scholarly journals Pituitary Macroadenoma and Severe Hypothyroidism: The Link between Brain Imaging and Thyroid Function

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Silvia Ciancia ◽  
Silvia Cesari ◽  
Barbara Predieri ◽  
Sergio Bernasconi ◽  
Lorenzo Iughetti

In case of primary hypothyroidism, reactive pituitary hyperplasia can manifest as pituitary (pseudo) macroadenoma. We report the case of a 12-year-old boy who was evaluated for impaired growth velocity and increased body weight. Because of low insulin-like growth factor 1 levels and poor response to the growth hormone stimulation test, brain magnetic resonance imaging was performed and a pituitary macroadenoma was found. Treatment with levothyroxine was started, and thyroid function was evaluated approximately every 40 days to titrate the dosage. After few months of therapy, the size of the macroadenoma decreased and growth hormone secretion normalized. The pituitary returned to normal size in approximately 5 years. The boy went through puberty spontaneously and reached a normal adult height. In a patient affected by primary hypothyroidism, reactive pituitary hyperplasia can cause growth hormone deficiency; however, growth hormone secretion usually normalizes after starting levothyroxine treatment. Pituitary macroadenoma can be difficult to distinguish from severe pituitary hyperplasia; however, pituitary macroadenomas are rare in childhood, and our clinical case underlines how the hormonal evaluation is essential to achieve a correct diagnosis and prevent unnecessary surgery in a context of pituitary mass.

Author(s):  
Marion Kessler ◽  
Michael Tenner ◽  
Michael Frey ◽  
Richard Noto

AbstractBackground:The objective of the study was to describe the pituitary volume (PV) in pediatric patients with isolated growth hormone deficiency (IGHD), idiopathic short stature (ISS) and normal controls.Methods:Sixty-nine patients (57 male, 12 female), with a mean age of 11.9 (±2.0), were determined to have IGHD. ISS was identified in 29 patients (20 male, 9 female), with a mean age of 12.7 (±3.7). Sixty-six controls (28 female, 38 male), mean age 9.8 (±4.7) were also included. Three-dimensional (3D) magnetic resonance images with contrast were obtained to accurately measure PV.Results:There was a significant difference in the mean PV among the three groups. The IGHD patients had a mean PV 230.8 (±89.6), for ISS patients it was 286.8 (±108.2) and for controls it was 343.7 (±145.9) (p<0.001). There was a normal increase in PV with age in the ISS patients and controls, but a minimal increase in the IGHD patients.Conclusions:Those patients with isolated GHD have the greatest reduction in PV compared to controls and the patients with ISS fall in between. We speculate that a possible cause for the slowed growth in some ISS patients might be related to diminished chronic secretion of growth hormone over time, albeit having adequate pituitary reserves to respond acutely to GH stimulation. Thus, what was called neurosecretory GHD in the past, might, in some patients, be relative pituitary hypoplasia and resultant diminished growth hormone secretion. Thus, PV determinations by magnetic resonance imaging (MRI) could assist in the diagnostic evaluation of the slowly growing child.


Author(s):  
Jan M. Wit ◽  
Wilma Oostdijk

In the five decades in which growth hormone has been prescribed for children with growth hormone deficiency (GHD) there has been definite progress, but on the other hand there is still insufficient evidence to answer many basic questions. From an evidence-based perspective the present situation with respect to growth hormone treatment for GHD is therefore far from optimal. First, the diagnosis GHD cannot be defined precisely, because there is a wide range of growth hormone secretion in normally growing individuals, which overlaps with the range observed in children clinically suspected of GHD. Furthermore, all test parameters available have serious drawbacks (1). Therefore, the term GHD stands for a heterogeneous group of congenital or acquired deficiencies (or apparent deficiency). Most patients have an idiopathic isolated GHD, but particularly in that subgroup retesting at the end of growth often shows a normal stimulated growth hormone peak. Of the acquired (organic) GHD, malignancies are the most frequent aetiology, but the incidence of traumatic brain injury may be underestimated.


