Systematic review and meta-analysis of prophylaxis use with intravenous contrast exposure to prevent contrast-induced nephropathy.

PURPOSE: Iodinated radiographic contrast media has been associated with an acute deterioration in renal function, termed contrast induced nephropathy (CIN). This review aims to establish the efficacy of prophylaxis interventions used in adult patients prior to intravenous exposure to iodinated contrast to reduce the risk of CIN. METHODS: An electronic search for published peer-reviewed articles was performed, supplemented with manual review of references from previous systematic reviews and the National Institute for Health and Care Excellence guidelines. Risk of bias was assessed using the Cochrane Collaboration's tool for assessing risk of bias. Random-effect meta-analyses were used to assess CIN incidence, need for kidney replacement therapy (KRT), mortality, fluid overload and persistent kidney dysfunction. RESULTS: 22 studies assessing a range of interventions were included in the qualitative analysis. The incidence of CIN was reduced by the use of N-acetylcysteine compared to a control group of saline (risk difference = -0.07, 95% CI -0.13 to -0.01) but not by sodium bicarbonate compared to control group of saline (risk difference = -0.02, 95% CI -0.04 to 0.01). Published studies give no indication that prophylactic interventions have significant impact on the need for KRT, mortality or persistent renal impairment. CONCLUSION: Evidence for prophylaxis against CIN in patients receiving intravenous iodinated contrast is limited. There was an association with the use of NAC with reduced incidence of CIN following intravenous contrast but there was no impact on other clinical outcomes assessed. The clinical significance of these findings remains unclear and further research focusing on these clinical outcomes is required.

An unusual cause of metabolic alkalosis: hiding in plain sight.

BACKGROUND: Sodium bicarbonate, in the form of baking soda, is widely used as a home remedy, and as an additive for personal and household cleaning products. Its toxicity has previously been reported following oral ingestion in the setting of dyspepsia. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity. CASE PRESENTATION: We are reporting a case of an 80-year-old woman who presented with chronic metabolic alkalosis and hypokalemia secondary to exogenous alkali exposure from baking soda as a toothpaste additive, which might have represented an underreported ingestion of the substance. CONCLUSIONS: Considering that one teaspoon of baking soda provides approximately 59 m-equivalents (mEq) of bicarbonate, specific questioning on its general use should be pursued in similar cases of chloride resistant metabolic alkalosis.

Kidney Injury from Recurrent Heat Stress and Rhabdomyolysis: Protective Role of Allopurinol and Sodium Bicarbonate.

BACKGROUND: Heat stress and rhabdomyolysis are major risk factors for the occurrence of repeated acute kidney injury in workers exposed to heat and strenuous work. These episodes, in turn, may progress to chronic kidney disease. OBJECTIVE: The purpose of this study was to test the effect of allopurinol (AP) and sodium bicarbonate on the kidney injury induced by recurrent heat stress dehydration with concomitant repeated episodes of rhabdomyolysis. METHODS: The model consisted of heat stress exposure (1 h, 37°C) plus rhabdomyolysis (R) induced by repetitive IM injections of glycerol (7.5 mL/kg BW days) in the rat. In addition, to replicate the human situation, uricase was inhibited (oxonic acid [OA] 750 mg/K/d) to increase uric acid (UA) levels. Additional groups were treated either with AP 150 mg/L, n = 10, bicarbonate (BC; 160 mM, n = 10), or both (AP + BC, n = 10) in drinking water. We also included 2 control groups consisting of normal controls (N-Ref, n = 5) and uricase-inhibited rats (OA, n = 5) that were not exposed to heat or muscle injury. Groups were studied for 35 days. RESULTS: Uricase-inhibited rats exposed to heat and rhabdomyolysis developed pathway and increased intrarenal oxidative stress and inflammasome activation. Kidney injury could be largely prevented by AP, and also BC, although the treatments were not synergistic. CONCLUSION: Increased levels of UA may play an important role in the renal alterations induced by heat stress and continuous episodes of rhabdomyolysis. Therefore, treatments aimed to reduce hyperuricemia may help to decrease the renal burden in these conditions. Clinical trials are suggested to test whether this is also true in humans.

