Endocrine dysfunction following traumatic brain injury: a 5-year follow-up nationwide-based study

Abstract

Post-traumatic endocrine dysfunction is a complication of traumatic brain injury (TBI). However, there is lack of long-term follow-up and large sample size studies. This study included patients suffering from TBI registered in the Health Insurance Database. Endocrine disorders were identified using the ICD codes: 244 (acquired hypothyroidism), 253 (pituitary dysfunction), 255 (disorders of the adrenal glands), 258 (polyglandular dysfunction), and 259 (other endocrine disorders) with at least three outpatient visits within 1 year or one admission diagnosis. Overall, 156,945 insured subjects were included in the final analysis. The 1- and 5-year incidence rates of post-traumatic endocrinopathies were 0.4% and 2%, respectively. The risks of developing a common endocrinopathy (p < 0.001) or pituitary dysfunction (P < 0.001) were significantly higher in patients with a TBI history. Patients with a skull bone fracture had a higher risk of developing pituitary dysfunction at the 1-year follow up (p value < 0.001). At the 5-year follow up, the association between intracranial hemorrhage and pituitary dysfunction (p value: 0.002) was significant. The risk of developing endocrine dysfunction after TBI increased during the entire 5-year follow-up period. Skull bone fracture and intracranial hemorrhage may be associated with short and long-term post-traumatic pituitary dysfunction, respectively.

Risk of Erectile Dysfunction After Traumatic Brain Injury: A Nationwide Population-Based Cohort study in Taiwan

“…ED was classified as psychogenic ED (ICD-9-CM 302.74) and organic ED (ICD-9-CM 607.84). Comorbidities in this study included dementia (ICD-9-CM 290, 294.1-294.2, 331.0), schizophrenia (ICD-9-CM 295), anxiety (ICD-9-CM 300.0, 300.2-300.3, 308.3, 309.31), bipolar disorder (ICD-9-CM 296.0-296.1, 296.4-296.8), depression (ICD-9-CM 296.2-296.3, 300.1, 311), stroke (ICD-9-CM 430-438), coronary artery disease (CAD) (ICD-9-CM 410-414), chronic obstructive pulmonary disease (COPD) (ICD-9-CM 491-492, 496), chronic kidney disease (CKD) (ICD-9-CM 580-589), hypertension (ICD-9-CM 401-405), diabetes mellitus (DM) (ICD-9-CM 250), hyperlipidemia (ICD-9-CM 272), asthma (ICD-9-CM 493), alcohol-related illness (ICD-9-CM 291, 303, 305, 571.0-571.3, 790.3, V11.3), fracture (ICD-9-CM 800-829), dislocation (ICD-9-CM 830-839), sprains and strains (ICD-9-CM 840-849), open wound (ICD-9-CM 870-899), injury to blood vessels (ICD-9-CM 900-904), superficial injury/contusion (ICD-9-CM 910-92), crushing (ICD-9-CM 925-929), foreign body entering through orifice (ICD-9-CM 930-939), burns (ICD-9-CM 940-949), injury to nerves and spinal cord (ICD-9-CM 950-957), poisoning (ICD-9-CM 960-989), with the references to previous studies about ED ( Chao, Chen, Wang, Li, & Kao, 2015 ; Chen, Liang, Lin, Liao, & Kao, 2016 ; Kao et al, 2016 ; Wang, Chao, Lin, Tseng, & Kao, 2016 ; Wu et al, 2016 ) or TBI ( Chi et al, 2016 ; Wimo et al, 2016 ; Wu et al, 2017 ; Yang et al, 2016 ). This was a retrospective cohort study.…”

Microglial cell‐derived interleukin‐6 influences behavior and inflammatory response in the brain following traumatic brain injury

“…Concerning neuroinflammatory conditions, upregulated Il6 expression in brain and increased IL‐6 protein levels in cerebrospinal fluid have been observed in people who suffered traumatic brain injury (TBI) (Frugier, Morganti‐Kossmann, O'Reilly, & McLean, ; R. G. Kumar et al, ). TBI refers to brain damage caused by an external physical force and it is one of the most common public health issues in terms of disability and death (Dewan et al, ; Yang et al, ). Although TBI subtypes differ in their pathology and consequences, the major hallmark of TBI at the lesion zone is a contusion core due to cell death and inflammatory processes (Raghupathi, ).…”

Extracranial Complications of Traumatic Brain Injury: Pathophysiology—A Review

“…This endocrine dysfunction occurs after moderate to severe head injury; however, it is not commonly recognized in the acute phase but becomes evident in the chronic stage beyond 6 months. 10 In a study by Yang et al, 58 endocrine dysfunction was noticed in 0.4%, as compared with 0.3% in non-TBI patients at 1-year follow-up, and the incidence increased to 2% over 5-year follow-up.…”

“…However, gonadotrophins and growth hormone abnormalities are also reported during recovery and in the late phase of head injury. 10 In a study by Yang et al, 58 in a follow-up of 31,389 patients with head injuries for 5 years, endocrine dysfunction was noticed in 0.4% as compared with 0.3% in non-TBI patients at 1-year follow-up, and the incidence increased to 2% over 5-year follow-up. Direct injury to the pituitary gland due to base of the skull fracture, disruption of the infundibulum, and interruption in blood supply due to damage to hypophyseal blood vessels may result in pituitary hemorrhage or infarction, and hypothalamic damage, and has been responsible for hypopituitarism.…”

“…Recurrent infections, hyponatremia, and hypotension are common in chronic phase. 10,58 Hypothyroidism due to pituitary cause has been reported in 17 to 24% of patients on days 1 and 2, after TBI. The peripheral conversion of thyroxine (T 4 ) to triiodothyronine (T 3 ) is impaired, and abnormal form of T3 known as reverse T3 (rT3) has been found to be elevated.…”