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PubMed1982

Treatment of lactic acidosis with dichloroacetate in dogs.

Lactic acidosis is a clinical condition due to accumulation of H(+) ions from lactic acid, characterized by blood lactate levels >5 mM and arterial pH <7.25. In addition to supportive care, treatment usually consists of intravenous NaHCO(3), with a resultant mortality >60%. Dichloroacetate (DCA) is a compound that lowers blood lactate levels under various conditions in both man and laboratory animals. It acts to increase pyruvate oxidation by activation of pyruvate dehydrogenase. We evaluated the effects of DCA in the treatment of two different models of type B experimental lactic acidosis in diabetic dogs: hepatectomy-lactic acidosis and phenformin-lactic acidosis. The metabolic and systemic effects examined included arterial blood pH and levels of bicarbonate and lactate; the intracellular pH (pHi) in liver and skeletal muscle; cardiac index, arterial blood pressure and liver blood flow; liver lactate uptake and extrahepatic splanchnic (gut) lactate production; and mortality. Effects of DCA were compared with those of either NaCl or NaHCO(3). The infusion of DCA and NaHCO(3), delivered equal amounts of volume and sodium, although the quantity of NaHCO(3) infused (2.5 meq/kg per h) was insufficient to normalize arterial pH. In phenformin-lactic acidosis, DCA-treated animals had a mortality of 22%, vs. 89% in those treated with NaHCO(3). DCA therapy increased arterial pH and bicarbonate, liver pHi and cardiac index, with increased liver lactate uptake and a fall in blood lactate. With NaHCO(3) therapy, there were decrements of cardiac index and liver pHi, with an increase in venous pCO(2) and gut production of lactate. Dogs with hepatectomy-lactic acidosis were either treated or pretreated with DCA. Treatment with DCA resulted in stabilization of cardiac index, a fall in blood lactate, and 17% mortality. NaHCO(3) was associated with a continuous decline of cardiac index, rise in blood lactate, and 67% mortality. In dogs pretreated with NaCl, mortality was 33%, but all dogs pretreated with DCA survived. Dogs pretreated with DCA also had lower blood lactate and higher arterial pH and bicarbonate than did those pretreated with NaCl.Thus, in either of two models of type B experimental lactic acidosis, treatment with DCA improves cardiac index, arterial pH, bicarbonate and lactate, and liver pHi. The mortality in dogs with type B lactic acidosis was significantly less in DCA-treated animals than in those treated with other modalities.

Acetates↗
PubMed1985

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Metabolic acidosis due to organic acids infusion fails to elicit hyperkalemia. Although plasma potassium levels may rise, the increase is smaller than in mineral acid acidosis. The mechanisms responsible for the different effects of organic acid acidosis and mineral acid acidosis remain undefined, although dissimilar hormonal responses by the pancreas may explain dissimilar hormonal responses by the pancreas may explain the phenomena. To test this hypothesis, beta-hydroxybutyric acid (7 meq/kg) or hydrochloric acid (3 meq/kg) was infused over 30 min into conscious dogs (n = 12) with chronically implanted catheters in the portal, hepatic, and systemic circulation, and flow probes were placed around the portal vein and hepatic artery. Acid infusion studies in two groups of anesthetized dogs were also done to assess the urinary excretion of potassium (n = 14), and to evaluate the effects of acute suppression of renal electrolyte excretion on plasma potassium and on the release/uptake of potassium in peripheral tissues of the hindleg (n = 17). Ketoacid infusion caused hypokalemia and a significant increase in portal vein plasma insulin, from the basal level of 27 +/- 4 microU/ml to a maximum of 84 +/- 22 microU/ml at 10 min, without changes in glucagon levels. By contrast, mineral acid acidosis of similar severity resulted in hyperkalemia and did not increase portal insulin levels but enhanced portal glucagon concentration from control values of 132 +/- 25 pg/ml to 251 +/- 39 pg/ml at 40 min. A significant decrease in plasma glucose levels due to suppression of hepatic release was observed during ketoacid infusion, while no changes were observed with mineral acid infusion. Plasma flows in the portal vein and hepatic artery remained unchanged from control values in both acid infusion studies. Differences in renal potassium excretion were ruled out as determinants of the disparate kalemic responses to organic acid infusion compared with HCl acidosis. Evaluation of the arteriovenous potassium difference across the hindleg during ketoacid infusion demonstrates that peripheral uptake of potassium is unlikely to be responsible for the observed hypokalemia. Although the tissue responsible for the different kalemic responses could not be defined with certainty, the data are compatible with an hepatic role in response to alterations in the portal vein insulin and/or glucagon levels in both acid infusion studies. We propose that cellular uptake of potassium is enhanced by hyperinsulinemia in ketoacid infusion, and release of potassium results from increased glucagon levels in HCl acidosis. Whether the changes in plasma potassium that other types od organic acid acidosis produce are accounted for by a similar hormonal mechanism remains to be determined.

