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Nutrients Nov 2020Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among...
Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid-base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride-bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2-4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a "mendicant" ion, plays a crucial role in acid-base and salt balance.
Topics: Acid-Base Imbalance; Adult; Chlorides; Dietary Supplements; Humans; Infant; Infant Formula; Syndrome; Water-Electrolyte Imbalance
PubMed: 33182508
DOI: 10.3390/nu12113436 -
Pediatric Research Jul 2021Congenital chloride diarrhea (CLD) is a rare autosomal recessive disorder characterized by watery diarrhea with a high level of fecal Cl, metabolic alkalosis, and...
INTRODUCTION
Congenital chloride diarrhea (CLD) is a rare autosomal recessive disorder characterized by watery diarrhea with a high level of fecal Cl, metabolic alkalosis, and electrolyte alterations. Several intestinal and extraintestinal complications and even death can occur. An optimal knowledge of the clinical features and best therapeutic strategies is mandatory for an effective management.
METHODS
Articles published between 1 January 1965 and 31 December 2019, reported in PUBMED and EMBASE, were evaluated for a systematic review analyzing four categories: anamnestic features, clinical features, management, and follow-up strategies.
RESULTS
Fifty-seven papers reporting information on 193 CLD patients were included. The most common anamnestic features were positive family anamnesis for chronic diarrhea (44.4%), consanguinity (75%), polyhydramnios (98.3%), preterm delivery (78.6%), and failure to pass meconium (60.7%). Mean age at diarrhea onset was 6.63 days. Median diagnostic delay was 60 days. Prenatal diagnosis, based on molecular analysis, was described in 40/172 (23.3%). All patients received NaCl/KCl-substitutive therapy. An improvement of diarrhea during adulthood was reported in 91.3% of cases. Failure to thrive (21.6%) and chronic kidney disease (17.7%) were the most common complications.
CONCLUSIONS
This analysis of a large population suggests the necessity of better strategies for the management of CLD. A close follow-up and a multidisciplinary approach is mandatory to manage this condition characterized by heterogeneous and multisystemic complications.
IMPACT
In this systematic review, we describe data regarding anamnestic features, clinical features, management, and follow-up of CLD patients obtained from the largest population of patients ever described to date. The results of our investigation could provide useful insights for the diagnostic approach and the management of this condition.
Topics: Diarrhea; Feces; Humans; Infant, Newborn; Meconium; Metabolism, Inborn Errors; Mutation, Missense
PubMed: 33173177
DOI: 10.1038/s41390-020-01251-2 -
Journal of Dietary Supplements 2021The aim of this systematic review was to investigate the effects of sodium bicarbonate supplementation on electromyographic (EMG) muscle activity in healthy, physically...
AIM
The aim of this systematic review was to investigate the effects of sodium bicarbonate supplementation on electromyographic (EMG) muscle activity in healthy, physically active individuals.
METHODS
A systematic review of cross-sectional studies, crossover studies and randomized controlled trials was performed to investigate the effects of sodium bicarbonate supplementation on EMG muscle activity in healthy, physically active individuals. Potentially eligible for the systematic review were identified through searches conducted in the PubMed/MEDLINE, Science Direct and Scopus, considering publications from January 1980 to August 2019. The terms used in the search were: sodium bicarbonate, NaHCO, alkalosis, alkaloses, electromyography, surface electromyography, electromyographies, electromyogram and EMG. Two independent assessors extracted data from the selected articles. Bias analysis was conducted using the Cochrane Risk of Bias tool and methodological quality was appraised using a checklist created based on the guidelines of the Consolidated Standards of Reporting Trials and the International Society of Electrophysiology and Kinesiology.
RESULTS
A total of 67 studies were retrieved and seven were included in this review. Only two studies showed significant differences in muscle activity after sodium bicarbonate supplementation. The different EMG signal capturing, processing, and analysis methods used constitute an important limitation to the comparative analyses of the results reported in the studies selected for the present review.
CONCLUSION
The results found do not allow us to affirm whether EMG may or may not be a safe tool to assess the effects of sodium bicarbonate supplementation on muscle activity.
Topics: Cross-Sectional Studies; Dietary Supplements; Electromyography; Humans; Muscle, Skeletal; Randomized Controlled Trials as Topic; Sodium Bicarbonate
PubMed: 32449633
DOI: 10.1080/19390211.2020.1766633 -
Paediatric Anaesthesia Jul 2020Infantile hypertrophic pyloric stenosis (IHPS) leads to excessive vomiting and metabolic alkalosis, which may subsequently cause apnea. Although it is generally assumed... (Review)
Review
BACKGROUND
Infantile hypertrophic pyloric stenosis (IHPS) leads to excessive vomiting and metabolic alkalosis, which may subsequently cause apnea. Although it is generally assumed that metabolic derangements should be corrected prior to surgery to prevent apnea, the exact incidence of perioperative apneas in infants with IHPS and the association with metabolic alkalosis are unknown. We performed this systematic review to assess the incidence of apnea in infants with IHPS and to verify the possible association between apnea and metabolic alkalosis.
METHODS
We searched MEDLINE, Embase, and Cochrane library to identify studies regarding infants with metabolic alkalosis, respiratory problems, and hypertrophic pyloric stenosis. We conducted a descriptive synthesis of the findings of the included studies.
RESULTS
Thirteen studies were included for analysis. Six studies described preoperative apnea, three studies described postoperative apnea, and four studies described both. All studies were of low quality or had other research questions. We found an incidence of 27% of preoperative and 0.2%-16% of postoperative apnea, respectively. None of the studies examined the association between apnea and metabolic alkalosis in infants with IHPS.
CONCLUSIONS
Infants with IHPS may have a risk to develop perioperative apnea. However, the incidence rates should be interpreted with caution because of the low quality and quantity of the studies. Therefore, further studies are required to determine the incidence of perioperative apnea in infants with IHPS. The precise underlying mechanism of apnea in these infants is still unknown, and the role of metabolic alkalosis should be further evaluated.
Topics: Apnea; Humans; Incidence; Infant; Pyloric Stenosis, Hypertrophic
PubMed: 32298502
DOI: 10.1111/pan.13879