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European Journal of Pediatric Surgery :... Dec 2023Normalization of metabolic alkalosis is an important pillar in the treatment of infantile hypertrophic pyloric stenosis (IHPS) because uncorrected metabolic alkalosis...
BACKGROUND
Normalization of metabolic alkalosis is an important pillar in the treatment of infantile hypertrophic pyloric stenosis (IHPS) because uncorrected metabolic alkalosis may lead to perioperative respiratory events. However, the evidence on the incidence of respiratory events is limited. We aimed to study the incidence of peroperative hypoxemia and postoperative respiratory events in infants undergoing pyloromyotomy and the potential role of metabolic alkalosis.
MATERIALS AND METHODS
We retrospectively reviewed all patients undergoing pyloromyotomy between 2007 and 2017. All infants received intravenous fluids preoperatively to correct metabolic abnormalities close to normal. We assessed the incidence of perioperative hypoxemia (defined as oxygen saturation [SpO] < 90% for > 1min) and postoperative respiratory events. Additionally, the incidence of difficult intubations was evaluated. We performed a multivariate logistic regression analysis to evaluate the association between admission or preoperative serum pH values, bicarbonate or chloride, and peri- and postoperative hypoxemia or respiratory events.
RESULTS
Of 406 included infants, 208 (51%) developed 1 or more episodes of hypoxemia during the perioperative period, of whom 130 (32%) experienced it during induction, 43 (11%) intraoperatively, and 112 (28%) during emergence. About 7.5% of the infants had a difficult intubation and 17 required more than 3 attempts by a pediatric anesthesiologist. Three patients developed respiratory insufficiency and 95 postoperative respiratory events were noticed. We did not find a clinically meaningful association between laboratory values reflecting metabolic alkalosis and respiratory events.
CONCLUSIONS
IHPS frequently leads to peri- and postoperative hypoxemia or respiratory events and high incidence of difficult tracheal intubations. Preoperative pH, bicarbonate, and chloride were bad predictors of respiratory events.
Topics: Infant; Humans; Child; Pyloric Stenosis, Hypertrophic; Retrospective Studies; Bicarbonates; Chlorides; Hypoxia; Alkalosis
PubMed: 36417975
DOI: 10.1055/a-1984-9803 -
Translational Animal Science 2023() is an endemic zoonotic pathogen still lacking adequate prevention in pigs. The present case study looked back to the occurrence and consequences of outbreaks in our...
() is an endemic zoonotic pathogen still lacking adequate prevention in pigs. The present case study looked back to the occurrence and consequences of outbreaks in our swine research facilities in search of new metabolic and physiological insight. From a series of outbreaks, a dataset was created including 56 pigs sampled during disease detection based on clinical signs. Pigs suspected with infection were defined as diseased ( = 28) and included pigs defined as neurologically diseased ( = 20) when severe neurological signs (central nervous system dysfunctions, i.e., opisthotonos, ataxia, and generalized tremor) were observed. Another set of 28 pigs included respective pen mates from each case and were defined as control. Representative deaths were confirmed to be caused by Tonsillar swabs were collected and analyzed by quantitative polymerase chain reaction () for total bacteria, total , and serotypes () 2 (and/or 1/2) and 9. Blood and sera were analyzed to quantify blood gases, minerals, and reactive immunoglobulins against current isolates. Data collected included litter sibling associations, birth and weaning body weight (), and average daily gain () 7 d after the disease detection. In general, the disease increased pH, sO and the incidence of alkalosis, but reduced pCO, glucose, Ca, P, Mg, K, and Na in blood/serum compared to control. The SS2 (and/or SS1/2) prevalence was significantly ( < 0.05) increased in neurologically diseased pigs and its relative abundance tended ( < 0.10) to increase in tonsils. In contrast, the relative abundance of total was lower ( > 0.05) in diseased pigs than control pigs. Levels of reactive IgG2 were lower, but IgM were higher ( < 0.03) in neurologically affected pigs compared to control. Furthermore, there was an increased proportion of sibling pigs that were diseased compared to control. In conclusion, our results evidence that naturally affected pigs were associated to average performing pigs without any predisease trait to highlight but a sow/litter effect. Besides, neurologically affected pigs had increased (SS2 and/or 1/2) prevalence and relative abundance, a respiratory alkalosis profile, and mineral loss.
PubMed: 38023423
DOI: 10.1093/tas/txad126 -
Cureus Sep 2023In a patient with persistent hypokalemia, it is important to consider Gitelman syndrome, a rare, salt-wasting tubulopathy inherited in an autosomal recessive pattern....
