Testicular responses to hCG stimulation at varying doses in men with spinal cord injury.

STUDY DESIGN: Prospective. OBJECTIVES: To test whether provocative stimulation of the testes identifies men with chronic spinal cord injury (SCI), a population in which serum testosterone concentrations are often depressed, possibly due to gonadal dysfunction. To accomplish this objective, conventional and lower than the conventional doses of human chorionic gonadotropin (hCG) were administered. METHODS: Thirty men with chronic SCI (duration of injury >1 year; 18 and 65 years old; 16 eugonadal (>12.1 nmol l-1) and 14 hypogonadal (⩽12.1 nmol l-1)) or able-bodied (AB) men (11 eugonadal and 27 hypogonadal) were recruited for the study. Stimulation tests were performed to quantify testicular responses to the intramuscular administration of hCG at three dose concentrations (ithat is, 400, 2000 and 4000 IU). The hCG was administered on two consecutive days, and blood was collected for serum testosterone in the early morning prior to each of the two injections; subjects returned on day 3 for a final blood sample collection. RESULTS: The average gonadal response in the SCI and AB groups to each dose of hCG was not significantly different in the hypogonadal or eugonadal subjects, with the mean serum testosterone concentrations in all groups demonstrating an adequate response. CONCLUSIONS: This work confirmed the absence of primary testicular dysfunction without additional benefit demonstrated of provocative stimulation of the testes with lower than conventional doses of hCG. Our findings support prior work that suggested a secondary testicular dysfunction that occurs in a majority of those with SCI and depressed serum testosterone concentrations.

Provocative stimulation of the hypothalamic-pituitary-testicular axis in men with spinal cord injury.

STUDY DESIGN: Prospective study. OBJECTIVE: To determine the integrity of the hypothalamic-pituitary-testicular axis in healthy men with spinal cord injury (SCI). METHODS: Thirty healthy men with chronic SCI (37±10 years) and thirty-eight able-bodied (AB) controls (36±10 years) participated. Gonadotropin-releasing hormone (GnRH; 100 µg IV) was administered to determine gonadotropin release, and human chorionic gonadotropin (hCG; 4000 IU IM) was administered to determine testosterone (T) secretion. Responses to stimulation were categorized as 'responder' or 'non-responder' by clinical criteria. Single factor ANOVA with repeated measures was performed to identify group differences. RESULTS: The proportion of responders to pituitary GnRH stimulation was similar in the SCI group (22 subjects (73%) for the follicular-stimulating hormone (FSH) and 23 subjects (76%) for the luteinizing hormone (LH) to that of the AB group. The SCI-responder group had an increased FSH response after stimulation compared with the AB-responder group (P<0.05). The SCI-responder group had a greater LH area under the curve to GnRH stimulation than the AB-responder group (P=0.06). The peak FSH response was at 60 min and the peak LH response at 30 min, regardless of group designation. All groups had similar increases in serum T concentration to hCG stimulation. CONCLUSIONS: The pituitary response to stimulation in healthy men with SCI revealed an augmented FSH response; LH response only trended higher. The testicular response to provocative stimulation was similar in hypogonadal and eugondal subjects and in GnRH responders and non-responders. These findings suggest a lack of hypothalamic drive of pituitary gonadotropin release in healthy people with chronic SCI.

SmartPill technology provides safe and effective assessment of gastrointestinal function in persons with spinal cord injury.

