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Metabolic Laboratory Data
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Like sodium, chloride is a mostly extracellular electrolyte. Unlike sodium it is an anion, not a cation. Chloride actually accounts for most of the measured anion content in our blood. Our bodies contain about 1.6 g of chloride per kg. An average male has about 112 g of chloride in his body, 90% of which is extracellular.
Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Chloride is found in the form of anion (Cl-) in all organisms and combines with cations like sodium (Na+) or potassium (K+) to form a salt such as sodium chloride (NaCl) or potassium chloride (KCl). After sodium, chloride is the most abundant mineral in the body. Chloride is the principal extracellular and intracellular anion (Cl−) in the body, where it represents 60–70% of the total negative ion content (6, 8, 15–16). Chloride is vital for maintenance of serum electrical neutrality, muscular activity, osmotic pressure, electrolyte balance, acid-base status, renal function, regulation of body fluids (fluid homeostasis), and hydrochloric acid (HCl) production in the gastrointestinal tract (6, 8, 15–16). In addition, it is an essential component for the assessment of many pathological conditions. It maintains the electrical balance in the nervous system and is involved in intracellular and extracellular transport (8, 15–16).
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Chloride: In human physiology, chloride ions help in the maintenance of regulating fluid balance, blood volume, electrolyte homeostasis, intracellular and extracellular fluid homeostasis, blood pressure, preservation of electrical neutrality, and pH of body fluids in a human body.125–127 The chloride ion is an important biomarker for a vast range of clinical conditions and, as a routine practice, is analytically determined in the sweat, urine, feces, and blood. Following intake of edible salt from diverse food sources, a human body gets chloride, which is absorbed in the intestine, while the excess amount gets excreted in the urine.125–128 However, excessive chloride levels indicate serious metabolic disorders, including metabolic acidosis or alkalosis, and a disruption in chloride channel expression and function, leading to multiple diseases and disorders in diverse organs.126–128
Associations between serum electrolyte and short-term outcomes in patients with acute decompensated heart failure
Published in Annals of Medicine, 2023
Kai Zhao, Qun Zheng, Jiang Zhou, Qi Zhang, Xiaoli Gao, Yinghua Liu, Senlin Li, Weichao Shan, Li Liu, Nan Guo, Hongsen Tian, Qingmin Wei, Xitian Hu, Yingkai Cui, Xue Geng, Qian Wang, Wei Cui
A total of 5145 participants (58.3% men; median age 69 y) comprised the potassium-related study population, with 631, 1784, 1726, 720 and 284 patients classified as internal 1 (K: <3.50 mmol/L), internal 2 (K: 3.50–4.00 mmol/L), interval 3 (K: 4.01–4.50 mmol/L), interval 4 (K: 4.51–5.00 mmol/L) and interval 5 (K: >5.00 mmol/L), respectively. Meanwhile, the sodium-related study population (58.3% men; median age 69 y) included 5135 participants categorized into five groups according to their serum sodium levels. Furthermore, 4966 patients from the chloride-related study population (58.0% men; median age 69 y) were divided into four different groups based on their serum chloride concentrations. Finally, differing from the above, the STC-related study population (58.7% men; median age 68 y) was composed of 4143 patients stratified into three groups on the basis of their STC levels.
Assessing accuracy of testing and diagnosis in cystic fibrosis
Published in Expert Review of Respiratory Medicine, 2023
Malina Barillaro, Tanja Gonska
In a study combining data of eight phase two and three clinical studies examining the effect of the CFTR-modulator, ivacaftor, a significant correlation was observed between the improved sweat chloride levels and the ppFEV1%, predicted forced expiratory volume in 1 second, a classic lung fucntion parameter [35]. Unfortunately, at an individual level, an association between sweat chloride levels and CF-associated symptoms is lacking. In pwCF, sweat chloride levels were not found to correlate to severity of pulmonary disease [36], nor were changes in sweat chloride levels from the baseline, correlated to improvements in lung function with CFTR modulator drug treatment [37]. Thus, sweat chloride levels provide a robust assessment of the CFTR function, and at a population level associate with symptom severity, but association is limited at the individual patient level.
Transient diabetes insipidus after vasopressin discontinuation in cystic fibrosis with septic shock
Published in Baylor University Medical Center Proceedings, 2023
Natnicha Leelaviwat, Juthipong Benjanuwattra, Ahmed Elkheshen, Nouran Eshak, Marawan Elmassry, Mahmoud Abdelnabi
Interestingly, central DI seems to occur even in those with low or normal serum sodium levels, as seen in our patient; therefore, attention should also be given to alteration in sodium levels when a diagnosis is suspected. These paradoxical findings could be explained in our patient by a long history of cystic fibrosis causing excessive loss of sodium and chloride. The pathophysiologic mechanism of transient DI after discontinuation of vasopressin is not well understood. It was hypothesized that a depletion of the body’s own vasopressin during an episode of shock and hypoperfusion of the hypothalamus resulted in a transient deficiency of vasopressin when the infusion was discontinued.16 Other hypotheses were attributed to the suppression of vasopressin production by exogenous vasopressin and the transient down-regulation of V2 receptor in the kidneys following continuous exposure to a supraphysiologic dose of vasopressin, causing transient nephrogenic DI that was still responsive to exogenous vasopressin treatment.2,17,18