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Abstract

Studies on head injury-induced pituitary dysfunction are limited in number and conflicting results have been reported. To further clarify this issue, 29 consecutive patients (24 males), with severe (n = 21) or moderate (n = 8) head trauma, having a mean age of 37 ± 17 years were investigated in the immediate post-trauma period. All patients required mechanical ventilatory support for 8-55 days and were enrolled in the study within a few days before ICU discharge. Basal hormonal assessment included measurement of cortisol, corticotropin, free thyroxine (fT4), thyrotropin (TSH), testosterone (T) in men, estradiol (E2) in women, prolactin (PRL), and growth hormone (GH). Cortisol and GH levels were measured also after stimulation with 100 µg human corticotropin releasing hormone (hCRH) and 100 µg growth hormone releasing hormone (GHRH), respectively. Cortisol hyporesponsiveness was considered when peak cortisol concentration was less than 20 µg/dl following hCRH. TSH deficiency was diagnosed when a subnormal serum fT4 level was associated with a normal or low TSH. Hypogonadism was considered when T (males) or E2 (women) were below the local reference ranges, in the presence of normal PRL levels. Severe or partial GH deficiencies were defined as a peak GH below 3 µg/l or between 3 and 5 µg/l, respectively, after stimulation with GHRH. Twenty-one subnormal responses were found in 15 of the 29 patients (52%) tested; seven (24%) had hypogonadism, seven (24%) had cortisol hyporesponsiveness, five (17%) had hypothyroidism, and two patients (7%) had partial GH deficiency. These preliminary results suggest that a certain degree of hypopituitarism occurs in more than 50% of patients with moderate or severe head injury in the immediate post-trauma period, with cortisol hyporesponsiveness and hypogonadism being most common. Further studies are required to elucidate the pathogenesis of these abnormalities and to investigate whether they affect long-term morbidity. P2 Cortisol reserve in head trauma victims: evaluation with the low-dose (1 µ µg) corticotropin (ACTH) stimulation test

Paramyxovirus replication induces the hexosamine biosynthetic pathway and mesenchymal transition via the IRE1α-XBP1s arm of the unfolded protein response

“…In response to TGFβ stimulation, the HBP pathway is induced at least partially via the IRE1α-XBP1s arm of the unfolded protein response (UPR) pathway (18). To further characterize the effect of RSV infection on GFPT2 and test whether GFPT2 expression was IRE1α dependent, we performed immunofluorescence microscopy for GFPT2 in RSV-infected cells with or without the IRE1α RNAase inhibitor, KIRA8.…”

“…Through an interconnected network of cellsurface and cytoplasmic pattern recognition receptors, RSV replication triggers a robust innate anti-viral response consisting of secretion of cytokine (49, 64), interferon (30), and damageassociated patterns (22). These factors act in paracrine manner to initiate leukocytic inflammation (18,22,35), mucous production (60) and reduce viral replication (59).…”