STUDY DESIGN: Spinal cord injury (SCI) results in gastrointestinal (GI) complications, including gastroesophageal reflux disease and constipation, but much of the data is based on older technology. OBJECTIVE: GI transit times were determined in subjects with SCI using a new device called a SmartPill. Our principal goal was to assess whether this new technology can be applied in persons with SCI. METHODS: SCI and age- and gender-matched able-bodied (AB) control subjects not taking proton pump inhibitors were studied. Following an 8-h overnight fast, subjects consumed 120 g EggBeaters (60 kcal), two slices of white bread (120 kcal) and 30 g strawberry jam (74 kcal). A pH calibrated SmartPill capsule was swallowed with 8 ounces of water, after which subjects fasted for an additional 6 h prior to consuming an Ensure Plus nutrition shake (350 kcal). Subjects remained fasted for an additional 2 h, after which time they resumed their regular diets. RESULTS: Twenty subjects with SCI and 10 AB control subjects were studied. Data are expressed as mean±s.d. Comparing the group with SCI to the AB control group, gastric emptying time (GET), colonic transit time (CTT) and whole gut transit time (WGTT) were prolonged (GET: 10.6±7.2 vs 3.5±1.0 h, P<0.01; CTT: 52.3±42.9 vs 14.2±7.6 h, P=0.01; WGTT: 3.3±2.5 vs 1.0±0.7 days, P<0.01). No complications or side effects were reported. CONCLUSION: Our results indicate that the SmartPill technology is a safe, non-invasive assessment technique that provides valid diagnostic information in persons with SCI.

A small-scale clinical trial to determine the safety and efficacy of testosterone replacement therapy in hypogonadal men with spinal cord injury.

Men with spinal cord injury are at an increased risk for secondary medical conditions, including metabolic disorders, accelerated musculoskeletal atrophy, and, for some, hypogonadism, a deficiency, which may further adversely affect metabolism and body composition. A prospective, open label, controlled drug intervention trial was performed to determine whether 12 months of testosterone replacement therapy increases lean tissue mass and resting energy expenditure in hypogonadal males with spinal cord injury. Healthy eugonadal (n = 11) and hypogonadal (n = 11) outpatients with chronic spinal cord injury were enrolled. Hypogonadal subjects received transdermal testosterone (5 or 10 mg) daily for 12 months. Measurements of body composition and resting energy expenditure were obtained at baseline and 12 months. The testosterone replacement therapy group increased lean tissue mass for total body (49.6 ± 7.6 vs. 53.1 ± 6.9 kg; p < 0.0005), trunk (24.1 ± 4.1 vs. 25.8 ± 3.8 kg; p < 0.005), leg (14.5 ± 2.7 vs. 15.8 ±2.6 kg; p = 0.005), and arm (7.6 ± 2.3 vs. 8.0 ± 2.2 kg; p < 0.005) from baseline to month 12. After testosterone replacement therapy, resting energy expenditure (1328 ± 262 vs. 1440 ± 262 kcal/d; p < 0.01) and percent predicted basal energy expenditure (73 ± 9 vs. 79 ± 10%; p < 0.05) were significantly increased. In conclusion, testosterone replacement therapy significantly improved lean tissue mass and energy expenditure in hypogonadal men with spinal cord injury, findings that would be expected to influence the practice of clinical care, if confirmed. Larger, randomized, controlled clinical trials should be performed to confirm and extend our preliminary findings.

A prospective assessment of renal impairment after preparation for colonoscopy: oral sodium phosphate appears to be safe in well-hydrated subjects with normal renal status.

BACKGROUND: The outcome of colonoscopy is highly dependent upon the quality of bowel cleansing prior to the procedure. Oral sodium phosphate solutions (OSPS) or preparations containing polyethylene glycol (PEG) are generally employed. However, the safety of administering OSPS prior to colonoscopy has been questioned because of the potential for renal failure. AIM: To compare rates of renal failure after OSPS and PEG in a randomized, prospective trial and to assess the quality of colonoscopy after these two bowel preparations. METHODS: Subjects with eGFR >or= 60 ml/min/1.73 m(2) and expressed willingness to adhere to hydration recommendations were randomized to OSPS or PEG solutions. Renal function was assessed 1 week prior to, immediately prior to, and 1 week after colonoscopy. RESULTS: No subject had acute kidney failure after OSPS or PEG. OSPS was associated with significant increases in the serum phosphate and sodium levels and significant decreases in the calcium and potassium levels. These values returned to normal limits in all subjects by 1 week after colonoscopy. The quality of colonic cleansing was superior after OSPS than after PEG (Ottawa score 2.5 +/- 2.2 vs. 3.5 +/- 2.3, respectively, P < 0.05). The detection of one or more adenomatous polyps was higher after OSPS than after PEG. CONCLUSIONS: Renal failure was not detected after the use of OSPS for colonoscopy preparation in subjects with recently documented normal renal function who were able to consume the required amounts of water after each dose. However, based on the number of subjects studied, the theoretical risk of this complication is still between 0 and 6.3%. Thus, it is appreciated that only a very large prospective trial would have yielded a more accurate estimate of the likelihood of renal compromise after OSPS. Despite this caveat, OSPS has advantages over PEG in terms of the adequacy of colonic visualization and the number of polyps detected.

