Systematic screening of pituitary function is recommended for all patients with moderate-to-severe TBI at risk of developing pituitary deficits. Patients with hypopituitarism benefit from appropriate hormonal replacement and prospects for rehabilitation of patients with TBI-induced hypopituitarism may be enhanced by appropriate HRT. Further exploration of this possibility requires: (1) active collaboration between divisions of endocrinology and rehabilitation at the local level to perform a screening of pituitary function in patients after TBI, (2) creation of a consultancy service by endocrine societies for use by rehabilitation centres, (3) development of continuing medical education (CME) programmes that can be offered as crossover training to the physicians who manage the care of patients with TBIs, (4) targeting of patient organizations with educational information for dissemination to patients and their families, (5) continued efforts to more clearly define the population at greatest risk of TBI-induced hypopituitarism and (6) monitor results of efficacy studies as they become available to evaluate whether and how much replacement therapy can improve the symptoms of individuals with TBI-induced hypopituitarism.

No abstract

No abstract

Intravenous application of 100 micrograms synthetic ovine corticotropin releasing factor (CRF) led to stimulation of ACTH-secretion in nine normal controls, with a maximum 30 min after CRF. Cortisol, corticosterone, cortisone and 11-deoxycortisol increased with a maximum at 60 min after CRF, whereas no rise was seen in aldosterone, 11-deoxycorticosterone, 17-alpha-hydroxyprogesterone, progesterone, DHEA-S and testosterone. The specificity of CRF-stimulation was also shown by unchanged TSH, LH, FSH, hGH, prolactin and thyroid hormone levels, als well as unchanged insulin and gastrin levels. No serious side-effects were observed during the test period and afterwards. CRF-tests were performed in ten patients with disturbances of the hypothalamo pituitary adrenal axis (HPAA). Preliminary findings show hyperresponsiveness of ACTH in all situations of ACTH-hypersecretion (two patients with Cushing's disease, one patient with Nelson's syndrome, and one with Addison's disease). In contrast, one patient with successful microadenomectomy showed no response of ACTH to CRF, whereas in another patient with a macroadenoma ACTH and cortisol-levels still increased postoperatively. Divergent patterns in ACTH-responsiveness to CRF were seen in four patients with secondary adrenal insufficiency, allowing the localization of the defect. These data point to the possible importance of the "CRF-test" as a differential diagnostic tool and prognostic factor in diseases of the HPAA.

To evaluate the dynamics of GH-secretion after infusion of growth hormone releasing factor, human pancreatic growth hormone releasing factor (hpGRF1-44) was infused over 2 and 5 h at a dosage of 100 \ g=m\ ghpGRF1-44/h into 11 healthy subjects. The infusion was started and terminated with a 50 \g=m\ghpGRF1-44 bolus injection. In 5 subjects 200 \ g=m\ g TRH was given 4 h after starting the infusion. In addition, 4 healthy subjects received 50 \g=m\ghpGRF1-44 bolus injection every 2 h. GRF, somatostatin, GH, Prl, and TSH were measured by radioimmunoassay. The initial 50 \ g=m\ g GRF bolus increased GH-levels in all 11 subjects with a maximum at 30 min (24.1 \ m=+-\5.1 ng/ml \ m=+-\ SE). However, though hpGRF1-44 was continuously infused and GFR-levels remained elevated, GH decreased to a minimum 270 min after start of infusion (2.6 \m=+-\0.6 ng/ml). The GH-response to the second bolus at the end of the infusion was lower compared to the first response (14.6 \ m=+-\ 3.4 ng/ml after 2 h and 7.6 \ m=+-\ 2.5 ng/ml after 5 h). TRH did not lead to a GH-increase during hpGRF1-44 infusion though Prl and TSH rose normally. The intermittent bolus injection of 50 \g=m\ghpGRF1-44 led to continuously decreasing GH-responses to the same GRF\x=req-\ dosage (I. bolus: 16.5 \ m=+-\1.6 ng/ml; II. bolus: 4.2 \ m=+-\ 0.8 ng/ml; III. bolus: 3.4 \m=+-\0.5 ng/ml). No change in somatostatin levels was observed.These findings show that GRF infusion or bolus injection in short intervals does not sustain elevated GH-levels.Pituitary GH is either not readily available for continuous GRF-stimulation or GH-secretion may be antagonized by increasing portal somatostatin levels which are not reflected in the peripheral circulation.