Clinical Implications, Evaluation, and Management of Hyponatremia in Cirrhosis.

Hyponatremia is the most common electrolyte abnormality in patients with decompensated cirrhosis on Liver Transplantation (LT) waiting list. Most of these patients have dilutional or hypervolemic hyponatremia secondary to splanchnic vasodilatation. Excessive secretion of the antidiuretic hormone also plays an important role. Hypervolemic hyponatremia is commonly associated with refractory ascites, spontaneous bacterial peritonitis, and hepatic encephalopathy. Although uncommon, the use of diuretics and laxatives can cause hypovolemic hyponatremia that is characterized by the striking absence of ascites or pedal edema. Clinical features are often nonspecific and depend on the acuity of onset rather than the absolute value of serum sodium. Symptoms may be subtle, including nausea, lethargy, weakness, or anorexia. However, rarely patients may present with confusion, seizures, psychosis, or coma. Treatment includes discontinuation of diuretics, beta-blockers, and albumin infusion. Hypertonic saline (3%) infusion may be used in patients with very low serum sodium (<110 mmol/L) or when patients present with seizures or coma. Short-term use of Vasopressin (V2) receptor antagonists may also be used to normalize sodium levels prior to LT. However, all these measures may be futile, and LT remains the definite treatment in these patients to improve survival. In this review, we describe the classification, pathogenesis of hyponatremia, and its clinical implications in patients with cirrhosis. Approach to these patients along with management will also be discussed briefly.

Effect of Estriol Sodium Succinate on Colony-Stimulating Factor Level in the Serum of Mice / 第二军医大学学报

We studied the changes of colony-stimu lating factor (CSF) level, the type of CSF after intraperi-toncal injection of estriol sodium succinate (E3?SNa) and the effect of E3?SNa itself on the proliferation of bone marrow precursors with the use of both agar colony assay and [3H]-TdR incorporation assay. Our experiment shows that CSF was at high level 6 h after E3?SNa administration and reached a peak by 24 h, and that elevation of CSF in the serum was maintained for at least 30 d. Using 0.14-28 mg of E3?SNa there was a dose-dependent increase in serum CSF when tested 24 h after E3?SNa treatment. The main type of CSF was GM-CSF. There was no direct stimulation of E32?SNa itself on the proliferation of mouse bone marrow precursors. So we think that the effect of estrogens on the hematopoiesis may, at least in part, be mediated by altered CSF activity.