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Artículos de revistas sobre el tema "Lactic acidosis in ruminants"

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Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 12 de febrero de 2022

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1

Dunlop, Robert H. y Paul B. Hammond. "D-LACTIC ACIDOSIS OF RUMINANTS*†". Annals of the New York Academy of Sciences 119, n.º 3 (16 de diciembre de 2006): 1109–32. http://dx.doi.org/10.1111/j.1749-6632.1965.tb47466.x.

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2

Lorenz, Ingrid y Arcangelo Gentile. "d-Lactic Acidosis in Neonatal Ruminants". Veterinary Clinics of North America: Food Animal Practice 30, n.º 2 (julio de 2014): 317–31. http://dx.doi.org/10.1016/j.cvfa.2014.03.004.

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3

Clayton, E. H. y G. P. D. Jones. "Preliminary observations of tumour necrosis factor-alpha in the faeces of sheep following acute lactic acidosis". Australian Journal of Agricultural Research 52, n.º 9 (2001): 869. http://dx.doi.org/10.1071/ar00118.

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Lactic acidosis resulting from excessive fermentation of starch by ruminants can lead to many deleterious effects on the animal including shock and death in severe cases. The exact mechanisms mediating this response are still relatively unknown and the present study has examined the influence of lactic acidosis in sheep on the production of tumour necrosis factor-alpha (TNFα), a pro-inflammatory cytokine. Lactic acidosis was induced in 6 Merino sheep by feeding 2 kg of barley-based pellets. Lactic acid levels rose in rumen fluid and faeces from 0.5 to 32.1 mmol/L and 0.5 to 48.0 mmol/L, respectively (P < 0.05); whereas, pH in both rumen fluid and faeces decreased from 8.22 to 5.18 and 7.05 to 5.00, respectively (P < 0.05), after lactic acidosis. TNF-· levels increased in faeces from 15 ng/g to 75 ng/g (P < 0.05) 24 h and 12 h after ruminal and hind gut lactic acidosis incidence, respectively. These preliminary findings suggest the possibility of an immune response in the body to lactic acidosis indicated by increasing TNFα levels. TNFα may be a mediator of lactic acidosis and its presence may explain many of the secondary effects observed after acidosis including laminitis and liver abscesses.

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4

Park, Seon Young, Mingyung Lee, Se Ra Lim, Hyemin Kwon, Ye Seul Lee, Ji Hyung Kim y Seongwon Seo. "Diversity and Antimicrobial Resistance in the Streptococcus bovis/Streptococcus equinus Complex (SBSEC) Isolated from Korean Domestic Ruminants". Microorganisms 9, n.º 1 (4 de enero de 2021): 98. http://dx.doi.org/10.3390/microorganisms9010098.

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S. bovis/S. equinus complex (SBSEC) includes lactic acid-producing bacteria considered as the causative agent associated with acute rumen lactic acidosis in intensive ruminants. Considering the limited information on the detailed characteristics and diversity of SBSEC in Korea and the emergence of antimicrobial resistance (AMR), we investigated the diversity of SBSEC from domestic ruminants and verified the presence of antimicrobial resistance genes (ARGs) against several antimicrobials with their phenotypic resistance. Among 51 SBSEC isolates collected, two SBSEC members (S. equinus and S. lutetiensis) were identified; sodA-based phylogenetic analyses and comparisons of overall genome relatedness revealed potential plasticity and diversity. The AMR rates of these SBSEC against erythromycin, clindamycin, and tetracycline were relatively lower than those of other SBSEC isolates of a clinical origin. An investigation of the ARGs against those antimicrobials indicated that tetracycline resistance of SBSECs generally correlated with the presence of tet(M)-possessing Tn916-like transposon. However, no correlation between the presence of ARGs and phenotypic resistance to erythromycin and clindamycin was observed. Although a limited number of animals and their SBSEC isolates were examined, this study provides insights into the potential intraspecies biodiversity of ruminant-origin SBSEC and the current status on antimicrobial resistance of the bacteria in the Korean livestock industry.