3-Hydroxybutyric Acid↗
PubMed2005

A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study.

INTRODUCTION: Metabolic acidosis is common in patients with cardiac arrest and is conventionally considered to be essentially due to hyperlactatemia. However, hyperlactatemia alone fails to explain the cause of metabolic acidosis. Recently, the Stewart-Figge methodology has been found to be useful in explaining and quantifying acid-base changes in various clinical situations. This novel quantitative methodology might also provide useful insight into the factors responsible for the acidosis of cardiac arrest. We proposed that hyperlactatemia is not the sole cause of cardiac arrest acidosis and that other factors participate significantly in its development. METHODS: One hundred and five patients with out-of-hospital cardiac arrest and 28 patients with minor injuries (comparison group) who were admitted to the Emergency Department of a tertiary hospital in Tokyo were prospectively included in this study. Serum sodium, potassium, ionized calcium, magnesium, chloride, lactate, albumin, phosphate and blood gases were measured as soon as feasible upon arrival to the emergency department and were later analyzed using the Stewart-Figge methodology. RESULTS: Patients with cardiac arrest had a severe metabolic acidosis (standard base excess -19.1 versus -1.5; P < 0.0001) compared with the control patients. They were also hyperkalemic, hypochloremic, hyperlactatemic and hyperphosphatemic. Anion gap and strong ion gap were also higher in cardiac arrest patients. With the comparison group as a reference, lactate was found to be the strongest determinant of acidosis (-11.8 meq/l), followed by strong ion gap (-7.3 meq/l) and phosphate (-2.9 meq/l). This metabolic acidosis was attenuated by the alkalinizing effect of hypochloremia (+4.6 meq/l), hyperkalemia (+3.6 meq/l) and hypoalbuminemia (+3.5 meq/l). CONCLUSION: The cause of metabolic acidosis in patients with out-of-hospital cardiac arrest is complex and is not due to hyperlactatemia alone. Furthermore, compensating changes occur spontaneously, attenuating its severity.

Acidosis↗
PubMed1985

Effects of acidosis on fetal and maternal blood coagulation: a fetal lamb model.

The effects of fetal acidosis (mean pH 6.93) on fetal and maternal blood coagulation were measured. Test results from 10 fetal lambs and mother ewes (127 +/- 2 days mean gestation) before and after fetal lactic acid infusions were compared to test results from eight control fetal lambs and mother ewes (127 +/- 3 days mean gestation) before and after control glucose infusion. Significant changes found in acidotic fetal lambs not seen in control fetuses included an increase in the white blood cell count (mean 2800/mm3 before to 3600/mm3 after acidosis; p = 0.0009), a shortening of the thrombin time (mean 17.8 s before to 11.2 s after acidosis; p = 0.0001), and decreases in the activities of factor V (mean 57% before to 37% after acidosis; p = 0.0014) and factor IX (mean 35% before to 29% after acidosis; p = 0.0128). There was also a reduction in the concentration of fibrinogen (mean 147 mg/100 ml before to 125 mg/100 ml after acidosis; p = 0.0492) but no significant changes in the levels of fibrin monomer, fibrinogen/fibrin degradation products, or antithrombin III. In vitro exposure of five different fetal whole blood samples to a pH of 6.9 for 2 h at 37 degrees C did not result in significant changes in any of the coagulation factor activities. A significant decrease in the level of factor V was also found in the mother ewes of the acidotic fetuses (mean 141% before to 113% after acidosis; p = 0.006) and a decrease in the level of maternal factor IX approached significance (mean 119% before to 102% after acidosis; p = 0.0564).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1997

Developmental changes in the effect of acidosis on contraction, intracellular pH, and calcium in the rabbit mesenteric small artery.