The Effect of a New Sodium Bicarbonate Loading Regimen on Anaerobic Capacity and Wrestling Performance.

Gastrointestinal side effects are the main problem with sodium bicarbonate (SB) use in sports. Therefore, our study assessed the effect of a new SB loading regimen on anaerobic capacity and wrestling performance. Fifty-eight wrestlers were randomized to either a progressive-dose regimen of up to 100 mg∙kg-1 of SB or a placebo for 10 days. Before and after treatment, athletes completed an exercise protocol that comprised, in sequence, the first Wingate, dummy throw, and second Wingate tests. Blood samples were taken pre- and post-exercise. No gastrointestinal side effects were reported during the study. After SB treatment, there were no significant improvements in the outcomes of the Wingate and dummy throw tests. The only index that significantly improved with SB, compared to the placebo (p = 0.0142), was the time-to-peak power in the second Wingate test, which decreased from 3.44 ± 1.98 to 2.35 ± 1.17 s. There were also no differences in blood lactate or glucose concentrations. In conclusion, although the new loading regimen eliminated gastrointestinal symptoms, the doses could have been too small to elicit additional improvements in anaerobic power and wrestling performance. However, shortening the time-to-peak power during fatigue may be particularly valuable and is one of the variables contributing to the final success of a combat sports athlete.

Nutritional Strategies to Modulate Intracellular and Extracellular Buffering Capacity During High-Intensity Exercise.

Intramuscular acidosis is a contributing factor to fatigue during high-intensity exercise. Many nutritional strategies aiming to increase intra- and extracellular buffering capacity have been investigated. Among these, supplementation of beta-alanine (~3-6.4 g/day for 4 weeks or longer), the rate-limiting factor to the intramuscular synthesis of carnosine (i.e. an intracellular buffer), has been shown to result in positive effects on exercise performance in which acidosis is a contributing factor to fatigue. Furthermore, sodium bicarbonate, sodium citrate and sodium/calcium lactate supplementation have been employed in an attempt to increase the extracellular buffering capacity. Although all attempts have increased blood bicarbonate concentrations, evidence indicates that sodium bicarbonate (0.3 g/kg body mass) is the most effective in improving high-intensity exercise performance. The evidence supporting the ergogenic effects of sodium citrate and lactate remain weak. These nutritional strategies are not without side effects, as gastrointestinal distress is often associated with the effective doses of sodium bicarbonate, sodium citrate and calcium lactate. Similarly, paresthesia (i.e. tingling sensation of the skin) is currently the only known side effect associated with beta-alanine supplementation, and it is caused by the acute elevation in plasma beta-alanine concentration after a single dose of beta-alanine. Finally, the co-supplementation of beta-alanine and sodium bicarbonate may result in additive ergogenic gains during high-intensity exercise, although studies are required to investigate this combination in a wide range of sports.

[Self-treatment with baking soda can lead to severe metabolic alkalosis].

This case report describes a 66-year-old man, previously healthy besides mild hypertension. He ingested a self-made folk remedy consisting of baking soda and water against acid reflux in dosages that resulted in severe metabolic alkalosis (pH 7.8). Diagnosing and treating MA is easy and cheap, but if the condition is not treated, consequences can be severe. The challenge is to uncover patients' use of non prescription medications and folk remedies in the diagnostic process. Having this information it is possible to prevent MA in both high- and low-risk patients.

Baking soda misuse as a home remedy: case experience of the California Poison Control System.

WHAT IS KNOWN AND OBJECTIVE: Baking soda is a common household product promoted by the manufacturer as an antacid. It contains sodium bicarbonate and has the potential for significant toxicity when ingested in excessive amounts. Characterizing the patterns and outcomes from the misuse of baking soda as a home remedy can guide the clinical assessment and preventative counselling of patients at risk for use of this product. METHODS: We conducted a retrospective review of all symptomatic cases involving ingestion and misuse of a baking soda powder product that were reported to the California Poison Control System between the years 2000 and 2012. RESULTS AND DISCUSSION: Of the 192 cases we identified, 55·8% were female, ages ranged 2 months to 79 years, and the most common reasons for misuse included antacid (60·4%), 'beat a urine drug test' (11·5%) and treat a UTI (4·7%). Most cases (55·2%) had significant symptoms warranting a medical evaluation, whereas 12 patients required hospital admission developed either electrolyte imbalances, metabolic alkalosis or respiratory depression. WHAT IS NEW AND CONCLUSION: Misuse of baking soda can result in serious electrolyte and acid/base imbalances. Patients at highest risk of toxicity may include those who chronically use an antacid, those who use the method to 'beat' urine drug screens, pregnant women and young children. Self-treatment with baking soda as a home remedy may also mask or delay medical care thereby complicating or exacerbating an existing medical problem. We suggest that healthcare providers counsel high-risk patients about the potential complications of misuse of baking soda as a home remedy.