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5

Valente, Tiago Neves Pereira, Cláudia Batista Sampaio, Erico da Silva Lima, Bruno Borges Deminicis, Andréia Santos Cezário y Wallacy Barbacena Rosa dos Santos. "Aspects of Acidosis in Ruminants with a Focus on Nutrition: A Review". Journal of Agricultural Science 9, n.º 3 (13 de febrero de 2017): 90. http://dx.doi.org/10.5539/jas.v9n3p90.

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An increased risk of acidosis in animals is associated with a high dry matter intake (DMI), which in turn results in the consumption of more fermentable organic matter (OM) in the rumen leading to a high production of volatile fatty acids (VFA). This is observed in lactating dairy cows and animals in a feedlot. Acute acidosis occurs when there is a severe drop in the pH of the rumen. A prolonged period when pH of in rumen remains low, it leads to sub-acute ruminal acidosis (SARA), which is a temporary imbalance between acid production and absorption. An associated change of an acute increase in the ruminal osmolarity and the accumulation of glucose and lactate in its stereoisomeric forms (D-lactate and L-lactate), is observed in the rumen fluid. However, in the sub-acute form, the accumulation of lactic acid occurs in the rumen. To a great extent, these changes in the rumen are due to high concentrations of VFA. The best way to avoid problems with ruminal acidosis is an adequate supply of neutral detergent fiber (NDF) in the diet, preferentially with large particle size and length to stimulate rumination and consequently greater buffering efficiency, thus maintaining the balance between pH and microorganisms in the rumen.

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6

Abeysekara, Saman, Jonathan M. Naylor, Andrew W. A. Wassef, Ulyana Isak y Gordon A. Zello. "d-Lactic acid-induced neurotoxicity in a calf model". American Journal of Physiology-Endocrinology and Metabolism 293, n.º 2 (agosto de 2007): E558—E565. http://dx.doi.org/10.1152/ajpendo.00063.2007.

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-Lactic acidosis (DAC) occurs as a complication of short-bowel syndrome in humans and in a variety of other gastrointestinal disorders in monogastrics and ruminants. DAC is associated with signs of impaired central nervous system (CNS) function including ataxia and coma. The objective of this experiment was to determine whether either acidification of nervous tissue or d-lactic acid is responsible for decreased neurological function. Eight Holstein calves (32 ± 11 days, 70 ± 10 kg) were surgically catheterized with indwelling intravenous jugular and atlanto-occipital space cerebrospinal fluid (CSF) catheters and infused for 6 h in random order with isomolar dl-lactic acid (dl-LA), l-lactic acid (l-LA), hydrochloric acid (HCl), or saline. dl-LA induced ataxia after 4 h of infusion and produced the greatest obtunding of CNS function (at 7 h, score 8.0 ± 0.4), whereas the other infusions caused neither ataxia nor scores over 1.5 ( P < 0.01 from dl-LA). dl-LA induced significantly less acidemia than HCl (at 6 h pH 7.13 ± 0.06 and 7.00 ± 0.04, base excess −16 ± 1 and −23 ± 3 mmol/l, bicarbonate 11 ± 1 and 8 ± 1 mmol/l respectively, all P < 0.01) but greater than l-LA and saline ( P < 0.01). CSF changes followed a similar but less pronounced pattern. Although HCl infusion produced a severe acidemia and CSF acidosis, only minor effects on neurological function were evident suggesting that d-lactate has a direct neurotoxic effect that is independent of acidosis. Conversely, l-LA produced only minor neurological changes.

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7

Ghali, M. B., P. T. Scott, G. A. Alhadrami y R. A. M. Al Jassim. "Identification and characterisation of the predominant lactic acid-producing and lactic acid-utilising bacteria in the foregut of the feral camel (Camelus dromedarius) in Australia". Animal Production Science 51, n.º 7 (2011): 597. http://dx.doi.org/10.1071/an10197.