In a patient with persistent hypokalemia, it is important to consider Gitelman syndrome, a rare, salt-wasting tubulopathy inherited in an autosomal recessive pattern. Gitelman syndrome leads to electrolyte abnormalities like hypokalemia, hypomagnesemia, and metabolic alkalosis. Typical clinical features include muscle cramps, fatigue, polydipsia, and salt cravings. Our case involves a female patient in her early 40s who visited the endocrinology clinic with symptoms of polyuria, constipation, muscle weakness, and fatigue. Electrolyte abnormalities included hypokalemia, hypomagnesemia, hypochloremia, and hyperreninemia. Initial tests, such as renal function tests, renal ultrasound, and CT scan, yielded normal results. Differential diagnosis of Gitelman syndrome and Bartter syndrome was considered due to the mutual electrolyte abnormalities of hypokalemia and metabolic alkalosis. Bartter syndrome was ruled out in our patient due to the presence of hypomagnesemia, which indicates a different defective receptor. Ultimately, genetic testing would be necessary to confirm the diagnosis of Gitelman syndrome considering the characteristic electrolyte disturbances and classic clinical presentation of fatigue, weakness, and salt craving.
PubMed: 37795074
DOI: 10.7759/cureus.44590 -
Journal of the American Society of... Aug 2023During acute base excess, the renal collecting duct β -intercalated cells ( β -ICs) become activated to increase urine base excretion. This process is dependent on...
SIGNIFICANCE STATEMENT
During acute base excess, the renal collecting duct β -intercalated cells ( β -ICs) become activated to increase urine base excretion. This process is dependent on pendrin and cystic fibrosis transmembrane regulator (CFTR) expressed in the apical membrane of β -ICs. The signal that leads to activation of this process was unknown. Plasma secretin levels increase during acute alkalosis, and the secretin receptor (SCTR) is functionally expressed in β -ICs. We find that mice with global knockout for the SCTR lose their ability to acutely increase renal base excretion. This forces the mice to lower their ventilation to cope with this challenge. Our findings suggest that secretin is a systemic bicarbonate-regulating hormone, likely being released from the small intestine during alkalosis.
BACKGROUND
The secretin receptor (SCTR) is functionally expressed in the basolateral membrane of the β -intercalated cells of the kidney cortical collecting duct and stimulates urine alkalization by activating the β -intercalated cells. Interestingly, the plasma secretin level increases during acute metabolic alkalosis, but its role in systemic acid-base homeostasis was unclear. We hypothesized that the SCTR system is essential for renal base excretion during acute metabolic alkalosis.
METHODS
We conducted bladder catheterization experiments, metabolic cage studies, blood gas analysis, barometric respirometry, perfusion of isolated cortical collecting ducts, immunoblotting, and immunohistochemistry in SCTR wild-type and knockout (KO) mice. We also perfused isolated rat small intestines to study secretin release.
RESULTS
In wild-type mice, secretin acutely increased urine pH and pendrin function in isolated perfused cortical collecting ducts. These effects were absent in KO mice, which also did not sufficiently increase renal base excretion during acute base loading. In line with these findings, KO mice developed prolonged metabolic alkalosis when exposed to acute oral or intraperitoneal base loading. Furthermore, KO mice exhibited transient but marked hypoventilation after acute base loading. In rats, increased blood alkalinity of the perfused upper small intestine increased venous secretin release.
CONCLUSIONS
Our results suggest that loss of SCTR impairs the appropriate increase of renal base excretion during acute base loading and that SCTR is necessary for acute correction of metabolic alkalosis. In addition, our findings suggest that blood alkalinity increases secretin release from the small intestine and that secretin action is critical for bicarbonate homeostasis.
Topics: Animals; Mice; Rats; Alkalosis; Bicarbonates; Mice, Knockout; Receptors, G-Protein-Coupled; Secretin; Sulfate Transporters
PubMed: 37344929
DOI: 10.1681/ASN.0000000000000173 -
Kidney International Reports Nov 2023Excessive dialytic potassium (K) and acid removal are risk factors for arrhythmias; however, treatment-to-treatment dialysate modification is rarely performed. We...
INTRODUCTION
Excessive dialytic potassium (K) and acid removal are risk factors for arrhythmias; however, treatment-to-treatment dialysate modification is rarely performed. We conducted a multicenter, pilot randomized study to test the safety, feasibility, and efficacy of 4 point-of-care (POC) chemistry-guided protocols to adjust dialysate K and bicarbonate (HCO3) in outpatient hemodialysis (HD) clinics.
