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Table 6 Outcomes antileukotrienes animals

From: Antileukotrienes for the prevention and treatment of chronic lung disease in very preterm newborns: a systematic review

 

Chen 2018

Demir 2008

Jouvencel 2003

Kertesz 1992

Park 2011

Phillips 1995

Schreiber 1985

Xiao-Yan 2020

Mortality

Not reported

See note 1

See note 2

See note 3

See note 4

See note 5

Not reported

See note 6

Somatic growth

Not reported

See note 7

See note 8

Not reported

Not reported

Not reported

Not reported

Not reported

Lung volume to body weight

See note 9

Not reported

See note 10

See note 11

Not reported

Not reported

Not reported

Not reported

Lung histology

See note 12

See note 13

See note 14

Not reported

See note 15

See note 16

Not reported

Not reported

Inflammation markers for lungs

See note 17

Not reported

Not reported

See note 18

Not reported

See note 19

Not reported

Not reported

Lung injury

See note 20

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Airway hyperresponsiveness, fibrosis and smooth muscle actin expression

Not reported

See note 21

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Behavioral tests

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

See note 22

Pulmonary vascular resistance

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

See note 23

Not reported

  1. None of the included studies reported on the following outcomes: Harms, lung function, markers for apoptosis, Fulton index, arterial wall structure
  2. Schreiber 1987 and Cassin 1989 are not listed in the table as they reported none of the outcomes specified in our review
  3. Intervention: montelukast 0/10 combination: 0/6 Control: clarithromycin 0/8 pentoxifylline 0/8 placebo 0/6
  4. Intervention 0/12. Control 0/12
  5. Experiment 1: not reported Experiment 2: intervention: the percent mortality of the rabbits at any given number of hours of exposure to > 95% (%) (48 h: 0; 60 h: 43; 84 h: 65 108 h: 88 132 h: 88). Control: experiment 2: The percent mortality of the rabbits at any given number of hours of exposure to > 95% (%) (48 h: 0; 60 h: 41; 84 h: 59 108 h: 79 132 h: 100). There were no significant differences at any time between the ICI and the control group
  6. There was no mortality among study animals
  7. In the prevention study (normoxia), 3 out of 19 and 1 out of 6 pups died in the antileukotriene and control group, respectively. In the treatment study (hyperoxia), 3 out of 22 and 0 out of 6 pups died in the antileukotriene and control group, respectively
  8. This outcome cannot be calculated because “any loss of sample size due to deaths was made up for by random sampling
  9. Intervention: montelukast: Me 13 SD 0.6 g; combination: Me 10.1 SD 1.1 g;:control clarithromycin: Me 9.3 SD 0.7 g; pentoxifylline: Me 9.2 SD 3.2; placebo: Me 11.6 SD 2.2 g; montelukast vs placebo p = 0.07; montelukast vs. clarithromycin p < 0.0001; montelukast vs. pentoxifylline p = 0.0019; combination vs. placebo p = 0.1661
  10. Intervention: mean 28.8 SD 0.5(g) (not relevant); control: Mean 28.5 SD 0.4 g (not relevant)
  11. LW/BW intervention: Not reported, → lung weight/body weight (LW/BW): It is impossible to extract the data due to wrong values on y-axis)
