expression and mutation analysis in corticotropin-secreting tumors. J Clin Endocrinol Metab 1996; 81:1768.
  39. Arlt W, Dahia PL, Callies F, et al. Ectopic ACTH production by a bronchial carcinoid tumour responsive to desmopressin in vivo and in vitro. Clin Endocrinol (Oxf) 1997; 47:623.
  40. Antoni FA. Novel ligand specificity of pituitary vasopressin receptors in the rat. Neuroendocrinology 1984; 39:186.
  41. Arnaldi G, de Keyzer Y, Gasc JM, et al. Vasopressin receptors modulate the pharmacological phenotypes of Cushing's syndrome. Endocr Res 1998; 24:807.
  42. Pecori Giraldi F, Marini E, Torchiana E, et al. Corticotrophin-releasing activity of desmopressin in Cushing's disease: lack of correlation between in vivo and in vitro responsiveness. J Endocrinol 2003; 177:373.
  43. Dickstein G, DeBold CR, Gaitan D, et al. Plasma corticotropin and cortisol responses to ovine corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), CRH plus AVP, and CRH plus metyrapone in patients with Cushing's disease. J Clin Endocrinol Metab 1996; 81:2934.
  44. Tsagarakis S, Kaskarelis IS, Kokkoris P, et al. The application of a combined stimulation with CRH and desmopressin during bilateral inferior petrosal sinus sampling in patients with Cushing's syndrome. Clin Endocrinol (Oxf) 2000; 52:355.
  45. Pasquali R, Gagliardi L, Vicennati V, et al. ACTH and cortisol response to combined corticotropin releasing hormone-arginine vasopressin stimulation in obese males and its relationship to body weight, fat distribution and parameters of the metabolic syndrome. Int J Obes Relat Metab Disord 1999; 23:419.
  46. Kaltsas GA, Giannulis MG, Newell-Price JD, et al. A critical analysis of the value of simultaneous inferior petrosal sinus sampling in Cushing's disease and the occult ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab 1999; 84:487.
  47. Booth GL, Redelmeier DA, Grosman H, et al. Improved diagnostic accuracy of inferior petrosal sinus sampling over imaging for localizing pituitary pathology in patients with Cushing's disease. J Clin Endocrinol Metab 1998; 83:2291.
  48. Virú-Loza MA, Quispe AV. Diagnostic Power of Bilateral Inferior Petrosal Sinus Sampling with Desmopressin in Paediatric Cushing’s Disease. J Clin Res Pediatr Endocrinol 2022; 14:334.
  49. Lacroix A, Feelders RA, Stratakis CA, Nieman LK. Cushing's syndrome. Lancet 2015; 386:913.
  50. Tsagarakis S, Vassiliadi D, Kaskarelis IS, et al. The application of the combined corticotropin-releasing hormone plus desmopressin stimulation during petrosal sinus sampling is both sensitive and specific in differentiating patients with Cushing's disease from patients with the occult ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab 2007; 92:2080.
  51. Findling JW, Raff H. Newer diagnostic techniques and problems in Cushing's disease. Endocrinol Metab Clin North Am 1999; 28:191.
  52. Deipolyi AR, Alexander B, Rho J, et al. Bilateral inferior petrosal sinus sampling using desmopressin or corticotropic-releasing hormone: a single-center experience. J Neurointerv Surg 2015; 7:690.
  53. Feng M, Liu Z, Liu X, et al. Tumour lateralization in Cushing's disease by inferior petrosal sinus sampling with desmopressin. Clin Endocrinol (Oxf) 2018; 88:251.
  54. Valizadeh M, Ahmadi AR, Ebadinejad A, et al. Diagnostic accuracy of bilateral inferior petrosal sinus sampling using desmopressin or corticotropic- releasing hormone in ACTH-dependent Cushing's syndrome: A systematic review and meta-analysis. Rev Endocr Metab Disord 2022; 23:881.