Measuring partial body potassium in the legs of patients with spinal cord injury: a new approach.

Patients with acute spinal cord injury (SCI) with paralysis experience rapid and marked muscle atrophy below the level of the lesion. Muscle is lost above the lesion due to enforced bed rest associated with immobilization. Presently, there is no viable method to quantify muscle loss between the time of injury to the initiation of rehabilitation and remobilization. Furthermore, to assess the efficacy of any physical or pharmacological intervention necessitates the ability to accurately determine the impact of these treatments on muscle mass and function. Our results are presented from measurements of regional potassium (K) in the legs of persons with chronic SCI. The intracellular body K, comprising approximately 97% of the total body K, is indicative of the metabolically active cell mass, of which over 50% is located in the skeletal muscle (SM). To assess regional variations in SM mass in the legs, a partial body K (PBK) system designed for this purpose was placed on a potentially mobile cart. The SM mass measured by PBK in an able-bodied control cohort (n = 17) and in patients with chronic SCI (n = 21) was 17.6 +/- 0.86 and 11.0 +/- 0.65 kg, respectively, a difference of approximately 37.5%. However, the difference in the lean tissue mass of the legs obtained by dual-energy absorptiometry (DXA) in the same cohorts was 20.5 +/- 0.86 and 15.5 +/- 0.88 kg, respectively, or a difference of approximately 24.4%. PBK offers a novel approach to obtain regional K measurements in the legs, thus allowing the potential for early and serial assessment of muscle loss in SCI subjects during the acute and subacute periods following paralysis. The basic characteristics and performance of our PBK system and our calibration procedure are described in this preliminary report.

Dual-energy X-ray absorptiometry overestimates bone mineral density of the lumbar spine in persons with spinal cord injury.

BACKGROUND: Bone mineral density (BMD) of the lumbar spine (L-spine) has been reported to be normal or increased in persons with chronic spinal cord injury (SCI). OBJECTIVE: To determine BMD of the L-spine by dual-energy X-ray absorptiometry (DXA) and quantitative computerized tomography (qCT) in men with chronic SCI compared with able-bodied controls. DESIGN: Cross-sectional, comparative study. SETTING: Clinical research unit, Veterans Affairs Medical Center, Bronx, NY, USA and Kessler Institute of Rehabilitation, West Orange, NJ, USA. METHODS: Measurements of the L-spine were made in 20 men with SCI and compared with 15 able-bodied controls. The DXA images were acquired on a GE Lunar DPX-IQ. The qCT images of the L-spine were acquired on a Picker Q series computerized tomographic scanner. RESULTS: The mean ages for the SCI and control groups were 44+/-13 vs 42+/-9 years, and the duration of injury of the group with SCI was 14+/-11 years. There were no significant differences between the SCI and control groups for L-spine DXA BMD (1.391+/-0.210 vs 1.315+/-0.178 g/m(2)) or for L-spine DXA T-score (1.471+/-1.794 vs 0.782+/-1.481). L-spine qCT BMD was significantly lower in the SCI compared with the control group (1.296+/-0.416 vs 1.572+/-0.382 g/m(2), P=0.05); the T-score approached significance (-1.838+/-1.366 vs -0.963+/-1.227, P=0.059). Subjects with moderate degenerative joint disease (DJD) had significantly higher T-scores by DXA than those without or with mild DJD. CONCLUSION: Individuals with SCI who have moderate to severe DJD may have bone loss of the L-spine that may be underestimated by DXA, reducing awareness of the risk of fracture.