METHODS
Participants received implantable cardiac loop monitors and crossed over to four 4-week periods with adjustment of dialysate K or HCO3 at each treatment according to pre-HD POC values: (i) K-removal minimization, (ii) K-removal maximization, (iii) Acidosis avoidance, and (iv) Alkalosis avoidance. The primary end point was percentage of treatments adhering to the intervention algorithm. Secondary endpoints included pre-HD K and HCO variability, adverse events, and rates of clinically significant arrhythmias (CSAs).
RESULTS
Nineteen subjects were enrolled in the study. HD staff completed POC testing and correctly adjusted the dialysate in 604 of 708 (85%) of available HD treatments. There was 1 K ≤3, 29 HCO3 <20 and 2 HCO3 >32 mEq/l and no serious adverse events related to study interventions. Although there were no significant differences between POC results and conventional laboratory measures drawn concurrently, intertreatment K and HCO3 variability was high. There were 45 CSA events; most were transient atrial fibrillation (AF), with numerically fewer events during the alkalosis avoidance period (8) and K-removal maximization period (3) compared to other intervention periods (17). There were no significant differences in CSA duration among interventions.
CONCLUSION
Algorithm-guided K/HCO3 adjustment based on POC testing is feasible. The variability of intertreatment K and HCO3 suggests that a POC-laboratory-guided algorithm could markedly alter dialysate-serum chemistry gradients. Definitive end point-powered trials should be considered.
PubMed: 38025214
DOI: 10.1016/j.ekir.2023.07.039 -
Current Opinion in Pediatrics Apr 2024Hypertension, commonly known as high blood pressure, is a widespread health condition affecting a large number of individuals across the globe. Although lifestyle... (Review)
Review
PURPOSE OF REVIEW
Hypertension, commonly known as high blood pressure, is a widespread health condition affecting a large number of individuals across the globe. Although lifestyle choices and environmental factors are known to have a significant impact on its development, there is growing recognition of the influence of genetic factors in the pathogenesis of hypertension. This review specifically focuses on the hereditary causes of hypertension that are associated with increased sodium transport through the thiazide-sensitive NaCl cotransporter (NCC) or amiloride-sensitive epithelial sodium channel (ENaC), crucial mechanisms involved in regulating blood pressure in the kidneys. By examining genetic mutations and signaling molecules linked to the dysregulation of sodium transport, this review aims to deepen our understanding of the hereditary causes of hypertension and shed light on potential therapeutic targets.
RECENT FINDINGS
Liddle syndrome (LS) is a genetic disorder that typically manifests early in life and is characterized by hypertension, hypokalemic metabolic alkalosis, hyporeninemia, and suppressed aldosterone secretion. This condition is primarily caused by gain-of-function mutations in ENaC. In contrast, Pseudohypoaldosteronism type II (PHAII) is marked by hyperkalemia and hypertension, alongside other clinical features such as hyperchloremia, metabolic acidosis, and suppressed plasma renin levels. PHAII results from overactivations of NCC, brought about by gain-of-function mutations in its upstream signaling molecules, including WNK1 (with no lysine (K) 1), WNK4, Kelch-like 3 (KLHL3), and cullin3 (CUL3).
SUMMARY
NCC and ENaC are integral components, and their malfunctions lead to disorders like LS and PHAII, hereditary causes of hypertension. Current treatments for LS involve ENaC blockers (e.g., triamterene and amiloride) in conjunction with low-sodium diets, effectively normalizing blood pressure and potassium levels. In PHAII, thiazide diuretics, which inhibit NCC, are the mainstay treatment, albeit with some limitations and potential side effects. Ongoing research in developing alternative treatments, including small molecules targeting key regulators, holds promise for more effective and tailored hypertension solutions.
Topics: Humans; Protein Serine-Threonine Kinases; Amiloride; Hypertension; Kidney; Pseudohypoaldosteronism; Sodium
PubMed: 37909881
DOI: 10.1097/MOP.0000000000001304 -
Nutrition Reviews Oct 2023Salicylates are generally present in plants as part of their defense system against pathogens and environmental stress. Major dietary sources of salicylates were found...
Salicylates are generally present in plants as part of their defense system against pathogens and environmental stress. Major dietary sources of salicylates were found in spices and herbs, such as curry and paprika (hot powder). Several studies suggest that these natural salicylates offer health benefits in the human body, such as antidiabetic, anticancer, antiviral, and anti-inflammatory properties. However, despite their advantages, salicylates can be harmful to people with allergies, and high doses of salicylates may cause respiratory alkalosis and gastrointestinal bleeding. Additionally, salicylates can interact with certain drugs, such as nonsteroidal anti-inflammatory drugs and warfarin. This narrative review aimed to consolidate recent information on the content of salicylates in food based on the literature, while also highlighting the benefits and risks associated with salicylate consumption in humans. Based on the literature review and analysis of results, it can be concluded that the dietary intake of salicylates in vegetarians can be relatively high, resulting in concentrations of salicylic acid in the blood and urine that are comparable to those observed in patients taking a low dose of aspirin (75 mg). This suggests that a diet rich in salicylates may have potential benefits in preventing and treating some diseases that require low doses of aspirin.
