11 Pituitary gland
<p><a href="https://www.meassociation.org.uk/2014/05/the-brain-injury-that-could-be-behind-30000-case-of-chronic-fatigue-mail-online-18-may-2014/">‘The brain injury that could be behind 30,000 case of chronic fatigue’ | Mail Online | 18 May 2014 | ME Association</a></p>
<p>Numerous studies have shown that between 20 and 30 per cent of the 135,000 patients who suffer a serious head injury also experience damage to the pituitary gland, which is situated below the brain, behind the nasal cavity.</p>
<p>The gland produces vital hormones that govern many bodily functions, including growth and repair, the sleep-wake cycle and how we react to stress. If the pea-sized organ is damaged, it may stop producing one or more of the essential hormones, triggering the wide-ranging symptoms of hypopituitarism.</p>
<p>Studies suggest there could be between 18,000 and 30,000 cases in the UK each year.</p>
<p>Treatment involves lifelong hormone replacement therapy, which is said to be highly effective but costs up to £6,000 a year.</p>
<p>During her illness, Jill was screened for deficiency in the hormone cortisol, a characteristic of hypopituitarism. However, the test – known as the short synacthen test (SST) – produced a normal result. ‘That was when I was told I had CFS,’ she says.</p>
<p>Yet SST misses two of out every five cases where the cause of cortisol deficiency is damage to the pituitary. In 2007, Jill came across a magazine article about Christine Wrighton, who was incorrectly diagnosed with CFS when in fact she was suffering from hypopituitarism.</p>
<p>‘Eventually, after huge persistence, Christine was able to pay privately for a test which the NHS would accept. This proved she had been right all along – her pituitary was faulty. Her story opened my eyes,’ says Jill.</p>
<p>Dr John Newell Price, consultant endocrinologist at the Royal Hallamshire Hospital in Sheffield and chairman of the Pituitary Foundation Medical Committee, says: ‘A “pass” on an SST may not always mean cortisol deficiency is excluded.’ He recommends referral to an endocrinologist if symptoms persist, so that the glucagon test can be carried out.</p>
<p>From: <a id="null" class="null" href="https://onlinelibrary.wiley.com/doi/full/10.1046/j.1365-2265.2000.01049.x">https://onlinelibrary.wiley.com/doi/full/10.1046/j.1365-2265.2000.01049.x</a></p>
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<p>Previous studies have revealed that hormonal disturbances may accompany the chronic fatigue syndrome (CFS). Changes in the secretion of the pituitary–adrenal axis have been demonstrated, as well as abnormalities in the GH‐IGF‐I axis. However, data have not always been well characterized and were sometimes conflicting. The small number of CFS patients investigated in earlier studies may have played a role in the interpretation of the results.</p>
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<h3 class="article-section__sub-title section1">SUBJECTS AND DESIGN</h3>
<p>Hormonal testing was performed in 73 nonobese CFS patients and nonobese 21 age‐and gender‐matched healthy controls. We investigated GH, ACTH and cortisol responses to insulin‐induced hypoglycaemia. In a subgroup of patients arginine and clonidine stimulation for GH was also performed. Nocturnal secretion of GH, ACTH and cortisol were determined. Serum levels of IGF‐I, prolactin, TSH, and free thyroxine were also measured. Visceral fat mass was assessed by CT scanning.</p>
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<h3 class="article-section__sub-title section1">RESULTS</h3>
<p>GH response to insulin induced hypoglycaemia assessed by peak value (17.0 ± 13.1 μg/l <em>vs</em>. 22.1 ± 9.8 μg/l; <em>P</em> = 0.01) and by AUC (450.0 ± 361.3 μg/l <em>vs</em>. 672.3 ± 393.0 μg/l; <em>P</em> = 0.002) was significantly decreased in CFS patients <em>vs</em>. controls. Nocturnal GH secretion assessed by GH peak value (5.4 ± 3.7 <em>vs</em>. 9.0 ± 5.1 μg/l; <em>P =</em> 0.44) and by AUC (34.4 ± 20.2 <em>vs</em>. 67.4 ± 43.1; <em>P</em> = 0.045) was also significantly impaired in CFS patients. Arginine and clonidine administration showed no differences in GH secretion between CFS patients and controls. In the CFS group, GH peak values were significantly higher after ITT than after arginine (<em>P</em> = 0.017) or clonidine (<em>P</em> = 0.001). No differences in serum IGF‐I levels were found between CFS patients and controls. Except for a significantly lower nocturnal cortisol peak value, no differences were found in ACTH and cortisol secretion between CFS patients and controls. Significantly higher serum prolactin levels (7.4 ± 4.7 μg/l <em>vs</em>. 4.4 ± 1.3 μg/l; <em>P</em> = 0.004) and significantly higher serum TSH levels (1.6 ± 1.0 mU/l <em>vs</em>. 1.0 ± 0.4 mU/l; <em>P</em> = 0.011) were found in CFS patients. Serum free thyroxine was comparable in both groups. Visceral fat mass was significantly higher in CFS patients (86.6 ± 34.9 cm2vs. 51.5 ± 15.7 cm2; <em>P</em> < 0.001).</p>
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<h3 class="article-section__sub-title section1">CONCLUSIONS</h3>
<p>We observed a significant impairment of GH response during insulin‐induced hypoglycaemia and a low nocturnal GH secretion in CFS patients. These changes did, however, not lead to different concentrations in serum IGF‐I. The clinical expression of this inadequate GH secretion can thus be questioned, although the alteration in body composition may be related to this relative GH deficiency. Significantly increased prolactin and TSH levels were found when compared to controls. These findings give support to the hypothesis of a decreased dopaminergic tone in CFS. Further investigations are required in order to identify specific adaptations within the neurotransmitter system in CFS and to determine the clinical importance of the impaired GH homeostasis.</p>
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