肝硬化腹水低钠血症173例分析

目的　探讨肝硬化腹水低钠血症的临床特点及治疗。方法　分析 173例肝硬化腹水病人低钠血症程度与肝性脑病、肾功能减退及病情预后的关系。结果　肝硬化腹水病人低钠血症的发生率为 49.13 % (85 / 173 ) ;重度低钠血症患者中肝性脑病及肾功能损害的发生率显著高于中、轻度者 (χ2 分别为 7.5 0 7、5 .5 97,P均 <0 .0 1) ;其病死率也明显增多(χ2 =7.782 ,P <0 .0 1) ;不同程度低钠血症的child分级不同 (χ2 =4.482 ,P <0 .0 5 )。结论　正确诊治肝硬化腹水低钠血症 ,对预后至关重要。     

Dilutional hyponatremia due to diazoxide-produced polydipsia

Subcutaneous injection of diazoxide every 3 hr for a total of 5 doses in 15 hr produced a state of elevated drinking and antidiuresis in rats resulting in a massive, positive, self-imposed water load. Dilutional hyponatremia was present, but not serum hyposmolality, owing to the increased serum glucose and BUN. The mechanism by which diazoxide produces a polydipsia even in the presence of an accumulating water load may illuminate the genesis of other pathophysiological dilutional states.     

Brugada pattern electrocardiographic changes associated with profound electrolyte disturbance

Only a few case reports of Brugada pattern ECG changes caused by electrolyte disturbance exist in the literature, all of which lack adequate electrophysiological exclusion (or inclusion) of an underlying Brugada syndrome. This report describes a case of an otherwise healthy 38-year-old man who presented to the hospital with diabetic ketoacidosis, profound electrolyte disturbance, and Brugada pattern ECG changes. Subsequent flecanide drug challenge and electrophysiological studies ruled out an underlying Brugada syndrome.     

Chronic hypoosmolality induces a selective decrease in magnocellular neurone soma and nuclear size in the rat hypothalamic supraoptic nucleus

The magnocellular neurones of the hypothalamo-neurohypophysial system (HNS) play a vital role in the maintenance of body homeostasis by regulating oxytocin (OT) and vasopressin (VP) secretion from the posterior pituitary. During hyperosmolality, OT and VP mRNA levels are known to increase by approximately two-fold, whereas during chronic hypoosmolality, OT and VP mRNA levels decrease to approximately 10-20% of basal levels. In these studies, we evaluated changes in cell size associated with these physiological conditions. Cell and nuclear sizes of neurones in the supraoptic nucleus (SON), the nucleus of the lateral olfactory tract (LOT) and the medial habenular nucleus (MHB) were measured from neurones identified by in situ hybridization histochemistry for beta(III)-tubulin mRNA, and measurements were made from OT and AVP magnocellular neurones in the SON after phenotypic identification by immunohistochemistry. Under hypoosmolar conditions, the cell and nuclear sizes of OT and VP magnocellular neurones decreased to approximately 60% of basal values, whereas cell and nuclear sizes of OT and VP neurones in hyperosmolar rats increased to approximately 170% of basal values. In contrast, neither hyperosmolality, nor hypoosmolality significantly affected cell and nuclear sizes in the LOT and MHB. These results confirm previous studies that showed that magnocellular neurones increase cell size in response to hyperosmolar conditions and, for the first time, demonstrate a marked decrease in cell size in the SON in response to chronic hypoosmolar conditions. These dramatic changes in cell and nuclear size directly parallel changes in OT and VP gene expression in the magnocellular neurones of the SON and, consequently, are consistent with the pronounced bidirectional changes in gene expression and cellular activity found during these osmotic perturbations. Our results therefore support the concept of global alterations in the synthetic activity of magnocellular OT and AVP neurones in response to extracellular osmolality.     

THE ROLE OF ACTIVE SODIUM AND POTASSIUM TRANSPORT IN HYPONATREMIC STATES IN INFANCY AND CHILDHOOD

ABSTRACT. Sigström, L. (Department of Paediatrics I, University of Goteborg, östra Sjukhuset, Göteborg, Sweden). The role of active sodium and potassium transport in hyponatremia states in infancy and childhood. Acta Psediatr Scand, 70:353, 1981.–Erythrocytes from 14 infants and children with serum sodium concentrations of 125 mmol/1 or less were analyzed for total and Na⁺, K⁺-ATPase, sodium and potassium content and ATP concentrations to evaluate the role of active Na⁺-K⁺ transport in hyponatremia. In six out of nine patients, with a duration of hyponatremia of more than 48 hours low Na⁺, K -ATPase activities and high erythrocyte sodium concentrations and Na⁺-K⁺ ratios were found indicating that a decreased Na⁺, K⁺-ATPase activity leading to an increased intracellular accumulation of sodium ions may have reduced the extracellular sodium concentration. Three subjects with large sodium losses had high Na⁺, K⁺-ATPase activities and normal erythrocyte sodium concentrations. In five cases of hyponatremia with a duration of less than 24 hours the variables indicating active Na⁺-K⁺ transport were normal. The therapeutic implications with sodium substitution and the use of drugs affecting active Na⁺-K⁺ transport are discussed.     

Screening for Spinal Defects

Second-trimester diagnosis of most open neural tube defects has become clinically feasible in the past five years. Alpha fetoprotein is the common denominator in a two-stage screening program. Maternal serum analysis identifies high-risk pregnancies; amniotic fluid analysis is diagnostic. The biochemical basis for these tests and findings of clinical studies are reviewed.     

老年颅脑损伤后脑性盐耗损综合征

目的　探讨老年急性颅脑损伤脑性盐耗损综合征的诊断及治疗。方法　回顾分析 2 1例 6 0岁以上老年颅脑损伤后脑性盐耗损综合征 (CSWS)的临床表现、实验室检查和诊治方法。结果　除早期的 3例死于脑水肿和脑梗塞外 ,其余18例水电解质代谢紊乱均得到纠正。结论　低血钠、低血容量、高尿钠、高尿量、高比重尿 (二低三高 )是CSWS的诊断依据 ,补高渗盐水和水化治疗是行之有效的方法。     

Natriuretic factors and lithium clearance in patients with the syndrome of inappropriate antidiuretic hormone (SIADH)

Because the syndrome of inappropriate antidiuretic hormone (SIADH) is a state of disturbed body fluid volume regulation and altered sodium balance we sought to determine if recently described volume regulatory factors were stimulated in SIADH. We measured atrial natriuretic peptide (ANP), endogenous digitalis-like natriuretic factor (EDNF) and urinary free dopamine in SIADH (n = 27). We also determined fractional clearance of lithium (FCLi). The data obtained in SIADH were compared with similar measurements performed in sodium retaining hyponatremias, such as those of heart failure (n = 26), liver cirrhosis (n = 19) and volume contraction (n = 28). We observed: ANP was 19.5 +/- 2.7 fM/ml in SIADH; it was significantly lower than ANP in cardiac failure, but no different from ANP in volume contraction. Urinary free dopamine was 2.2 +/- 0.8 microM/24 h in SIADH; this was significantly higher than in volume contraction and liver cirrhosis. EDNF (259 +/- 42 nM/24 h) and FCLi (21.4 +/- 2%) were both numerically higher in SIADH than in other hyponatremic disorders; however, the differences did not achieve significance. In conclusion, our observations did not establish a specific role of ANP in chronic stable SIADH. As to the importance of EDNF, dopamine and proximal tubular fluid reabsorption (FCLi) additional work using acute volume changes may demonstrate their participation in the renal sodium handling of SIADH more clearly than our study did.