An exaggerated diurnal weight gain is a feature of idiopathic edema; normal women gain approximately 0.6 kg during the day, whereas women with idiopathic edema gain more than 1.4 kg [1], Concern about weight can lead to intermittent fasting and binging in some patients which may be a factor in causing the edema. Fasting suppresses the sympathetic nervous system, and the natriuresis of fasting is in part due to decreased renal sympathetic nerve activity. Carbohydrate feeding results in increased sympathetic activity with subsequent sodium reabsorption. Edema can occur in normal women going from a low to a high carbohydrate diet if sodium intake is high [ 12].

The possible role of prolactin in the disease was engendered by the report of one patient with galactorrhea and idiopathic edema. Although prolactin is important in salt and water retention in some vertebrates, particularly birds, there is no evidence that it plays a similar role in humans. However, since prolactin secretion is inhibited by dopaminergic receptors in the hypothalamus, bromocriptine has been used to treat idiopathic edema, without uniform success [4]. There is no convincing evidence that estrogen plays a role in idiopathic edema even though estradiol in high doses, 10-20 mg daily, decreases sodium excretion. Some patients with idiopathic edema are postmenopausal, and normal estrogen and progesterone excretion have been documented in affected patients.

Although angioedema is clinically dissimilar to idiopathic edema in that the episodes of edema are acute and episodic, some have postulated a change in capillary permeability to protein in women with idiopathic edema [11]. In one series comparing normal subjects and patients with idiopathic edema, plasma albumin concentrations were lower in women with the disorder. A greater fractional turnover of albumin was deemed the cause in some, while a lower rate of albumin synthesis was observed in others. However, there is no convincing evidence that the disappearance rate of 125I-labeled albumin is greater in patients with idiopathic edema, although women have greater transcapillary protein flux than men when venous pressure is raised artificially. The decrease in plasma volume reported in some series may reflect obesity, which reduces calculated plasma volume when expressed as milliliters per kilogram of body weight.

Recently a syndrome has been described which may have relevance to idiopathic edema. In approximately 2% of women undergoing induction of ovulation prior to in vitro fertilization, the development of ascites with edema of the legs, hands, and face occurs. In some patients this has caused volume depletion with hemoconcentration and renal failure [2], It has been postulated that endothelial cell damage due to administration of high doses of follicle-stimulating hormone and luteinizing hormone during pituitary suppression with a gonadotropin-releasing hormone analog causes a capillary leak syndrome. However, when a large series of women with this syndrome were studied only half were hemoconcentrated, while all demonstrated increased cardiac output and low peripheral vascular resistance. Elevated plasma levels of renin, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide were noted in conjunction with elevated urinary PGE2 and 6-keto-PGFia:. The syndrome seems to result from endothelial cell dysfunction which may increase capillary permeability to plasma protein in some women, but cause vasodilation in all, the latter a stimulus to renal sodium absorption. This syndrome provides a striking demonstration of the effect of hormonal stimuli on endothelial cell function.

There is little evidence that a diminished effective blood volume occurs with idiopathic edema since plasma renin, a sensitive indicator of volume perception by the juxtaglomerular apparatus, is not elevated. Moreover, studies in women with idiopathic edema have demonstrated salt retention during normal suppression of renin and aldosterone secretion [9] and with normal increased secretion of atrial natriuretic hormone [ 1].

DeWardener suggested that idiopathic edema was caused by diuretic abuse based on the observation that when diuretics are discontinued in these women intense salt retention occurs, followed by normalization of sodium excretion with time [5], Although chronic diuretic intake may certainly exacerbate sodium retention, this hypothesis would not explain why the women take diuretics initially, nor why many with the disorder have been documented never to have taken diuretics [ 13]. In trying to wean patients from diuretics, it is important to recognize the role of potassium deficiency in the rebound sodium retention which can occur, perhaps exacerbating edema [10].


