Ureteral stricture rate after endoscopic treatments for urolithiasis and related risk factors: systematic review and meta-analysis.

PURPOSE: We aimed to accurately determine ureteral stricture (US) rates following urolithiasis treatments and their related risk factors. METHODS: We conducted a systematic review and meta-analysis following the PRISMA guidelines using databases from inception to November 2023. Studies were deemed eligible for analysis if they included ≥ 18 years old patients with urinary lithiasis (Patients) who were subjected to endoscopic treatment (Intervention) with ureteroscopy (URS), percutaneous nephrolithotomy (PCNL), or shock wave lithotripsy (SWL) (Comparator) to assess the incidence of US (Outcome) in prospective and retrospective studies (Study design). RESULTS: A total of 43 studies were included. The pooled US rate was 1.3% post-SWL and 2.1% post-PCNL. The pooled rate of US post-URS was 1.9% but raised to 2.7% considering the last five years' studies and 4.9% if the stone was impacted. Moreover, the pooled US rate differed if follow-ups were under or over six months. Patients with proximal ureteral stone, preoperative hydronephrosis, intraoperative ureteral perforation, and impacted stones showed higher US risk post-endoscopic intervention with odds ratio of 1.6 (P = 0.05), 2.6 (P = 0.009), 7.1 (P < 0.001), and 7.47 (P = 0.003), respectively. CONCLUSIONS: The overall US rate ranges from 0.3 to 4.9%, with an increasing trend in the last few years. It is influenced by type of treatment, stone location and impaction, preoperative hydronephrosis and intraoperative perforation. Future standardized reporting and prospective and more extended follow-up studies might contribute to a better understanding of US risks related to calculi treatment.

Insulin Growth Factor-I in Protein-Energy Malnutrition during Rehabilitation in Two Nutritional Rehabilitation Centres in Burkina Faso.

Objective. To investigate the relationship between IGF-I and the nutritional status of West-African children hospitalised for nutritional rehabilitation. Patients and methods. A cohort study was performed in two centres for nutritional rehabilitation and education (CREN) in Burkina Faso. Children were followed and the anthropometric data as well as the capillary blood samples were taken on the 7th and on the 14th days after their admission. IGF-I levels were determined from dried blood spots on filter paper on IGF-I RIA, after separation of the IGF-I from its binding proteins, using Sep-Pak chromatography. Results. A total of 59 children was included in the cohort. The IGF-I mean geometric values (SD) were 6.3 (1.4) mug/L on admission, 8.6 (1.8) mug/L at day 7 and 13.6 (2.0) mug/L at day 14. The differences between these values were statistically significant (P < .001). There is a significant correlation between the changes of IGF-I with the change of weight for height Z-score (P = .01). Conclusion. These results suggest that IGF-I can be considered as a potential marker to follow the nutritional status of children admitted in hospital for protein and energy malnutrition.

Reference values of IGF-I in children from birth to 5 years of age, in Burkina Faso, using blood samples on filter paper.

OBJECTIVES: The aims of this study were to validate the use of filter paper to measure insulin-like growth factor-I (IGF-I) and to establish normal levels of IGF-I in children appearing healthy, from birth to 5 years of age in an African population. METHODS: We determined IGF-I from blood collected on filter paper. We validated this method by comparing the IGF-I values from dried blood spots on filter paper (kept at 4 degrees C and ambient temperature) and from serum among 13 children under 5. IGF-I were measured by the classical IGF-I RIA, after separation of the IGF-I from its binding proteins, using Sep-Pak chromatography. To establish normal levels of IGF-I, we conducted a cross-sectional study and collected blood samples with filter paper among 360 children in Ouagadougou (Burkina Faso). RESULTS: IGF-I determined from dried blood spots on filter paper were in good agreement with IGF-I levels obtained from blood serum, whether the filter papers were kept at 4 degrees C or at ambient temperature. The results of IGF-I-levels in apparently healthy children showed that geometric mean IGF-I ranged from 27 microg/l in boys younger than five months to 31 microg/l in 5-year-old boys. In girls, mean IGF-I ranged from 29 microg/l for girls younger than five months to 45 microg/l at the age of 5. From birth to 24 months, IGF-I decreased by 0.32+/-0.08 microg/l/month in boys and by 0.27+/-0.06 microg/l/month in girls and these decreases were not significantly different (p=0.95). After the age of 24 months, there was an increase in IGF-I of 4.9+/-1.3 microg/l/year in boys and of 8.4+/-0.8 microg/l/year in girls. This increase was indeed significantly different (p<0.001). CONCLUSIONS: Reference values of IGF-I for African boys and girls were determined. They will be used for endocrine evaluations and nutritional monitoring.

Insulin-like growth factor-I gene transfer by electroporation prevents skeletal muscle atrophy in glucocorticoid-treated rats.

Catabolic states caused by injury are characterized by a loss of skeletal muscle. The anabolic action of IGF-I on muscle and the reduction of its muscle content in response to injury suggest that restoration of muscle IGF-I content might prevent skeletal muscle loss caused by injury. We investigated whether local overexpression of IGF-I protein by gene transfer could prevent skeletal muscle atrophy induced by glucocorticoids, a crucial mediator of muscle atrophy in catabolic states. Localized overexpression of IGF-I in tibialis anterior (TA) muscle was performed by injection of IGF-I cDNA followed by electroporation 3 d before starting dexamethasone injections (0.1 mg/kg.d sc). A control plasmid was electroporated in the contralateral TA muscle. Dexamethasone induced atrophy of the TA muscle as illustrated by reduction in muscle mass (403 +/- 11 vs. 461 +/- 19 mg, P < 0.05) and fiber cross-sectional area (1759 +/- 131 vs. 2517 +/- 93 mum(2), P < 0.05). This muscle atrophy was paralleled by a decrease in the IGF-I muscle content (7.2 +/- 0.9 vs. 15.7 +/- 1.4 ng/g of muscle, P < 0.001). As the result of IGF-I gene transfer, the IGF-I muscle content increased 2-fold (15.8 +/- 1.2 vs. 7.2 +/- 0.9 ng/g of muscle, P < 0.001). In addition, the muscle mass (437 +/- 8 vs. 403 +/- 11 mg, P < 0.01) and the fiber cross-sectional area (2269 +/- 129 vs. 1759 +/- 131 mum(2), P < 0.05) were increased in the TA muscle electroporated with IGF-I DNA, compared with the contralateral muscle electroporated with a control plasmid. Our results show therefore that IGF-I gene transfer by electroporation prevents muscle atrophy in glucocorticoid-treated rats. Our observation supports the important role of decreased muscle IGF-I in the muscle atrophy caused by glucocorticoids.