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临床上由于某些疾病和危重病使下丘脑-垂体受损,导致抗利尿激素(antidiuretic hormone,ADH)分泌异常增多或肾脏对ADH超敏引起水、钠紊乱而出现一组相应的临床综合征称之为抗利尿激素分泌异常综合征或抗利尿激素分泌不当综合征(SIADH)。儿科许多疾病,特别是危重患儿常合并抗利尿激素分泌的异常,因而充分认识这一综合征,给予恰当的处理和治疗至关重要。1基本概念ADH又称精氨酸加压素(AVP),是下丘脑视上核和室旁核神经元胞体合成的激素,经下丘脑-垂体束神经纤维运输到神经垂体,储存在轴突末梢的囊泡内。当视上核神经元兴奋时,神经冲动经…     

Syndrome of inappropriate secretion of antidiuretic hormone in enteroviral meningitis

In nine of 102 children admitted to the Montreal Children's Hospital with a diagnosis of aseptic meningitis, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) developed. Patients with and without SIADH were similar with respect to clinical symptoms, duration of illness, and CSF inflammatory response. The SIADH group differed in that the largest age group was 1 to 5 years.     

Ecstasy (3,4-methylenedioxymethamphetamine)-induced inappropriate antidiuretic hormone secretion

3,4-Methylenedioxymethamphetamine (MDMA), popularly known as the illicit drug "Ecstasy," is an amphetamine derivative that has become widely abused throughout the United States and other industrialized nations. 3,4-Methylenedioxymethamphetamine has an undeserved reputation as a "safe" drug among its users, but MDMA shares the toxicity profile of other amphetamines. Its use may result in lethal cardiovascular, hepatic, metabolic, or neurological toxicity. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a unique toxicity that may occur after isolated MDMA use. Although the phenomenon is well described in adults, reports of MDMA-induced SIADH and symptomatic hyponatremia in children are rare. We describe a 13-year-old girl who experienced MDMA-induced SIADH with symptomatic hyponatremia. Toxicity of MDMA, in particular, the pathophysiology and treatment of MDMA-induced hyponatremia, is discussed.     

Idiopathic syndrome of inappropriate secretion of antidiuretic hormone

The authors report a case of idiopathic, chronic inappropriate secretion of antidiuretic hormone (S I A D H) in a 31 months old boy. This inappropriate secretion of ADH was demonstrated by three water tolerance tests and by the bioassays of ADH in urine. These findings were detected five months later suggesting chronic S I A D H. After a review of the literature the mechanism and the treatment of this disease are discussed.     

Chronic syndrome of inappropriate secretion of antidiuretic hormone in childhood

Chronic forms of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) occur infrequently in childhood. We describe three pediatric patients with chronic SIADH. In two patients the persistent SIADH was associated with neoplasms of the central nervous system while in the third patient it was due to congenital anomalies of the central nervous system. We describe the clinical course and management of each patient, including the long-term use of furosemide taken orally once a day.     

Hypouricemia in neonates with syndrome of inappropriate secretion of antidiuretic hormone

A prospective study of serum levels of uric acid in 23 hyponatremic neonates was performed. Infants on diuretic medications or with renal failure were excluded. The infants were separated into two groups: group I consisted of 11 neonates with clinical evidence of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), (mean +/- SD serum sodium 127 +/- 1.36 mEq/liter). Group II included 12 infants with hyponatremia (mean serum sodium 128 +/- 1.10 mEq/liter) associated with decreased effective vascular volume manifest by a fractional sodium excretion less than 1%. The groups were similar for gestational and postnatal ages, birth weight, clinical conditions, and concurrent use of drugs. The serum urate concentration in neonates with SIADH was 2.46 +/- 0.54 mg/dl; serum urate concentration in group II infants was 8.49 +/- 2.45 mg/dL (p less than 0.001). Water restriction in the group I infants with SIADH resulted in a rise in mean serum urate concentration (p less than 0.001). Fractional excretion of urate was elevated during hyponatremia in the group I infants (to 78 +/- 0.13%) and fell to 51 +/- 0.08% after correction (p less than 0.001). In group I infants, a direct correlation was found between fractional excretion of urate and sodium (r = 0.7667, p less than 0.001). These results indicate that hypouricemia is common in infants with suspected SIADH and seems to be due to increased urate clearance secondary to volume expansion.     

The syndrome of inappropriate antidiuretic hormone secretion with carcinoma of the tongue

A 64-year-old male developed symptomatic recurrent syndrome of inappropriate ADH secretion in association with locally advanced squamous cell carcinoma of the tongue. His SIADH was managed successfully with saline infusion, frusemide, and maintenance treatment with demeclocycline.     

Suprasellar arachnoid cyst resulting in the syndrome of inappropriate antidiuretic hormone secretion

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is occasionally seen after hypothalamic injury or dysfunction, although it typically occurs in association with other endocrine disturbances. It is has never been described as a presenting feature of a suprasellar arachnoid cyst (SAC) in the pediatric population. The authors describe the case of an enlarging SAC resulting in SIADH as the only presenting feature, with an otherwise normal hypothalamic-pituitary axis. An SAC was diagnosed in utero in this 5-month-old girl who had a normal functioning hypothalamic-pituitary axis on presentation. Because of cyst enlargement and hydrocephalus, the patient was scheduled for surgery; however, preoperative labs revealed SIADH. After stabilizing the serum sodium concentration with fluid restriction and the administration of 3% sodium chloride, the patient underwent endoscopic cyst fenestration. Postoperatively, she had complete resolution of the SIADH. Syndrome of inappropriate antidiuretic hormone secretion as the presenting symptom of an SAC has not been previously described. In the aforementioned patient, the proposed mechanism for SIADH was enlargement of the suprasellar arachnoid cyst causing compression of the supraoptic and paraventricular nuclei and thus overstimulating the secretion of arginine vasopressin, which resulted in SIADH. The association of SIADH with an SAC is reportable, as is the resolution of the SIADH via cyst fenestration. The authors suggest that SIADH is an uncommon presenting feature of SACs and that syndrome resolution is possible with cyst decompression.