The Diagnosis and Treatment of Childhood and Adolescent Growth Hormone Deficiency—Consensus or Confusion?

The consensus guidelines of the Growth Hormone Research Society (GRS) for the diagnosis and treatment of childhood and adolescent GH deficiency, which appear in this issue of the journal (1), are the latest in a series of attempts to refine these components of patient management (2‐ 4). The publication of these, or any other, guidelines raises questions on several levels. First, are the guidelines, as presented, helpful to the clinician? In addition, what is the overall usefulness of consensus guidelines? The answer to the first question is clearly positive. However, there are several features, both general and specific, that may limit the application of the GRS recommendations. The lack of supporting literature, while understandable, greatly lessens the usefulness of the overall presentation. At the very least, the inclusion of references to various pertinent reviews would have strengthened the recommendations. They would have been less opinion-based and more based on the available evidence. Clearly, the report was written by a committee with an attempt to represent all views. A number of contentious points that have sparked vigorous discussion at scientific meetings over the past 30 ‐35 yr are glossed over. Although this makes for a stronger consensus, legitimate competing viewpoints may be lost to the ultimate detriment of patient care. Throughout the presentation, height and height velocity are expressed as sd and sd score. Whereas this is politically correct and well and good for investigators and for most clinicians, it is not what patients and parents readily understand. The use of height percentiles and growth velocity expressed as cm/yr still deserves a place in the definition of criteria for the evaluation of growth and the response to GH therapy. Reference to normative data, despite its imperfections, would have been helpful. Several additional specifics are deserving of comment. Listing the more common chronic systemic illnesses that may lead to growth failure would make it more likely that the laboratory tests that would uncover these conditions would be part of the initial patient evaluation. These would include chronic renal failure, renal tubular acidosis, inflammatory bowel disease, celiac disease, and liver disease. Because prolonged neonatal jaundice due to deficient conjugation of bilirubin is extremely common and is not a hallmark of GH deficiency, prolonged elevation of direct bilirubin should be specified. Congenital nystagmus is another neonatal physical finding that may indicate GH deficiency and that deserves inclusion. As stated in the guidelines, the preferable imaging technique to detect underlying intracranial pathology is magnetic resonance imaging. This should be carried out both with and without contrast. Indeed, the guidelines recommend this procedure for all patients shown to have GH deficiency. This approach is far superior to computerized tomography and infinitely superior to plane skill films. The latter should probably be abandoned as simply providing an unnecessary exposure to radiation rather than tolerated as it is in the guidelines. Listing the other causes of low insulin-like growth factor I, particularly pointing out the effect of malnutrition, would add to the suggested interpretation of low insulin-like growth factor concentrations. Measurement of GH in the presence of neonatal or infantile hypoglycemia should be carried out as part of the so-called “critical sample” analysis. In general, this should be done as an initial step in the evaluation of hypoglycemia rather than after the elimination of metabolic disease from consideration.