Effect of oral sodium bicarbonate supplementation on progression of chronic kidney disease in patients with chronic metabolic acidosis: study protocol for a randomized controlled trial (SoBic-Study).

BACKGROUND: Overt chronic metabolic acidosis in patients with chronic kidney disease develops after a drop of glomerular filtration rate to less than approximately 25 mL/min/1.73 m2. The pathogenic mechanism seems to be a lack of tubular bicarbonate production, which in healthy individuals neutralizes the acid net production. As shown in several animal and human studies the acidotic milieu alters bone and vitamin D metabolism, induces muscle wasting, and impairs albumin synthesis, aside from a direct alteration of renal tissue by increasing angiotensin II, aldosteron and endothelin kidney levels. Subsequent studies testing various therapeutic approaches in very selected study populations showed that oral supplementation of the lacking bicarbonate halts progression of decline of renal function. However, due to methodological limitations of these studies further investigations are of urgent need to ensure the validity of this therapeutic concept. METHODS/DESIGN: The SoBic-study is a single-center, randomized, controlled, open-label clinical phase IV study performed at the nephrological outpatient service of the Medical University of Vienna. Two-hundred patients classified to CKD stage 3 or 4 with two separate measurements of HCO3- of <21 mmol/L will be 1:1 randomized to either receive a high dose of oral sodium bicarbonate with a serum target HCO3- level of 24±1 mmol/L or receive a rescue therapy of sodium bicarbonate with a serum target level of 20±1 mmol/L. The follow up will be for two years. The primary outcome is the effect of sodium bicarbonate supplementation on renal function measured by means of estimated glomerular filtration rates (4-variable-MDRD-equation) after two years. Secondary outcomes are change in markers of bone metabolism between groups, death rates between groups, and the number of subjects proceeding to renal replacement therapy across groups. Adverse events, such as worsening of arterial hypertension due to the additional sodium consumption, will be accurately monitored. DISCUSSION: We hypothesize that sufficiently balanced acid-base homeostasis leads to a reduction of decline of renal function in patients with chronic kidney disease. The concept of an exogenous bicarbonate supplementation to substitute the lacking endogenous bicarbonate has existed for a long time, but has never been investigated sufficiently to state clear treatment guidelines. TRIAL REGISTRATION: EUDRACT Number: 2012-001824-36.

Additive effects of beta-alanine and sodium bicarbonate on upper-body intermittent performance.

We examined the isolated and combined effects of beta-alanine (BA) and sodium bicarbonate (SB) on high-intensity intermittent upper-body performance in judo and jiu-jitsu competitors. 37 athletes were assigned to one of four groups: (1) placebo (PL)+PL; (2) BA+PL; (3) PL+SB or (4) BA+SB. BA or dextrose (placebo) (6.4 g day⁻¹) was ingested for 4 weeks and 500 mg kg⁻¹ BM of SB or calcium carbonate (placebo) was ingested for 7 days during the 4th week. Before and after 4 weeks of supplementation, the athletes completed four 30-s upper-body Wingate tests, separated by 3 min. Blood lactate was determined at rest, immediately after and 5 min after the 4th exercise bout, with perceived exertion reported immediately after the 4th bout. BA and SB alone increased the total work done in +7 and 8 %, respectively. The co-ingestion resulted in an additive effect (+14 %, p < 0.05 vs. BA and SB alone). BA alone significantly improved mean power in the 2nd and 3rd bouts and tended to improve the 4th bout. SB alone significantly improved mean power in the 4th bout and tended to improve in the 2nd and 3rd bouts. BA+SB enhanced mean power in all four bouts. PL+PL did not elicit any alteration on mean and peak power. Post-exercise blood lactate increased with all treatments except with PL+PL. Only BA+SB resulted in lower ratings of perceived exertion (p = 0.05). Chronic BA and SB supplementation alone equally enhanced high-intensity intermittent upper-body performance in well-trained athletes. Combined BA and SB promoted a clear additive ergogenic effect.

