Tuberculous Scleritis and Multidrug Resistance

Agarwal, Mamta; Patnaik, Gazal; Agarwal, Shweta; Iyer, Geetha; Anand, Appakkudal R.; Ar, Gayathri; Biswas, Jyotirmay; Zierhut, Manfred

doi:10.1080/09273948.2020.1853176

Cited by 5 publications

(2 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In particular, mitochondrial function in type II alveolar epithelial cells (AECs) is critical to produce acetyl-CoA for de novo fatty acid (FA) synthesis, supporting the generation of phospholipid-rich surfactant. Metabolic alterations in FA synthesis and phospholipid production reflects lung mitochondrial stress, and disruption has profound pathogenic effects in deterioration of lung function and host defense against pathogens [21][22][23][24][25]. In fact, several mitochondrial derived damage-associated molecular patterns (DAMPs) cause pathological inflammation and irreversible lung injury, one of which is mitochondrial cardiolipins [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung

Chandler

Park

et al. 2019

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Cadmium (Cd) causes acute and chronic lung toxicities at occupational exposure levels, yet the impacts of Cd exposure at low levels through dietary intake remain largely uncharacterized. Health concerns arise because humans do not have an effective Cd elimination mechanism, resulting in a long (10-to 35-y) biological half-life. Previous studies showed increased mitochondrial oxidative stress and cell death by Cd yet the details of mitochondrial alterations by low levels of Cd remain unexplored. In the current study, we examined the impacts of Cd burden at a low environmental level on lung metabolome, redox proteome, and inflammation in mice given Cd at low levels by drinking water (0, 0.2, 0.6 and 2.0 mg Cd/L) for 16 weeks. The results showed that mice accumulated lung Cd comparable to non-smoking humans and showed inflammation in lung by histopathology at 2 mg Cd/L. The results of high resolution metabolomics combined with bioinformatics showed that mice treated with 2 mg Cd/L increased levels of lipids in the lung, accompanied by disruption in mitochondrial energy metabolism. In addition, targeted metabolomic analysis showed that these mice had increased accumulation of mitochondrial carnitine and citric acid cycle intermediates. The results of redox proteomics showed that Cd at 2 mg/L stimulated oxidation of isocitrate dehydrogenase, malate dehydrogenase and ATP synthase. Taken together, the results showed impaired mitochondrial function and accumulation of lipids in the lung with a Cd dose response relevant to non-smokers without occupational exposures. These findings suggest that dietary Cd intake could be an important variable contributing to human pulmonary disorders.

show abstract

Section: Introductionmentioning

confidence: 99%

Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung

Chandler

Park

et al. 2019

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…The diagnosis of tuberculous scleritis is a clinical challenge due to the varied presentations, it is often presumptive based on a bundle of arguments includinga rigorous anamnesis, guiding clinical signs, positive tuberculin skin test (> 15 mm or more of induration) or QTB, evidence of healed or active pulmonary or extrapulmonary tuberculosis, exclusion of other causes of scleritis, and a favorable therapeutic response to anti-tuberculosis treatment. Definitive diagnosis is based on the detection of acid-fast bacilli on smears, growth on culture medium, demonstration of the Mycobacterium tuberculosis genome by PCR and histopathological evidence; The majority of the cases described occur in isolation without any detectable systemic involvement of tuberculosis [5].…”

Section: Discussion:-mentioning

confidence: 99%

Case Report: Tuberculous Scleritis a Challenging Diagnostic

Ouail¹,

Soukaina²,

Bennis³

et al. 2022

IJAR

View full text Add to dashboard Cite

Scleritis is a severe painful inflammatory process localized in the sclera. Scleritis may be the revealer of many systemic diseases so that it is important to exclude multisystem disease. We present a case of non-necrotizing antero-posterior scleritis revealing a systemic tuberculosis which is an uncommon manifestation of tuberculosis. Diagnosing and managing the disease can be difficult. However, a good anamnesis, a careful clinical evaluation, an adequate interpretation of the investigations and an appropriate management allow a good prognosis.

show abstract