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The camel is emerging as a new and important animal in the Australian livestock industry. However, little is known regarding the microbial ecosystem of the gastrointestinal tract of this ruminant-like animal. This study was carried out to determine the diversity of lactic acid-producing and lactic acid-utilising bacteria in the foregut of the feral camel (Camelus dromedarius) in Australia. Putative lactic acid bacteria were isolated from the foregut contents of camels by culturing on De Man, Rogosa, Sharpe and lactic acid media. Identification of representative isolates was based on the analysis of 16S rRNA gene sequences. Fermentation end products of glucose (i.e. volatile fatty acids and lactate) were also measured in vitro. The key predominant bacteria identified in this study were closely related to Streptococcus bovis, Selenomonas ruminantium, Butyrivibrio fibrisolvens, Lachnospira pectinoschiza and Prevotella ruminicola. The main L-lactate producers were those isolates closely related to S. bovis, S. ruminantium and Lactococcus garvieae, while the efficient lactate utilisers were S. ruminantium-related isolates. D-lactate was produced by isolates closely related to either L. pectinoschiza or S. ruminantium. The predominant bacteria isolated and characterised in this study are identical and/or closely related to those typically found in true ruminants (e.g. S. ruminantium, B. fibrisolvens, S. bovis). In addition, some of the bacteria isolated represent novel species of Lachnospira and Clostridium in the context of lactic acid bacteria from a large herbivorous host. The results from this study have contributed to our understanding and provide opportunities to reduce foregut acidosis in the camel.

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8

Hutton, P., C. L. White, Z. Durmic y P. E. Vercoe. "Eremophila glabra is an Australian plant that reduces lactic acid accumulation in an in vitro glucose challenge designed to simulate lactic acidosis in ruminants". Animal 3, n.º 9 (2009): 1254–63. http://dx.doi.org/10.1017/s1751731109004789.

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9

Bacha, Flávia Barbieri, Rayane Chitolina Pupin, Paula Velozo Leal, Nilton Marques Carvalho, Gumercindo Loriano Franco, Camila Celeste Brandão Ferreira Ítavo, Franklin Riet-Correa y Ricardo Antônio Amaral de Lemos. "Experimental poisoning by Enterolobium contortisiliquum in sheep". Pesquisa Veterinária Brasileira 37, n.º 1 (enero de 2017): 23–30. http://dx.doi.org/10.1590/s0100-736x2017000100004.

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ABSTRACT: Ingestion of Enterolobium contortisiliquum pods causes digestive disturbances, secondary hepatogenous photosensitization and abortions in ruminants. Pods were administered to sheep via a ruminal cannula to characterize acute poisoning. In Experiment 1, a single dose of 12g/kg of body weight (BW) was administered to three sheep in one experiment. One sheep died, and the other two recovered after presenting clinical signs. In Experiment 2, 10g/kg BW were administered daily to 15 sheep until the onset of clinical signs or for three consecutive days. Fourteen sheep showed mild to severe signs after the ingestion of 1-3 doses. Two sheep died, and the others recovered. Clinical signs in both experiments were diarrhea, anorexia, rumen atony, apathy, dehydration and tachypnea. The main macroscopic findings were an orange, frothy ruminal content witch contained pods fragments. The intestinal content was liquid. Detachment of the mucosa from the submucosa and ballooning degeneration of mucosal cells were observed histologically in the forestomachs. Evaluation of ruminal contents revealed acute lactic ruminal acidosis (ALRA). Bromatological analysis of E. contortisiliquum pods revealed 537.8g/kg DM (dry matter) of non-fibrous carbohydrates, which is sufficient to cause ALRA. Only one sheep in Experiment 2 had liver failure, characterized by jaundice, elevated serum activity of liver enzymes and histological lesions in liver biopsies. It is concluded that the administration of E. contortisiliquum pods in forage-fed sheep at doses of 10g/kg BW or higher may cause ALRA. The induction of liver failure in one sheep suggests that liver damage may occur in those sheep that do not develop acidosis.

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10

McAllister, T. A., K. A. Beauchemin, A. Y. Alazzeh, J. Baah, R. M. Teather y K. Stanford. "Review: The use of direct fed microbials to mitigate pathogens and enhance production in cattle". Canadian Journal of Animal Science 91, n.º 2 (junio de 2011): 193–211. http://dx.doi.org/10.4141/cjas10047.