Increased intake of calcium reverses vitamin B12 malabsorption induced by metformin.

OBJECTIVE: Of patients who are prescribed metformin, 10-30% have evidence of reduced vitamin B12 absorption. B12-intrinsic factor complex uptake by ileal cell surface receptors is known to be a process dependent on calcium availability Metformin affects calcium-dependent membrane action. The objective of this study was to determine the magnitude and mechanism of the reduction in serum vitamin B12 after metformin administration. RESEARCH DESIGN AND METHODS: A comparative study design was employed using 2 groups (metformin and control). A total of 21 patients with type 2 diabetes received sulfonylurea therapy; 14 of these 21 patients were switched to metformin. Monthly serum total vitamin B12 measurements and holotranscobalamin (holoTCII) (B12-TCII) were performed. After 3 months of metformin therapy, oral calcium supplementation was administered. RESULTS: Serial serum vitamin B12 determinations revealed a similar decline in vitamin B12 and holoTCII. Oral calcium supplementation reversed the metformin-induced serum holoTCII depression. CONCLUSIONS: Patients receiving metformin have diminished B12 absorption and low serum total vitamin B12 and TCII-B12 levels because of a calcium-dependent ileal membrane antagonism, an effect reversed with supplemental calcium.

Chronic baclofen therapy improves the blunted growth hormone response to intravenous arginine in subjects with spinal cord injury.

Human GH (hGH) secretion is stimulated by vigorous physical activity, whereas immobilization reduces its release. In paralyzed subjects with spinal cord injury (SCI), it has recently been shown that the release of hGH to provocative stimulation and plasma insulin-like growth factor-I (IGF-I) levels are reduced. The acute administration of baclofen, a gamma-aminobutyric acid derivative, has been shown to stimulate hGH release. The present study investigated the effect of chronic administration of baclofen on the provocative testing of hGH secretion and plasma IGF-I levels. Sixteen subjects with SCI were studied; eight subjects were treated (40-80 mg/day; > 6 months) with baclofen (Bac+), and eight were not (Bac-). Additionally, 8 non-SCI subjects were studied as controls. The groups were matched for gender and age. The subjects were not receiving any medications known to influence hGH secretion. After an overnight fast, arginine hydrochloride (30 g/subject) was infused iv over 30 min, with blood drawn for hormone determinations at baseline and 30, 60, 90, and 120 min. In the Bac- group compared with the Bac+ group, the arginine-stimulated mean plasma hGH levels at 30 and 60 min (P < 0.05) and peak and sum plasma hGH levels (P < 0.01) were reduced. There were no significant differences in the plasma hGH response between the Bac+ group and the control group. Plasma IGF-I levels may reflect the integrated tissue response to hGH. A significant inverse relationship was present between age and plasma IGF-I levels for the control and Bac+ groups, but not for the Bac- group. The mean plasma IGF-I level was significantly reduced in the Bac- compared with the Bac+ group. No significant differences in mean plasma IGF-I levels were noted between the Bac+ and control groups. SCI is associated with body composition changes and metabolic alterations that may be exacerbated by reduced activity of the hGH-IGF-I axis. Oral chronic baclofen therapy appears to reverse the deleterious effects of paralysis and immobilization on hGH physiology.

Inhibition of bronchial hyperresponsiveness by the GABA-agonist baclofen.

