Cerebral salt wasting syndrome (CSW-cerebral salt wasting) was first described in 1950 by Peters. This syndrome can occur in patients who have sustained damage to the central nervous system (e.g. patients with subarachnoid bleeding, bacterial meningitis or after neurosurgery). Patients present with excessive natriuresis and hyponatremic dehydration. Differentiating this syndrome with the syndrome of inappropriate antidiuretic hormone secretion (SIADH-syndrome of inappropriate antidiuretic hormone secretion), which may occur in the same group of patients, is necessary in order to administer the correct treatment which consists of fluid restriction and sodium replacement in SIADH and fluid and sodium replacement as well as occasional mineralocorticoid therapy in CSW.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Background: A new pathophysiologic approach to evaluating hyponatremic patients identified the different causes of hyponatremia, including non-hyponatremic patients with renal salt wasting (RSW). RSW was considered a rare to nonexistent syndrome until we found 24 (38%) of 62 hyponatremic patients in a general medical ward to have RSW. We induced RSW in rats by injecting plasma from 18 AD patients suspected to have RSW.
View Article and Find Full Text PDFThe microbiota-derived bile acid taurodeoxycholic acid improves hepatic cholesterol levels in mice with cancer cachexia.
Gut Microbes
December 2025
Metabolism and Nutrition Research Group, Louvain Drug Research Institute, UCLouvain, Université catholique de Louvain, Brussels, Belgium.
Alterations in bile acid profile and pathways contribute to hepatic inflammation in cancer cachexia, a syndrome worsening the prognosis of cancer patients. As the gut microbiota impinges on host metabolism through bile acids, the current study aimed to explore the functional contribution of gut microbial dysbiosis to bile acid dysmetabolism and associated disorders in cancer cachexia. Using three mouse models of cancer cachexia (the C26, MC38 and HCT116 models), we evidenced a reduction in the hepatic levels of several secondary bile acids, mainly taurodeoxycholic (TDCA).
View Article and Find Full Text PDFIntroduction: Screening for congenital adrenal hyperplasia through the measurement of 17-hydroxyprogesterone on the neonatal blood spot aims to: a) prevent neonatal deaths; b) allow earlier identification and thereby decrease the severity of the initial salt-wasting episode; and c) shorten the time during which a severely virilized genetic female newborn may be assigned the male sex. It is now practiced in the majority of high-income countries, although the positive predictive value of the test is very low in infants born preterm, who seem to be infrequently affected. In almost all low- and middle-income countries, it has not yet been implemented.
View Article and Find Full Text PDFA Rare Cause of Neonatal Salt Wasting Syndrome: Clinical Management of a Case Diagnosed with Pseudohypoaldosteronism Due to a Novel Homozygous Variant in the Gene.
J Clin Res Pediatr Endocrinol
December 2024
Department of Pediatric Endocrinology, Akdeniz University Hospital, Antalya, Turkey.
Pseudohypoaldosteronism (PHA) is a rare disorder that, if not promptly recognized and treated, can lead to life-threatening hyperkalemia resulting in cardiac arrest and death. Systemic PHA is caused by variants that deactivate the epithelial sodium channel (ENaC) subunits. Management is challenging due to high-dose oral replacement therapy, and patients with systemic PHA require lifelong treatment.
View Article and Find Full Text PDFRare Types of Congenital Adrenal Hyperplasias Other Than 21-hydroxylase Deficiency.
J Clin Res Pediatr Endocrinol
December 2024
University of Health Science, Dr Sami Ulus Child Health and Diseases Health Implementation and Research Center, Clinics of Pediatric Endocrinology, Ankara, Türkiye.
Although the most common cause of congenital adrenal hyperplasia (CAH) worldwide is 21-hydroxylase deficiency (21OHD), which accounts for more than 95% of cases, other rare causes of CAH such as 11 beta-hydroxylase deficiency (11βOHD), 3 beta-hydroxy steroid dehydrogenase (3β-HSD) deficiency, 17 hydroxylase deficiency and lipoid CAH may also be encountered in clinical practice. 11βOHD is the most common type of CAH after 21OHD, and CYP11B1 deficiency in adrenal steroidogenesis causes the inability to produce cortisol and aldosterone and the excessive production of adrenal androgens. Although the clinical and laboratory features are similar to 21OHD, findings of mineralocorticoid deficiency are not observed.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!