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McAllister, T. A., Beauchemin, K. A., Alazzeh, A. Y., Baah, J., Teather, R. M. and Stanford, K. 2011. Review: The use of direct fed microbials to mitigate pathogens and enhance production in cattle. Can. J. Anim. Sci. 91: 193–211. Direct-fed microbials (DFM) have been employed in ruminant production for over 30 yr. Originally, DFM were used primarily in young ruminants to accelerate establishment of the intestinal microflora involved in feed digestion and to promote gut health. Further advancements led to more sophisticated mixtures of DFM that are targeted at improving fiber digestion and preventing ruminal acidosis in mature cattle. Through these outcomes on fiber digestion/rumen health, second-generation DFM have also resulted in improvements in milk yield, growth and feed efficiency of cattle, but results have been inconsistent. More recently, there has been an emphasis on the development of DFM that exhibit activity in cattle against potentially zoonotic pathogens such as Escherichia coli O157:H7, Salmonella spp. and Staphylococcus aureus. Regulatory requirements have limited the microbial species within DFM products to organisms that are generally recognized as safe, such as lactic acid-producing bacteria (e.g., Lactobacillus and Enterococcus spp.), fungi (e.g., Aspergillus oryzae), or yeast (e.g., Saccharomyces cerevisiae). Direct-fed microbials of rumen origin, involving lactate-utilizing species (e.g., Megasphaera elsdenii, Selenomonas ruminantium, Propionibacterium spp.) and plant cell wall-degrading isolates of Butyrivibrio fibrisolvens have also been explored, but have not been commercially used. Development of DFM that are efficacious over a wide range of ruminant production systems remains challenging because[0] comprehensive knowledge of microbial ecology is lacking. Few studies have employed molecular techniques to study in detail the interaction of DFM with native microbial communities or the ruminant host. Advancements in the metagenomics of microbial communities and the genomics of microbial–host interactions may enable DFM to be formulated to improve production and promote health, responses that are presently often achieved through the use of antimicrobials in cattle.

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11

Chuprina, E. G., A. B. Vlasov, D. A. Yurin y N. A. Yurina. "Feed product in the rations of freshly calved cows consisting of protected soybean and sunfl ower protein". Kormlenie sel'skohozjajstvennyh zhivotnyh i kormoproizvodstvo (Feeding of agricultural animals and feed production), n.º 10 (1 de octubre de 2020): 24–32. http://dx.doi.org/10.33920/sel-05-2010-03.

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Conducting dairy cattle breeding in modern environments is impossible without a deep understanding of all the physiological processes occurring in the body of a highly productive animal. It is well known that the realization of the genetic potential of cows is impossible without the use of high-quality feed products and feeds. The issue of complete feeding of ruminants is particularly acute during the period of increasing the milk yield. The purpose of the researches was to study the feeding of the PassPro Balance feed product consisting of protected soybean and sunfl ower protein in the rations of freshly calved highly productive cows. It has been found as a result of the experiment that the input of the studied additive in the amount of 2 kg in the ration of cows of the experimental group contributed to the increased consumption of feed dry matter by 3,4 %. For the period of experiment from the experimental animals by 12,0 % more milk (P < 0,05) has been received in comparison with the control group. It has been found that the yield of milk fat in the experimental group was signifi cantly higher than the control one by 13,3 % (P < 0,05). In the experimental group of cows there was a tendency to increase the milk protein content by 10,8 %. By adjusting milk yield by 4,0 % in the experimental group of cows this indicator signifi cantly exceeded the control by 12,8 % (P < 0,05). When analyzing the rumen fl uid for microbiological indicators, a certain decrease in enterobacteria and staphylococci has been found in samples of cows of the experimental group with the increase in lactic acid microorganisms by 1,6 times. The pH of the rumen fl uid of cows of both groups was at the level of 6,2, which excludes the development of acidosis in animals during the fresh calving period.

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12

Martín, Elizabeth, Edward Pérez, Solains Cañón, Jorge Rodríguez y Fernando Rodríguez. "Sonda oro-ruminal experimental como alternativa para la obtención de microorganismos anaeróbicos del rumen". Corpoica Ciencia y Tecnología Agropecuaria 6, n.º 1 (2 de junio de 2005): 39. http://dx.doi.org/10.21930/rcta.vol6_num1_art:34.

