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- Author: Aleksandra Gilis-Januszewska x
Endocrinology Department, University Hospital in Krakow, Krakow, Poland
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Endocrinology Department, University Hospital in Krakow, Krakow, Poland
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Endocrinology Department, University Hospital in Krakow, Krakow, Poland
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Traumatic brain injury affects many people each year, resulting in a serious burden of devastating health consequences. Motor-vehicle and work-related accidents, falls, assaults, as well as sport activities are the most common causes of traumatic brain injuries. Consequently, they may lead to permanent or transient pituitary insufficiency that causes adverse changes in body composition, worrisome metabolic function, reduced bone density, and a significant decrease in one’s quality of life. The prevalence of post-traumatic hypopituitarism is difficult to determine, and the exact mechanisms lying behind it remain unclear. Several probable hypotheses have been suggested. The diagnosis of pituitary dysfunction is very challenging both due to the common occurrence of brain injuries, the subtle character of clinical manifestations, the variable course of the disease, as well as the lack of proper diagnostic algorithms. Insufficiency of somatotropic axis is the most common abnormality, followed by presence of hypogonadism, hypothyroidism, hypocortisolism, and diabetes insipidus. The purpose of this review is to summarize the current state of knowledge about post-traumatic hypopituitarism. Moreover, based on available data and on our own clinical experience, we suggest an algorithm for the evaluation of post-traumatic hypopituitarism. In addition, well-designed studies are needed to further investigate the pathophysiology, epidemiology, and timing of pituitary dysfunction after a traumatic brain injury with the purpose of establishing appropriate standards of care.
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Objective
Cushing’s syndrome (CS) is associated with an 18-fold greater risk of venous thromboembolism (VTE). We aimed to identify factors which provoke VTE among patients with CS and VTE and to describe the anticoagulant regimen used in these cases.
Methods
In this retrospective observational study, patients included in the European Registry on CS (ERCUSYN) in Krakow center, Poland, were followed for the occurrence of VTE and anticoagulant treatment. We identified factors provoking VTE according to the International Society of Thrombosis and Hemostasis (ISTH), along with factors included in the Padua score and CS-VTE score.
Results
Of the 128 patients followed for a median of 4.3 years, there were nine patients who experienced ten VTE episodes (prevalence of 7.8% and incidence of 13.4 per 1000 patient-years). All VTEs were classified as provoked according to the ISTH guidance, predominantly due to the transient major and minor (50% and 20%, respectively) factors, while they were less commonly due to persistent (30%) factors. In 2/9 patients, we could not identify any risk factor for VTE according to the Padua score, while in 2/6 patients according to the CS-VTE score. Patients were mostly anticoagulated with vitamin K antagonists (4/8 patients), followed by direct oral anticoagulants (3/8) and low-molecular-weight heparin (1/8). The median duration of anticoagulation was 2.75 years and exceeded beyond the primary treatment in 28% of episodes provoked by transient factors.
Conclusion
Further, multicenter studies are required to create a validated thrombotic risk score and guidelines regarding VTE treatment in CS patients.
