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Thread: relationship re:SCI & thyroid

  1. #1
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    relationship re:SCI & thyroid

    Somewhere in a spinal cord injury site I recall reading about a certain relationship between SCI & thyroid hormones or the like. I can't find it now. My husband has incomplete SCI and was told his TSH is elevated, the rest of the thyroid panel was normal. Any ideas????

  2. #2
    franroty, I think that I had posted several of the studies showing changes in the pituitary axis hormones (which would include TSH). The mechanism of these effects are unclear. Likewise, some women have changes in their FSH and LH, and other pituitary hormones.

    If your husbands T3 and T4 levels are normal, you probably don't need to worry about his thyroid function. The following are some recent studies on thyroid and I threw in an abstract on parathyroid as well. To tell you the truth, I don't understand the mechanisms or the consequences of the various hormonal changes described. Some of it may be medication related but others appear to be spinal cord injury and severity related.

    • Bauman WA and Spungen AM (2000). Metabolic changes in persons after spinal cord injury. Phys Med Rehabil Clin N Am. 11 (1): 109-40. Summary: Persons with chronic SCI have several metabolic disturbances. As a consequence of inactivity and the body compositional changes of decreased skeletal muscle with a relative increase in adiposity, a state of insulin resistance and hyperinsulinemia has been demonstrated to exist, associated with abnormalities in oral carbohydrate handling. Elevated plasma insulin levels in persons with SCI probably contribute to the cause of frequent dyslipidemia and hypertension. This constellation of metabolic changes represents an atherogenic pattern of CHD risk factors with many of the distinctive features of a cardiovascular dysmetabolic syndrome that is called syndrome X. Reduction in modifiable risk factors for CHD should decrease the occurrence of catastrophic cardiovascular events. There is evidence to suggest that endogenous anabolic hormone levels are depressed in a proportion of individuals with SCI. Depression of serum testosterone and growth hormone/IGF-I levels may exacerbate the adverse lipid and body compositional changes, reduce exercise tolerance, and have deleterious effects on quality of life. Because of immobilization, individuals with paraplegia have osteoporosis of the pelvis and lower extremities, and those with tetraplegia also have osteoporosis of the upper extremities. In addition, there is evidence to suggest that bone loss progresses with time in persons with chronic SCI. This may be caused by chronic immobilization per se or may be a consequence of adverse hormonal changes, including deficiency of anabolic hormones or deficiency of vitamin D and calcium with secondary hyperparathyroidism. Serum thyroid function abnormalities resembling the euthyroid sick "low T3 syndrome" have been reported in those with acute and chronic spinal cord injury. Depressed serum T3 and elevated rT3 in chronic SCI may be caused by associated illness. Current practice has been hesitant to treat abnormal serum thyroid chemistries associated with nonthyroidal illness. Recognition of metabolic abnormalities in individuals with SCI is vital as a first step in improving clinical care. The application of appropriate interventions to correct or ameliorate these abnormalities promises to improve longevity and quality of life in persons with SCI. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10680161> Department of Medicine, Mount Sinai Medical Center, New York, USA. Bauman.W@Bronx.VA.GOV