  55. Wind JJ, Lonser RR, Nieman LK, et al. The lateralization accuracy of inferior petrosal sinus sampling in 501 patients with Cushing's disease. J Clin Endocrinol Metab 2013; 98:2285.
  56. Mulligan GB, Faiman C, Gupta M, et al. Prolactin measurement during inferior petrosal sinus sampling improves the localization of pituitary adenomas in Cushing's disease. Clin Endocrinol (Oxf) 2012; 77:268.
  57. Sharma ST, Raff H, Nieman LK. Prolactin as a marker of successful catheterization during IPSS in patients with ACTH-dependent Cushing's syndrome. J Clin Endocrinol Metab 2011; 96:3687.
  58. Findling JW, Kehoe ME, Raff H. Identification of patients with Cushing's disease with negative pituitary adrenocorticotropin gradients during inferior petrosal sinus sampling: prolactin as an index of pituitary venous effluent. J Clin Endocrinol Metab 2004; 89:6005.
  59. Qiao X, Ye H, Zhang X, et al. The value of prolactin in inferior petrosal sinus sampling with desmopressin stimulation in Cushing's disease. Endocrine 2015; 48:644.
  60. Qiao J, Li J, Zhang W, et al. The usefulness of the combined high-dose dexamethasone suppression test and desmopressin stimulation test in establishing the source of ACTH secretion in ACTH-dependent Cushing's syndrome. Endocr J 2021; 68:839.
  61. Tirabassi G, Papa R, Faloia E, et al. Corticotrophin-releasing hormone and desmopressin tests in the differential diagnosis between Cushing's disease and pseudo-Cushing state: a comparative study. Clin Endocrinol (Oxf) 2011; 75:666.
  62. Coiro V, Volpi R, Capretti L, et al. Desmopressin and hexarelin tests in alcohol-induced pseudo-Cushing's syndrome. J Intern Med 2000; 247:667.
  63. Pecori Giraldi F, Pivonello R, Ambrogio AG, et al. The dexamethasone-suppressed corticotropin-releasing hormone stimulation test and the desmopressin test to distinguish Cushing's syndrome from pseudo-Cushing's states. Clin Endocrinol (Oxf) 2007; 66:251.
  64. Colombo P, Dall'Asta C, Barbetta L, et al. Usefulness of the desmopressin test in the postoperative evaluation of patients with Cushing's disease. Eur J Endocrinol 2000; 143:227.
  65. Romanholi DJ, Machado MC, Pereira CC, et al. Role for postoperative cortisol response to desmopressin in predicting the risk for recurrent Cushing's disease. Clin Endocrinol (Oxf) 2008; 69:117.
  66. Valéro R, Vallette-Kasic S, Conte-Devolx B, et al. The desmopressin test as a predictive factor of outcome after pituitary surgery for Cushing's disease. Eur J Endocrinol 2004; 151:727.
  67. Dall'Asta C, Barbetta L, Bonavina L, et al. Recurrence of Cushing's disease preceded by the reappearance of ACTH and cortisol responses to desmopressin test. Pituitary 2004; 7:183.
  68. Ambrogio AG, Andrioli M, De Martin M, et al. Usefulness of desmopressin testing to predict relapse during long-term follow-up in patients in remission from Cushing's disease. Endocr Connect 2017; 6:791.
  69. Castinetti F, Martinie M, Morange I, et al. A combined dexamethasone desmopressin test as an early marker of postsurgical recurrence in Cushing's disease. J Clin Endocrinol Metab 2009; 94:1897.
  70. Danet-Lamasou M, Asselineau J, Perez P, et al. Accuracy of repeated measurements of late-night salivary cortisol to screen for early-stage recurrence of Cushing's disease following pituitary surgery. Clin Endocrinol (Oxf) 2015; 82:260.
  71. Vassiliadi DA, Balomenaki M, Asimakopoulou A, et al. The Desmopressin Test Predicts Better Than Basal Cortisol the Long-Term Surgical Outcome of Cushing's Disease. J Clin Endocrinol Metab 2016; 101:4878.
Topic 158 Version 21.0

References

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