Pituitary Magnetic Resonance Imaging in Idiopathic and Genetic Growth Hormone Deficiency

Mohamad Maghnie, Sandro Loche and Marco Cappa

Department of Pediatrics (M.M.), Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Matteo, University of Pavia, 27100 Pavia, Italy; Servizio di Endocrinologia Pediatrica (S.L.), Ospedale Regionale per le Microcitemie, 09121 Cagliari, Italy; Unità Operativa di Auxologia (M.C.), Ospedale Bambino Gesù, IRCCS, Palidoro, 00050 Rome, Italy

Address correspondence to: Mohamad Maghnie, M.D., Ph.D., Department of Pediatrics, IRCCS Policlinico S. Matteo, Viale Golgi 2, 27100 Pavia, Italy. E-mail: maghnie{at}smatteo.pv.it.

To the editor:

We read with great interest the paper by Osorio et al. (1). The authors have carefully reported pituitary function, gene analysis, and magnetic resonance imaging (MRI) findings in a large cohort of patients with GH deficiency (GHD). Most patients had combined hormone deficiency (CPHD). In addition, the authors have reviewed the currently available data regarding the role of MRI in the work-up of patients with hypo-pituitarism. These findings have important clinical implications for patients with GHD of different etiologies. However, we wish to make some comments.

In the study, 14 patients, all with a high degree of consanguinity, showed molecular defects in the GH-1, GHRH-R, PIT-1, and PROP-1 genes. Fifty-three patients, 17 with isolated GHD and 36 with CPHD, had ectopic posterior pituitary at MRI, and only 9 patients had no evidence of genetic or pituitary abnormalities (1). GHD is heterogeneous, and often the cause is not recognized. However, the cause of hypopituitarism was identified in the majority of the patients in the study, thus indicating a possible bias in patient selection. Are the patients all consecutive from the time of the diagnosis? Were they previously selected on the basis of the MRI findings, or rather on the severity of GH deficiency? Several studies have found that between 40% and 70% of children diagnosed with GHD normalized their GH secretion after growth completion (2), suggesting that a high proportion of patients with childhood-onset GHD may have transitory GHD, or they just do not have this condition (3, 4). Our data suggest that GHD is more severe and more frequently associated with multiple pituitary hormone deficiencies in patients with ectopic posterior pituitary, indicating that the abnormal MRI finding is highly predictive of severe GHD (2).

There is considerable evidence that GH responses to stimulation in patients with hypothalamic-pituitary abnormalities vary according to the particular secretagogue chosen, as well as to age and time of evaluation (5). The distinction between pituitary or hypothalamic dysfunction in patients with CPHD and ectopic posterior pituitary cannot rely solely on the results of GH and TRH stimulation tests. It is our opinion that the complexity of the defect depends on multiple factors, including the presence or absence of the vascular component of the pituitary stalk (observed after contrast medium injection), pituitary size, time of evaluation (progressive impairment of somatotrope function), and the number of hormone deficits (5). Eventual perinatal adverse events could further affect the already altered pituitary anatomy and function, thus indicating that both hypothalamic and pituitary defects may coexist. In this regard, what is the authors’ definition of hypothalamic or pituitary defect in patients with anterior pituitary hypoplasia and ectopic posterior pituitary? What is the contribution of the morphological abnormality of the anterior pituitary gland (hypoplasia) to the diagnosis of hypopituitarism?

The prevalence of hypothalamic-pituitary abnormalities in idi-opathic GHD and the clear site of damage are still unknown, and thus far no conclusions can be drawn on the prevalence of ectopic posterior pituitary in patients with GHD of childhood-onset. Multicenter studies involving a large number of patients with idiopathic GHD are needed to elucidate the frequency of such MRI abnormalities.

Received November 25, 2002.

References

  1. Osorio MGF, Marui S, Jorge AAL, Latronico AC, Lo LSS, Leite CC, Estefan V, Mendonca BB, Arnhold IJP 2002 Pituitary magnetic resonance imaging and function in patients with growth hormone deficiency with and without mutations in GHRH-R, GH-1, or prop-1 genes. J Clin Endocrinol Metab 87:5076–5084[Abstract/Free Full Text]
  2. Maghnie M, Strigazzi C, Tinelli C, Autelli M, Cisternino M, Loche S, Severi F 1999 Growth hormone (GH) deficiency (GHD) of childhood onset: reassessment of GH status and evaluation of the predictive criteria for permanent GHD in young adults. J Clin Endocrinol Metab 84:1324–1328[Abstract/Free Full Text]
  3. Loche S, Bizzarri C, Maghnie M, Faedda A, Tzialla C, Autelli M, Casini MR, Cappa M 2002 Results of early re-evaluation of growth hormone (GH) secretion in short children with apparent GH deficiency. J Pediatr 140:445–449[CrossRef][Medline]
  4. Carel JC, Ecosse E, Nicolino M, Tauber M, Leger J, Cabrol S, Bastié-Sigeac I, Chaussain JL, Coste J 2002 Adult height after long term treatment with recombinant growth hormone for idiopathic growth hormone deficiency: observational follow-up of the French population based registry. BMJ 325:70–76[Abstract/Free Full Text]
  5. Maghnie M, Salati B, Bianchi S, Rallo M, Tinelli C, Autelli M, Aimaretti GL, Ghigo E 2001 Relationship between the morphological evaluation of the pituitary and the growth hormone (GH) response to GH-releasing hormone plus arginine in children and adults with congenital hypopituitarism. J Clin Endocrinol Metab 86:1574–1579[Abstract/Free Full Text]




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