A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate.

BACKGROUND AND OBJECTIVES: Current guidelines recommend Na(+)-based alkali for CKD with metabolic acidosis and plasma total CO2 (PTCO2) < 22 mM. Because diets in industrialized societies are typically acid-producing, we compared base-producing fruits and vegetables with oral NaHCO3 (HCO3) regarding the primary outcome of follow-up estimated GFR (eGFR) and secondary outcomes of improved metabolic acidosis and reduced urine indices of kidney injury. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Individuals with stage 4 (eGFR, 15-29 ml/min per 1.73 m(2)) CKD due to hypertensive nephropathy, had a PTCO2 level < 22 mM, and were receiving angiotensin-converting enzyme inhibition were randomly assigned to 1 year of daily oral NaHCO3 at 1.0 mEq/kg per day (n=35) or fruits and vegetables dosed to reduce dietary acid by half (n=36). RESULTS: Plasma cystatin C-calculated eGFR did not differ at baseline and 1 year between groups. One-year PTCO2 was higher than baseline in the HCO3 group (21.2±1.3 versus 19.5±1.5 mM; P<0.01) and the fruits and vegetables group (19.9±1.7 versus 19.3±1.9 mM; P<0.01), consistent with improved metabolic acidosis, and was higher in the HCO3 than the fruits and vegetable group (P<0.001). One-year urine indices of kidney injury were lower than baseline in both groups. Plasma [K(+)] did not increase in either group. CONCLUSIONS: One year of fruits and vegetables or NaHCO3 in individuals with stage 4 CKD yielded eGFR that was not different, was associated with higher-than-baseline PTCO2, and was associated with lower-than-baseline urine indices of kidney injury. The data indicate that fruits and vegetables improve metabolic acidosis and reduce kidney injury in stage 4 CKD without producing hyperkalemia.

Metabolic alkalosis from unsuspected ingestion: use of urine pH and anion gap.

Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis.

Increased blood pH but not performance with sodium bicarbonate supplementation in elite rugby union players.

PURPOSE: This study investigated the effect of ingesting 0.3 g/kg body weight (BW) of sodium bicarbonate (NaHCO3) on physiological responses, gastrointestinal (GI) tolerability, and sprint performance in elite rugby union players. METHODS: Twenty-five male rugby players, age 21.6 (2.6) yr, participated in a randomized, double-blind, placebo-controlled crossover trial. Sixty-five minutes after consuming 0.3 g/kg BW of either NaHCO3 or placebo, participants completed a 25-min warm-up followed by 9 min of high-intensity rugby-specific training followed by a rugby-specific repeated-sprint test (RSRST). Whole-blood samples were collected to determine lactate and bicarbonate concentrations and pH at baseline, after supplement ingestion, and immediately after the RSRST. Acute GI discomfort was assessed by questionnaire throughout the trials, and chronic GI discomfort was assessed during the 24 hr postingestion. RESULTS: After supplement ingestion and immediately after the RSRST, blood HCO3⁻ concentration and pH were higher for the NaHCO3 condition than for the placebo condition (p < .001). After the RSRST, blood lactate concentrations were significantly higher for the NaHCO3 than for the placebo condition (p < .001). There was no difference in performance on the RSRST between the 2 conditions. The incidence of belching, stomachache, diarrhea, stomach bloating, and nausea was higher after ingestion of NaHCO3 than with placebo (all p < .050). The severity of stomach cramps, belching, stomachache, bowel urgency, diarrhea, vomiting, stomach bloating, and flatulence was rated worse after ingestion of NaHCO3 than with placebo (p < .050). CONCLUSIONS: NaHCO3 supplementation increased blood HCO3⁻ concentration and attenuated the decline in blood pH compared with placebo during high-intensity exercise in well-trained rugby players but did not significantly improve exercise performance. The higher incidence and greater severity of GI symptoms after ingestion of NaHCO3 may negatively affect physical performance, and the authors strongly recommend testing this supplement during training before use in competitive situations.