The purpose of the present study was to determine developmental changes in the effect of respiratory acidosis on vascular smooth muscle contraction. Vessel diameter, intracellular pH (pHi), and calcium concentration ([Ca]i) were measured in a cannulated preparation of the small mesenteric artery of newborn and adult rabbits. In the artery precontracted by high KCl, acidosis caused a vasorelaxation both in the newborn and the adult; the vasorelaxation was greater in the newborn than in the adult. The fura-2 fluorescence ratio, an indicator of [Ca]i, decreased transiently during acidosis and the decrease was similar in the two age groups. In the artery precontracted by norepinephrine, acidosis caused a transient vasoconstriction in the adult and a vasorelaxation in the newborn. In these vessels, the fura-2 fluorescence ratio increased transiently during acidosis; the increase was similar in the two groups. Upon induction of acidosis, pHi fell rapidly in the artery precontracted by norepinephrine or high KCl, and the depression of pHi was similar in the two groups. In the skinned smooth muscle preparation, a tension-[Ca] relationship curve at pH 7.1 was not significantly different from that at pH 6.8 in the adult. In the newborn, the tension-[Ca] curve at pH 6.8 was shifted to the right, compared with that at pH 7.1. These data suggest that the vasorelaxant effect of respiratory acidosis in the premature vessel is greater than in the adult. The greater vasorelaxation in the newborn cannot be explained by the age-related difference in pHi or [Ca]i during acidosis. The greater sensitivity of myofibrils to low pHi in the newborn may, at least in part, be responsible for the greater vasorelaxation in this age group.

Acidosis, Respiratory↗
PubMed2003

Metabolic acidosis stimulates RANKL RNA expression in bone through a cyclo-oxygenase-dependent mechanism.

UNLABELLED: Metabolic acidosis inhibits osteoblastic bone formation and stimulates osteoclastic resorption. To determine whether acidosis alters expression of RNA for the osteoclastic differentiation factor RANKL, mouse calvariae were incubated in neutral or physiologically acidic media. Acidosis resulted in a significant cyclo-oxygenase-dependent increase in RANKL RNA levels, which would be expected to induce the associated increase in bone resorption. INTRODUCTION: Metabolic acidosis increases net calcium efflux from bone, initially through physicochemical mechanisms and later through predominantly cell-mediated mechanisms. Acidosis decreases osteoblastic bone formation and increases osteoclastic resorption. The growth and maturation of osteoclasts, derived from hematopoietic precursors in the monocyte/macrophage lineage, are dependent on the interplay of a number of factors. Commitment of pre-osteoclasts to osteoclasts is induced by the interaction of the osteoclastic cell-surface receptor RANK with a ligand expressed by osteoblasts, RANKL. The RANK/RANKL interaction not only initiates a differentiation cascade that culminates in mature bone-resorbing osteoclasts but also increases osteoclastic resorptive capacity and survival. METHODS: To test the hypothesis that metabolic acidosis increases expression of RANKL, we cultured neonatal mouse calvariae in acidic (initial medium pH approximately 7.1 and [HCO3-] approximately 11 mM) or neutral (initial medium pH approximately 7.5 and [HCO3-] approximately 25 mM) medium for 24 and 48 h. We determined the relative expression of RANKL RNA by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitated the expression by Northern analysis. RESULTS: In this model of metabolic acidosis, there was significantly increased expression of RANKL RNA at both 24 (2-fold) and 48 h (5-fold) compared with respective controls. Net calcium efflux from bone was also increased in acidic medium compared with control medium. At 48 h, net calcium efflux correlated directly with RANKL expression (r = 0.77, n = 15, p < 0.001). Inhibition of prostaglandin synthesis with indomethacin blocked the acid-induced increase in RANKL RNA as well as the increased calcium efflux. CONCLUSIONS: Metabolic acidosis induces osteoblastic prostaglandin synthesis, followed by autocrine or paracrine induction of RANKL. This increase in RANKL would be expected to augment osteoclastic bone resorption and help explain the increase in cell-mediated net calcium efflux.