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<p>Estudios sobre el ecosistema microbiano ruminal, han requerido tradicionalmente el uso de la canulación de los animales. El alto costo de la cirugía y su mantenimiento ha limitado a muchos laboratorios a tener fácil acceso a las muestras del rumen y a explorar su diversidad microbiana. Métodos como el uso de sondas de oro- ruminales se han utilizado tradicionalmente para transformación de animales sanos y otros que tienen enfermedades metanbólicas; que también han sido utilizadas en para el diagnóstico de enfermedades severas: síndrome de abomaso reflejo, acidosis láctica aguda, la acidosis crónica latente, putrefacción y la inactividad microbiana. La primera sonda oro- ruminal fue utilizada por Pounden en 1954, que consistió en un simple tubo que desciende desde la boca o la nariz hasta el rumen. Una jeringa grande se incluyó más tarde para succión de líquido ruminal. A veces se han utilizado accesorios de metal perforados para aspiración. Otra técnica ha permitido a las pequeños cantidades de fluido ruminal ser obtenidos por aspiración caudo ventral del rumen usando una jeringa sencilla. Aunque la rumenocentesis (como se conoce a este proceso) conduce al riesgo de producir una peritonitis localizada en un animal, que es actualmente uno de los métodos más utilizados en grandes granjas lecheras de producción para el seguimiento de los cambios abruptos y frecuentes en el pH ruminal que por lo general se asocian con lacto-acidosis. Este estudio se propone la utilización de una sonda oro-rumial para la obtención de muestras de contenido ruminal de animales no canulados y su uso en el aislamiento de microorganismos anaerobios habituales. Evaluando e implementando la metodología de la sonda oro-ruminal surgió la necesidad creciente de más estudios orientados hacia la obtención de conocimiento de los microorganismos de las vías gastrointestinales y aumentar el banco de germoplasma recolectado por CORPOICA de bacterias ruminales y hongos de las razas criollas colombianas.</p><p> </p><p class="Default"><strong>Ruminal anaerobic microorganism recovery using an experimental oro-ruminal probe</strong></p><p class="Default">Ruminal microbial ecosystem studies have traditionally required the use of canulado animals. The high cost of animal surgery and their maintenance has limited many laboratories having easy access to rumen samples and exploring their microbial diversity. Methods like using oro-ruminal probes have been traditionally used for transfaunactions from healthy animals to others having digestive disorders and metabolic diseases; they have also been used in diagnosing several diseases: abomasum reflex syndrome, acute lactic acidosis, chronic-latent acidosis, putrefaction and microbial inactivity. The earliest oro-ruminal probe was used by Pounden in 1954, consisting of a simple tube descending from the mouth or nose to the rumen. A large syringe was included later on for suc-king up the flow of ruminal liquid. Perforated metal suction accessories have sometimes been used. Another technique has allowed small quantities of ruminal fluid to be obtained by caudo-ventral aspiration of the rumen using a simple syringe. Even though rumenocentesis (as this process is known) leads to the risk of producing loca-lized peritonitis in an animal, it is currently one of the most used methods on large-scale production dairy farms for monitoring abrupt and frequent changes in ruminal pH which are usually associated with lactoacidosis. This study proposes using an oro-ruminal probe for obtaining samples of ruminal content from non-canulado animals and its use in isolating customary anaerobic microorganisms. Evaluating and implementing the oro-ruminal probe methodology became necessary due to the growing need for further studies orientated towards gaining know-ledge of microorganisms from the gastrointestinal tract and increasing CORPOICA’s germoplasm bank collection of ruminal bacteria and fungi from Colombian creole breeds.</p>

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13

Rumbak, Mark J. "Lactic Acidosis". Annals of Internal Medicine 113, n.º 3 (1 de agosto de 1990): 254. http://dx.doi.org/10.7326/0003-4819-113-3-254_2.