gamma-Aminobutyric acid (GABA) is a well-known inhibitory transmitter of the central nervous system. Recently, the presence of GABA and its receptors has been confirmed in peripheral tissues, including lung tissue. gamma-Aminobutyric acid and the GABA-agonist baclofen have been shown in animal studies to inhibit airway responsiveness to various bronchoconstricting agents. The results of these investigations suggest the possibility of a role for baclofen in the therapy of human airway hyperreactivity. We recently showed that subjects with cervical spinal cord injury (quadriplegia) uniformly exhibit hyperresponsiveness to methacholine. The interruption of sympathetic airway innervation and resultant unopposed cholinergic tone occurring after transection of the cervical spine are thought to explain this phenomenon. We compared bronchial responsiveness with methacholine (PC20) in a control group of otherwise healthy quadriplegic nonsmokers (n = 8) with a similar group of subjects (n = 6) maintained on baclofen for the relief of muscle spasm. Mean PC20 (mg/ml) among the control group was 1.42 +/- 1.6(SD) vs 15.0 +/- 9.1 in the baclofen group (p = 0.001). The inhibition of bronchial hyperresponsiveness in subjects with cervical spinal cord injury maintained on chronic baclofen therapy suggests the drug's ability to block neuronal acetylcholine release within airways, as well as a possible direct effect on airway smooth muscle. This action of baclofen, along with its documented ability in animal lung to inhibit release of other inflammatory mediators, supports further investigation of this drug as a potential therapeutic agent for asthma treatment.

Bronchial hyperresponsiveness after cervical spinal cord injury.

Cervical spinal cord injury results in interruption of sympathetic airway innervation, which originates from the upper thoracic spine, whereas parasympathetic nerve supply, arising in the vagal nuclei of the brainstem, remains intact. To assess the effect of such an altered neural environment on airway reactivity, bronchoprovocation testing was performed on eight subjects with nonacute traumatic lesions of the cervical spine, all of whom were lifetime nonsmokers without history of respiratory symptoms prior to their injury. Bronchial challenge was subsequently repeated after pretreatment with the anticholinergic agent, ipratropium bromide, an inhibitor of airway muscarinic receptors. All subjects demonstrated hyperresponsiveness to methacholine (the concentration of methacholine producing a fall in FEV1 of 20 percent from baseline [PC20] = 1.42 +/- 1.61 [SD] mg/ml). Airway hyperreactivity was completely blocked by pretreatment with inhaled ipratropium bromide (mean PC20 > 25 mg/ml [p < 0.0001]). The bronchial hyperresponsiveness observed in this population most likely reflects the loss of sympathetic airway innervation and resultant unopposed cholinergic bronchoconstrictor tone which results from transection of the cervical spine. Blockade of methacholine hyperresponsiveness with ipratropium bromide suggests a muscarinic receptor-mediated phenomenon.

Airway hyperresponsiveness to methacholine in subjects with spinal cord injury.

Previously, we found that never-smokers with quadriplegia were hyperresponsive to aerosolized methacholine. To further explore the phenomenon, we compared responsiveness to methacholine in never-smokers with that of smokers and ex-smokers. We also evaluated responsiveness in subjects with high paraplegia (lesions at T-1 to T-6) or low paraplegia (lesions at T-7 and below). We found that smokers and ex-smokers with quadriplegia were hyperresponsive to methacholine (provocative concentration causing a 20% fall in FEV1 = 1.9 mg/mL), and that the response was comparable to that found in never-smokers, revealing that hyperresponsiveness among never-smokers cannot be attributed to preinjury airway hyperreactivity that precluded cigarette use. In contrast, subjects with low paraplegia were not hyperresponsive to methacholine. Among subjects with high paraplegia, the three subjects demonstrating airway hyperresponsiveness had significantly lower FEV1 (percent predicted). The findings support the hypothesis that airway hyperresponsiveness in subjects with quadriplegia represents loss of sympathetic innervation of the lung, thereby leaving intact unopposed bronchoconstrictor cholinergic activity. However, reduced lung volumes in these subjects also suggest the possibility that airway hyperresponsiveness is due to loss of ability to stretch airway smooth muscle by deep breathing.

Disorders of carbohydrate and lipid metabolism in veterans with paraplegia or quadriplegia: a model of premature aging.

