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Respiratory, endocrine, cardiac, and renal topics
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
The thiazides have been successfully used in children with nephrogenic diabetes insipidus. By inducing volume contraction, they enhance the proximal tubular reabsorption of water and electrolytes, thus significantly decreasing urine output. While usefully decreasing urine output, volume contraction may inhibit growth in young children with nephrogenic diabetes insipidus.
The Clinical Approach to Sepsis and Its Mimics in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Abdullah Chahin, Steven M. Opal
Hypovolemia is the state of decrease in blood volume or a decrease in intravascular component. This loss leads to volume contraction. Causes are loss of blood, loss of plasma (severe burns and oozing wounds), or loss of sodium with consequent loss of intravascular and extravascular water (diarrhea, vomiting, heat stroke, etc.). For hypovolemia to result in hypotension, around 30%–40% of intravascular volume would typically be lost [24].
Rheology of Cardiovascular Disease
Published in Gordon D. O. Lowe, Clinical Blood Rheology, 2019
Gordon D. O. Lowe, C. D. Forbes
Some studies have found significantly increased hematocrit levels in patients with ischemic heart disease,125,127–129,133,134 but others have not126,130–132,135–137 In a study of 12 patients, all had significant plasma volume depletion (mean 82% of predicted) but normal red cell mass (mean 95% of predicted).138 Coronary artery bypass grafting did not alter this contracted plasma volume, despite relief of angina.138 Hence from the limited data available, the increased hematocrit in coronary artery disease appears to result from contracted plasma volume rather than increased red cell mass, as with essential hypertension (see above). This syndrome may merge with relative polycythemia, in which the incidence of cardiovascular events is increased (Chapter 9, Volume II). The cause of plasma volume contraction is obscure. It may reflect an adaptive mechanism to decrease left ventricular volume and systolic wall tension, decreasing myocardial oxygen consumption and relieving angina, since venesection increases the angina threshold and volume expansion decreases it.138 However, reduced plasma volume does not appear to be a result of myocardial ischemia, since it was unaltered by bypass grafting.138 Chronically increased adrenergic activity may be responsible, since catecholamines decrease plasma volume in the short-term.138 This would fit with the hypothesis of increased “stress” in coronary artery disease and hypertension.
Association between polycythemia and risk of ischemic stroke in males based on the national health insurance service-health screening cohort
Published in Expert Review of Hematology, 2023
Hyo-Sun You, Sang-Jun Shin, Joungyoun Kim, Hee-Taik Kang
Hematologic disorders are common causes of ischemic stroke but are frequently neglected [3]. Polycythemia is a hematological disorder that can cause ischemic stroke. Polycythemia refers to a state in which the hematocrit or hemoglobin concentration in peripheral blood is increased. Polycythemia, or erythrocytosis, is classified into spurious polycythemia and true polycythemia according to its etiology. Spurious polycythemia is induced by volume contraction, severe dehydration, and Gaisbock syndrome. True polycythemia is divided into primary and secondary polycythemia according to serum erythropoietin (EPO) levels. Polycythemia vera and primary familial and congenital polycythemia are the types of primary polycythemia with low serum EPO levels. Secondary polycythemia is caused by various diseases that cause hypoxia in cells, which induces EPO release. High altitude, respiratory diseases such as chronic obstructive pulmonary disease (COPD), cyanotic heart disease, elevated carboxyhemoglobin, hemoglobinopathies, and EPO-secreting tumors can also cause secondary polycythemia [4].
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
It has been postulated that natriuresis, in part, may contribute to the SGLT2 mediated anti-hypertensive effect. Specifically, an acute and transient increase in natriuresis is observed in the early stages of SGLT2 inhibition [71]. Maximal natriuresis is reported within the first 3 days of treatment and eventually returns to baseline over time. Partially by the process of osmoregulation, acute sodium excretion is accompanied by a sustained 7.3% plasma volume contraction, as observed in patients following 8 weeks of dapagliflozin treatment [72,73]. Although the exact mechanisms outlining the transient nature of natriuresis are still unclear, it may be explained by way of a compensatory increase in distal tubule sodium reabsorption to offset the initial increase in sodium excretion at the proximal tubule and may suggest minimal contribution of natriuresis to BP reduction. Despite this, an acute increase in urinary sodium excretion by 10–20% was demonstrated in patients with T2D in response to SGLT2 inhibitor therapy, emphasizing a potential role for natriuresis [74].
A comparative safety review between GLP-1 receptor agonists and SGLT2 inhibitors for diabetes treatment
Published in Expert Opinion on Drug Safety, 2018
Agostino Consoli, Gloria Formoso, Maria Pompea Antonia Baldassarre, Fabrizio Febo
SGLT2i, on the other end, are, in regard to HF, not only safe, but able to reduce its risk, independently from improvement in glycemic control [14,16,38]. Of the many mechanisms potentially involved in these beneficial effects, none has been convincingly proven. It has been postulated that reductions in cardiac preload (both via circulating volume contraction and via natriuresis/osmotic diuresis), BP, and arterial stiffness might all play a role [28]. These hemodynamic effects seem to persist even in the presence of renal impairment, despite the fact that GFR deterioration reduces SGLT2i efficacy on glucose lowering [45]. The EMPAREG OUTCOME trial [14] offers the strongest data on the effect of SGLT2 inhibition on CV outcomes and in particular on HF. In this study, diabetic subjects with established CV disease receiving empagliflozin (10 or 25 mg) exhibited significantly and markedly lower HHF rates as compared to placebo (2.7% vs. 4.1%; 35% risk ratio (RR) reduction). The CANVAS trial [39] yielded similar results with patients randomized to canagliflozin (100 or 300 mg) showing a lower risk for HHF as compared to placebo (HR 0.67; 95% CI 0.52–0.87). Finally, initiation of a SGLT-2i was associated with a lower risk of HHF (pooled HR 0.61; 95% CI 0.51–0.73; p < 0.001) compared to other glucose-lowering drugs in real world-evidence study (CVD-REAL) [38].