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14

Stacpoole, Peter W. "Lactic Acidosis". Endocrinology and Metabolism Clinics of North America 22, n.º 2 (junio de 1993): 221–45. http://dx.doi.org/10.1016/s0889-8529(18)30163-4.

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15

Madias, Nicolaos E. "Lactic acidosis". Kidney International 29, n.º 3 (marzo de 1986): 752–74. http://dx.doi.org/10.1038/ki.1986.62.

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16

Gill, G. V. y K. G. M. M. Alberti. "Lactic acidosis". Practical Diabetes International 2, n.º 4 (julio de 1985): 15–19. http://dx.doi.org/10.1002/pdi.1960020405.

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17

Kraut, Jeffrey A. y Nicolaos E. Madias. "Lactic Acidosis". New England Journal of Medicine 371, n.º 24 (11 de diciembre de 2014): 2309–19. http://dx.doi.org/10.1056/nejmra1309483.

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18

De Backer, Daniel. "Lactic acidosis". Intensive Care Medicine 29, n.º 5 (mayo de 2003): 699–702. http://dx.doi.org/10.1007/s00134-003-1746-7.

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19

Mizock, Barry A. "Lactic acidosis". Disease-a-Month 35, n.º 4 (abril de 1989): 237–300. http://dx.doi.org/10.1016/0011-5029(89)90021-7.

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20

Kuroda, Yasuhiro, Etsuo Naito, Eiji Takeda, Ichiro Yokota y Masuhide Miyao. "Congenital Lactic Acidosis". Enzyme 38, n.º 1-4 (1987): 108–14. http://dx.doi.org/10.1159/000469196.

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21

Landow, Laurence. "Hypoxic Lactic Acidosis". Chest 106, n.º 2 (agosto de 1994): 653–54. http://dx.doi.org/10.1378/chest.106.2.653b.

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22

Hayat, Muhammad S., Soon-IL Song, Zandra K. Ferrufino-Ponce, Nausheen Naz y Frederick W. Ruymann. "D-Lactic Acidosis". American Journal of Gastroenterology 101 (septiembre de 2006): S377. http://dx.doi.org/10.14309/00000434-200609001-00947.

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23

Petersen, Craig. "D-Lactic Acidosis". Nutrition in Clinical Practice 20, n.º 6 (diciembre de 2005): 634–45. http://dx.doi.org/10.1177/0115426505020006634.

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24

Johnson, R. N. "Lactic Acidosis Revisited". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 26, n.º 2 (marzo de 1989): 113–14. http://dx.doi.org/10.1177/000456328902600202.

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25

Kinney, Evlin L. "Dichloroacetate and Lactic Acidosis". Annals of Internal Medicine 109, n.º 5 (1 de septiembre de 1988): 435. http://dx.doi.org/10.7326/0003-4819-109-5-435_1.

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26

Cohen, R. D. y H. F. Woods. "Metformin and lactic acidosis". Diabetes Care 22, n.º 6 (1 de junio de 1999): 1010–11. http://dx.doi.org/10.2337/diacare.22.6.1010.

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27

Jackson, M., S. Nussey y S. Mudan. "Metformin induced lactic acidosis". Clinical Intensive Care 11, n.º 4 (agosto de 2000): 209–13. http://dx.doi.org/10.3109/tcic.11.4.209.213.

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28

HOLLANDER, ROBERT G. "Lactic Acidosis in Pheochromocytoma". Annals of Internal Medicine 107, n.º 2 (1 de agosto de 1987): 259. http://dx.doi.org/10.7326/0003-4819-107-2-259.

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Haupt, Marilyn T. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00020.

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30

Fulop, Milford. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00021.

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31

Coyle, Thomas. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00022.

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32

Chariot, Patrick. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00023.

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33

Baram, Daniel. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00024.

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34

Chattha, Geetinder. "Lactic Acidosis and AIDS". Annals of Internal Medicine 119, n.º 4 (15 de agosto de 1993): 343. http://dx.doi.org/10.7326/0003-4819-119-4-199308150-00025.

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35

Hulisz, D. T., M. F. Bonfiglio y R. D. Murray. "Metformin-Associated Lactic Acidosis". Journal of the American Board of Family Medicine 11, n.º 3 (1 de mayo de 1998): 233–36. http://dx.doi.org/10.3122/15572625-11-3-233.

