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PubMed1995

Antibiotic-induced D-lactic acidosis.

OBJECTIVE: To describe a case of oral antibiotic-induced D-lactic acidosis in a patient with enteric overgrowth of Lactobacillus acidophilus. DESIGN: Single case study. SETTING: University-affiliated community hospital. INTERVENTION: Oral carbohydrate challenge test with 4000 kcal/d. MAIN RESULTS: A patient had several episodes of D-lactic acidosis after receiving oral antibiotics. Stool cultures yielded Lactobacillus acidophilus resistant to the implicated agents. Provocative challenge with dietary carbohydrate alone, in the absence of antibiotics, failed to reproduce the syndrome. CONCLUSIONS: Oral antibiotics may induce D-lactic acidosis in patients with the short-bowel syndrome by promoting the overgrowth of resistant D-lactate-producing organisms. Interactions between carbohydrate intake and antibiotic use are likely determinants in the development of this syndrome. Periodic use of stool cultures with antimicrobial susceptibility testing may assist in the management of these patients by optimizing the selection of antimicrobial agents.

Acidosis, Lactic↗
PubMed2000

Lactic acidosis and hepatic steatosis associated with use of stavudine: report of four cases.

BACKGROUND: An association between use of zidovudine and didanosine and a rare but life-threatening syndrome of hepatic steatosis, lactic acidosis, and myopathy has been reported. OBJECTIVE: To describe the syndrome of hepatic steatosis, lactic acidosis, and myopathy in four patients taking stavudine. DESIGN: Case series. SETTING: A community hospital in Washington, D.C., and National Institutes of Health Clinical Center, Bethesda, Maryland. PATIENTS: Two men and two women with HIV-1 infection who were taking stavudine presented with lactic acidosis and elevated levels of aminotransferases. All patients required intensive care. MEASUREMENTS: Levels of lactic acid, alanine aminotransferase, aspartate aminotransferase, amylase, and lipase; computed tomography of the abdomen; liver biopsy (two patients); and muscle biopsy (two patients). RESULTS: Histologic findings consistent with mitochondrial injury confirmed the diagnosis of hepatic or muscle abnormality. CONCLUSION: Because hepatic steatosis may be life-threatening, physicians should consider it as a possible cause of elevated hepatic aminotransferase levels among patients taking stavudine.

Acidosis, Lactic↗
PubMed1975

Lactic acidosis from carboxyhemoglobinemia after smoke inhalation.

Tissue hypoxia as a result of a wide variety of clinical situations had frequently been implicated as a cause of systemic acidosis due to the accumulation of lactic acid. Four patients suffering from smoke inhalation had lactic acidosis in association with carboxyhemoglobinemia. There was no evidence of decreased tissue perfusion, hypotension, arterial hypoxemia, or anemia. The following were tested in all patients: arterial pH (7.25 to 7.40), Pco-2 (19 to 27 mm Hg), Po (63 to 116 mm Hg), HCO-2- (11 to 19 meq/litre), carboxyhemoglobin (13% to 37%), and lactic acid (5.1 to 9.3 meq/litre). After therapy with oxygen and intravenous corticosteroids, there was prompt return of lactic acid levels, carboxyhemoglobin values, and arterial pH to normal. It is concluded that the cause of lactic acidosis in the presence of carboxyhemoglobinemia during smoke inhalation is tissue hypoxia. This tissue hypoxia is due to the reduction of the oxygen-carrying capacity of the blood and the concomitant shift of the oxyhemoglobin dissociation curve to the left, both known to result from carboxyhemoglobinemia.

Acidosis↗
PubMed1979

Spironolactone-induced hyperchloremic acidosis in cirrhosis.

Six patients with alcoholic cirrhosis developed a reversible metabolic acidosis during treatment with the aldosterone antagonist spironolactone. Mean serum bicarbonate concentration decreased significantly with spironolactone therapy (100 to 200 mg/day) from 18.2 +/- 4.5 to 10.9 +/- 3.2 meq/litre (P less than 0.001). Upon withdrawal of spironolactone, serum bicarbonate concentration increased from 10.9 +/- 3.2 to 18.1 +/- 3.5 meq/litre (P less than 0.001). During the development of this hyperchloremic metabolic acidosis, serum potassium concentration rose from 3.7 +/- 0.5 to 5.0 +/- 0.8 meq/litre (P less than 0.005); this reversed after cessation of spironolactone therapy. These effects of spironolactone treatment were not associated with significant alterations in serum creatinine or sodium concentration. Thus, even though an aldosterone antagonist in the treatment of sodium and water retention in cirrhotic patients may prevent hypokalemia and rapid diuresis, it may also induce or worsen another complication: hyperchloremic metabolic acidosis.