  12. Intervention: Mean 5.3 SD 0.13(ml/100 g) (not relevant) control: Mean 5.15 SD 0.13 (not relevant)
  13. LW/BW intervention: not reported(Lung water expressed as lung wet weight to body weight ratios 0.1 µM/kg/h ICI 48 h: 1.3 SD ?; 72 h: 5,7 SD 0.2; 84 h: 7.6 SD 0,4 96 h: 7.5 SD 0.5; 1.0 µM/kg/h ICI 84 h: 7.5 SD ?; 96 h: 6,6 SD 0.3). Control: lung wet weight: body weight ratios began to increase at 72 h and continued to increase slowly after 84 and 96 h of hyperoxic exposure. No differences between intervention and control group (Fig. 3b) Control Lung water expressed as lung wet weight to body weight ratios control 48 h: 1.7 SD ?; 72 h: 5.4 SD 0.2; 84 h: 6.2 SD 0.4 96 h: 6.3 SD 0.5
  14. Intervention: mean linear intercept (MLI): 93 SD .5; radial alveolar count (RAC) mean: 4.28 SD 0.24—both p < 0.01 vs hyperoxia model. Control: mean linear intercept (MLI): 130 SD 7.7; radial alveolar count (RAC): 1.94 SD 0.1
  15. Intervention: alveolar surface area (%): group 3 montelukast Me 41.6 SD 4.8; group 5 combination: Me 64.0 SD 3; control: alveolar surface area (%); clarithromycin Me 50.9 SD 4.2; pentoxifylline Me 59.4 SD 6.8; placebo Me 50.2 SD 10.4. montelukast vs. placebo p = 0.0389 montelukast vs. clarithromycin p = 0.0005 montelukast vs. pentoxifylline p < 0.0001 combination vs. placebo p = 0.0093
  16. Intervention: surface density of parenchymal tissue mean 24.2 SD 1.2 (%) (not relevant); mean linear chord length mean 53.3 SD 1.3 (µm) (not relevant) septal attachments (/mm bronchi) mean 29.1 SD 1.0 (not relevant). Control: surface density of parenchymal tissue mean 22.8 SD 0.5 (not relevant); mean linear chord length mean 52.7 SD 1.3(not relevant) septal attachments (/mm bronchi) mean31.7 SD 0.9 (not relevant)
  17. Number of airspaces intervention: treatment group: (dose 40 mg/kg, P10-14): mean 20 SD 2. Prevention group (dose 40 mg/kg, p1–4): mean 19 SD 1 control treatment group (dose 0 mg/kg, P10–14): mean 11 SD ? prevention: (dose 0 mg/kg, p1–4): mean 6 SD 2
  18. 95% oxygen + treatment: airspace (%) (37.0 SD 6.0) neutrophils (No mm−2) (198 SD 10.9 (Different from 95% O, control, p < 0.05)) lung sections from pre-term guinea pig pups. 21% oxygen + treatment: airspace (%) (43.5 SD 3.5) neutrophils (No mm2) (108 SD 8.5) lung sections from pre-term guinea pig pup
  19. Intervention: relative TNF-α mRNA level mean: 2.0 SD 0.15; relative IL-6 mRNA level mean: 1.7 SD 0.06; relative IL-1β mRNA level: 1.9 SD 0.12; [not sure about p value, in the text: "Montelukast treatment significantly reduced the levels of TNF-a, IL-6, and IL-1b in the lung tissues of the BPD mice. control: relative TNF-α mRNA level mean: 3.3 SD 0.1; relative IL-6 mRNA level mean: 3.5 SD 0.2; relative IL-1β mRNA level mean: 2.9 SD 0.1
  20. Intervention: Dose 0.1 μM/kg/h: Total protein recovered from BAL mean (µg/ml) (48 h and 72 h: 90 SD 20; 84 h: 250 SD 120; 96 h: 330 SD 40); PMNS represented as a percentage of the total (48 h: 0; 72 h: 1,3 SE 7; 84 h: 10 SE 5; 96 h: 18 SE 5) white cells recovered from BAL mean (%); PMNs, represented as the absolute number recovered from BAL of the left lung (× 100,000) (48 h and 72 h: 0.5 SE 0.2; 84 h: 2,4 SE 0.3 96 h: 2.9 SE 0.3); 6-Keto-PGF 1 alfa the stable metabolite of PGI, in pg/ml (48 h: 71 SE no info; 72 h: 54 SE 28; 84 h: 144 SE 50; 96 h: 347 SE 463); TXB, the stable metabolite of TXA, in pg/ml mean (48 h: 115 SE no