This is the most important part of the Letter to the Editor that we sent (without references). If you have additional problems during experiments, new ideas for experiments or additional methodological problems, please state.
1. Man is unique in his bipedal stance and no animal model can precisely replicate the complex anatomic and structural forces placed on the human inguinal canal.
2. Ordinarily, spermatic vein testosterone levels are markedly higher than peripheral blood levels. One cannot completely exclude the possibility of sampling error despite samples being obtained as close to the gonad as possible to avoid any dilutional effects from the extensive collateral flow around the testes.
3. Subtle changes in number of Leydig cells might be difficult to quantify with light microscopy alone. Ordinarily, Leydig cell function is well preserved despite spermatogenic cell dysfunction or loss. Whether these findings represent an early or progressive defect remains unknown.
4. The vas sits between the external and internal spermatic fascia and involvement may depend on the amount of cremaster muscle or the presence of a cord lipoma, both of which can serve to buffer the vas from involvement by the mesh reaction. In addition, the vas is sometimes found in intimate association with the hernia sac and may require careful and complete dissection away from all surrounding structures leaving it with little adjacent tissue.
5. The same hernia classification system should be used for the comparison of the preoperative and postoperative results. Most studies have hernia-dependent exclusion criteria - bilateral, relapsed, femoral, incarcerated or strangulated hernias, and systemic disease exclusion criteria - cirrhosis, heart deficiency, diabetes mellitus hypertension, collagen vascular diseases.
6. Giant scrotal hernias or large hernias have predisposition for testicular atrophy but are not suitable for laparoscopic hernioplasty by many institutions. Therefore, in these most important groups comparison of methods is not possible.
7. Difficulty in comparing the results of different studies due to modifications of mesh composition, mesh placement technique and mesh size in open repair, slit mesh or non-slit mesh methods of TEP repair, performance by different surgeons.
8. Direct and indirect thermal injury and other types of direct damage to the vas deference and surrounding vascularization mostly not recorded in medical records. This significant underestimation can falsely indicate the mesh as the main cause of partial/complete vasal damage/obstruction.
9. Tremendous variability with adhesion formation and tissue fibroblastic responses to mesh (patient heterogeneity)
10. Tremendous time variability (3 days to 2 years) of postoperative investigations of testicular function/perfusion changes and vasal obstruction.
11. The vast majority of testicular nerves are sympathetic axons with vasomotor function and innervate the small vessels supplying cluster of Leydig cells and regulate testicular LH receptors and blood flow. Therefore, interruption or damage of innervation, not perfusion could cause changes in hormone production and blood flow.
12. Lichtenstein repair, contrary to the TAPP procedure, induced a higher (probably reactive) perfusion at the groin on a pig model, even 6 months after operation.
13. Ultrasonographic examination should be performed in the supine position, and the patients holding the penis suprapubically in a temperature controlled room after resting for at least 10 minutes.
14. There are no studies about the long-term potential effect of mesh placement on testicular function. RI may be a useful marker in research going forward in the male population subjected to mesh repairs at a young age.
15. Many animal studies have small number of animal groups for the power of statistical analysis.
extremly importsnt question we had a master thesis about the open hernia fixation and testicular function and now we have another master thesis on laparoscopic mesh repair and testicular function .if you are asking for extreme fixation of all variants in order to proper elicit the effect of the mesh on the testicular function tha answer is definitely no one can because you must have the sme preoperative testicular function in the tested and control groupbefore mesh fixation regarding testicular size ,testicular blood flow and veinous drainage (varicocele or not and what degree if it is present) same level of spermatogenesis and same level of endocrine function .then you should fix mesh type ,method of fixation ,the area between the mesh and the cord,fix single surgeon and have exactly the same criteria of the sudieded hernia in all the patient groupr egarding type ,size,also the history or whether ther was complication or not likr irreducability or not and forced reduction or not,and after fixing all these parameters which i think no one can do you have to know for sure that the degree of fibrosis induced by the mesh is the same inall patients then you have to do your investigation after 2 years to all patients and control group
Maybe some intermediate layer can be introduced to minimize contact of the deferential duct and the mesh - like oxidized cellulose, tachosil, etc.
presently what we know that all meshes do produce fibosis and adhesive barriers like ORC,TACHOCILor Seprafilm will not protect.
Dear Prasanna do you have any references for this statements. Thank you in advance
- Badges
- Science topic
- Similar topics
- Social Psychology
- Attitude