Due to the poorly understood nature of the disorder and its many postulated mechanisms, no single treatment for idiopathic edema exists. Some patients benefit from conservative measures such as the avoidance of prolonged periods of standing and moderate salt restriction. Additionally, the use of elastic stockings may be particularly helpful in patients in whom orthostatic sodium and water retention is excessive. However, diuretics are sometimes required to adequately control edema. Diuretics should be limited to alternate days if possible and potassium supplementation administered appropriately. Given the long held theory that idiopathic edema could result from an exaggerated response of aldosterone to upright posture, some clinicians have suggested that spironolactone, an aldosterone antagonist, is the preferred agent. This is based on anecdotal evidence, however, and it is not clear whether there is any benefit over a thiazide diuretic. Loop diuretics have been avoided by some clinicians in large part due to the findings of worsening renal function in some patients on long-term furosemide therapy [ 14]. Sympathomimetic drugs such as ephedrine have been employed with some success, perhaps by lowering aldosterone secretion [8]. Likewise, angiotensin converting enzyme inhibitors have shown promising results in some small series [6]. It is important in the treatment of women with idiopathic edema to emphasize the benign nature of the disorder. The patient should be reassured that there are various factors controlling sodium retention that are not completely understood. Likewise, the physician should not be threatened or confused by the failure to understand the pathophysiology of the disorder. To infer that the problem is psychologic or to imply that the disease has been caused by surreptitious diuretic abuse only causes guilt feelings that become counterproductive to proper treatment. As with all chronic diseases, a relationship of trust and confidence between patient and doctor is of utmost therapeutic value.


1. Anderson, G. H., and Streeten, D. H. (1990). Effect of posture on plasma atrial natriuretic hormone and renal function during salt loading in patients with and without idiopathic edema. J. Clin. Endo. Metab. 71, 243-246.

2. Balasch, J., e£ al (1994). Hemohormonal and hemodynamic change in severe cases of the ovarian hyperstimulationsyndrome. Ann. Int. Med. 121, 27-33.

3. BihunJ. A. P., McSherry, J., and Marciano, D. (1993). Idiopathic edema and eating disorders: Evidence for an association, int. J. Eating Disorders 14,197-201.

4. Cateria, R. A., et al. (1984). Altered dopaminergic modulation of sympathetic nervous system activity in idiopathic edema. J. Endo. Invest. 7, 461-466.

5. DeWardenerJ. E. (1981). Idiopathic edema: Role of diuretic abuse. Kidney Int. 19, 881.

6. Docci, D., Turci, F., and Salvi, G. (1983). Therapeutic response of idiopathic edema to Captopril. Nephron 34, 198-200.

7. Dunnigan, M. G., and Pelosi, A. J. (1993). Familial idiopathic edema in pre-pubertal children: a new syndrome. Q.J. Med. 86, 301-313.

8. Edwards, B. D., and Hudson, W. A. (1991). A novel treatment for idiopathic oedema of women. Nephron 58, 369-370.

9. Ferris, T. F., et al. (1973). Studies of the mechanism of sodium retention in idiopathic edema. Trans. Assoc. Am. Physicians 86, 310.

10. Galvez, O. G., et al. (1977). The hemodynamic effects of potassium deficiency in the dog. Circ. Res. 40,(Suppl. 1), 5.

11. Gill, J. R.,Jr., et al. (1972). Idiopathic edema. I. The occurrence of hypoalbuminemia and abnormal albumin metabolism in women with unexplained edema. Am. J. Med. 52, 444.

12. Landsberg, L., and Young, J. B. (1978). Fasting, feeding, and regulation of the sympathetic nervous system. N. Engl. J. Med. 298,1295.

13. Pelosi, A. J., et al (1995). The role of diuretics in the aetiology of idiopathic oedema. Q.J. Med. 88,49-54.

14. Shichiri, M., Shiigai, T., and TakeuchiJ. (1984). Long-term furosemide treatment in idiopathic edema. Arch. Intern. Med. 144, 2161.


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