Pituitary Dysfunction as a Result of Traumatic Brain Injury

A victim of brain injury can experience many consequences and complications as a result of brain damage. Unfortunately, the problems caused by a traumatic brain injury can extend even beyond what most people think of as the standard symptoms of a brain injury, like mood change and cognitive impairment. One issue which can occur is pituitary dysfunction. If the pituitary gland is damaged due to injury to the brain, the consequences can be dramatic as the pituitary gland works together with the hypothalamus to control every hormonal aspect of a person’s body.

Pituitary dysfunction as a result of a brain injury can be difficult to diagnose, as you may not immediately connect your symptoms to the head injury you experienced. If you did suffer injury to the pituitary gland, you need to know about it so you can get proper treatment. If someone else caused your brain injury to occur, you also want to know about your pituitary dysfunction so you can receive compensation for costs and losses associated with this serious health problem.

The pituitary is a small area of the center of your brain that is about the size of the uvula. The pituitary is surrounded and guarded by bone, but it does hang down.  When it becomes damaged as a result of a brain injury, the damage normally occurs as a result of the fact the pituitary was affected by reduced by reduced blood flow. It can also be harmed directly from the trauma, and only a tiny amount of damage can cause profound consequences.

Many of the important hormones that your body needs are controlled by the pituitary working with the hypothalamus. If the pituitary is damaged, the result can include a deficiency of Human Growth Hormone (HGH). This deficiency can affect your heart and can impact bone development.  Thyroid Stimulating Hormone (TSH) can also be affected, which could result in hypothyroidism. Sex hormones (gonodotropin); Adrenocorticotopic hormone; and many other hormones could be impacted as well, causing fertility problems; muscle loss; sexual dysfunction; kidney problems; fatigue; or even death.

Unfortunately, problems with the pituitary gland may not always be visible on MRIs or other imaging tests because the pituitary is so small. Endocrinologists who handle hormone therapy frequently are not familiar with brain injuries, and may not make the connection that your brain injury was the cause of the problem.

If you begin to experience hormonal issues following an accident, you should be certain to get an accurate diagnosis to determine if your brain injury played a role. If it did, those responsible for causing the accident could be responsible for compensating you for the harm you have experienced to your pituitary and to the body systems which malfunction as a result of your new hormonal issues.

Nelson Blair Langer Engle, PLLC

From http://www.nblelaw.com/posts/pituitary-dysfunction-result-of-traumatic-brain-injury

“My feet are killing me!” An unusual presentation of Cushing’s syndrome

Adverse effects of steroid excess on bone metabolism are well established but presentation of Cushing’s syndrome with metabolic bone disease is reported to be uncommon. We describe a case of Cushing’s syndrome presenting with pathological fractures probably present for 8 years before diagnosis.

A 33 year old nurse first sustained spontaneous stress fractures of her metatarsals in 1994, with repeated fractures occurring up to 2002. In 2001 she developed hypertension, acute lumbar back pain and gained weight.

In 2002 she was admitted to hospital with chest/back pain. Lumbar spine X-ray showed new fracture of L3,old fractures of L4/5,with fractured ribs on CXR. Isotope bone scan revealed multiple hot spots. MRI showed collapse of T8 with features consistent with malignant disease. The primary malignancy was sought and a left-sided 1.5 centimetre thyroid nodule detected.

Suspicious cytology prompted thyroid lobectomy revealing follicular variant of papillary carcinoma. T8 biopsy revealed chronic infection with Propionobacteria rather than metastatic carcinoma. Despite antibiotic therapy further spontaneous vertebral fractures developed. Bone densitometry revealed Z scores of minus 2.4 at L2-4, minus 2.5 and 2.9 at the hips.

Referral to our centre prompted investigations for Cushing’s syndrome. Serum potassium was 4.1 millimols per litre, androgens, calcitonin and urinary catecholamines all normal. TSH was suppressed by T4 therapy. Urinary free cortisol values were raised,(563-959 nanomols per 24hours) with loss of diurnal rhythm in cortisol secretion (9am 429-586,midnight 397-431 nanomols per litre)and no suppression on low or high dose dexamethasone. Abdominal CT showed a 3.5 centimetre adrenal mass. These findings were consistent with adrenal dependent Cushing’s syndrome. Risedronate and metyrapone were commenced before adrenalectomy, completion thyroidectomy and ablative radioiodine.
Comment: Cushing’s syndrome may present with spontaneous fractures in both axial and appendicular skeleton in the absence of marked clinical features. This case demonstrates the importance of thorough investigation of unexplained fractures.