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36

BORNEMANN, MICHAEL. "Lactic Acidosis in Pheochromocytoma". Annals of Internal Medicine 105, n.º 6 (1 de diciembre de 1986): 880. http://dx.doi.org/10.7326/0003-4819-105-6-880.

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37

Kruse, James A. "Metformin-associated lactic acidosis". Journal of Emergency Medicine 20, n.º 3 (abril de 2001): 267–72. http://dx.doi.org/10.1016/s0736-4679(00)00320-6.

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Suh, Sunghwan. "Metformin-Associated Lactic Acidosis". Endocrinology and Metabolism 30, n.º 1 (2015): 45. http://dx.doi.org/10.3803/enm.2015.30.1.45.

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Neale, R. "Statin precipitated lactic acidosis?" Journal of Clinical Pathology 57, n.º 9 (1 de septiembre de 2004): 989–90. http://dx.doi.org/10.1136/jcp.2004.015958.

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Fitzgerald, E., S. Mathieu y A. Ball. "Metformin associated lactic acidosis". BMJ 339, sep16 2 (16 de septiembre de 2009): b3660. http://dx.doi.org/10.1136/bmj.b3660.

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Stemar, Andrew, Yvan Mardy, Yizhak Kupfer y Sidney Tessler. "LACTIC ACIDOSIS IN ASTHMA". Critical Care Medicine 22, n.º 1 (enero de 1994): A94. http://dx.doi.org/10.1097/00003246-199401000-00175.

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&NA;. "CRITICAL CARE Lactic Acidosis". AJN, American Journal of Nursing 94, n.º 10 (octubre de 1994): 10–11. http://dx.doi.org/10.1097/00000446-199410000-00005.

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Vici, C. Dionisi, E. Bertini, A. Bartuli y G. Sabetta. "Carnitine in lactic acidosis". Journal of Pediatrics 112, n.º 4 (abril de 1988): 678. http://dx.doi.org/10.1016/s0022-3476(88)80202-6.

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Pasquel, Francisco J., Ziad Hinedi, Guillermo E. Umpierrez, Robin Klein, Adaeze Adigweme, Richard Coralli, Juan L. Pimentel y Fred A. Lopez. "Metformin-Associated Lactic Acidosis". American Journal of the Medical Sciences 349, n.º 3 (marzo de 2015): 263–67. http://dx.doi.org/10.1097/maj.0b013e3182a562b7.

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Ramakrishna, Karan N., Jaswinder Virk y Harvir Singh Gambhir. "Albuterol-Induced Lactic Acidosis". American Journal of Therapeutics 26, n.º 5 (2019): e635-e636. http://dx.doi.org/10.1097/mjt.0000000000000843.

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Pearlman, Brian L., Andrew Z. Fenves y Michael Emmett. "Metformin-associated lactic acidosis". American Journal of Medicine 101, n.º 1 (julio de 1996): 109–10. http://dx.doi.org/10.1016/s0002-9343(97)89422-3.

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Liem, Edwin B., Stephen C. Mnookin y Michael E. Mahla. "Albuterol-induced Lactic Acidosis". Anesthesiology 99, n.º 2 (1 de agosto de 2003): 505–6. http://dx.doi.org/10.1097/00000542-200308000-00036.

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Briggs, Deborah. "Metformin-associated lactic acidosis". Emergency Nurse 22, n.º 5 (3 de septiembre de 2014): 20–25. http://dx.doi.org/10.7748/en.22.5.20.e1332.

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Apodaca, Aaron A. y Robert M. Rakita. "Linezolid-Induced Lactic Acidosis". New England Journal of Medicine 348, n.º 1 (2 de enero de 2003): 86–87. http://dx.doi.org/10.1056/nejm200301023480123.

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Ashall, V. y T. Dawes. "Metformin and lactic acidosis". British Journal of Anaesthesia 101, n.º 6 (diciembre de 2008): 876–77. http://dx.doi.org/10.1093/bja/aen286.

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