Disorders of Calcium Metabolism: Hypocalcemia and Hypercalcemia

Tinawi, Mohammad

doi:10.7759/cureus.12420

Cited by 29 publications

(30 citation statements)

References 44 publications

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“…Aminoglycoside use in patients with CF can result in metabolic alkalosis due to a Bartter-like syndrome. Aminoglycosides activate the calcium-sensing receptor (CaSR), resulting in inhibition of the Na + -K + -2Cltransporter in the TAL with subsequent increase in urinary Na + , K + , Ca +2 , and Mg +2 [32][33]. The intact PTH level is low despite hypocalcemia due to the activation of CaSR.…”

Section: Table 3: Causes Of Metabolic Alkalosismentioning

confidence: 99%

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Pathophysiology, Evaluation, and Management of Metabolic Alkalosis

Tinawi¹

2021

Cureus

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Metabolic alkalosis is an increase in blood pH to >7.45 due to a primary increase in serum bicarbonate (HCO 3 − ). Metabolic alkalosis results from alkali accumulation or acid loss, and it is associated with a secondary increase in carbon dioxide arterial pressure (P a CO 2 ). Metabolic alkalosis is a common acid-base disorder, especially in critically ill patients. The pathogenesis of chronic metabolic alkalosis includes two derangements, generation of metabolic alkalosis via gain of alkali or loss of acid and maintenance of metabolic alkalosis by increased tubular HCO 3 − reabsorption (failure of the kidneys to excrete excess alkali). Metabolic alkalosis is the most common acid-base disorder in hospitalized patients, particularly in the surgical critical care unit. Mortality increases as pH increases.

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Section: Table 3: Causes Of Metabolic Alkalosismentioning

confidence: 99%

“…The manifestations are usually due to concomitant hypokalemia, hypophosphatemia, hypoventilation, volume depletion, and hypocalcemia. Metabolic alkalosis decreases ionized calcium levels [33]. Severe metabolic alkalosis (serum HCO3 − >45 mmol/l) can lead to tetany, seizures, cardiac arrhythmias, and delirium [3].…”

Section: Manifestations Of Metabolic Alkalosismentioning

confidence: 99%

Pathophysiology, Evaluation, and Management of Metabolic Alkalosis

Tinawi¹

2021

Cureus

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“…Low serum calcium is a common finding in patients with sepsis and critical illness, with reported prevalence rates of up to 80%[ 72 ]. Hypocalcemia may be due to one or more of various causes[ 73 ]. However, during sepsis, calcium is shifted into red blood cells with significant increases in erythrocyte calcium of more than twice the control value[ 74 ].…”

Section: Clinical Manifestations Of H2o2 Induced Oxidative Stressmentioning

confidence: 99%

Sepsis: Evidence-based pathogenesis and treatment

Pravda¹

2021

WJCCM

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Sepsis can develop during the body’s response to a critical illness leading to multiple organ failure, irreversible shock, and death. Sepsis has been vexing health care providers for centuries due to its insidious onset, generalized metabolic dysfunction, and lack of specific therapy. A common factor underlying sepsis is the characteristic hypermetabolic response as the body ramps up every physiological system in its fight against the underlying critical illness. A hypermetabolic response requires supraphysiological amounts of energy, which is mostly supplied via oxidative phosphorylation generated ATP. A by-product of oxidative phosphorylation is hydrogen peroxide (H 2 O 2 ), a toxic, membrane-permeable oxidizing agent that is produced in far greater amounts during a hypermetabolic state. Continued production of mitochondrial H 2 O 2 can overwhelm cellular reductive (antioxidant) capacity leading to a build-up within cells and eventual diffusion into the bloodstream. H 2 O 2 is a metabolic poison that can inhibit enzyme systems leading to organ failure, microangiopathic dysfunction, and irreversible septic shock. The toxic effects of H 2 O 2 mirror the clinical and laboratory abnormalities observed in sepsis, and toxic levels of blood H 2 O 2 have been reported in patients with septic shock. This review provides evidence to support a causal role for H 2 O 2 in the pathogenesis of sepsis, and an evidence-based therapeutic intervention to reduce H 2 O 2 levels in the body and restore redox homeostasis, which is necessary for normal organ function and vascular responsiveness.

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“…A decrease in PTH levels may induce a clinically detectable hypocalcemia delayed for up to 48 h after the hypoparathyroidism. The development of hypocalcemia depends on several factors, including the catabolism of PTH (some PTH particles continue to have biological activity), vitamin D levels, and the presence of bone mineral disorders [11,12]. These factors are important for surgeons to take into account in order to prevent the development of post-thyroidectomy hypocalcemia.…”

Section: Introductionmentioning

confidence: 99%

PTH after Thyroidectomy as a Predictor of Post-Operative Hypocalcemia

Metere¹,

Biancucci

Natili³

et al. 2021

Diagnostics

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Post-thyroidectomy hypocalcemia is a frequent complication with significant morbidity, and has been shown to increase hospital stay and readmission rates. The evaluation of serum parathyroid hormone (PTH) levels after thyroidectomy represents a reliable method to predict post-thyroidectomy hypocalcemia, but it remains infrequently used. This retrospective study investigates serum PTH values 3 h after thyroidectomy as a predictor of hypocalcemia. In this study, we enrolled 141 patients aged between 27 and 71 years eligible for total thyroidectomy who presented with multinodular goiter, suspicious nodule on cytological examination, Graves’ disease, or toxic multinodular goiter. Three hours after total thyroidectomy, 53 patients (37.6%) showed a reduction in serum PTH. Of these patients 75.5% developed hypocalcemia by 24 h after surgery and 100% were hypocalcemic after 48 h (p < 0.001). There was no significant difference attributable to the different thyroid diseases, nor to the age of the patients. PTH at 3 h after total thyroidectomy accurately predicts post-operative hypocalcemia. The early detection of patients at risk of developing post-operative hypocalcemia allows for prompt supplementation of calcium and Vitamin D in order to prevent symptoms and allows for a safe and timely discharge.

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Disorders of Calcium Metabolism: Hypocalcemia and Hypercalcemia

Cited by 29 publications

References 44 publications

Pathophysiology, Evaluation, and Management of Metabolic Alkalosis

Pathophysiology, Evaluation, and Management of Metabolic Alkalosis

Sepsis: Evidence-based pathogenesis and treatment

PTH after Thyroidectomy as a Predictor of Post-Operative Hypocalcemia

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