Hyponatremia in visceral leishmaniasis.

There are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kala-azar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H2O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H2O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

Hyponatremia in visceral leishmaniasis / Hiponatremia no calazar

There are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100 percent of kala-azar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H2O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H2O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8 percent of patients and increased fractional urinary uric acid excretion was detected in 74.5 percent of them. Increased glomerular filtration rate was present in 25.4 percent of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

Existem poucos relatos relacionando hiponatremia com a leshmaniose visceral (calazar). Este é um estudo de 55 pacientes portadores de calazar e um grupo controle de 20 indivíduos normais. Hiponatremia e hipo-osmolalidade sérica foram detectados em 100 por cento dos pacientes portadores de calazar. A presença de alta osmolalidade da primeira urina da manhã (750,0 ± 52,0 vs. 894,5 ± 30 mOsm/Kg H2O, p < 0,05) e da urina de 24h (426,0 ± 167,0 vs. 514,6 ± 132,0 mOsm/Kg H2O, p < 0,05), demonstraram a presença de persistente secreção de hormônio antidiurético. A concentração de sódio urinário foi elevada (82,3 ± 44,2 vs. 110,3 ± 34,7 mEq/L, p < 0,05). Hipouricemia ocorreu em 61,8 por cento dos pacientes e aumento da fração de excreção urinária de ácido úrico foi detectada em 74,5 por cento dos casos. Aumento da velocidade de filtração glomerular estava presente em 25,4 por cento dos pacientes. Não havia evidência clínica de depleção de volume extracelular. Valores normais de ADH plasmático foram observados nos pacientes com calazar. Não foi detectada disfunção renal ou endócrina. É provável, que a maioria dos pacientes com calazar apresente uma síndrome de secreção inapropriada de hormônio antidiurético.

Syndrome of inappropriate secretion of antidiuretic hormone associated with strongyloidiasis.

We report a case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) with accompanying severe strongyloidiasis in a 52-year-old male. On admission, he showed drowsiness and emaciation with severe hyponatremia. We gave sodium (saline or salts) in an i.v. drip infusion and orally without improvement. A urinalysis and plasma osmotic pressure test indicated SIADH, therefore, treatment was changed to restrict his sodium intake. The hyponatremia gradually improved initially, but the appetite loss, nausea, and hyponatremia continued. Endoscopy revealed white patches on the stomach wall and histopathological examination revealed infestation of the mucosal epithelium with numerous Strongyloides stercoralis larvae. Ivermectin treatment was then initiated and the abdominal symptoms and hyponatremia gradually resolved. We carefully investigated the underlying cause of the SIADH, such as disease of the central nervous system, lung cancer, and other malignancies, but no abnormality or clear cause could be found. We concluded that the patient developed SIADH secondary to severe S. stercoralis infection.

Case report: severe acute symptomatic hyponatraemia in falciparum malaria.

Hyponatraemia is a common finding in malaria, but rarely appears to be of clinical significance. We describe a case of acute, profound, hyponatraemia with confusion and convulsions developing in the context of seemingly uncomplicated Plasmodium falciparum malaria. We draw attention to this rarely reported and poorly documented life-threatening complication and review the limited literature on the subject.

Clinical study of cerebral malaria in African children.

Of 51 consecutive children with cerebral malaria, fever, convulsions, and drowsiness were the commonest presenting symptoms. Decerebrate and decorticate postures and absent cornea reflex were the commonest brain stem signs. Opening lumbar cerebrospinal (CSF) pressure was raised in all but one of 24 children in whom it was reliably measured [mean 15.2 +/- 5.7 mmHg, range 6-24]. Hyponatraemia occurred in 17 (33%). Acute renal failure was not uncommon; the combination of hypercreatininaemia (plasma creatinine > 100 mumol/L) and hyperkalaemia (plasma potassium > 6.0 mumol/L) was fatal in 5 out of 7 patients in whom it occurred. Disturbances of acid-base status were present in all 40 children in whom it was assessed on admission. Mortality rate was 16% (8 patients). Neurological deficits occurred in 7 (14%) of the survivors and included cortical blindness [3], aphasia [3], hypertonia [3], hearing loss [2], and dystonia [1]. In addition to the present measures aimed at reducing morbidity and morality in children with cerebral malaria, efforts should be directed at rapid assessment of renal function and prompt correction of such dysfunction if found.

Hyponatraemia in severe falciparum malaria: a clinical study of nineteen comatose African children.

In a prospective study, hyponatraemia was observed in 52.6% of 19 children with cerebral malaria on admission, the plasma sodium ranging from 117 to 129 mumol/l. In addition, a further 10% developed hyponatraemia between 48 and 96 hrs after admission; in half of these, there was continuing urinary sodium loss. The clinical presentation of hypo- and normonatraemic children was similar except for vomiting and hypoglycaemia which were commoner in the normonatraemic and irritability and signs of lower respiratory tract infection which were commoner in the hyponatraemic groups. In hyponatraemic and normonatraemic children, there was a negative correlation between hyponatraemia and parasite density (r = -0.503, P < 0.05) and (r = -0.14, P < 0.05 respectively) and between parasite density and urinary sodium concentration during the first 24 hours of admission (r = -0.034; P < 0.05 and r = -0.045, P > 0.05 respectively). Irrespective of group, a relative increase in plasma sodium in the first 24 hours of admission (positive delta Na 24 h) was associated with a reduction in seizure frequency during this period as compared to the reported 24 hour of pre-admission seizure frequency, and, vice-versa. It is concluded that hyponatraemia is not uncommon in childhood cerebral malaria; urinary sodium loss may be contributory to the hyponatraemia seen in this condition.