LM Albon, JD Rippin & JA Franklyn

From http://www.endocrine-abstracts.org/ea/0005/ea0005p26.htm

Day 2 Coverage of ENDO 2015

ENDO_2015

 

OR22-Osteoporosis–Winner: Outstanding Abstract Award

Effects of teriparatide on bone microarchitecture in postmenopausal women with osteoporosis
S Orlov, R Ridout, L Tile, M Kapral, S Cardew, MR Werb, SD Sandler, J Chang, H Hu, E Szabo, C Derzko, A Cheung


FRI 224-247-Metabolic and Genetic Bone Disorders

The effect of vitamin D supplementation on falls and physical performance in elderly women. A randomized clinical trial
S Yousefian, JC Gallagher, SH Tella


The etiology and risk factors analysis in hypercalcemic crisis
H Liao, DL Lorber, E Cohen


LBF 001-014-Late-breaking Thyroid/HPT Axis II

Diagnostic lobectomy for thyroid nodules >4 cm with benign cytology after fine-needle aspiration is associated with improved outcomes at an acceptable cost compared to observation: …
L Lee, E Theodosopoulos, EJ Mitmaker, JA Lee, J Chabot, JH Kuo


LBF 015-023-Late-breaking Reproductive Endocrinology II

Effect of testosterone treatment on cardiac biomarkers in a randomized controlled trial of men with type 2 diabetes
EJ Gianatti, R Hoermann, Q Lam, P Dupuis, JD Zajac, M Grossmann


OR17-Novel Aspects of Adrenal Tumors and the HPA Axis

Epigenetic modulation of DNA Is associated with fatigue, depression and anxiety in patients with Cushing’s syndrome in remission: A genome-wide methylation study
CAM Glad, JC Andersson-Assarsson, P Berglund, R Bergthorsdottir, O Ragnarsson, G Johannsson


Pharmacogenetic analysis of glucocorticoid gene polymorphisms and prediction of daily dexamethasone doses in adults with congenital adrenal hyperplasia
JS Frassei, LG Gomes, RP Moreira, G Madureira, BB Mendonca, TA Bachega


OR20-Pituitary Tumors-New Clinical Considerations

Reduced mortality in patients with GH replacement therapy – a Swedish study based on more than 4,000 patient-years
DS Olsson, AG Nilsson, P Trimpou, B-A Bengtsson, E Andersson, G Johannsson


OR22-Osteoporosis

Denosumab restores cortical bone loss at the 1/3 radius associated with aging and reduces wrist fracture risk: Analyses from the Freedom extension cross-over group
JP Bilezikian, CL Benhamou, CJF Lin, JP Brown, NS Daizadeh, PR Ebeling, A Fahrleitner-Pammer, E Franek, N Gilchrist, PD Miller, JA Simon1, I Valter, AF Zerbini, C Libanati


OR22-Osteoporosis–Winner Clinical Fellows Abstract Award Travel Grants in Womens Health

Estrone may be more important than testosterone and estradiol for bone health and prevention of fractures in post-menopausal women
G Toraldo, TG Travison, X Zhang, KE Broe, S Bhasin, DP Kiel, AD Coviello

Bone Complications in Patients with Cushing’s Syndrome: Looking for clinical, biochemical, and genetic determinants

Osteoporosis International, 11/14/2013  Clinical Article

Trementino L, et al. – Bone loss and fractures are a common complication of CS.

The authors investigate the role of gender, disease etiology, duration, and degree of hypercortisolism as well as the impact of glucocorticoid receptor (GR) polymorphisms on the development of bone complications in CS.

While GR gene variants as well as gender and disease etiology seem not to play a role, the degree and duration of hypercortisolism seem to be the major determinants of bone loss and fractures in this group of patients.

More investigations are needed to understand the real impact of these determinants on the development of bone complications in patients with hypercortisolism.

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