    • Mechanick JI, Pomerantz F, Flanagan S, Stein A, Gordon WA and Ragnarsson KT (1997). Parathyroid hormone suppression in spinal cord injury patients is associated with the degree of neurologic impairment and not the level of injury. Arch Phys Med Rehabil. 78 (7): 692-6. Summary: OBJECTIVE: To demonstrate that after spinal cord injury (SCI) suppression of the parathyroid-vitamin D axis is associated with the degree of neurologic impairment and not the level of injury. DESIGN: A retrospective analysis of clinical and biochemical data obtained from hospital records of patients with SCI compared to a control group of patients with traumatic brain injury (TBI). SETTING: The inpatient rehabilitation unit of a tertiary care hospital. SUBJECTS: The medical records of 82 consecutive admissions to the rehabilitation unit with a diagnosis of SCI or TBI were reviewed. Patients with SCI were classified by the American Spinal Injury Association (ASIA) impairment scale and then grouped based on the completeness and level of injury. MAIN OUTCOME MEASURE: Comparisons of serum parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D (1,25-D) were planned. Multiple comparisons were performed for total and ionized serum calcium levels, serum phosphorus levels, and 24-hour urinary calcium excretion rates to reflect changes in mineral homeostasis. Multiple comparisons were also performed for serum albumin, prolactin, thyroid function tests, and AM cortisol levels, as well as 24-hour urinary urea nitrogen and cortisol excretion rates to reflect metabolic responses to stress. RESULTS: Patients with SCI had significant suppression in PTH (p < .000009) and 1,25-D [p < .02) levels with elevated phosphorus [p < 0.03) and prolactin [p < .03) levels compared to patients with TBI. Also, more patients with SCI were hypoalbuminemic [p < .003) than patients with TBI. Patients with complete SCI [ASIA A) had more suppressed PTH [p < .03) and higher urinary urea nitrogen [p < .05) levels than SCI patients with incomplete injuries [ASIA B-D). Patients with complete, but not incomplete, SCI had lower albumin levels than patients with TBI [p < .05). These differences were not found between patients with tetraplegic and paraplegic SCI. ASIA motor scores did not correlate with any of the measured parameters but when used as a covariate did abolish differences in PTH and 1,25-D among the study groups by ANOVA. CONCLUSION: In patients with SCI, the degree of neurologic impairment, and not the level of injury, is associated with PTH suppression and markers of metabolic stress. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9228870> Division of Endocrinology and Metabolism, Mount Sinai School of Medicine, New York, NY 10029, USA.

    • Huang TS, Wang YH, Lai JS, Chang CC and Lien IN (1996). The hypothalamus-pituitary-ovary and hypothalamus-pituitary-thyroid axes in spinal cord-injured women. Metabolism. 45 (6): 718-22. Summary: Sixteen women with spinal cord injury (SCI) underwent studies of the hypothalamus-pituitary-ovary (HPO) and hypothalamus-pituitary-thyroid (HPT) axes with luteinizing hormone (LH) releasing hormone (LHRH) and thyrotropin (TSH) releasing hormone (TRH) stimulation tests during the early follicular phase. The mean interval from injury to participation in this study was 7.5 years (range, 1.5 to 13.1). All subjects were menstruating regularly. Five (35.7%) SCI subjects who were menstruating before injury had postinjury amenorrhea for 1 to 12 months, and the other nine (64.3%) SCI subjects had no interruption of menstruation after injury. Two SCI subjects whose injury occurred in preadolescence proceeded to menarche without any delay. The amount of menstrual flow was noted to be reduced in nine (64.3%) SCI subjects. Two and three SCI subjects had elevated follicle-stimulating hormone (FSH) and prolactin (PRL) levels, respectively. LH responses to LHRH were significantly higher in the SCI group (P < .001). Ten [62.6%) SCI subjects had enhanced LH responses to LHRH. The mean TSH, PRL, and FSH responses to TRH and LHRH of the SCI group were not significantly different from those of age-matched controls. However, five [31.2%), four [25.0%), and five [31.2%) SCI subjects had enhanced TSH, PRL, and FSH responses to TRH and LHRH, respectively. Six [37.5%) SCI subjects had a delayed FSH response to LHRH. In total, 13 [81.2%) SCI subjects had at least one axis abnormality. These findings are consistent with the hypothesis that changes of central neurotransmitters may occur after SCI. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8637446> Department of Medicine, National Taiwan University Hospital, Taipei, Republic of China.


