Department of Internal Medicine, Medical School, University of Ioannina, 45110 Ioannina, Greece
Received 21 March 2000; in revised form 5 June 2000; accepted 13 June 2000
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ABSTRACT |
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INTRODUCTION |
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MATERIALS AND METHODS |
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In patients with hyponatraemia (serum sodium < 134 mmol/l, reference range: 136145 mmol/l), the detection of the underlying pathogenetic mechanisms was our primary task. Diagnostic approach was based on the patients' history and their physical examination, with emphasis on extracellular volume status and on the correct interpretation of laboratory tests. The first step in this approach was to confirm the presence of hypo-osmolality (Posm < 280 mOsm/kg) (Fig. 1). In the setting of normal or elevated effective serum osmolality [measured Posm blood urea (mg/dl)/6], evaluation of one of the causes of pseudohyponatraemia was carried out (severe hyperlipidaemia or hyperproteinaemia) (Weisberg, 1989
; Rose, 1994
). Once it was demonstrated that the patient was hypo-osmolar, the evaluation of the Uosm was used to determine whether water excretion was normal or impaired. A value of Uosm < 100 mOsm/kg was indicative of a complete and appropriate suppression of antidiuretic hormone (ADH) secretion, a finding seen with either primary polydipsia (including beer potomania) or reset osmostat (Gillum and Linas, 1984
). The criteria used to diagnose the beer potomania syndrome included a history of binge beer drinking and poor dietary intake along with decreased serum sodium levels in the absence of other known causes of hyponatraemia (Hilden and Svendsen, 1975
; Fenves et al., 1996
). When Uosm exceeded 100 mOsm/kg, hyponatraemia due to impaired water excretion was diagnosed. Since patients with ascites or peripheral oedema were excluded, normovolaemic or hypovolaemic hyponatraemia was established. In such cases, the urine sodium was evaluated in addition to assessing adrenal and thyroid function. Taking into account that patients with renal failure as well as patients receiving diuretics were excluded, a urine sodium less than 20 mmol/l was indicative of hypovolaemia, while a urine sodium greater than 40 mmol/l was suggestive of the syndrome of inappropriate antidiuresis (SIADH), reset osmostat, and of salt wasting conditions (Chung et al., 1987
). In patients with equivocal findings (urine sodium 2040 mmol/l), the correct diagnosis was based on the response of serum sodium levels following the i.v. administration of sodium chloride (2 l of NaCl 0.9% w/v/day for 2 days). Hypovolaemia was diagnosed if the serum sodium concentration increased by 5 mmol/l or more as a response to this test (Chung et al., 1987
). The reset osmostat syndrome was suspected in patients with persistent hyponatraemia accompanied by an appropriate decrease in Uosm (<100 mOsm/kg) but inappropriate natriuresis (>40 mmol/l). In this setting, the diagnosis was confirmed by calculating free-water clearance (CH2O) (Defronzo et al., 1976
; Elisaf et al., 1996
). Finally, the changes of serum uric acid levels and uric acid FE were evaluated in the differential diagnosis between salt wasting syndrome and SIADH. The restoration of the serum sodium levels by salt supplementation and fluid restriction followed by a reduction in urinary urate excretion pointed to the diagnosis of SIADH, whereas the persistence of hypo-uricaemia and uric acid wasting following normalization of serum sodium levels was suggestive of salt wasting (Maesaka, 1996
).
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RESULTS |
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DISCUSSION |
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The syndrome of beer potomania was diagnosed in two patients. These patients were malnourished binge drinkers and presented with profound hyponatraemia. In beer potomania, hyponatraemia is due to a large consumption of beer (which has a poor salt content) together with a minimal intake of ordinary food. A diet poor in salt and protein compounds (i.e. urea precursors) results in reduced excretion of urinary solutes, which limits the ability to excrete free water (Hilden and Svendsen, 1975; Fenves et al., 1996
; Blaustein and Schwenk, 1997
). In both patients, there was an appropriate renal response to the large fluid intake by maximally diluting the urine (Uosm
100 mOsm/kg). Binge drinkers typically produce less than 250 mOsm of solutes a day; hence, our patients could probably excrete no more than 2.5 l of urine daily (250/100 = 2.5 l). Since they were drinking about 3 l of beer daily, about 0.5 l of fluid was retained leading to dilutional hyponatraemia.
In one patient presenting hyponatraemia with inappropriate natriuresis, the syndrome of SIADH was implicated. However, the patient fulfilled the criteria for the diagnosis of the reset osmostat syndrome (Defronzo et al., 1976; Wall et al., 1992
; Elisaf et al., 1996
). Specifically, this patient had:
(1) normovolaemic hyponatraemia and could maintain sodium balance without correcting the existing hyponatraemia when sodium chloride intake was increased; (2) an intact urinary diluting ability, as his urine osmolality was lower than 100 mOsm/kg; (3) normal excretion of a standard water load (>80% within 4 h); (4) normal adrenal, renal, and thyroid function together with no evidence of cardiac or hepatic disease. Nevertheless, we cannot disregard the fact that this patient may have had a mild degree of volume depletion. Thus, ADH secretion adjusted for hypo-osmolality as well as (to some extent) for hypovolaemia could be responsible for the patient's clinical presentation.
Hyponatraemia due to reset osmostat has not been reported in alcoholic patients. There is evidence that this syndrome is present in approximately one-third of patients with SIADH and may occur in several other conditions, including chronic malnutrition, as was the case in our patient (Defronzo et al., 1976). In this setting, defective cellular metabolism may be responsible for the abnormal osmoreceptor function. Interestingly, correction of the underlying problem and hyperalimentation were effective in returning the serum sodium concentration towards normal.
Finally, one patient with alcohol-induced cerebral atrophy and dementia presented with hyponatraemia related to cerebral salt-wasting syndrome. The diagnosis was based on a recently proposed diagnostic work-up taking into account uric acid metabolism and the patient's response to saline infusion (Maesaka, 1996). It is of interest that patients with this syndrome develop hyponatraemia with all the SIADH-associated findings (including inappropriate natriuresis and hypo-uricaemia). However, these patients are volume depleted and have a high urine sodium concentration due to urinary sodium wasting and not to volume expansion (Al Mufti and Arief, 1984; Ishikawa et al., 1987
; Tanneau et al., 1987
). The correction of hyponatraemia after saline infusion and the persistence of hypouricaemia (and inappropriate uric acid wasting) despite normalization of sodium levels suggest salt wasting (Maesaka, 1996
). The cerebral salt-wasting syndrome is observed in patients with cerebral diseases and its pathogenesis remains unclear. It has been proposed that there is an increased release of natriuretic peptides from specific hormone-producing neurons in the brain stimulated by disorders of the central nervous system (Tanneau et al., 1987
).
In conclusion, hyponatraemia is a frequently observed electrolyte abnormality in hospitalized chronic alcoholic patients and is related to various pathophysiological mechanisms.
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FOOTNOTES |
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