Table 8.
Studies with evaluation performed in the early phase of Traumatic Brain Injury.
| Ref | Patients | Methods | Pertinent results |
|---|---|---|---|
| 18 | 48 consecutive patients aged 15–70 years, with severe TBI, (GCS score ≤ 8), who were referred within 24 h after head trauma. | Blood sampled at day 1 and day 4 after TBI twice per day: in the morning (8–10 am) and in the evening (5–7 pm). Cortisol, GH, IGF-1, PRL, TSH, FT3, FT4, FSH, LH, testosterone, SHBG (only in men) were measured in the morning, whereas cortisol and GH were also measured in the evening. | Day 1- Low cortisol (<10 µg/dl) in 54.5% of patients sampled in the morning and in 52.3% of patients sampled in the evening. Very low cortisol (<3.6 µg/dl) in 18.6% and 15.9%, respectively. Low TSH (<0.27 mU/L) in 4.5%; low FT4 (<12 pmol/L or < 0.93 ng/dl) in 5.5%. Low age-related IGF-1 values in 30.2%. Day 4- Low cortisol in 70.5% of patients sampled in the morning and in 59.1% of patients sampled in the evening. Very low cortisol in 22.7% and 24.4%, respectively. Low TSH in 15.9% of patients; low FT4 27.3% of patients; Low age-related IGF-1 values in 2.3% of patients. |
| 19 | 50 consecutive patients admitted with severe or moderate TBI (initial GCS score 3–13) | Stimulation test for cortisol and GH, baseline thyroid function, PRL, IGF-1, gonadotrophins, testosterone or estradiol and glucagon evaluated at a median of 12 days (range 7–20) following TBI. | Low baseline cortisol (<50 nmol/L or 1.8 μg/dl) in 40% of patients; low cortisol peak after glucagon challenge (<450 nmol/L or 16.3 μg/dl) in 16% of patients. Low GH (peak after glucagon challenge <5 ng/ml) in 18% of patients. No statistical difference in plasma IGF-1 levels between the GH-sufficient and GH-deficient subjects. TSH deficiency (<0.5 mU/L) in 2% of patients. |
| 20 | 81 subjects with primary ES (70 females, 11 males; mean age 49.9 ± 14.5 years) | All patients with TES (n = 34) and PES (n = 47) underwent endocrinological evaluation. This consisted of measurement of fasting morning GH, IGF-1, FSH, LH, 17β estradiol (females), total testosterone (males), cortisol, ACTH, TSH, FT3 and FT4. |
TES vs. PES:
|
| 21 | 58 children and adolescents (21 females, 37 males median age 11.3 years) evaluated after a TBI (GCS range 3–12) | Measurement of TSH, FT4, IGF-1, PRL, morning cortisol, FSH, LH, and testosterone (in boys) or estradiol (in girls) in the early post-traumatic period (2–14 days, T0), at 3 months (T3), 6 months (T6) and 12 months (T12) | At T0, 45% of patients had central hypothyroidism. At T3, 3% of patients showed combined pituitary hormone deficiency. At T6, only one patient (2%) was diagnosed with GH deficiency. At T12, two girls and one boy (5%) had GH deficiency. The boy had also central hypothyroidism. ES was detected in two boys with GH deficiency. |
| 12 | 89 patients (23 females, 66 males; mean age 36 years) evaluated after a TBI (GCS range 3–14) | TSH and FT4 in the acute stage of TBI; cortisol, TSH, FT4, IGF-1, and testosterone and SHBG (in men) at 3–6 months after TBI; morning cortisol, TSH, FT4 and stimulation tests (ACTH, arginine, glucagon) in case of clinical suspicion at one year after TBI | ES was more frequent in patients with major deficits compared to those without (78% vs. 20%) Acute phase: 53% of patients with ≥1 deficiency of one axis (37% GH axis, 10% ACTH axis, 3% TSH axis). At 3 and 6 months, recovery of normal function was documented in 55% and 37%, respectively. At 12 months 19 patients (21%) still had major hormonal deficiencies (63% GH axis, 0% TSH axis, 0% ACTH axis). |
| 22 | 56 consecutive patients (44 females, 12 males, aged 18–45 years) with diagnosis of head trauma | All patients were sampled for total and free T3, total and free T4, TSH, ACTH, cortisol, DHEA, DHEAS, GH, IGF-1, PRL, LH, FSH and testosterone (in males) or estradiol (females) in the early post-traumatic phase (0–10 days), at 6 and 12 months. Stimulation tests (ACTH test, insulin tolerance test), performed only in selected cases. | Hormonal dysfunction seen in 39 patients (70%) in the early phase. One, two and three axis dysfunction was reported in 26, 8 and 5 patients, respectively. Central hypothyroidism, hypocortisolism and GH deficiency was seen in 16 (29%), 7 (13%) and 11 (20%) patients, respectively. Pituitary deficiencies persisted in 7 (13%) and 8 (15%) patients at 6 and 12 months post TBI. |
| 23 | 63 patients (11 females, 52 males, 37.5 ± 17.0 years) with severe head injury (GCS < 8) | Measurement of serum TSH, FT4, ACTH, cortisol, GH, IGF-1, LH, FSH, and testosterone (in men) on admission, at the intensive care unit, and subsequently for 10 years. | Overall, hypopituitarism was diagnosed in 68% of patients, but in 38% in the early phase (<1 year post TBI). GH deficiency, central hypothyroidism and secondary adrenal failure were found in 51%, 22% and 9%, respectively. No correlation between hypopituitarism and clinical parameters on admission or at intensive care unit. |
| 24 | 163 patients admitted to neurorehabilitation, of whom 111 after severe TBI (28 females, 83 males) | Measurement of FSH, LH, testosterone (in men), estrogen (women), TSH, and ACTH stimulation test at admission and at 1-year follow-up | Central hypothyroidism diagnosed in 9% of patients. |
Abbreviations: ES = empty sella; GCS = Glasgow Coma Scale; TBI = traumatic brain injury; PES = partial empty sella; TES = total empty sella; SHBG = sex hormone-binding globulin; PRL = prolactin. GH = growth hormone; IGF-1 = insulin-like growth factor 1; TSH = thyrotropin; FT3 = free triiodothyronine; FT4 = free thyroxine; FSH = follicle stimulating hormone; LH = luteinizing hormone; ACTH = adrenocorticotropic hormone; DHEA = dehydroepiandrosterone; DHEAS = Dehydroepiandrosterone sulfate.
Only data on hypothalamus-pituitaryadrenal/thyroid axis and GH-IGF-1 axis are reported.