One hundred veterans with paralysis due to spinal cord injury (SCI), equally divided between those with paraplegia and quadriplegia, and 50 able-bodied veteran controls underwent a 75-g oral glucose tolerance test (OGTT). In subjects with SCI, 22% were diabetic by criteria established by the World Health Organization (WHO), whereas only 6% of the control group were diabetic. Eighty-two percent of the controls had normal (NL) oral glucose tolerance, compared with 38% of those with quadriplegia and 50% of those with paraplegia. Subjects with diabetes mellitus (DM) were older in both the SCI and control groups, but those with SCI developed carbohydrate disorders at younger ages than did the control group. SCI subjects had significantly higher mean glucose and insulin values at several points during the OGTT when compared with controls, suggesting an accentuated state of insulin resistance in those with SCI. Mean fasting plasma glucose (FPG) values for both SCI and control groups were significantly higher in subjects with DM compared with those with NL glucose tolerance. When the FPG value was compared between SCI or control subjects with abnormalities in glucose tolerance, the subgroups with SCI and NL or impaired glucose tolerance (IGT) had significantly lower FPG levels than the respective control subgroups, suggestive of decreased hepatic glucose output in SCI.(ABSTRACT TRUNCATED AT 250 WORDS)

Soft tissue body composition differences in monozygotic twins discordant for spinal cord injury.

To determine the effect of paralysis on body composition, eight pairs of male monozygotic twins, one twin in each pair with paraplegia, were studied by dual-energy X-ray absorptiometry. Significant loss of total body lean tissue mass was found in the paralyzed twins compared with their able-bodied co-twins: 47.5 +/- 6. 7 vs. 60.1 +/- 7.8 (SD) kg (P < 0.005). Regionally, arm lean tissue mass was not different between the twin pairs, whereas trunk and leg lean tissue masses were significantly lower in the paralyzed twins: -3.0 +/- 3.3 kg (P < 0.05) and -10.1 +/- 4.0 kg (P < 0.0005), respectively. Bone mineral content of the total body and legs was significantly related to lean tissue mass in the able-bodied twins (R = 0.88 and 0.98, respectively) but not in the paralyzed twins. However, the intrapair difference scores for bone and lean tissue mass were significantly related (R = 0.80 and 0.81, respectively). The paralyzed twins had significantly more total body fat mass and percent fat per unit body mass index than the able-bodied twins: 4.8 kg (P < 0.05) and 7 +/- 2% (P < 0.01). In the paralyzed twins, total body lean tissue was significantly lost (mostly from the trunk and legs), independent of age, at a rate of 3.9 +/- 0.2 kg per 5-yr period of paralysis (R = 0.87, P < 0.005). Extreme disuse from paralysis appears to contribute to a parallel loss of bone with loss of lean tissue in the legs. The continuous lean tissue loss may represent a form of sarcopenia that is progressive and accelerated compared with that in ambulatory individuals.

Treatment with an anabolic agent is associated with improvement in respiratory function in persons with tetraplegia: a pilot study.

BACKGROUND: Pulmonary complications are a major cause of morbidity and mortality among individuals with cervical spinal cord lesions. Strengthening of the respiratory musculature may reduce these complications. Anabolic steroids have been used to increase muscle mass and improve muscle performance. Oxandrolone, an anabolic steroid, may have beneficial effects on breathing in persons with tetraplegia. METHODS: The effect of one-month treatment with oxandrolone on weight gain and pulmonary function was studied in ten subjects with complete motor tetraplegia. Spirometry, maximal inspiratory and expiratory pressures, and resting self-rating of dyspnea (Borg Scale) were measured at baseline and repeated again at the end of one month of oxandrolone therapy (20 mg/day). Serum lipid profiles and liver function tests were performed before and after treatment. A paired t-test was used to determine pre- and post-treatment differences on the dependent variables. Percent change from baseline was calculated for each variable and tested using a one-sample t-test. RESULTS: On average, the subjects gained 1.4+/-1.5 kg, a 2+/-2% increase in weight (p=0.01). A significant, 9+/-2% improvement was found in the combined measures of spirometry (p<0.005). Maximal inspiratory pressure improved an average of 10+/-7% (p<0.001). Maximal expiratory pressure improved 9+/-13% (non-significant). Subjective self-rating of dyspnea decreased an average of 37+/-28% (p<0.01). CONCLUSIONS: In healthy subjects with tetraplegia, the use of oxandrolone was associated with significant improvements in weight and pulmonary function, and a subjective reduction in breathlessness. Therefore, oxandrolone may be indicated to strengthen respiratory musculature in individuals who have tetraplegia and ventilatory insufficiency aggravated by superimposition of pneumonia or other such conditions. However, long-term use of oxandrolone may not be indicated, due to the adverse complications associated with this class of agents.