The safety and effectiveness of different methods of earwax removal: a systematic review and economic evaluation.

BACKGROUND: Build-up of earwax is a common reason for attendance in primary care. Current practice for earwax removal generally involves the use of a softening agent, followed by irrigation of the ear if required. However, the safety and benefits of the different methods of removal are not known for certain. OBJECTIVES: To conduct evidence synthesis of the clinical effectiveness and cost-effectiveness of the interventions currently available for softening and/or removing earwax and any adverse events (AEs) associated with the interventions. DATA SOURCES: Eleven electronic resources were searched from inception to November 2008, including: The Cochrane Library; MEDLINE (OVID), PREMEDLINE In-Process & Other Non-Indexed Citations (OVID), EMBASE (OVID); and CINAHL. METHODS: Two reviewers screened titles and abstracts for eligibility. Inclusion criteria were applied to the full text or retrieved papers and data were extracted by two reviewers using data extraction forms developed a priori. Any differences were resolved by discussion or by a third reviewer. Study criteria included: interventions - all methods of earwax removal available and combinations of these methods; participants - adults/children presenting requiring earwax removal; outcomes - measures of hearing, adequacy of clearance of wax, quality of life, time to recurrence or further treatment, AEs and measures of cost-effectiveness; design - randomised controlled trials (RCTs) and controlled clinical trials (CCTs) for clinical effectiveness, cohort studies for AEs and cost-effectiveness, and costing studies for cost-effectiveness. For the economic evaluation, a deterministic decision tree model was developed to evaluate three options: (1) the use of softeners followed by irrigation in primary care; (2) softeners followed by self-irrigation; and (3) a 'no treatment' option. Outcomes were assessed in terms of benefits to patients and costs incurred, with costs presented by exploratory cost-utility analysis. RESULTS: Twenty-six clinical trials conducted in primary care (14 studies), secondary care (8 studies) or other care settings (4 studies), met the inclusion criteria for the review - 22 RCTs and 4 CCTs. The range of interventions included 16 different softeners, with or without irrigation, and in various different comparisons. Participants, outcomes, timing of intervention, follow-up and methodological quality varied between studies. On measures of wax clearance Cerumol, sodium bicarbonate, olive oil and water are all more effective than no treatment; triethanolamine polypeptide (TP) is better than olive oil; wet irrigation is better than dry irrigation; sodium bicarbonate drops followed by irrigation by nurse is more effective than sodium bicarbonate drops followed by self-irrigation; softening with TP and self-irrigation is more effective than self-irrigation only; and endoscopic de-waxing is better than microscopic de-waxing. AEs appeared to be minor and of limited extent. Resuts of the exploratory economic model found that softeners followed by self-irrigation were more likely to be cost-effective [24,433 pounds per quality-adjusted life-year (QALY)] than softeners followed by irrigation at primary care (32,130 pounds per QALY) when compared with no treatment. Comparison of the two active treatments showed that the additional gain associated with softeners followed by irrigation at primary care over softeners followed by self-irrigation was at a cost of 340,000 pounds per QALY. When compared over a lifetime horizon to the 'no treatment' option, the ICERs for softeners followed by self-irrigation and of softeners followed by irrigation at primary care were 24,450 pounds per QALY and 32,136 pounds per QALY, respectively. LIMITATIONS: The systematic review found limited good-quality evidence of the safety, benefits and costs of the different strategies, making it difficult to differentiate between the various methods for removing earwax and rendering the economic evaluation as speculative. CONCLUSIONS: Although softeners are effective, which specific softeners are most effective remains uncertain. Evidence on the effectiveness of methods of irrigation or mechanical removal was equivocal. Further research is required to improve the evidence base, such as a RCT incorporating an economic evaluation to assess the different ways of providing the service, the effectiveness of the different methods of removal and the acceptability of the different approaches to patients and practitioners.

