scholarly journals In Unexplained Altered Sensorium - Look for Arterial Ammonia Level

2018 ◽  
Vol 39 (3) ◽  
Author(s):  
Usha Dutta
2021 ◽  
Vol 11 (6) ◽  
pp. 478
Author(s):  
Ching Chang ◽  
Chien-Hao Huang ◽  
Hsiao-Jung Tseng ◽  
Fang-Chen Yang ◽  
Rong-Nan Chien

Background: Hepatic encephalopathy (HE), a neuropsychiatric complication of decompensated cirrhosis, is associated with high mortality and high risk of recurrence. Rifaximin add-on to lactulose for 3 to 6 months is recommended for the prevention of recurrent episodes of HE after the second episode. However, whether the combination for more than 6 months is superior to lactulose alone in the maintenance of HE remission is less evident. Therefore, the aim of this study is to evaluate the one-year efficacy of rifaximin add-on to lactulose for the maintenance of HE remission in Taiwan. Methods: We conducted a real-world single-center retrospective cohort study to compare the long-term efficacy of rifaximin add-on to lactulose (group R + L) versus lactulose alone (group L, control group). Furthermore, the treatment efficacy before and after rifaximin add-on to lactulose was also analyzed. The primary endpoint of our study was time to first HE recurrence (Conn score ≥ 2). All patients were followed up every three months until death, and censored at one year if still alive. Results and Conclusions: 12 patients were enrolled in group R + L. Another 31 patients were stratified into group L. Sex, comorbidity, ammonia level, and ascites grade were matched while age, HE grade, and model for end-stage liver disease (MELD) score were adjusted in the multivariable logistic regression model. Compared with group L, significant improvement in the maintenance of HE remission and decreased episodes and days of HE-related hospitalizations were demonstrated in group R + L. The serum ammonia levels were significantly lower at the 3rd and 6th month in group 1. Concerning changes before and after rifaximin add-on in group R + L, mini-mental status examination (MMSE), episodes of hospitalization, and variceal bleeding also improved at 6 and 12 months. Days of hospitalization, serum ammonia levels also improved at 6th month. Except for concern over price, no patients discontinued rifaximin due to adverse events or complications. The above results provide evidence for the one-year use of rifaximin add-on to lactulose in reducing HE recurrence and HE-related hospitalization for patients with decompensated cirrhosis.


Antibiotics ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 145 ◽  
Author(s):  
Kosuke Kaji ◽  
Soichiro Saikawa ◽  
Hiroaki Takaya ◽  
Yukihisa Fujinaga ◽  
Masanori Furukawa ◽  
...  

Rifaximin is a poorly absorbable antibiotic against hepatic encephalopathy (HE). This observational study aimed to elucidate the effect of rifaximin on intestinal permeability and gut microbiota in patients with decompensated cirrhosis. Thirty patients with decompensated cirrhosis were assessed by ammonia level, neuropsychological testing, endotoxin activity (EA), and serum proinflammatory cytokines at baseline and after four weeks of rifaximin treatment (1200 mg/day). Intestinal permeability was indicated by serum soluble CD163 (sCD163), mannose receptor (sMR), and zonulin levels. To evaluate the gut microbiome, 16S ribosomal RNA gene sequencing was applied. Rifaximin ameliorated hyperammonemia and cognitive dysfunction, although it did not change the serum proinflammatory cytokine levels. It decreased EA levels as well as serum levels of sCD163 and sMR, but not zonulin, and both decreases in sCD163 and sMR showed positive correlations with EA decrease (ΔsCD163: Correlation coefficient (R) = 0.680, p = 0.023; ΔsMR: R = 0.613, p = 0.014, vs. ΔEA). Gut microbial analysis revealed that the richness and complexity of species were unchanged while the abundance of the Streptococcus genus was reduced after treatment with rifaximin. Collectively, rifaximin alleviated HE and endotoxemia with improved intestinal hyperpermeability in patients with decompensated cirrhosis, and this effect is partially involved in a gut microbial change.