Acidosis↗
PubMed1988

Metabolic acidosis during exercise in patients with chronic obstructive pulmonary disease. Use of the V-slope method for anaerobic threshold determination.

Patients with chronic obstructive pulmonary disease (COPD) usually have limited exercise tolerance owing to low ventilatory capacity. Because metabolic acidosis induced by exercise increases ventilatory drive, decreasing the hydrogen ion stimulus may improve exercise capacity. However, in those with mechanical limitation to ventilation or chemoreceptor insensitivity, identifying metabolic acidosis may be difficult using gas exchange methods that depend on the ventilatory response to the acidosis. We compared a modification of a gas exchange method (V-slope) for determining the lactate (anaerobic) threshold (AT), which is independent of ventilatory response with a method using the change in blood standard bicarbonate (HCO3-) level in COPD and normal subjects during cycle incremental exercise. In 43 normal subjects, the VO2 at which metabolic acidosis was identified using the two method correlated (r = 0.75), although mean values differed. In 22 patients with moderately severe to severe COPD, eight who had a change in standard HCO3- less than 2.0 mEq/L between rest and 2 min of recovery from exercise (group 1) were contrasted with 14 whose blood standard HCO3- fell by greater than 2.5 mEq/L (group 2). Mean VC was higher and FEV1/VC was lower in group 2, but mean FEV1, maximal voluntary ventilation, and diffusing capacity for carbon monoxide were not different. The degree of obstruction did not correlate strongly with the degree of exercise metabolic acidosis. The AT determined by the V-slope method was compared with that from standard HCO3-; good correlation between these methods was found (r = 0.98), although mean values were different. The V-slope method predicted metabolic acidosis in 10/14 who had a fall in HCO3- more than 2.5 mEq/L. A significant proportion of patients with COPD seem to develop metabolic acidosis during exercise. The V-slope gas exchange method may be useful in selecting those patients with COPD who develop exercise metabolic acidosis and might therefore benefit from exercise training.

Acidosis↗
PubMed1987

Cholestasis in late metabolic acidosis of prematurely born infants.

Serum concentrations of bile acids and tyrosine were determined in 14 premature infants with late metabolic acidosis and in 13 comparable controls without acidosis (protein intake 2 g/kg X d). At the same time the bile acids and the catalytic activity concentrations of lipase and trypsin were estimated in the duodenal juice. The daily faecal excretion and the percentage of fat eliminated were measured. In 8 patients with late metabolic acidosis the duodenal studies were repeated one week after late metabolic acidosis. Infants with late metabolic acidosis showed significantly higher concentrations of bile acids and tyrosine in the serum than the controls (p less than 0.0005). In the duodenal juice the activities of lipase and trypsin and the concentration of bile acids--especially of dihydroxy bile acids--were decreased (p less than 0.001). The faecal excretion during late metabolic acidosis was significantly increased, with high percentage of fat. Eight days after late metabolic acidosis all duodenal parameters equalled the range of the control group. The relations between acidosis, cholestasis, and amino acid transport to the liver are discussed.

Acidosis↗
PubMed2001

Is intrapartum vibroacoustic stimulation an effective predictor of fetal acidosis?

