PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 17187319

[Isoniazid intoxication].

J Graf·N Scheffold·W Radunz·J Cyran
View original source ↗Export metadata ↓

Abstract

HISTORY AND ADMISSION FINDINGS: A 55-year-old woman presented with sustained convulsions after the ingestion of an at first unknown amount of isoniazid, rifampin, ethambutol and alcohol. INVESTIGATION: At admission the patient had a severe metabolic acidosis. Blood tests showed changes caused by the hepatotoxicity of isoniazid. TREATMENT AND COURSE: Because diazepam was not efficacious in controlling the convulsions the patient was intubated. In response to the therapautic measures the convulsions stopped and metabolic acidosis was quickly compensated. Pyridoxine was given intravenously as an antidote. CONCLUSION: The rare intoxication with isoniazid demands immediate administration of pyridoxine and aggressive treatment of the convulsions.

Explore related subjects

AcidosisAnticonvulsantsAntidotesAntitubercular AgentsDiazepamFemaleHumansInfusions, IntravenousIsoniazidMiddle AgedPyridoxineRecurrenceSeizuresSuicide, AttemptedVitamin B ComplexCase ReportsEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Graf, N Scheffold, W Radunz, J Cyran. 2007-01-05. [Isoniazid intoxication].. https://doi.org/10.1055/s-2007-959283

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Grave acidosis after severe anaphylactic bronchospasm: friend or foe?

In a 20-year-old woman with known asthma, anaphylactic bronchospasm induced a grave combined respiratory and metabolic acidosis (pH(a) 6.66) with marked hypoxaemia (S(a)O(2) 45%). The beneficial effects of the rightward shift of the oxyhaemoglobin dissociation curve on tissue O(2) unloading at such pH was more than offset by the negative effect on S(a)O(2) at the reduced P(a)O(2) (7.0 kPa) found in this patient. This case illustrates the detrimental effect of grave acidosis on arterial blood oxygen content at subnormal P(a)O(2) values, the beneficial effect of a supranormal P(a)O(2) on the S(a)O(2) in such patients, and the rapid remission rate of life-threatening acidosis and blood lactate after adequate ventilation and tissue oxygenation were secured. The initial treatment of the patient and clinically relevant considerations are discussed.

Acidosis↗
PubMed2007

Mitogen-activated protein kinase-dependent activation of the Na+/H+ exchanger is mediated through phosphorylation of amino acids Ser770 and Ser771.

We investigated regulation of the type 1 isoform of the Na(+)/H(+) exchanger by phosphorylation. Four specific groups of serine and threonine residues in the regulatory carboxyl-terminal tail were mutated to alanine residues: group 1, S693A; group 2, T718A and S723A/S726A/S729A; group 3, S766A/S770A/S771A; and group 4, T779A and S785A. The proteins were expressed in Na(+)/H(+) exchanger-deficient cells, and the activity was characterized. All of the mutants had proper expression, localization, and normal basal activity relative to wild type NHE1. Sustained intracellular acidosis was used to activate NHE1 via an ERK-dependent pathway that could be blocked with the MEK inhibitor U0126. Immunoprecipitation of (32)P-labeled Na(+)/H(+) exchanger from intact cells showed that sustained intracellular acidosis increased Na(+)/H(+) exchanger phosphorylation in vivo. This was blocked by U0126. The Na(+)/H(+) exchanger activity of mutants 1 and 2 was stimulated similar to wild type Na(+)/H(+) exchanger. Mutant 4 showed a partially reduced level of activation. However, mutant 3 was not stimulated by sustained intracellular acidosis, and loss of stimulation of activity correlated to a loss of sustained acidosis-mediated phosphorylation in vivo. Mutation of the individual amino acids within mutant 3, Ser(766), Ser(770), and Ser(771), showed that Ser(770) and Ser(771) are responsible for mediating increases in NHE1 activity through sustained acidosis. Both intact Ser(770) and Ser(771) were required for sustained acidosis-mediated activation of NHE1. Our results suggest that amino acids Ser(770) and Ser(771) mediate ERK-dependent activation of the Na(+)/H(+) exchanger in vivo.

Acidosis↗
PubMed2007

Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning.

We have previously reported that the prolonged transient acidosis during early reperfusion mediates the cardioprotective effects in canine hearts. Recently, postconditioning has been shown to be one of the novel strategies to mediate cardioprotection. We tested the contribution of the prolonged transient acidosis to the cardioprotection of postconditioning. Open-chest anesthetized dogs subjected to 90-min occlusion of the left anterior descending coronary artery and 6-h reperfusion were divided into four groups: 1) control group; no intervention after reperfusion (n = 6); 2) postconditioning (Postcon) group; four cycles of 1-min reperfusion and 1-min reocclusion (n = 7); 3) Postcon + sodium bicarbonate (NaHCO(3)) group; four cycles of 1-min reperfusion and 1-min reocclusion with the administration of NaHCO(3) (n = 8); and 4) NaHCO(3) group; administration of NaHCO(3) without postconditioning (n = 6). Infarct size, the area at risk (AAR), collateral blood flow during ischemia, and pH in coronary venous blood were measured. The phosphorylation of Akt and extracellular signal-regulated kinase (ERK) in ischemic myocardium was assessed by Western blot analysis. Systemic hemodynamic parameters, AAR, and collateral blood flow were not different among the four groups. Postconditioning induced prolonged transient acidosis during the early reperfusion phase. Administration of NaHCO(3) completely abolished the infarct size-limiting effects of postconditioning. Furthermore, the phosphorylation of Akt and ERK in ischemic myocardium induced by postconditioning was also blunted by the cotreatment of NaHCO(3). In conclusion, postconditioning mediates its cardioprotective effects possibly via prolonged transient acidosis during the early reperfusion phase with the activation of Akt and ERK.

Acidosis↗