HYPONATREMIC NATRIURETIC SYNDROME IN TUBERCULOUS MENINGITIS - THE PROBABLE ROLE OF ATRIAL-NATRIURETIC-PEPTIDE

HYPONATREMIA HAS BEEN reported in up to one third of patients with int racranial disease and has frequently been associated with tuberculous meningitis, often complicated by hydrocephalus. The lowered plasma sod ium levels were previously attributed to the syndrome of inappropriate secretion of antidiuretic hormone. A controlled prospective study of 24 patients with tuberculous meningitis and hydrocephalus was carried out. Analyses of serum electrolytes and cerebrospinal fluid were perfo rmed. Plasma and cerebrospinal fluid levels of atrial natriuretic pept ide (ANP) and antidiuretic hormone (ADH) were measured by radioimmunoa ssay. Fifteen patients were found to be hyponatremic (plasma sodium < 130 mmol/L) and ANP levels of 12 to 1,488 pg/ml were present (median, 26 pg/ml). The remaining 9 patients had normal plasma sodium values be tween 130 and 145 mmol/L, and in these, plasma ANP values varied betwe en 12 and 21.7 pg/ml (median, 12 pg/ml). The difference between these two groups was not statistically significant. (Control values from pat ients undergoing myelography were established to range between 12 and 40 pg/ml; median, 14.4 pg/ml.) ANP levels were undetectable in the cer ebrospinal fluid in all. Plasma ADH levels in the hyponatremic group w ere between 7 and 159 pg/ml (median, 40 pg/ml). In the normonatremic g roup, plasma ADH levels of 25 to 250 pg/ml (median, 29 pg/ml) were obt ained. (The controls ranged between 3.6 and 35 pg/ml; median, 10.4 pg/ ml). In the hyponatremic group, there was a moderate negative correlat ion (r = -0.683) between plasma ANP and plasma sodium (P = 0.02). No c orrelation between plasma ADH and plasma sodium was found (r = -0.168; P = 0.62). It therefore appears that plasma ANP accounted for 65% of the variation in plasma sodium (P = 0.0085), while ADH accounted for o nly 3% (P = 0.489). These findings suggest that elevations in plasma A NP account for the major proportion of the hyponatremic states in tube rculous meningitis with hydrocephalus, while ADH, initially thought to be important, seems to play a negligible role. A more accurate and us eful description of the hyponatremic state in tuberculous meningitis w ould be ''hyponatremic natriuretic syndrome.''