OBJECTIVE: The hypothesis of this prospective study is that intrapartum vibroacoustic stimulation (VAS) is an effective predictor of fetal acidosis during labor. Various clinical conditions, such as term versus preterm gestation, first stage versus second stage of labor, and fetal heart rate (FHR) variable decelerations versus late decelerations will be tested. METHODS: During the study period, 113 patients were studied prospectively in either active phase of first stage (n = 53) or during the second stage of labor (n = 60). They were selected from cases exhibiting moderate to severe FHR variable decelerations or late decelerations. The fetuses of study subjects received a VAS for three seconds and FHR changes were recorded. Fetal scalp blood pH or umbilical arterial blood pH was obtained within 15 minutes of VAS. The relationship between FHR responses to VAS and fetal blood pH in term and preterm gestations, the relationship of two tests (VAS and fetal blood pH) to type of FHR decelerations, and the predictability of neonatal morbidity by two tests were analyzed. Where appropriate, Fisher's exact test (p < 0.05 was considered statistically different) and the odd ratio with 95% confidence intervals were used for statistical analyses. RESULTS: Excellent association between acceleration response to VAS and pH > or = 7.20, and between a negative response to VAS (no acceleration or decelerations) and pH < 7.20 were found in the first stage of labor, the second stage of labor, and the combination of both stages together (p = 0.0001, OR = 10.6 [3.3-34.0]). It was observed that negative VAS responses for predicting fetal acidosis (pH < 7.20) were comparable between term (> or = 37 weeks) and preterm (< 37 weeks, > or = 34 weeks) fetuses. Since the preterm fetuses enrolled in the study were limited in number, it is difficult to draw adequate conclusions. The positive predictive value (PPV) of fetal acidosis was 67% in both groups of FHR variable decelerations and late decelerations, but the false negative rate of acceleration VAS response for predicting no acidosis was significantly higher in the group of late decelerations (29% vs 8%, p = 0.034). Finally, both a negative VAS response and fetal acidosis (pH < 7.20) have equal predictability for neonatal morbidity. The PPV of NICU admission by a negative VAS response was two times higher than that of fetal acidosis (PPV = 61% vs 29%, p = 0.038). CONCLUSION: We found that intrapartum VAS was an effective predictor of fetal acidosis in cases of FHR variable decelerations, but its predictability for fetal acidosis in cases of FHR late decelerations was limited. Both VAS and fetal blood pH are good predictors of neonatal morbidity.

Acidosis↗
PubMed1996

Acidosis effects on insulin response during glucose tolerance tests in Jersey cows.

The effect of metabolic alkalosis and acidosis on insulin response to glucose tolerance tests was determined for cows fed a high cation diet to induce a state of metabolic acidosis. The anion diet to induce a state of metabolic acidosis. The glucose tolerance test (500 mg of glucose/kg of BW infused i.v. over 10 min) caused a rapid increase in plasma glucose and insulin concentrations. Plasma glucose concentrations were highest, and plasma insulin concentrations were lowest, during metabolic acidosis. These results suggest that insulin secretion is impaired during metabolic acidosis, which may reduce tissue uptake of glucose. Correction of metabolic acidosis by oral administration of sodium bicarbonate prior to glucose tolerance testing increased blood pH and bicarbonate concentrations and partially restored insulin response to the glucose tolerance test. Interestingly, sodium bicarbonate also caused an elevation in plasma cortisol concentrations. We concluded that glucose utilization is altered in cows with metabolic acidosis. The correction of acidosis associated with diseases such as diarrhea and ketosis may improve the therapeutic benefit of glucose infusions used to treat these diseases.

Acidosis↗
PubMedDate not supplied

Impaired acidification of urine in children aged two months to two years with acute gastroenteritis complicated by acidosis.

BACKGROUND: In some children with acute gastroenteritis and acidosis, the urine pH may be abnormally high thus simulating distal Renal Tubular Acidosis (dRTA). This inability to acidify urine properly in the presence of metabolic acidosis has been shown to be due to poor delivery of sodium to the distal nephron which prevents full excretion of a hydrogen ion load, instead of an intrinsic defect in the ability of the distal tubule to acidify urine. The aim of this study is to determine the prevalence of transient urinary acidification defect in children aged two months to two years with acute gastroenteritis, dehydration and acidosis, and the relationship between urine pH and urine sodium concentration. METHOD: A prospective study of children aged two months to two years admitted for the treatment of acute gastroenteritis and dehydration at the Children's Emergency Ward (CHEW) of the University of Port Harcourt Teaching Hospital, Rivers State. RESULTS: Of the 196 children (140 males and 56 females) studied with spontaneous acidosis which developed as a result of acute gastroenteritis, seventy-three of them had impaired acidification of urine, giving a prevalence of 37.2%. There was no significant difference in the age, duration of symptoms, degree of acidosis, degree of dehydration and serum potassium concentration between the children with impaired and those with proper urine acidification. Those with impaired acidification of urine however had a significantly lower serum sodium and urine sodium concentrations and a significantly higher urine potassium concentration and urine anion gap than those children with proper urine acidification. All urine samples with sodium concentration less than or equal to 25 mmol/L (52) had urine pH greater than 5.5. CONCLUSION: Mere presence of acidosis and high urine pH should not lead to a diagnosis of Distal Renal Tubular Acidosis (dRTA). The urine anion gap (UAG) should be calculated using the formula: urine [Na+] + [K+] [Cl], and if negative, it suggests a high ammonium excretion, which makes the diagnosis of dRTA unlikely.

