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A case of bilateral inguinal hernia recurrence in infancy: investigations on collagen metabolism
1Department of Surgery, University Hospital Aachen, Germany. r.rosch@chir.rwth-aachen.de
Insights
Bilateral inguinal hernia recurrence in infants is rare. This study found no significant collagen abnormalities or altered matrix metalloproteinase 2 activity, suggesting connective tissue pathology is unlikely to explain recurrent hernias.
Area of Science:
- Pediatric Surgery
- Connective Tissue Diseases
- Biochemistry
Background:
- Recurrent inguinal hernias are uncommon in infants.
- A 3-month-old male infant presented with bilateral inguinal hernia recurrence.
- Altered collagen metabolism in hernia patients prompted investigation for connective tissue pathology.
Observation:
- Hernial sac tissue from the infant was compared to controls with primary inguinal hernias.
- Collagen types I and III distribution, and matrix metalloproteinase 2 (MMP-2) expression were analyzed.
- Fibroblast cultures were used to assess gene and protein expression of collagen and MMP-2.
Findings:
- No differences in collagen I/III ratios were observed between the recurrent hernia patient and controls.
- MMP-2 expression was lower in the recurrent hernia patient, but its activity was similar.
- Electron microscopy revealed no significant differences in fibroblast morphology.
Implications:
- A severe connective tissue pathology was not identified as the cause of inguinal hernia recurrence in this infant.
- The observed slight differences in MMP-2 expression warrant further investigation for a potential role in hernia genesis.
Background:
Recurrent inguinal hernias in early infancy are rare. We report on a case of a 3-month-old male infant suffering bilateral inguinal hernia recurrence (RINGH). Due to previous observations of an altered collagen metabolism in hernia patients, a severe connective-tissue pathology in the infant was hypothesised.
Methods:
Hernial sac tissue of the infant was analysed and compared to specimens from five children operated upon one-sided primary inguinal hernias (controls). In paraffin-embedded sections, we determined the distribution of collagen types I and III by crosspolarisation microscopy and the expression of matrix metalloproteinase 2 (MMP-2) by immunohistochemistry. In fibroblast cultures, expression of collagen types I and III and of MMP-2 was investigated by RT-PCR (real-time polymerase chain reaction) and zymography. Electron microscopical investigations were performed exemplarily in two fibroblast cultures to compare cell morphology.
Results:
No differences in collagen I/III ratios between RINGH and controls were found either on protein or on mRNA level. Immunohistochemical and RT-PCR analysis of MMP-2 showed a lowered expression in the RINGH patient, as compared to controls, whereas the gelatinolytic activity of MMP-2 did not differ between the groups. Electron microscopical investigations showed similar cell arrangement and morphology.
Conclusions:
To conclude, a marked biochemical correlate to a severe connective-tissue pathology in the infant suffering inguinal hernia recurrence could not be found. With regard to the slight differences in the expression of MMP-2, a possible role in the genesis of inguinal hernia recurrence cannot be ruled out.