Acidosis↗
PubMed1976

[Pathomorphologic changes in the ruminal acidosis of sheep].

Acute and subacute and spontaneous rumen acidosis was experimentally induced in 20 sheep and two lambs after feeding of barley, maize or glycose. The inner organs of those animals then were examined for morphological changes. The changes recorded from experimental acidosis were analogous to those observed after spontaneous outbreaks. Hyperaemia and blood leakage were macroscopically observed underneath the rumen mucous membrane which could be easily pulled off. The same signs sometimes were manifest in the third and second stomach as well. Pronounced edemas and hyperaemia occurred in the lungs, meninges (pia mater), and brain, and blood leakage was recorded from the epicardium. The histological findings included epithelial desquamation, infiltration of lymphocytes and leucocytes into rumen and fourth stomach (subacute) hepatitis (in 60 per cent of all cases), physical degeneration in the kidneys, and focal myocarditis (in 50 per cent of all cases). There were hyperaemia, edematisation, and blood leakage in the lungs, perivascular and pericellular edema in the brain, and severe hyperaemia of the meninges (pia mater) and thyroid gland. Those morphological changes were persistent and characteristic. Their relevance to diagnosis of rumen acidosis in sheep is undenied, provided that due consideration is given at the same time to the case history and paraclinical indices.

Acidosis↗
PubMed1999

[Giant placental angioma with polyhydramnios, high level of alpha-fetoprotein and neonatal congenital lactic acidosis].

Placental tumors are rare in pregnancy. They cause nonspecific complications such as polyhydramnios, fetal anemia, fetal thrombocytopenia and cardiac decompensation with non-immunological hydrops fetalis. In the presented case a very large placental hemangioma was connected with polyhydramnios, premature delivery, fetal anemia and thrombocytopenia, maternal serum alpha fetoprotein elevation and congenital lactic acidosis. After delivery a severe state of the newborn was caused by oligovolemic shock. In the course of the disease the neonatal state steadily deteriorated mainly because of sepsis, cerebral hemorrhage and metabolic acidosis despite adequate therapy. The organic acids assessment in the blood serum of a newborn child showed a very strong signal of lactic acid and an increase in parahydroksyfenylolactic acid. Postmortal examination confirmed prematurity, respiratory distress syndrome, sepsis and cerebral hemorrhage. These symptoms probably resulted from the presence of a placental tumor of considerable size of 12 cm and congenital lactic acidosis, which to our knowledge, have not been described in the available literature until now. In conclusion it should be underlined, that there exists difficult to explain relationship between the presence of a placental haemangioma and severe metabolic changes resulting in high mortality and morbidity of the newborn.

Acidosis, Lactic↗
PubMedDate not supplied

Fatal acidosis in a neonate with Pearson syndrome.

We report a neonate who presented with hypotonia, hypoglycemia, and severe lactic acidosis. The patient's acidosis did not respond to bicarbonate replacement and dialysis. Postmortem liver samples revealed portal dilatation, fibrosis, canalicular proliferation, cholestasis, and hepatocellular hemosiderosis. Vacuolization of bone marrow precursors suggested a diagnosis of Pearson syndrome. A common mitochondrial DNA deletion of 4,978 bp was found. We emphasize that Pearson syndrome should be considered in neonates with lactic acidosis despite absence of anemia.

Acidosis, Lactic↗
PubMed2000

Molecular and pathophysiologic mechanisms of hyperkalemic metabolic acidosis.

In summary, hyperkalemia may have a dramatic impact on ammonium production and excretion. Chronic hyperkalemia decreases ammonium production in the proximal tubule and whole kidney, inhibits absorption of NH4+ in the mTALH, reduces medullary interstitial concentrations of NH4+ and NH3, and decreases entry of NH4+ and NH3 into the medullary collecting duct. The potential for development of a hyperchloremic metabolic acidosis is greatly augmented when renal insufficiency with associated reduction in functional renal mass coexists with the hyperkalemia, or in the presence of aldosterone deficiency or resistance. Such a cascade of events helps to explain, in part, the hyperchloremic metabolic acidosis and reduction in net acid excretion characteristic of several experimental models of hyperkalemic-hyperchloremic metabolic acidosis including: obstructive nephropathy, selective aldosterone deficiency, and chronic amiloride administration (7.9).