Acidosis, Renal Tubular↗
PubMed2001

Lactic acidosis update for critical care clinicians.

Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO(3) increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO(3) is of little value. Carbicarb is a mixture of Na(2)CO(3) and NaHCO(3) that buffers similarly to NaHCO(3) but without net generation of CO(2). The results from animal studies are promising; however, clinical trials are sparse. Dichloroacetate stimulates pyruvate dehydrogenase and improves laboratory values, but unfortunately not survival rates, among patients with lactic acidosis. Hemofiltration has been advocated for the treatment of lactic acidosis, on the basis of anecdotal experiences. However, kinetic studies of lactate removal do not suggest that removal can counteract lactate production in any meaningful way. The ideal treatment is to stop acid production by treating the underlying disorder.

Acidosis, Lactic↗
PubMed2001

Preretinal neovascularization associated with acetazolamide-induced systemic acidosis in the neonatal rat.

PURPOSE: NH4Cl gavage in the neonatal rat produces a metabolic acidosis-induced retinopathy which serves as a model for retinopathy of prematurity (ROP). Acetazolamide induces a metabolic acidosis via an alternative biochemical mechanism (bicarbonate loss versus hydrogen ion load). In the present study, the following hypothesis was tested: acetazolamide-induced acidosis is associated with preretinal neovascularization in the neonatal rat. METHODS: All studies used newborn Sprague-Dawley rats raised in expanded litters of 25. Arterial blood pH was measured to determine the level of acidosis induced by intraperitoneal (IP) acetazolamide (50 or 200 mg/kg) or saline. In a separate retinopathy study, newborn rats (n = 75) were randomized to either IP acetazolamide, 50 mg/kg (low-dose), or IP saline twice daily from days 2 to 7. After 5 days of recovery, retinal vasculature was assessed using ADPase staining and light microscopy. The presence and severity (clock hours) of neovascularization were assessed by three masked observers. In an additional retinopathy study, newborn rats (n = 100) were randomized to either IP acetazolamide, 200 mg/kg (high-dose), or IP saline twice daily from days 2 to 7. After 5 days of recovery, the retinas were similarly analyzed. RESULTS: Neovascularization occurred in 59% of rats receiving high-dose acetazolamide (200 mg/kg). High-dose acetazolamide produced a severe acidosis (pH 7.13 +/- 0.06) during drug delivery. Low-dose acetazolamide (50 mg/kg) produced a pH (7.22 +/- 0.07) that was intermediate between high-dose (200 mg/kg) acetazolamide (P < 0.001) and saline controls (7.42 +/- 0.06, P < 0.001); however, neither low-dose acetazolamide nor saline induced preretinal neovascularization. CONCLUSIONS: Acidosis induced by high-dose acetazolamide, independent of hyperoxemia or hypoxemia, is associated with preretinal neovascularization in the neonatal rat. Induction of neovascularization appears to depend on a critical threshold of acidosis severity. This study further supports a proposed independent role for acidosis in the pathogenesis of ROP.

Acetazolamide↗
PubMed2001

Changes in serum leptin levels in chronic renal failure patients with metabolic acidosis.