info; 72 h: 81 SE 19; 84 h: 241 SE 121; 96 h: 207 SE 22). Dose 1.0 uM/kg/h: total protein recovered from BAL mean (µg/ml) (84 h: 475 SD 112; 96 h: 416 SD 56); PMNS represented as a percentage of the total (48 h: 0; 72 h: no info; 84 h: 20 SE 4; 96 h: 14 SE 5) white cells recovered from BAL mean (%); PMNs, represented as the absolute number recovered from BAL of the left lung (× 100,000) (48 h and 72 h: no info; 84 h: 2,9 SE 0.3 96 h: 2.1 SE 0.); 6-Keto-PGF, the stable metabolite of PGI, in pg/ml (48 h: no info; 72 h: no info; 84 h: 348 SE 32; 96 h: 315 SE 32); TXB, the stable metabolite of TXA, in pg/ml mean (48 h: no info; 72 h: no info; 84 h: 211 SE 19; 96 h: 259 SE 37)
  21. Control: total protein recovered from BAL mean (µg/ml) (48 h and 72 h: 90 SD 20; 84 h: 392 SD 61; 96 h: 420 SD 56) PMNS represented as a percentage of the total (48 h: 0; 72 h: 1,3 SE 8; 84 h: 22 SE 5; 96 h: 21 SE 4) white cells recovered from BAL mean (%); PMNs, represented as the absolute number recovered from BAL of the left lung (× 100 000) (48 h and 72 h: 0.5 SE 0.2; 84 h: 3,4 SE 0,3 96 h: 3,5 SE 0,2); 6-Keto-PGF, the stable metabolite of PGI, in (48 h: 71 SE no info; 72 h: 54 SE 28; 84 h: 222 SE 32; 96 h: 265 SE 44) TXB, the stable metabolite of TXA, in pg/ml mean (48 h: 115 SE no info; 72 h: 81 SE 19; 84 h: 241 SE 121; 96 h: 207 SE 22) pg/ml
  22. 95% oxygen + treatment: neutrophil and eosinophil numbers and protein concentration in bronchoalveolar lavage fluid (BALF) neutrophils (10 4 ml-’ BALF) 3.0: 1.85 SD 0.79 (Different from equivalent vehicle control, PcO.05.)) eosinophils (10 6 ml -’ BALF) 3,0: 0.88 SD 0.37 protein (mg ml -’ BALF) 3,0: 0.28 SD 0.127). 21% oxygen + treatment: neutrophil and eosinophil numbers and protein concentration in bronchoalveolar lavage fluid (BALF) neutrophils(10 4 ml-’ BALF) 3,0: 1.45 SD 1.56 eosinophils (10 6 ml -’ BALF) 3.0: 0.94 SD 0.31(Different from equivalent vehicle control, PcO.05.) protein (mg ml -’ BALF)3.0: 0.27 SD 0.08)
  23. Intervention: oxidative stress malondialdehyde 1.4 +—0.1 mcmol/g (mean, sd); SOD superoxide dismutase 22.0 +—1 IU/mg (mean, sd). Control: oxidative stress malondialdehyde 1.9 +—0.05 mcmol/g (mean, sd); SOD superoxide dismutase 16.5 + 1 IU/mg (mean, sd)
  24. Degree of fibrosis absent /mild /moderate /marked Intervention: group 3 montelukast 0/1/6/3 group 5 combination: 4/2/0/0. Control: clarithromycin 0/1/3/4 pentoxifylline 2/2/4/0 placebo0/2/3/1. Actin score (density x intensity) Intervention: group 3 montelukast: 5 (2–9) group 5 combination: 0 (0–1) Control: clarithromycin 7.5 (2–9) pentoxifylline 1.5 (0–6) placebo 7 (2–12)
  25. Compared with the PVL group, the escape latency of the rats in the Pran group was shortened (p < 0.05) (Table 2). On the 5th day of the experiment, there was a statistically significant difference in the number of times the rats in each group crossed the platform (F = 12.59, p < 0.001). Compared with the PVL group, the number of times (1.86 ± 0.23) of rats in the Pran group crossed the platform increased (p < 0.05)
  26. Intervention: me 44.0 SD 7.0 in mmHg 1-1 min−1 kg−1. Control: me 70.3 SD 15.5 (p < 0.05 vs hypoxia + FPL 57,231) in mmHg1-1 min−1 kg−1 p = 0.0086
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Respiratory Research

ISSN: 1465-993X

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