    • Cheville AL and Kirshblum SC (1995). Thyroid hormone changes in chronic spinal cord injury. J Spinal Cord Med. 18 (4): 227-32. Summary: Spinal cord injury (SCI) impacts metabolic function and deranges various hormonal axes. Previous studies characterizing thyroid hormones in SCI reported depressed triiodothyronine (T3) and thyroxin (T4), primarily in acute tetraplegics. These studies cited an 11-13 percent incidence of low T3 syndrome (LT3S) in SCI patients, with an increased incidence in tetraplegics (20-36 percent). The purpose of this study was to evaluate thyroid function and determine the incidence and clinical relevance of LT3S in the chronic SCI population. Thyroid function tests were performed on 30 chronic SCI patients (14 tetraplegics and 16 paraplegics) and 30 age- and gender-matched controls. Mean T3 and T4 levels were significantly depressed in SCI patients relative to controls, while T3 resin uptake (T3RU) values were significantly elevated. LT3S only occurred in the SCI population with an incidence of 23.3 percent. SCI patients with LT3S did not differ significantly from those without in the level or completeness of injury, age or the interval since injury. They did, however, have co- existent pathology: decubiti, urinary tract infections, etc. When SCI patients with normal T3 were compared with controls, they still had depressed mean T3 levels. We conclude that LT3S occurs frequently in the chronic SCI population and suggest that depressed serum T3 levels may predispose SCI patients to sick euthyroidism in the face of minor pathologic insult. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8591067> University of Medicine and Dentistry, New Jersey, Newark, USA.


    • Wang YH, Huang TS and Lien IN (1992). Hormone changes in men with spinal cord injuries. Am J Phys Med Rehabil. 71 (6): 328-32. Summary: The steady state profiles of 63 men with traumatic spinal cord injuries (24 quadriplegics and 39 paraplegics; average age of 31.2 +/- 6.8 yr; 18-44 yr) were studied. The average length of post-traumatic period was 6.2 +/- 5.0 yr, ranging from 8 months to 20 yr. It was found that all the subjects had normal serum thyroxine, thyrotropin, cortisol, growth hormone and plasma adrenocorticotropic hormone. Seven cases (11.1%) had low serum triiodothyronine and eight cases (12.7%) had low serum testosterone. On the other hand, 17 cases (27.0%) had hyperprolactinemia; 9 cases (14.3%) had elevated serum testosterone level; 6 cases (9.5%) had elevated serum follicle-stimulating hormone; and 4 cases (6.3%) had elevated serum luteinizing hormone. The level of spinal cord injury, injury period and patient age had no correlation with other serum hormone changes except that quadriplegic subjects had lower serum triiodothyronine than the paraplegic, with a mean of 1.42 +/- 0.30 v 1.70 +/- 0.36 nmol/liter (P < 0.005). Of the eight subjects who had low serum testosterone, none had elevated gonadotropin. There were also eight subjects with elevated follicle-stimulating hormone and/or luteinizing hormone, six of them had normal serum testosterone and two had elevated serum testosterone. This suggested their hypogonadism did not result primarily from classic primary gonadal failure. It could be speculated that other testicular paracrine factors and/or alteration of hypothalamus-pituitary-testicular axis are involved in the pathogenesis of hypogonadism. Further studies in this field will provide information regarding male reproductive physiology and may have impact on fertility enhancement options for men with spinal cord injuries. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1466870> Department of Physical Medicine and Rehabilitation, National Taiwan University Hospital, Taipei, Republic of China.

  3. #3

    empty sella and autonomic disturbances after SCI

    I had no autonomic problems prior to SCI,one year after surgery an empty sella was noted. Also developed symptoms of autonomic dysreflexia. Could the injury cause empty sella, then empty sella cause autonomic problems?

    Oh, after SCI developed low albumin which is only detected when serum SPEP test is done. Regular blood testing does not show the lower albumin.

    //

  4. #4
    I'm not familiar with "empty sella". Can you elaborate? (SAH)

  5. #5

    Empty Sella

    The pituitary gland is housed in the sella. For some reason the brain herniates (or the arachnoid)and the cerebral spinal fluid fills the pituitary area and smashes the gland.

    From what I have read, it occurs in obese, multiparious women. Of course those studies are 25 years old. I was not obese, but am becoming heavier which might be because of activity level.
    It can be caused by brain surgery or traumatic child birth (Sheehan's syndrom).

    I am now wondering if it is not caused by cerebral spinal fluid blockage (such as what might occur in SCI)

    My empty sella was not found until after my decompressive surgery when I started to develop autonomic signs and symptoms. Brain MRI reports done prior to surgery do not mention empty sella, it is only after the surgery that it is mentioned.
    A lot of my deficiets developed after surgery.

    I''m really curious and wonder if SCI causes this and if others have it.

    //

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