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Fulltext The role of serum insulin-like growth factor I (IGF-I) in neonatal outcome

Hayati AR, Cheah FC, Yong JF, Tan AE, Norizah WM

J Clin Pathol, 2004 Dec;57(12):1299-301.
PMID: 15563671

AIMS: To determine the role of serum insulin-like growth factor I (IGF-I) in predicting the occurrence of septal hypertrophic cardiomyopathy in infants of mothers with diabetes.
METHODS/MATERIALS: In this prospective study, 100 pregnant women (50 with diabetes and 50 controls), matched for age and race, were studied. One intrapartum blood sample was taken at 28 weeks of gestation from both groups of mothers and another sample at delivery. All samples were analysed for maternal IGF-I by an enzyme linked immunosorbent assay method. A chest radiograph and an electrocardiogram were performed on the babies of the mothers with diabetes within the first 24 hours of life. An echocardiogram was performed in the first 3 days of life to look for septal hypertrophy and to measure the myocardial thickness.
RESULTS: In the six cases of neonatal septal hypertrophic cardiomyopathy, all the mothers had greatly raised IGF-I concentrations of more than 400 ng/ml at the time of delivery compared with a mean (SD) of 302 (25) ng/ml in control mothers.
CONCLUSIONS: In the present study a crude analysis revealed that increased IGF-I concentrations correlate with neonatal septal hypertrophic cardiomyopathy.
Study site: Obstetric and gynaecology clinic, Pusat Perubatan Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia

Matched MeSH terms: Cardiomyopathy, Hypertrophic/etiology*
Hypertrophic obstructive cardiomyopathy: the mitral valve could be the key

Dulguerov F, Marcacci C, Alexandrescu C, Chan KM, Dreyfus GD

Eur J Cardiothorac Surg, 2016 Jul;50(1):61-5.
PMID: 26792931 DOI: 10.1093/ejcts/ezv473

OBJECTIVES: As we strongly believe that treating the mitral valve abnormalities is a key feature of hypertrophic obstructive cardiomyopathy (HOCM), we have systematically corrected both the anterior and posterior leaflet (PL) size and geometry. We have analysed our immediate results and at mid-term follow-up.
METHODS: From March 2010 until June 2015, 16 patients with HOCM underwent surgical correction of obstruction. The mean age was 51 years old (range, 32-72 years). All were symptomatic being New York Heart Association (NYHA) class 3 (n = 4) or 4 (n = 12). All had systolic anterior motion at echocardiogram with severe mitral regurgitation (MR). Intraventricular gradient preoperatively was 73.5 mmHg (range, 50-120 mmHg). All patients underwent a double-stage procedure: first septal resection through (i) the aortic valve and (ii) the detached anterior leaflet (AL) of the mitral valve and at second, mitral valve repair by (i) reducing PL height (leaflet resection or artificial neochordae) (ii) increasing AL height with pericardial patch.
RESULTS: There was no in-hospital or late death. All patients were Class 1 NYHA at latest follow-up. Control echocardiography showed no MR, mean rest intraventricular gradient was 15 mmHg (range, 9-18 mmHg).
CONCLUSIONS: Our good mid-term results support the concept that HOCM is not only a septal disease and that the mitral valve pathology is a key component that should be addressed. For most patients, the ideal surgical treatment should consist in a two-step procedure. It is even necessary to be studied whether treating the mitral valve alone could not suffice.

Matched MeSH terms: Cardiomyopathy, Hypertrophic/etiology*
Umbilical artery resistance index in diabetic pregnancies: the associations with fetal outcome and neonatal septal hypertrophic cardiomyopathy

Tan AE, Norizah WM, Rahman HA, Aziz BA, Cheah FC

J Obstet Gynaecol Res, 2005 Aug;31(4):296-301.
PMID: 16018775 DOI: 10.1111/j.1447-0756.2005.00291.x

Aim: To determine the incidence of an abnormal umbilical artery resistance index (UARI) in diabetic pregnancies and the relation to fetal outcome and the development of neonatal septal hypertrophic cardiomyopathy.

Methods: A case-control study with subjects comprising 50 randomly selected diabetic mothers and a matched control group of 50 non-diabetic pregnancies. Doppler studies of the UARI were carried out at least once per week, beginning from 36 weeks' gestation for both groups. Within 48 h post delivery, echocardiograms were carried out on the newborn infants to identify those with hypertrophic cardiomyopathy, particularly asymmetrical septal hypertrophy.

Results: The numbers of patients with abnormal UARI were similar in both the diabetic and control groups. A higher proportion of operative deliveries for intrapartum fetal distress was seen in patients with an abnormal UARI in the diabetic group. However, the groups did not differ in the numbers of infants who were small for gestational age, who had low Apgar scores or umbilical artery acidosis, and who required admission to the special care nursery. Six infants of diabetic mothers (12%) had septal hypertrophy, but none of these were associated with abnormal antenatal UARI.

Conclusion: Diabetic pregnancy is not associated with a significantly higher incidence of abnormal UARI on Doppler study than non-diabetic pregnancy. UARI is not a useful single indicator by which to predict subsequent fetal outcome or the development of neonatal septal hypertrophic cardiomyopathy in diabetic pregnancies.

Matched MeSH terms: Cardiomyopathy, Hypertrophic/etiology
Insulin-like growth factor-1 receptor expression in the placentae of diabetic and normal pregnancies

Hayati AR, Cheah FC, Tan AE, Tan GC

Early Hum Dev, 2007 Jan;83(1):41-6.
PMID: 16750336 DOI: 10.1016/j.earlhumdev.2006.04.002

BACKGROUND: Septal hypertrophic cardiomyopathy (sHCM) is a characteristic anomaly of the infant of diabetic mother (IDM). Insulin-like growth factor-1 (IGF-1) has been identified as a mediator of tissue overgrowth and we have previously shown that maternal IGF-1 levels were significantly elevated among neonates with asymmetrical sHCM. IGF-1 does not cross the placenta; it exerts physiologic action through binding to the IGF-1 receptor (IGF-1R). Localisation and expression of IGF-1R in term diabetic pregnancies are largely unclear. We have studied IGF-1R in the placentae of diabetic and normal pregnancies and this receptor expression in association with neonates with sHCM.
METHODS: IGF-1R localization and expression in the placentae of six diabetic pregnancies associated with neonatal sHCM were compared with six each of randomly selected diabetic and normal pregnancies without neonatal sHCM by immunohistochemistry. The staining for IGF-1R in the deciduas, cytotrophoblasts, syncytiotrophoblasts and villous endothelium for these 18 samples were assessed and scored by two pathologists who were blinded to the respective diagnoses.
RESULTS: Placental IGF-1R staining was negative in the villous endothelium for all three groups. IGF-1R staining was present in deciduas, cytotrophoblasts and syncytiotrophoblasts but the staining was weaker in the entire group of infants with sHCM compared to those without sHCM.
CONCLUSIONS: IGF-1R is localized in all cell types of the placenta except in villous endothelium. Weaker placental IGF-1R staining in the placentae of diabetic pregnancies associated with sHCM suggests reduced expression of IGF-1R. This may be a down-regulatory response to elevated maternal IGF with neonatal sHCM outcome.

Matched MeSH terms: Cardiomyopathy, Hypertrophic/etiology