Acidosis↗
PubMed2000

Lactic acidosis and antiretroviral therapy: a case report and literature review.

Antiretrovirals, particularly nucleoside analogue reverse transcriptase inhibitors (RTIs) - DDI, 3TC and D4T, are widely used to effectively control human immunodeficiency virus (HIV) infection. These drugs have several adverse effects including anemia, peripheral neuropathy, pancreatitis and, on rare occasions, lactic acidosis. We describe the case of a 39 year old patient who had severe lactic acidosis after receiving stavudine (D4T) and didanosine (DDI) for an 8 month period. She had never manifested an opportunistic infection and presented a CD4 count of 378 cells/mm3 and an undetectable viral load (< 400 copies/ml). The purpose of the following report is to alert clinicians and infectious diseases specialists to the occurrence of lactic acidosis in asymptomatic HIV patients receiving antiretrovirals for long periods of time.

Acidosis, Lactic↗
PubMed2000

Metabolic acidosis during urinary retention in a patient with an enterovesical fistula.

We report a patient known to have an enterovesical fistula who presented severe acute metabolic acidosis during an episode of urinary retention. The enterovesical fistula which had been intermittently symptomatic for 4 years, had developed after several intestinal surgical procedures and related intraperitoneal sepsis following resection of colon cancer 21 years previously. The patient who had a total colectomy and ileostomy, was admitted for hip replacement with the routine placement of a Foley bladder catheter. Three weeks post-operatively, the patient developed acute urinary retention following removal of the urinary catheter. The output from his ileostomy was immediately markedly increased, presumably from bladder urine diverted into the intestines through the enterovesical fistula. Within a few days he presented a normal anion gap metabolic acidosis with raised urea and stable creatinine; his clinical status deteriorated markedly with profound obtundation. These metabolic abnormalities were readily corrected by re-insertion of the Foley catheter with restoration of normal urine flow and immediate corresponding fall in the ileostomy output. Radiographic studies showed the presence of the enterovesical fistula originating from the jejunum. This is the first report of acute metabolic acidosis in association with an enterovesical fistula; the severe metabolic disturbances were triggered by the development of urinary retention resulting in the diversion of urine into the small bowel through the fistula.

Acidosis↗
PubMedDate not supplied

[Neurological evolution of asphyctic full-term newborns with severe umbilical acidosis (pHUA <7.00)].

INTRODUCTION AND OBJECTIVE: Umbilical arterial blood pH (pHUA) has become increasingly recognized as the most reliable indication of foetal oxygenation and acid-base condition at birth. In term infants pHUA is a poor predictor of newborn complications associated with perinatal asphyxia (PA), unless the pHUA is less than 7.00. The objective of this article is to analyse the neurologic evolution of asphyctic full-term newborns with severe umbilical acidosis (pHUA < or = 7.00). PATIENTS AND METHODS: One hundred and eighty consecutive asphyxiated term infants were studied during 64 months, and classified in two cohorts: G1 (pHUA < or = 7.00, n = 18) and G2 (pHUA > 7.00, n = 162). Variables prospectively obtained on standard protocol forms from the medical records were derived from a detailed review of the obstetric record, the delivery room management, the detailed neonatal clinical history and the postneonatal follow-up. The perinatal variables were graded as prenatal (gestational and obstetric), neonatal (resuscitation, general data of the newborn, and organic manifestations of asphyxia) and postneonatal (neurologic sequelae with at lest 24 months of follow-up). PA was graded as severe and non-severe, hypoxic-ischemic encephalopathy was based on Levene's criteria, and neurologic sequelae were based on Finer and Amiel-Tisson's criteria. RESULTS: An umbilical artery pH value < or = 7.00 occurred in 0.3% of the total live full-term newborns. In G1 the mean pHUA value was 6.93 +/- 0.06 (range 6.80-7.00) and in G2 the mean pHUA value was 7.17 +/- 0.09 (range 7.01-7.46). The incidence of severe PA was significantly increased in G1 (RR = 4.74, CI 95% = 2.62-8.55, p < 0.001), with more postasphyctic neurologic (RR = 3.72, CI 95% = 2.34-5.92, p < 0.001) and extraneurologic (RR = 3.13, CI 95% = 1.65-5.94, p < 0.01) involvement. But we do not found differences in the incidence of neurologic sequelae between both cohorts. CONCLUSIONS: Term asphyctic newborns with severe umbilical acidosis have worse evolution at short term (more clinical involvement during neonatal period), but not worse evolution at long term (neurologic sequelae). The poor correlation between umbilical acidosis and neurologic prognosis persist when pHUA cut-off is < or = 7.00.