Dietary supplementation with carbonate increases expression of ornithine decarboxylase and proliferation in gastric mucosa in a rat model of gastric cancer.

Dietary factors play essential roles in gastric carcinogenesis. We recently found that dietary supplementation with NaHCO(3) significantly increased the development of gastric cancer in a rat gastric stump model. Here, we analysed nontransformed gastric mucosa for expression of the cancer-related proteins cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC), and we examined the relationship between expression levels of those proteins and mucosal proliferation. Research has shown that COX-2 is upregulated in gastric mucosal inflammation and is strongly associated with gastrointestinal cancer. ODC is the key enzyme in polyamine synthesis and a regulator of cell proliferation. We performed gastric resections on 48 Wistar rats to induce spontaneous gastric cancer; half of these animals were given a normal diet, and the other half received a diet supplemented with NaHCO(3). Twenty-four unoperated rats served as a control group. The surgical procedure per se led to a significant rise in mucosal expression of COX-2 and an associated increase in cell proliferation. However, the COX-2 level in gastric mucosa was not further affected by dietary supplementation of carbonate. Interestingly, nontransformed gastric mucosa in the operated rats receiving a carbonate-supplemented diet showed a pronounced increase in ODC expression that was strongly correlated with a further enhanced cell proliferation. These results indicate that carbonate ions, which represent a major constituent of intestinal reflux into the stomach, increase the expression of ODC and thereby enhance cell proliferation in nontransformed mucosa, and consequently elevate the risk of gastric cancer.

Metabolic acidosis in childhood: why, when and how to treat.

OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

Acidose metabólica na infância: por que, quando e como tratá-la? / Metabolic acidosis in childhood: why, when and how to treat

OBJETIVO: Apresentar uma revisão atualizada e crítica sobre os mecanismos das principais patologias associadas e o tratamento da acidose metabólica, discutindo aspectos controversos quanto aos benefícios e riscos da utilização do bicarbonato de sódio e outras formas de terapia. FONTES DOS DADOS: Revisão da literatura publicada, obtida através de busca eletrônica com as palavras-chave acidose metabólica, acidose láctica, cetoacidose diabética, ressuscitação cardiopulmonar, bicarbonato de sódio e terapêutica nas bases de dados PubMed/MEDLINE, LILACS e Cochrane Library, entre 1996 e 2006, além de publicações clássicas referentes ao tema, sendo selecionadas as mais atuais e representativas, buscando-se consensos e diretrizes. SíNTESE DOS DADOS: A utilização de bicarbonato de sódio não demonstra benefícios no quadro hemodinâmico, evolução clínica, morbidade e mortalidade nos quadros de acidose metabólica de anion gap elevado, relacionados à acidose láctica, cetoacidose diabética e ressuscitação cardiorrespiratória. Assim, a sua utilização rotineira não é indicada. Devem ser considerados os potenciais efeitos colaterais. O tratamento da doença de base é fundamental para reversão do processo. Outras terapias alternativas não demonstram efetividade comprovada em grande escala. CONCLUSÕES: Apesar dos efeitos conhecidos da acidemia em situações críticas no organismo, discute-se o papel protetor da acidemia nas células sob hipoxemia e os riscos da alcalemia secundária à intervenção medicamentosa. Existe consenso na reposição de álcalis e bicarbonato de sódio nos casos de acidose de anion gap normal; entretanto, nos casos de acidose de anion gap elevado, particularmente na acidose láctica, cetoacidose diabética e na ressuscitação cardiorrespiratória, o uso de bicarbonato de sódio não demonstra benefícios, além dos potenciais efeitos adversos, o que torna restrita sua indicação. Apesar da controvérsia, o único ponto concordante refere-se à abordagem...

OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease...

Prospective randomized crossover trial comparing fibre with lactulose in the treatment of idiopathic chronic constipation.

