In an effort to characterize thyroid, gonadal and adrenal function following neurotrauma, the present study determined serum concentrations of thyroid-stimulating hormone (TSH), total triiodothyronine (T3), thyroxine (T4), testosterone and cortisol over a 7 day period in 31 patients with traumatic brain injury. The study group consisted of eight patients with mild closed head injury (Glasgow Coma Scale--GCS 13-15), 10 patients with extensive penetrating head injury (GCS 4-6) and 13 patients with blast injuries but without direct head trauma. The latter group was included in the study because the development of indirect brain trauma has previously been implicated in blast injuries. Patients with multiple injuries were not included. Following mild injury (GCS 13-15), TSH was increased up until day 3 after injury. T3 levels were elevated on days 1, 5 and 7 after injury while T4 remained unchanged throughout. While testosterone was decreased over only the first 2 days post-trauma, cortisol was increased over these first 2 days after injury. In contrast, following severe penetrating injury (GCS 4-6), there were significant declines in TSH, T3 and testosterone over the 7 day observation period post-trauma. Serum cortisol also declined in these patients between 1-3 days after injury, before increasing again on days 5 and 7 after injury. Following indirect neurotrauma, TSH was slightly decreased immediately after trauma but increased to above normal levels on days 5 and 7 post-trauma. Similarly, T3 initially declined after injury, but then increased to above normal levels between 5 and 7 days after injury. T4 and testosterone remained unchanged over the entire post-traumatic period. Serum cortisol was significantly increased after indirect neurotrauma but only up to day 2 post-trauma. In summary, patients with both direct and indirect traumatic brain injury demonstrated endocrine alterations after trauma, the dynamics of which may be a reflection of the severity of brain damage.

The results document the scope of the profession and will serve as a foundation for the next revision of the Certified Clinical Data Manager TM exam. A clear articulation of professional competencies and necessary foundational knowledge could inform the content of graduate degree programs or tracks in areas such as clinical research informatics that will develop the current and future clinical research data management workforce.

Tissue trauma leads to a complex hormonal response of pituitary end-organ axis. This response can be recorded by determining parameters that represent the functional integrity of these systems. The concentrations of serum prolactin (PRL), serum testosterone, and plasma adrenocorticotropin (ACTH) were measured in 62 adult male casualties from the recent war in former Yugoslavia. Patients with brain injury were not included. Venous blood samples were taken as soon as possible (2-18 hours) after admission and at 1, 2, 5, and 14 days after injury. The severity of gunshot/missile wounds was assessed by the Injury Severity Score (ISS). The control group consisted of healthy blood donors. Uninjured subjects who had undergone great stress on the battlefield (explosion in the vicinity without injury) served as the sham-control group. Tissue trauma leads to a severity-dependent decrease in serum testosterone concentrations during the first 5 days following injury. Significant correlations were observed between ACTH, prolactin, and ISS during the first 18 hours after injury. A strong negative correlation between testosterone and prolactin serum concentrations was found during the first 18 hours. In patients with additional complications or unsatisfactory outcome, the prolactin concentrations remained elevated, whereas testosterone concentrations were reduced. Our results support the usefulness of recording hormonal changes for determining trauma severity and monitoring the clinical course. Such monitoring also helps assess the efficacy of therapeutic strategies. The relation between testosterone and prolactin might be helpful for predicting the clinical course and trauma outcome.

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Concentrations of carcinoembryonic antigen (CEA) and carborhydrate antigen (CA) 50 were measured in pleural effusion and sera of 57 patients with bronchogenic carcinoma and in 73 patients in whom the effusion was the sequela of tuberculous pleurisy. In the group with bronchogenic carcinomas, planocellular was confirmed in 19, microcellular in 17, macrocellular in 2, and adenocarcinoma in 18, while in 1 patient it was not possible to determine the histopathologic structure. The diagnosis of pleural disease was established upon the cytologic examination of the effusion and histopathologic examination of the pleural sample obtained by blind percutaneous needle biopsy or following pleuroscopy. CEA concentration in the sera of patients with bronchogenic carcinoma was significantly higher than in the patients with tuberculosis (p < 0.001), with sensitivity of 44% and ideal specificity and positive predictive value of 100%. In the same group highly significant difference of mean values of CEA concentrations in pleural effusion (p < 0.001), was also found with sensitivity of 60%, significant specificity of 99% and positive predictive value of 97%. CA 50 concentrations in the sera of patients with lung carcinoma were significantly higher than those in the sera of patients with tuberculous pleurisy (p < 0.05), and the sensitivity was 50%, while the specificity was 94% and positive predictive value was 75%. Significantly higher was also the value in the pleural effusion (p < 0.05), but the sensitivity was slightly lower--40%, but specificity was favorable as well as the positive predictive value (94 and 86%, respectively). The results indicate the significance of the determination of CEA and CA 50 in the sera and pleural effusion in the differentiation of malignant from tuberculous pleural effusion.