Mechanisms of Altered Water Metabolism in Psychotic Patients with Polydipsia and Hyponatremia

Goldman, Michael; Luchins, Daniel J.; Robertson, Gary

doi:10.1056/nejm198802183180702

Cited by 289 publications

(140 citation statements)

References 41 publications

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“…Hariprasad et al (1980) described Type II SIADH. Goldman et al (1988), in a well controlled study, found that psychiatric patients with polydipsia had higher levels of vasopressin at any given level of osmolality. They noted that changes in A VP secretion and action were not sufficient to explain the altered sodium levels and osmolality.…”

Section: Arginine Vasopressin or Antidiuretic Hormonementioning

confidence: 96%

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

Verghese

León

Simpson

1993

Neuropsychopharmacol

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Polydipsia and water intoxication cause considerable morbidity and mortality in chronic psychiatric patients. Polydipsia in psychiatric patients has been described si nce the 1930s prior to the use of neuroleptics, but sys te matic study of the disorder has been done mostly in th e last two decades. There are many names for the dis order, which include psychogenic polydipsia (Bauer 1925), compulsive water drinking (Barlow and De Wardener 1959), psychosis, intermittent hyponatremia and polydipsia (PIP) syndrome (Vieweg et al. 1985) and self-induced water intoxication (Hobson and English 1963). The main purpose of this paper is to propose an hypothesis about the pathophysiology of the disorder and to reconceptualize some of the thinking about it.

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Section: Arginine Vasopressin or Antidiuretic Hormonementioning

confidence: 96%

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

Verghese

León

Simpson

1993

Neuropsychopharmacol

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“…Acute psychosis itself can also cause AVP secretion, which often appears to take the form of a reset osmostat. 45 Although no single mechanism can completely explain the occurrence of hyponatremia in psychiatric patients with polydipsia, the combination of higher than normal water intake plus even modest elevations of plasma AVP levels from a variety of potential sources appears to account for a significant portion of such cases.…”

Section: Eahmentioning

confidence: 99%

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

Verbalis

Goldsmith

Greenberg

et al. 2007

The American Journal of Medicine

519

498

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Although hyponatremia is a common, usually mild, and relatively asymptomatic disorder of electrolytes, acute severe hyponatremia can cause substantial morbidity and mortality, particularly in patients with concomitant disease. In addition, overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death, and optimal treatment strategies for such cases are not established. Hyponatremia is the most common disorder of electrolytes encountered in clinical practice, occurring in up to 15% to 30% of both acutely and chronically hospitalized patients. 1 Although most cases are mild and relatively asymptomatic, hyponatremia is important clinically because: (1) acute severe hyponatremia can cause substantial morbidity and mortality; (2) mortality is higher in patients with hyponatremia who have a wide range of underlying diseases; and (3) overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death.Despite knowledge of hyponatremia since the mid-20th century, this common disorder remains incompletely understood in many basic areas because of its association with a plethora of underlying disease states, and its multiple etiologies with differing pathophysiologic mechanisms. 2 Optimal treatment strategies have not been well defined, both for these reasons and because of marked differences in symptomatology and clinical outcomes based on the acuteness or chronicity of the hyponatremia. 3 Vasopressin receptor antagonists have long been anticipated as a more effective method to treat hyponatremia by virtue of their unique aquaretic effect to selectively increase solute-free water excretion by the kidneys. 4 The recent approval of the first such agent, conivaptan, for clinical use by the US Food and Drug Administration (FDA) heralds the beginning of a new era in the management of hyponatremic disorders. However, effective therapy with these agents will require intelligent guidelines for their use. To this end, a panel of experts in hyponatremia convened to review current therapies for hyponatremia and to evaluate the situations in which aquaretic agents should be considered as alternatives or supplements to accepted current therapies. This review is a summary of the conclusions of this panel.

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“…Furthermore, polydipsic patients with and without hyponatremia display impaired HPA axis negative feedback (Goldman et al, 1993) that is consistent with hippocampal pathology (Goldman et al, 2006). In addition, hyponatremic polydipsic (but not normonatremic polydipsic) patients exhibit an unexplained increase in AVP secretion that contributes to their water retention (Goldman et al, 1988(Goldman et al, , 1996. Finally, this defect worsens with the stress of acute psychosis in the hyponatremic subset, culminating in episodes of lifethreatening water intoxication (de Leon et al, 1994;Goldman et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

Goldman

Gnerlich

Hussain

2006

Neuropsychopharmacol

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Schizophrenia, many believe, reflects an enhanced vulnerability to psychological stress. Controlled exposure to stressors, however, has produced inconclusive results, particularly with regards to neurohormones. Some of the variability may be attributable to the nature and psychological significance of the stimulus and failure to control physiologic confounds. In addition, it is possible that the heterogeneity of schizophrenia is an important factor. In a carefully designed study and in a controlled setting, we measured the neuroendocrine response of eight polydipsic hyponatremic (PHS), seven polydipsic normonatremic (PNS), and nine nonpolydipsic normonatremic (NNS) (ie normal water balance) schizophrenic in-patients as well as 12 healthy controls (HC) to two different stressors: one of which appears to influence neuroendocrine secretion through its psychological (cold pressor) and the other (upright posture) through its systemic actions. Subjects in the three psychiatric groups were stabilized and acclimated to the research setting, and all received saline to normalize plasma osmolality. Following the cold pressor, plasma adrenocorticotropin and cortisol levels showed a more prolonged rise in PHS patients relative to PNS patients. NNS patients, in contrast, exhibited blunted responses relative to both of the polydipsic groups and the HC. Peak vasopressin responses were also greater in PHS and blunted in NNS patients. Responses to the postural stimulus were similar across patient groups. These findings provide a mechanism for life threatening water intoxication in schizophrenia; help to reconcile conflicting findings of stress responsiveness in schizophrenia; and potentially identify a discrete patient subset with enhanced vulnerability to psychological stress.

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Mechanisms of Altered Water Metabolism in Psychotic Patients with Polydipsia and Hyponatremia

Cited by 289 publications

References 41 publications

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

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