PubMed: 37897072
DOI: 10.1093/nutrit/nuad136 -
Clinical Practice and Cases in... May 2024Severe metabolic alkaloses are relatively rare but can carry a high mortality rate. Treatment involves supportive care and treatment of underlying causes.
INTRODUCTION
Severe metabolic alkaloses are relatively rare but can carry a high mortality rate. Treatment involves supportive care and treatment of underlying causes.
CASE REPORT
A 55-year-old male dependent on a gastrojejunostomy tube presented to the emergency department for altered mental status. The patient had metabolic alkalosis, electrolyte abnormalities, and prolonged QT interval on electrocardiogram. Examination and history revealed that chronic drainage of gastric fluid via malfunctioning a gastrojejunostomy tube resulted in profound alkalosis. The patient recovered with supportive care, electrolyte repletion, and gastrojejunostomy tube replacement.
CONCLUSION
This case highlights the importance of gastrointestinal acid-base pathophysiology.
PubMed: 38869337
DOI: 10.5811/cpcem.1519 -
AJP Reports Jan 2024We describe a pregnant patient with severe compulsive water ingestion and vomiting that lead to metabolic alkalosis and preterm delivery. A 21-year-old patient was...
We describe a pregnant patient with severe compulsive water ingestion and vomiting that lead to metabolic alkalosis and preterm delivery. A 21-year-old patient was hospitalized multiple times throughout pregnancy for symptoms initially thought to be related to hyperemesis gravidarum. Overtime, it became apparent that the patient induced vomiting by rapidly drinking large volumes of water. At 32 weeks' gestation, rapid ingestion of water caused 3 days of vomiting with findings of hyponatremia, hypokalemia, hypochloremia, metabolic alkalosis, and compensatory respiratory acidosis. Fetal monitoring showed minimal variability and recurrent decelerations; subsequent biophysical profile score of 2/10 prompted urgent cesarean section. A male newborn was delivered and cord blood gases reflected neonatal metabolic alkalosis and electrolyte imbalances identical to those of the mother. Compensatory hypoventilation in both mother and fetus were treated with assisted ventilation. With saline administration and repletion of electrolytes, metabolic alkalosis resolved for both patients within days. Metabolic alkalosis was transplacentally acquired by the fetus. This case demonstrates the development of metabolic alkalosis in a pregnant woman caused by vomiting severe enough to prompt preterm delivery for nonreassuring fetal status. It also demonstrates fetal dependence on both placenta and mother to maintain physiologic acid-base and electrolyte balance.
PubMed: 38269119
DOI: 10.1055/s-0043-1778113 -
Cureus Jan 2024Abiraterone acetate causes an adrenocorticotropic hormone (ACTH)-mediated mineralocorticoid excess. We present a 77-year-old man with prostate adenocarcinoma who...
Abiraterone acetate causes an adrenocorticotropic hormone (ACTH)-mediated mineralocorticoid excess. We present a 77-year-old man with prostate adenocarcinoma who developed signs and symptoms of mineralocorticoid excess while on abiraterone and discuss its pathophysiology and treatment options. The patient developed hypokalemia, metabolic alkalosis, and hypertension, indicative of increased mineralocorticoid activity, confirmed by elevated ACTH, corticosterone, and deoxycorticosterone levels. Abiraterone inhibits cytochrome P450c17 (CYP17A1), thus inhibiting testosterone and cortisol synthesis. Diminished cortisol synthesis, in turn, leads to excessive mineralocorticoid precursor production mediated by ACTH, leading to enhanced sodium absorption and potassium excretion. Abiraterone is often prescribed with low-dose prednisone to suppress ACTH; however, this strategy may not provide physiological glucocorticoid levels, resulting in ACTH-mediated mineralocorticoid excess in some patients. High-dose steroids or mineralocorticoid antagonists may activate mutant androgen receptors in prostate cancer tissue; therefore, amiloride is suggested for managing residual mineralocorticoid activity. This case highlights the importance of being vigilant for the signs and symptoms of mineralocorticoid excess in patients on abiraterone.
PubMed: 38318572
DOI: 10.7759/cureus.51757