OBJECTIVE: To examine the relationship between serum leptin levels (SLL) and metabolic acidosis in patients with chronic renal failure (CRF). DESIGN: SLL in control patients and in predialysis patients with CRF were measured and compared. SLL before and after correction of acidosis in patients with CRF were also compared. PATIENTS AND CONTROLS: Twenty-five patients with CRF (10 men and 15 women) aged 51.2 +/- 10.4 years and control patients (healthy subjects, 23 men and 25 women) aged 42.1 +/- 12.6 years were studied. INTERVENTION: Five percent sodium bicarbonate (NaHCO(3), 2 to 3 mL/kg) was intravenously infused on the morning of the first day of treatment. NaHCO(3) was taken orally at a dosage of 50 to 200 mg/kg/d for 3 to 5 days thereafter. MAIN OUTCOME MEASURE: SLL before and after NaHCO(3) treatment was measured by radioimmunoassay, and blood gas was measured before and after correction of metabolic acidosis in patients with CRF. RESULTS: SLL in the normal control group (n = 48) was 10.04 +/- 7.0 ng/mL and was realated to body mass index (BMI) (P =.0331). SLL in men (n = 23) was lower than that in female controls (n = 25, P <.01). SLL in patients with CRF (n = 25) before (plasma HCO(3)(-), 13.03 +/- 3.05 mmol/L) and immediately after improvement of metabolic acidosis (plasma HCO(3)(-), 18.35 +/- 4.21 mmol/L) was 14.52 +/- 9.27 ng/mL and 15.34 +/- 11.89 ng/mL (P >.05), respectively. SLL measured 3 to 5 days after treatment for metabolic acidosis (plasma HCO(3)(-), 20.46 +/- 4.03 mmol/L) was 19.33 +/- 14.58 ng/mL, which was significantly higher than that in the normal control group and that in acidotic patients before NaHCO(3) treatment (P <.01). CONCLUSIONS: SLL in acidotic patients with CRF were comparable to that in control subjects, and SLL was significantly increased after correction of metabolic acidosis in patients with CRF. The preliminary results suggest that hyperleptinemia in patients with CRF may be masked by metabolic acidosis and that metabolic acidosis may inhibit leptin synthesis or secretion. Further studies are needed to clarify the mechanisms.

Acidosis↗
PubMed1992

Biguanide related lactic acidosis: incidence and risk factors.

The objective of this study was to evaluate in an open population the incidence and risk factors of biguanide related lactic acidosis. All patients currently treated in the Department of Diabetes and Lipid Metabolism of the Instituto Nacional de la Nutrición and their records were reviewed for the present use or history of administration of biguanides. The study was complemented with a revision of all admissions of diabetic patients to the emergency room during 1987-1990. In the outpatient study, 235 cases were included. No case of lactic acidosis was found. A high percentage of the biguanide treated patients had one or more lactic acidosis related risk factors. In the emergency study, 609 admissions of 273 patients were included. In 17 patients a metabolic non-ketotic acidosis was diagnosed. The frequency of non-ketotic acidosis for the different treatments was: 29.4 cases x 1000 emergency admissions for sulphonylurea treated group, 32 for sulphonylurea plus phenformin treated and 47.94 for type II insulin treated patients. All cases had severe precipitant diseases that can cause lactic acidosis with or without associated biguanide administration. No metformin related cases were found. The conclusions of this study are that biguanides in general and metformin in particular are not associated with a high risk of lactic acidosis. Severe systemic dysfunction associated with intercurrent diseases, frequently observed in diabetic patients, is the main determinant for the appearance of lactic acidosis.

Acidosis, Lactic↗
PubMed1991

[Digestive manifestations and metabolic acidosis secondary to intravenous administration of cotrimoxazol].

BACKGROUND: Digestive features and metabolic acidosis have been observed in patients with Pneumocystis carinii pneumonia treated with intravenous high dose co-trimoxazole. METHODS: To evaluate this phenomenon, a retrospective study of 22 patients (group A) and a prospective study of 12 patients (group B) were carried out. Group B patients were investigated following a protocol lasting for the 21 days of treatment. RESULTS: Metabolic acidosis developed in 23 (67%) of the overall number of study patients, and it was associated with digestive features such as nausea, vomiting and epigastralgia in 12. One patient had digestive features without metabolic acidosis. Metabolic acidosis developed early, between the days 4 and 7 of administration of the drug. The mean value of bicarbonate at the onset of therapy was 24,55 mEq; the mean value in the patients with metabolic acidosis was 16,43 mEq. The overall mean value of base excess at the onset of therapy was -2,39, and it was -8,46 in the patients who developed metabolic acidosis. CONCLUSIONS: As in all patients other causes of metabolic acidosis were ruled out, it became obvious that intravenous co-trimoxazole was directly related to the development of digestive features and metabolic acidosis, which disappeared with bicarbonate administration or with cessation of therapy.

