Growth Hormone and Craniofacial Changes: Preliminary Data From Studies in Turner's Syndrome

PEDIATRICS ◽  
1999 ◽  
Vol 104 (Supplement_5) ◽  
pp. 1021-1024
Author(s):  
Kirt E. Simmons

Normal craniofacial and dental growth and development is dependent on growth hormone (GH) and insulin-like growth factor I (IGF-I). Deficiencies of either during childhood cause diminished growth of the maxilla and (to a greater degree) the mandible. Dental development/eruption also is compromised. Conversely, excessive GH/insulin-like growth factor I causes overgrowth, with the mandible again more affected than the maxilla. Replacement therapy in deficiency conditions generally normalizes craniofacial growth. Systemic GH also has been used in other disorders for which overt deficiency of GH has not been demonstrated. One such condition, Turner's syndrome, is now widely treated with GH. Although systemic GH in Turner's syndrome has been shown to positively affect stature, the effects on craniofacial growth and dental development/eruption are largely unknown. To explore these issues, standardized lateral radiographs of seven untreated patients with Turner's syndrome were analyzed and revealed hypoplasias of the cranial base, maxilla, and mandible. Dental development/eruption of patients with Turner's syndrome was found to be significantly advanced (by 0.63 years), relative to control subjects, in a separate study. Annual radiocephalometric measurements of 19 patients with Turner's syndrome treated with GH were compared with nonaffected control subjects over 1 year of treatment. Compared with age-matched historic control subjects, all maxillary—and most mandibular—growth measures were within 2 standard deviations of control. However, in our patients with Turner's syndrome, we found two measures of mandibular growth that deviated by more than 3 standard deviations from control. These data, although preliminary and only encompassing a short period, indicate that mandibular growth may be more affected than is maxillary growth by GH treatment and should be monitored over long-term-therapy.

1993 ◽  
Vol 129 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Klaas Hoogenberg ◽  
Wim I Sluiter ◽  
Robin PF Dullaart

Glomerular hyperfiltration is a characteristic feature of acromegaly but it is uncertain whether albuminuria is elevated in this disease. To investigate the role of abnormal growth hormone (GH) and insulin-like growth factor I (IGF-I) levels on urinary protein excretion, we measured the overnight urinary albumin excretion rate (UalbV) and creatinine clearance in 14 acromegalic patients with metabolically active disease (fasting GH > 5 μg/l and IGF-I > 2.2 kU/l), 8 GH-deficient patients and 20 control subjects. The UalbV was higher in the acromegalic patients (median 8.4 (range 4.2–68.2) μg/min) than in the GH-deficient patients (2.0(0.9–5.9) μg/min, p< 0.001) and control subjects (3.3 (1.0– 7.8) μg/min, p <0.01). Five acromegalic patients had UalbV levels above the normal upper normal limit of 10 μg/min. Only one patient with concomitant untreated hypertension had persistent microalbuminuria. Creatinine clearance also was higher in the acromegalic patients (p<0.05) and lower in the GH-deficient patients (p <0.05) than in the control subjects. In 11 of these acromegalic cases, the lowering of GH by 63% and of IGF-I by 48%, following treatment with the somatostatin analogue (N = 10) or spontaneous pituitary infarction (N=1), reduced the UalbV by 29% to 4.9 (3.1–45.2) μg/min (p<0.01). Among the acromegalic patients (25 observations), the UalbV was related to GH (r=0.61, p<0.01), IGF-I (r=0.57, p<0.01) and creatinine clearance (r=0.54, p<0.01). In conclusion, circulatory GH and IGF-I levels influence albuminuria. Because persistent microalbuminuria is uncommon in acromegaly, it is unlikely that GH elevation alone predisposes to clinically important glomerular damage.


1994 ◽  
Vol 35 (2) ◽  
pp. 218-222 ◽  
Author(s):  
Carol M Foster ◽  
Maria Borondy ◽  
Mara E Markovs ◽  
Nancy J Hopwood ◽  
Gad B Kletter ◽  
...  

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