2007 ◽  
Vol 54 (6) ◽  
pp. 1015-1019
Author(s):  
Ken-ichi KASHIMADA ◽  
Toshikazu ONISHI ◽  
Makoto ONO ◽  
Kentaro MIYAI ◽  
Masayasu OHTA ◽  
...  

2009 ◽  
Vol 53 (7) ◽  
pp. 853-858 ◽  
Author(s):  
Eduardo Micmacher ◽  
Roberto P. Assumpção ◽  
Renato G. Redorat ◽  
Luciana D. Spina ◽  
Ivan C. Cruz ◽  
...  

OBJECTIVE: To investigate the growth hormone (GH) response to glucagon stimulation test (GST) in a population of healthy men over 50 years old in comparison to insulin tolerance test (ITT), analysis of the spontaneous 24-hour GH profile and insulin-like growth factor 1 (IGF-I). METHODS: 27 healthy men aged between 51 and 65 years were tested. RESULTS: Using non-parametric correlation analysis, a positive correlation between GH peak after GST and mean IGF-I (r = 0.528; p = 0.005) was found, as well with GH peak in 24-hour profile (r = 0.494; p = 0.009). No correlation was found comparing GH peak after ITT with the same parameters. Ten subjects presented GH peak of less than 3.0 μg/L after GST, none confirmed in ITT. CONCLUSIONS: GH peak response to GST was lower than ITT, but it showed a positive correlation with mean IGF-I and also with GH peak in 24-hour profile. However, GST should not be used to differentiate organic growth hormone deficiency (GDH) from the expected decline on GH secretion due to aging.


2003 ◽  
Vol 58 (4) ◽  
pp. 456-463 ◽  
Author(s):  
Juliane Donaubauer ◽  
Wieland Kiess ◽  
Jürgen Kratzsch ◽  
Tanja Nowak ◽  
Heinz Steinkamp ◽  
...  

1977 ◽  
Vol 84 (1) ◽  
pp. 11-22 ◽  
Author(s):  
Olav Trygstad

ABSTRACT This study was carried out in order to determine whether children with a transitory type of growth hormone deficiency showed an accelerated growth in height velocity on treatment with human growth hormone (HGH). Following careful diagnostic routine procedures 13 extremely short children were diagnosed as having isolated growth hormone deficiency, and were successfully treated with HGH. A true isolated growth hormone deficiency was present in 5 of the children, whereas 8 showed a normal increase in serum growth hormone on repeated growth hormone stimulation tests after their development of puberty and termination of HGH treatment. Three boys with bone ages of 5.5, 8.0 and 9.5 years showed an undisputable effect following HGH administration. They showed an initial growth at the start of treatment, and a second growth spurt during development of puberty. Two of the boys reached final statures of 14 cm taller than the predicted heights. The other patients, including the children with true isolated growth hormone deficiency showed an initial spurt of growth at the start of the HGH treatment immediately followed by a pubertal growth spurt. The mean acceleration of height velocity for the children with true isolated growth hormone deficiency was from 3.4 cm during the year before treatment to 7.0 cm during the first year on treatment, as compared to 2.8 and 7.4 cm, respectively, for the children with transitory growth hormone deficiency. A girl with severe anorexia nervosa who had a transitory growth hormone deficiency, showed an accelerated high velocity from 1.1 cm to 7.6 cm during the first year following treatment with HGH. The question whether HGH treatment should be made available to all short children with no known syndrome, and presenting a height less than −3.5 sds, a bone age/chronological age ratio of less than ⅔, and a height velocity less than −2 sds is discussed. The only way to know if a child will respond to HGH treatment is to give it for a trial period of at least six months. At least a physiological stimulus to growth hormone secretion should be decisive in the selection of growth retarded children for HGH treatment. Different mechanisms seem to be responsible for physiological growth hormone secretion to sleep or exercise, and the secretion obtained with pharmacological stimuli.


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