2010 ◽  
Vol 39 (3) ◽  
pp. 549-555 ◽  
Author(s):  
Raul Franzolin ◽  
Fabrício Pini Rosales ◽  
Weber Vilas Bôas Soares

The effects were assessed of two energy sources in concentrate (ground grain corn vs. citrus pulp) and two nitrogen sources (soybean meal vs. urea) on rumen metabolism in four buffaloes and four zebu cattle (Nellore) with rumen cannula and fed in a 4 × 4 Latin square design with feeds containing 60% sugar cane. Energy supplements had no effect on the rumen ammonia concentration in cattle, but ground grain corn promoted higher ammonia level than citrus pulp in buffalo. Urea produced higher ammonia level than soybean meal in both animal species. On average, the buffaloes maintained a lower rumen ammonia concentration (11.7 mg/dL) than the cattle (14.5 mg/dL). Buffaloes had lower production of acetic acid than cattle (58.7 vs. 61.6 mol/100 mol) and higher of propionic acid (27.4 vs. 23.6 mol/100 mol). There was no difference in the butyric acid production between the buffaloes (13.6 mol/100 mol) and cattle (14.8 mol/100 mol) and neither in the total volatile fatty acids concentration (82.5 vs. 83.6 mM, respectively). The energy or nitrogen sources had no effect on rumen protozoa count in either animal species. The zebu cattle had higher rumen protozoa population (8.8 × 10(5)/mL) than the buffaloes (6.1 × 10(5)/mL). The rumen protozoa population differed between the animal species, except for Dasytricha and Charonina. The buffaloes had a lower Entodinium population than the cattle (61.0 vs 84.9%, respectively) and a greater percentage of species belonging to the Diplodiniinae subfamily than the cattle (28.6 vs. 1.4%, respectively). In cattle, ground corn is a better energy source than citrus pulp for use by Entodinium and Diplodiniinae. In the buffaloes, the Entodinium are favored by urea and Diplodiniinae species by soybean meal.


2017 ◽  
Vol 08 (04) ◽  
Author(s):  
Tushar Premraj Raut ◽  
Gaurav Baheti ◽  
Anupa Hinduja ◽  
Prashant Makhija ◽  
Khursheed Ansari ◽  
...  

2001 ◽  
Vol 86 (2) ◽  
pp. 836-844 ◽  
Author(s):  
Dominic Mort ◽  
Païkan Marcaggi ◽  
James Grant ◽  
David Attwell

A rise of brain ammonia level, as occurs in liver failure, initially increases glutamate accumulation in neurons and glial cells. We investigated the effect of acute exposure to ammonia on glutamate transporter currents in whole cell clamped glial cells from the salamander retina. Ammonia potentiated the current evoked by a saturating concentration ofl-glutamate, and decreased the apparent affinity of the transporter for glutamate. The potentiation had a Michaelis-Menten dependence on ammonia concentration, with a K m of 1.4 mM and a maximum potentiation of 31%. Ammonia also potentiated the transporter current produced by d-aspartate. Potentiation of the glutamate transport current was seen even with glutamine synthetase inhibited, so ammonia does not act by speeding glutamine synthesis, contrary to a suggestion in the literature. The potentiation was unchanged in the absence of Cl− ions, showing that it is not an effect on the anion current gated by the glutamate transporter. Ammonium ions were unable to substitute for Na+in driving glutamate transport. Although they can partially substitute for K+ at the cation counter-transport site of the transporter, their occupancy of these sites would produce a potentiation of <1%. Ammonium, and the weak bases methylamine and trimethylamine, increased the intracellular pH by similar amounts, and intracellular alkalinization is known to increase glutamate uptake. Methylamine and trimethylamine potentiated the uptake current by the amount expected from the known pH dependence of uptake, but ammonia gave a potentiation that was larger than could be explained by the pH change, and some potentiation of uptake by ammonia was still seen when the internal pH was 8.8, at which pH further alkalinization does not increase uptake. These data suggest that ammonia speeds glutamate uptake both by increasing cytoplasmic pH and by a separate effect on the glutamate transporter. Approximately two-thirds of the speeding is due to the pH change.