BACKGROUND: Fibre is often recommended as the first-choice treatment but its effects can be uneven. The aim of the study was to compare the clinical efficacy and tolerability of fibre versus lactulose in outpatients with chronic constipation. METHODS: In a prospective randomized crossover trial, patients were randomized to receive fibre or lactulose for four weeks. Between treatments, patients had at least one week free of laxatives. RESULTS: 50 patients, of median age 50 years (range, 18-85) were recruited and 39 patients completed the trial. Compared to fibre, lactulose resulted in significantly higher mean bowel frequency (7.3, 95% CI 5.7 to 8.9 vs. 5.5, 95% CI 4.4 to 6.5; p=0.001) and stool consistency score (3.4, 95% CI 3.1 to 3.7 vs. 2.9, 95% CI 2.5 to 3.3; p=0.018). Scores for ease of evacuation were similar. The frequencies of adverse effects were not significantly different, but greater in the lactulose group. Mean patients' recorded improvement score was significantly higher after taking lactulose than fibre (6.2, 95% CI 5.5 to 7.0 vs. 4.8, 95% CI 4.0 to 5.9; p=0.017). Of the 39 patients who completed the trial, 24 (61.5%) preferred lactulose and 14 (35.9%) preferred fibre. CONCLUSIONS: Lactulose had better efficacy than fibre for chronic constipation in ambulant patients, although both treatments were equally well tolerated in terms of adverse effects.

Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients.

OBJECTIVE: Milk-alkali syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of milk-alkali syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients' and syndrome characteristics. DESIGN AND PATIENTS: In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients' charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with milk-alkali syndrome, additional historical, clinical, laboratory and imaging data were collected. RESULTS: We identified 125 patients with hypercalcaemia, 11 (8.8%) of whom had milk-alkali syndrome, 42 (33.6%) had malignancy and 37 (29.6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium 3.5 mmol/l. Malignancy accounted for 13 of those patients (37.1%) and milk-alkali for nine (25.7%). Conditions prevalent among the milk-alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with milk-alkali syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0.047). CONCLUSION: Milk-alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In milk-alkali syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

A toxicity index of skin and wound cleansers used on in vitro fibroblasts and keratinocytes.

OBJECTIVE: To determine toxicity indexes of commercially available skin, wound, and skin/wound cleansers on in vitro fibroblasts and keratinocytes. DESIGN: Seventeen cleansers and 3 liquid bath soaps were evaluated for cytotoxic effect on human infant dermal fibroblasts and epidermal keratinocytes. Both skin cell types were exposed to serial 10-fold dilutions of each cleanser until treated cell viability was comparable to untreated controls. RESULTS: The experimental design allowed calculation of relative toxicity indexes ranging from 0 to 100,000. Shur-Clens, SAF-Clens, and saline were found to be the least toxic to fibroblasts (toxicity index 0); Dial Antibacterial Soap and Ivory Liqui-Gel were the most toxic (toxicity index 100,000). Biolex, Shur-Clens, and Techni-Care were the least toxic to keratinocytes (toxicity index 0); hydrogen peroxide, modified Dakin's solution, and povidone (10%) were found to be the most toxic (toxicity index 100,000). CONCLUSIONS: Successful cutaneous tissue repair depends on the viability of the principal cell types involved (fibroblasts and keratinocytes). Toxicity indexes provide helpful guidelines for subsequent in vivo evaluations and clinical applications. The study findings also suggest that judicious use of these supposedly innocuous agents should be considered in a clinical setting.

[Incidence of stomach ruptures after ingestion of sodium bicarbonate-containing or carbonated beverages]. / Zur inzidenz von Magen-Rupturen nach Ingestion kohlensäure- bzw. bikarbonathaltiger Getränke.

SUBJECT: Spontaneous rupture of the stomach is an uncommon condition with a usually poor prognosis. The questions of pathophysiologic factors and the possible role of carbonated or bicarbonate-containing beverages were addressed. METHODS AND RESULTS: A review of the literature based on a search of MEDLINE (1966-1998) was performed. Using the key word 'stomach rupture', we found 675 publications. 279 publications dealt with etiologic factors 15 of which mentioned the ingestion of bicarbonate preparations. No record of carbonated or bicarbonate-containing beverages as a single etiologic factor could be found. CONCLUSION: These beverages do not seem to play a significant role in the pathogenesis of stomach rupture, whereas in rare cases bicarbonate preparations can cause rupture of the previously overdistended stomach.