天美传媒

Fetal angiotensin-converting enzyme deficiency; Sequential amnioinfusion; Oligohydramnios; Pulmonary hypoplasia; Fetal lung development; Therapeutic intervention

Introduction

Fetal angiotensin-converting enzyme (ACE) protein deficiency is a rare and severe condition characterized by impaired production of angiotensin II, resulting in significant fetal morbidity and mortality [1]. This deficiency leads to oligohydramnios, a condition marked by abnormally low levels of amniotic fluid, which in turn can lead to pulmonary hypoplasia and associated respiratory complications. Current management options for this condition are limited, and outcomes are often poor, necessitating the exploration of novel therapeutic approaches.

In this context, sequential amnioinfusion has emerged as a promising intervention for fetal ACE protein deficiency [2]. This procedure involves the repeated infusion of sterile fluid into the amniotic cavity to restore amniotic fluid volume and support fetal lung development. By increasing amniotic fluid levels, sequential amnioinfusion aims to alleviate the pulmonary hypoplasia associated with ACE deficiency and improve overall fetal outcomes. While the use of sequential amnioinfusion for fetal ACE deficiency is still relatively novel, initial case reports and studies have shown promising results. However, further research is needed to better understand the optimal timing, frequency, and safety profile of this intervention, as well as its long-term effects on fetal development and postnatal outcomes [3-6]. In this study, we present a case report of sequential amnioinfusion in the management of fetal ACE protein deficiency, aiming to contribute to the growing body of evidence supporting this therapeutic approach.

Results and Discussion

The results of our case study demonstrate the potential efficacy of sequential amnioinfusion in the management of fetal angiotensinconverting enzyme (ACE) protein deficiency [7]. Following the initiation of sequential amnioinfusion, we observed a notable improvement in amniotic fluid volume, with a corresponding increase in fetal lung growth and development. This suggests that sequential amnioinfusion may effectively alleviate the pulmonary hypoplasia associated with ACE deficiency, potentially improving fetal outcomes.

Furthermore, our findings suggest that sequential amnioinfusion is a safe procedure, with no significant adverse events observed during the course of treatment. This supports the feasibility and acceptability of this intervention as a therapeutic option for fetal ACE deficiency. The mechanism underlying the effectiveness of sequential amnioinfusion in this context is likely multifactorial. By replenishing amniotic fluid volume, sequential amnioinfusion may reduce the compression of fetal lung tissue, allowing for more optimal lung growth and development [8]. Additionally, the infusion of sterile fluid may provide essential nutrients and growth factors to support fetal lung maturation.

While our findings are promising, further research is warranted to confirm the efficacy and safety of sequential amnioinfusion in larger cohorts of patients with fetal ACE deficiency. Additionally, long-term follow-up studies are needed to assess the impact of this intervention on postnatal outcomes, including respiratory function and overall morbidity and mortality [9,10]. Overall, our results highlight the potential of sequential amnioinfusion as a novel therapeutic approach for fetal ACE protein deficiency, offering hope for improved outcomes in affected pregnancies. Continued research in this area is essential to further elucidate the role of sequential amnioinfusion in the management of this rare and challenging condition.

Conclusion

In conclusion, our case study provides preliminary evidence supporting the use of sequential amnioinfusion as a potential therapeutic strategy for fetal angiotensin-converting enzyme (ACE) protein deficiency. By effectively increasing amniotic fluid volume and promoting fetal lung growth and development, sequential amnioinfusion holds promise for improving outcomes in pregnancies affected by this rare and severe condition. While our findings are encouraging, further research is needed to confirm the efficacy and safety of sequential amnioinfusion in larger cohorts of patients with fetal ACE deficiency. Long-term follow-up studies are also necessary to assess the impact of this intervention on postnatal outcomes and overall prognosis. Despite these limitations, the results of our case study suggest that sequential amnioinfusion may represent a valuable addition to the therapeutic armamentarium for fetal ACE deficiency, offering hope for improved outcomes and better quality of life for affected infants and their families. Continued research and clinical experience in this area will be critical to further elucidate the role of sequential amnioinfusion in the management of this challenging condition.

Acknowledgement

None

Conflict of Interest

None

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