Acidosis↗
PubMed1990

[Acute renal failure with lactic acidosis].

This study examined the acid base disturbances in 18 adults with acute renal failure (ARF) from one of new aspects, which is lactate metabolism and pathophysiology. 10 patients (55%) of them were accompanied by lactic acidosis and 9 patients (90%) of those with lactic acidosis also had severe hepatic failure. Mortality of patients with lactic acidosis was 80%, and much higher than that of ARF (66.7%). Lactate, pyruvate, lactate-to-pyruvate ratio (L/P) were 76.7 +/- 15.66 mg/dl, 3.30 +/- 0.74 mg/dl and 19.9 +/- 1.41, respectively. All of them significantly raised, compared to values of healthy adults, patients with liver cirrhosis, chronic renal failure and diabetes mellitus. Arterial pH and HCO3- levels were 7.20 +/- 0.04 and 10.6 +/- 1.20 mEq/l. Anion gap (AG) was 30.0 +/- 3.66 mEq/l. Significant correlations of lactate with pH, HCO3-, AG and L/P were demonstrated, while correlations of lactate with BUN, CR and prothrombin time were not significantly observed. Lactic acidosis results from two mechanisms. One is lactate overproduction (e.g tissue hypoxia) and the other is lactate underutilization (e.g severe liver and/or renal failure). Whenever lactic acidosis occurred, both mechanisms were present simultaneously and continuously. Especially, the latter mechanism had a very important role on it, and seemed to decide the prognosis of the patients with lactic acidosis. Therapy of lactic acidosis was very difficult. First of all, we tried to improve the circulatory failure and severe acidemia (pH less than 7.20) not to fall into vicious cycle. Then, CAVH, if combined with alkali infusion, seemed to be the most useful technique in managing lactic acidosis with ARF.

Acidosis, Lactic↗
PubMed1990

[Renal acidosis].

Normal adults with normal protein intakes have a urinary NH4 excretion of 40 to 50 mmol/24 hours and a variable urinary pH. In cases of metabolic acidosis a urinary pH less than 5.5 suggests an extra-renal origin whilst a urinary pH greater than 5.5 is in favour of renal acidosis, but there are many exceptions to this rule. On the other hand, urinary NH4 excretion is always greater than 70 mmol/24 hours in the first case and less than 40-50 mmol/24 hours in the second; and the use of the urinary anionic gap (Na + K - Cl), negative in the first case and positive in the second, enables the two situations to be distinguished. The acidosis of nephron reduction is easily recognised in cases of severe renal failure with an increase in unmeasured plasma anions whilst tubular acidoses are accompanied by a hyperchloremia. Measurement of fractional HCO3 excretion after an oral loading dose of NaHCO3, preferably by TmCHO3 with respect to GFR, distinguishes proximal tubular acidosis (low TmHCO3) from distal tubular acidosis (normal or high TmHCO3). In the latter case, the presence of hypokalemia suggests a distal tubular acidosis either due to deficiency of the H(+)-ATPase pumps (absence of increased urinary pCO2 after oral loading dose of NaHCO3) or to the inability of the kidney to maintain a normal H+ gradient (normal increase of urinary pCO2. The presence of hyperkalemia suggests diseases associated with hypoaldosteronism (low or inappropriate serum aldosterone concentrations), abnormal transepithelial voltages or with a pseudo-hypoaldosteronism syndrome (high plasma aldosterone concentration). The prevalence of distal tubular acidosis with hyperkalemia is on the increase whilst tubular acidosis with hypokalemia remains rare.

Acid-Base Equilibrium↗