Book Abstract
the book reports on the management of Langerhans cell histiocytosis (LCH)-induced central diabetes insipidus and its associated endocrinological/neurological sequelae in the national survey. The next chapter addresses DI and head injuries. Next, the management of neuroendocrine instability during maintenance of potential organ donors is described. Organ transplants have gradually increased worldwide. To have maintenance of appropriate potential organs, AVP is needed. Furthermore,nephrogenic DI-the potential therapeutic drugs and analysis of membrane protein stability is the topic of the next two chapters, followed by new insights into the diagnosis and management of pregnancy-related DI. The seventh chapter reports on the problems with differential diagnosis in a case of central DI in a female patient with bipolar disorder. The lithium treatment usually resulted in nephrogenic DI. Finally,over the last years, the development of MRI imaging on the pituitary gland with the stalk and hypothalamus has advanced. The final chapter interprets imaging techniques in DI in detail. Diabetes insipidus (DI) from post-TBI hypopituitarism was first reported in 1921 (Rouvillois, Reverchon et al. 1921) and, in the 1970s, multiple case reports were published, documenting posterior pituitary dysfunction (Massol,Humbert et al. 1987; Halimi, Sigaletal. 1988). DI may be of a central (neurogenic),nephrogenic, gestational, dipsogenic, adipsic, or psychogenic type. The most common DI, the central type, which follows brain injury or surgery to the region of the pituitary and hypothalamus, is noted in previous literature review. DI is characterized by a diminished secretion of antidiuretic hormone, also known as arginine vasopressin(AVP). Neuroendocrine abnormalities following brain injury may occur with a much higher prevalence than previously realized, and represent an underdiagnosed consequence of brain injury. The prevalence of central DI among all kinds of neuroendocrine derangements after TBI in acute to chronic phases was 1.7%-26%. The development of DI seems to correlate with the severity of trauma in spite of more cases of permanent DI being reported in mild TBI cases. Central DI caused by brain injury is detectable because of polyuria and polydipsia in patients, but the occasions of DI are almost transient, leading to ignorance of its precise diagnosis and adequate treatment. In this chapter, diabetes insipidus was considered as central diabetes insipidus, which is a result of TBI.