Acidosis↗
PubMed2000

Potentiation of a voltage-gated proton current in acidosis-induced swelling of rat microglia.

Microglia are equipped with a strong proton (H(+)) extrusion pathway, a voltage-gated H(+) channel, probably to compensate for the large amount of H(+) generated during phagocytosis; however, little is known about how this channel is regulated in pathological states. Because neural damage is often associated with intracellular and extracellular acidosis, we examined the regulatory mechanisms of the H(+) current of rat spinal microglia in acidic environments. More than 90% of round/amoeboid microglia expressed the H(+) current, which was characterized by slow activation kinetics, dependencies on both intracellular and extracellular pH, and blockage by Zn(2+). Extracellular lactoacidosis, pH 6.8, induced intracellular acidification and cell swelling. Cell swelling was also induced by intracellular dialysis with acidic pipette solutions, pH 5.5-6.8, at normal extracellular pH 7.3 in the presence of Na(+). The H(+) currents were increased in association with cell swelling as shown by shifts of the half-activation voltage to more negative potentials and by acceleration of the activation kinetics. The acidosis-induced cell swelling and the accompanying potentiation of the H(+) current required nonhydrolytic actions of intracellular ATP and were inhibited by agents affecting actin filaments (phalloidin and cytochalasin D). The H(+) current was also potentiated by swelling caused by hypotonic stress. These findings suggest that the H(+) channel of microglia can be potentiated via cell swelling induced by intracellular acidification. This potentiation might operate as a negative feedback mechanism to protect microglia from cytotoxic acidification and hence acidosis-induced swelling in pathological states of the CNS.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

[Severe lactic acidosis due to metformin therapy in a patient with contra-indications for metformin].

A 52-year-old woman with a medical history of diabetes mellitus type 2, chronic alcoholism and liver function disorders was hospitalized because of complaints of haematemesis, abdominal complaints and dyspnoea. This was due to a severe lactic acidosis caused by acute alcohol intoxication and the use of metformin. With bicarbonate infusion and haemofiltration, the lactic acidosis disappeared, but she developed a distributive shock with multiple organ failure and died 23 days after admission. Lactic acidosis is a rare but serious adverse effect of metformin. Almost all patients described had contraindications to the drug, like renal failure, liver disease, alcohol abuse, and intercurrent conditions causing hypoxia or ischaemia. It is important to be aware of the circumstances in which metformin should not be prescribed.

Acidosis, Lactic↗
PubMed1975

Blood flow to the human uterus during maternal metabolic acidosis.

Uterine blood flow and metabolism were estimated at cesarean section under general anesthesia in pregnant women at term with the use of the Fick principle with nitrous oxide as the test material. Observations were made without superimposed maternal metabolic acidosis and during the infusion of ammonium chloride. Increasing maternal metabolic acidosis was accompanied by a decreasing rate of blood flow in the uterine circulation. There were no statistically significant differences in the metabolic rate of the uterus and its contents during maternal metabolic acidosis induced by the infusion of ammonium chloride.

Acid-Base Equilibrium↗
PubMed2000

[New ways of correcting metabolic acidosis in experimental periodontitis].

Established prevention of atrophy of osseous cloth alveolar rats jaws sprouts and correction of metabolic acidosis of mineral concentrate "VITA" attached to modeling parodontit by dint of creation in them of fortune compensated metabolic acidosis. Mineral concentrate realizes normalization redoksfortune, thiol-disulphid system, lowering of relations SH/SS-group, multiplies maintenance oxidized and lowers maintenance restored of nicotinamid copherments, normalize relation HA[symbol: see text]/HA[symbol: see text]H in osseous jaws cloth of experimental rats attached to modeling in them metabolic acidosis and parodontit in distinction from fortune of alkalosis. Mineral complex will normalize in rats maintenance of regulators and orientation of exchange processes in cloths attached to parodontit, whereat indicates lowering of activity key gluconeogenesis processes enzyme fructosodiphosphatasa of liver cloths, mucous gum and alveolar sprouts of jaws.

