Amazoniac
Member
Guru, at least it confirms that potassium in great amounts is needed for recovery. The chlorid part is confusing to me.
Here they appoint the fingers to ketones:
VVhat's your opinion?
Here they appoint the fingers to ketones:
Acidosis-Induced Hypochloremic Alkalosis in Diabetic Ketoacidosis Confirmed by The Modified Base Excess Method | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
"The presence of chloride deficits and hypochloremic alkalosis in DKA without vomiting was demonstrated using the BECl of the modified BE method in our study. The mean BECl value was positive and significantly higher in DKA than in pre-DKA states (Table 2). BECl values ≧ 2 mEq/L were observed in 79.4% of patients with DKA, suggesting hypochloremic alkalosis due to chloride deficit (10, 11), and consistent with the low Cl/Na ratio and ClCorr values (Table 2). The alkalinizing effect of hypochloremia was substantial, effectively mitigating the base deficits in DKA by approximately 25% (Table 2). Furthermore, BECl tightly correlated with the total ketone concentration (Figure 1). That is, as hyperketonemia is more severe, the chloride deficit and hypochloremic alkalosis became greater. These results suggest the frequent coexistence of acidosis-induced hypochloremic alkalosis with DKA, and also the important roles of ketoacids in its pathogenesis. The strong correlations (P < .0001; n = 27) of BECl with SIG (r = 0.70) and sodium-corrected SIG (r = 0.75) support this conclusion."
"The mechanism of acidosis-induced hypochloremic alkalosis remains unclear. Based on the occurrence of acidosis-induced hypochloremia in nephrectomized and volume-controlled uremic rats, Madias et al (20) concluded that there was no reduction in Cl stores. Instead, they suggested the possibility that an internal ion shift occurred, either of chloride of the extracellular space or of sodium and water into the extracellular fluid. In the present study, the positive BECl might have occurred because of a chloride shift from plasma to erythrocytes or interstitial fluids, despite low bicarbonate state, and the negative BEFW might have followed an internal shift of free water (24, 25). Thus, our results support the argument proposed by Madias et al (20), and it is likely that these responses might be secondary to ketoacidosis, rather than being compensatory or adaptive (25)."
"In contrast, several factors including prior hypercapnea, volume contraction, potassium deficiency, chloruretic diuretics, persistent mineralocorticoid excess, etc., are responsible for the generation and maintenance of metabolic alkalosis (31–33)."
"The presence of chloride deficits and hypochloremic alkalosis in DKA without vomiting was demonstrated using the BECl of the modified BE method in our study. The mean BECl value was positive and significantly higher in DKA than in pre-DKA states (Table 2). BECl values ≧ 2 mEq/L were observed in 79.4% of patients with DKA, suggesting hypochloremic alkalosis due to chloride deficit (10, 11), and consistent with the low Cl/Na ratio and ClCorr values (Table 2). The alkalinizing effect of hypochloremia was substantial, effectively mitigating the base deficits in DKA by approximately 25% (Table 2). Furthermore, BECl tightly correlated with the total ketone concentration (Figure 1). That is, as hyperketonemia is more severe, the chloride deficit and hypochloremic alkalosis became greater. These results suggest the frequent coexistence of acidosis-induced hypochloremic alkalosis with DKA, and also the important roles of ketoacids in its pathogenesis. The strong correlations (P < .0001; n = 27) of BECl with SIG (r = 0.70) and sodium-corrected SIG (r = 0.75) support this conclusion."
"The mechanism of acidosis-induced hypochloremic alkalosis remains unclear. Based on the occurrence of acidosis-induced hypochloremia in nephrectomized and volume-controlled uremic rats, Madias et al (20) concluded that there was no reduction in Cl stores. Instead, they suggested the possibility that an internal ion shift occurred, either of chloride of the extracellular space or of sodium and water into the extracellular fluid. In the present study, the positive BECl might have occurred because of a chloride shift from plasma to erythrocytes or interstitial fluids, despite low bicarbonate state, and the negative BEFW might have followed an internal shift of free water (24, 25). Thus, our results support the argument proposed by Madias et al (20), and it is likely that these responses might be secondary to ketoacidosis, rather than being compensatory or adaptive (25)."
"In contrast, several factors including prior hypercapnea, volume contraction, potassium deficiency, chloruretic diuretics, persistent mineralocorticoid excess, etc., are responsible for the generation and maintenance of metabolic alkalosis (31–33)."
VVhat's your opinion?