2014 ◽  
Vol 1 (4) ◽  
pp. 274
Author(s):  
BinduT Nair ◽  
RK Sanjeev ◽  
Sumit Lakhanpal

2020 ◽  
Vol 92 (2) ◽  
pp. 55-60
Author(s):  
S. A. Kozhevnikova ◽  
L. V. Tribuntseva ◽  
A. V. Budnevsky

Chronic obstructive pulmonary disease (COPD) is a world-wide problem. It is characterized by comorbidity. Among the numerous comorbidity obesity is considered. The common pathogenetic factors cause the more severe course of COPD. Obesity is a complex metabolic condition affecting many physiological systems, in particular, the metabolic liver affection is developing in the type of non-alcoholic liver disease. In patients with different stages of non-alcoholic liver disease detoxification function is reduced. Toxic ammonia does not convert in urea. Ammonia begins to affect the whole organism. Aim.To identify the frequency of hyperammonemia in patients with COPD and obesity, to analyze the degree of its influence on the COPD course and the quality of patients life, to assess the possibility of hyperammonemia correction with L-ornithine L-aspartate (LOLA). Materials and methods.The study included 50 patients with non-acute COPD (GOLD 2), Group D, phenotype with frequent exacerbations, central-type obesity. At the 1st stage of the investigation, COPD course was evaluated, specific evaluation tests (mMRC, CCQ, CAT, SGRQ, SF-36) were used, the biochemical blood test was performed, hyperammoniemia was detected on a Pocket Chem BA PA-4140, and Number Connecting Test was performed. In the 2ndstage of the investigation, all patients were prescribed a course of treatment with LOLA and after 4 weeks the estimated parameters were compared in dynamics. Results.After 4 weeks, comparative analysis showed reliable positive dynamics of subjective assessment of weakness, 2 scales of SGRQ questionnaire, all scales of SF-36 questionnaire, as well as reliable reduction of ammonia level by 18.26 mol/l, normal value of Number Connecting Test. Conclusion.Detection of hyperammoniemia in patients with COPD and obesity and its correction with LOLA seems rational in order to reduce toxic effects of ammonia on organs and systems in this category of patients.


2020 ◽  
Vol 7 (10) ◽  
pp. 1537
Author(s):  
Sriramchandra Rahul Pulavarty ◽  
Nagabhushana Midathala

Background: Posterior reversible encephalopathy syndrome is a neurological disorder which can present with sudden onset headache, visual disturbances, seizures and altered sensorium which is potentially reversible with early detection and treatment of the precipitating factor. The range of presentations is being constantly widened and this endeavour is a step towards understanding the wide array of presentation and primary etiology.Methods: This is a prospective observational study of 25 patients presenting to a tertiary care hospital with symptoms and imaging features suggestive of PRES. Thorough clinical examination and MRI brain were performed in all patients.Results: Out of the 25 patients, 18 (72%) were females and 7 (28%) were males. Most common symptom was headache (84%) followed by seizures (56%), nausea (40%), visual blurring (36%) and altered sensorium (20%). In patients presenting with seizure, 28.57% had recurrent seizures.The most common precipitating cause was postpartum state without hypertension (40%) followed by accelerated hypertension (28%), eclampsia (16%), chronic kidney disease (12%) and one patient of chronic severe anaemia had PRES following blood transfusion (4%). Most of the patients improved with no residual neurological deficit.Conclusions: Good neurological outcomes can be achieved by early diagnosis and appropriate imaging in patients with PRES. In pregnant and postpartum patients, PRES should be always considered even with normal blood pressure. Rapid correction of chronic severe anaemia is a rare but preventable cause of PRES.


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