Acidosis↗
PubMed2001

[An autopsy case of neonatal lactic acidosis].

Defects in mitochondrial enzymes, such as pyruvate dehydrogenase and cytochrome oxidase, cause hereditary disorders which lead to modifications in cellular pH due to the accumulation of pyruvate and lactic acid. Mitochondrial diseases include severe neonatal diseases and less severe forms of adult diseases. We report the case of lactic acidosis in a newborn girl who was delivered at 36 weeks of gestation and who died 3 months after birth. Her family history revealed a relative with tetraparesis and mental retardation. Her clinical findings, such as tonic-clonic convulsions and accumulation of pyruvate and lactic acid in blood, urine and cerebrospinal fluid, were refractory to treatment and developed soon after birth. Ultrasound scans of the brain some days before death revealed cerebral atrophy with ventricular dilatation and thinning of the corpus callosum and septum pellucidum. The clinical diagnosis of metabolic lactic acidosis was confirmed by macroscopic, microscopic and ultrastructural findings seen at autopsy. On macroscopic examination, the heart was hypertrophic, and the brain was atrophic with ventricular dilatation and thinning of corpus callosum. Small cystic lesions were present in the basal ganglia. On microscopic examination, the latter were characterized by loss of neurons, gliosis and capillary proliferation. Ultrastructural examination of the heart and skeletal muscle showed lysis of myofibrils, mitochondrial pleomorphism and hyperplasia, and crystalline inclusion in mitochondria and in the matrix compartment. In reporting this case, we emphasize the importance of accurate postmortem examination and clinical data for the diagnosis of metabolic lactic acidosis.

Acidosis, Lactic↗
PubMed2001

[Osteopenia and renal calcification in a 4.5 year old child with primary distal renal tubular acidosis treated for idiopathic renal hypercalciuria].

We present a case of a 4.5 years old boy suffering from hypercalciuria caused by a not diagnosed distal renal tubular acidosis. In the age of 2.5 years, after a banal infection the routine analysis showed a presence of numerous calcium phosphates in urine. Other diagnostic procedures showed: hypercalciuria, hyperphosphaturia, rather high calcemia and high values of UCa/cr and UPO4/cr ratios. HCO3 in serum 21.2 mmol/l, pH of urine 7.0. Kidneys and urinary tract-usg normal. These results induced the family doctor to make the diagnosis: idiopathic renal hypercalciuria. He advised the therapy with hydrochlorothiazide and limitations of calcium and vitamins D3 oral supply. This decision caused an illusory positive effect: decreased the UCa/cr ratio (to 0.96 mmol/mmol) without any reduction of calcemia. After a period of 12 months the UCa/cr ratio increased up to 1.31 and calcification of renal pyramids appeared. We diagnosed the distal renal tubular acidosis (some medical informations suggested the essential distal renal tubular acidosis) and osteopenia (DXA BMD L1-L4 below -1 s.d.). The therapy with NaHCO3 (about 2.6 mmol/kg) normalized the levels of HCO3a and calcium in serum, decreased the UCa/cr ratio to values 0.09-0.16 mmol/mmol.

Acidosis, Renal Tubular↗
PubMed2001

Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure.

BACKGROUND AND PURPOSE: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. PATIENTS AND METHODS: Eighteen patients with chronic renal failure (creatinine clearance 12 +/- 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. RESULTS: After bicarbonate infusion, there were significant increases in plasma pH (7.31 +/- 0.04 to 7.40 +/- 0.03, p < 0.001), bicarbonate concentration (18.46 +/- 2.49 to 23.66 +/- 2.72, p < 0.001), serum total calcium concentration (2.01 +/- 0.24 to 2.12 +/- 0.24 mmol/L, p < 0.001), and PICP concentration (137.3 +/- 56.25 to 159.6 +/- 57.30 micrograms/L, p < 0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 +/- 88.6 to 111.5 +/- 78.7, p < 0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. CONCLUSION: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

Acidosis↗