Coronary artery disease: metabolic risk factors and latent disease in individuals with paraplegia.

Individuals with spinal cord injury (SCI) currently have a longer life span as a result of recent improvements in medical care. As in the able-bodied population, cardiovascular disease is the leading cause of death in persons with SCI, but it appears to occur at younger ages in those with SCI than in the able-bodied population. The reduction in level of activity and adverse changes in body composition caused by SCI have profound metabolic consequences that may influence the progression and severity of coronary artery disease. Metabolic sequelae of SCI include disorders of carbohydrate and lipid metabolism. Almost half of the 45 active, healthy subjects with paraplegia we studied have a disorder of carbohydrate tolerance, 1 in 5 subjects having a diabetic oral glucose tolerance test. Hyperinsulinemia is found in those with abnormal glucose tolerance. Subjects with paraplegia having impaired glucose tolerance or diabetes mellitus are significantly older than those with normal glucose tolerance. High-density lipoprotein cholesterol is markedly depressed, and low density lipoprotein is relatively elevated. Radionuclide myocardial perfusion imaging after upper body ergometry exercise reveals latent coronary artery disease in 12 of 19 subjects with paraplegia.

Carbohydrate and lipid metabolism in chronic spinal cord injury.

BACKGROUND: Abnormalities of carbohydrate and lipid metabolism are more common in the spinal cord injury (SCI) population than in the able-bodied population. This is an important consideration in the long-term care of individuals with SCI. DESIGN: Literature review. FINDINGS: When compared with the able-bodied population, people with SCI are more likely to have oral carbohydrate intolerance, insulin resistance, elevated low-density lipoprotein cholesterol, and reduced high-density lipoprotein cholesterol, associated with increased prevalences of diabetes mellitus and cardiovascular disease. CONCLUSIONS: Because of increased risk factors for diabetes mellitus and heart disease in individuals with SCI, modifiable risk factors should be addressed, eg, obesity, inactivity, dietary factors, and smoking. To reduce mortality and morbidity associated with these risk factors, periodic screening for carbohydrate and lipid abnormalities is recommended, with appropriate therapeutic interventions.

Viral hepatitis in patients with spinal cord injury is explained by known risk factors.

Spinal cord injury (SCI) has been reported to be associated with viral hepatitis. However, this association may be related to other confounding factors, such as intravenous drug abuse or blood transfusions. Screening for viral hepatitis associated risk factors and serum serologies, including HBsAg, anti-HBc, anti-HBs and anti-HCV testing, were performed in 78 randomly selected SCI patients and 93 non-alcoholic patients attending a general medical clinic. Hepatitis B and C seropositivies in SCI patients were 29.5 percent and 14.1 percent, respectively, and were significantly associated with a history of intravenous drug abuse. In contrast, hepatitis B and C seropositivities in non-alcoholic general medicine clinic patients were 22.6 percent and 2.2 percent, respectively. In the subgroup of patients without known viral hepatitis risk factors, there were no significant differences between SCI and non-alcoholic patients with respect to hepatitis B (21.4 percent vs. 22.1 percent) or hepatitis C (0 percent vs. 1.3 percent) seropositivity. Stepwise logistic regression also failed to detect an association of SCI with viral hepatitis. In conclusion, the increased seroprevalence of hepatitis C in SCI patients is secondary to intravenous drug use and blood transfusions. Further preventive measures such as improved hepatitis screening of blood donors and substance abuse treatment should decrease viral hepatitis exposure in SCI patients.

Prevalence of viral hepatitis B in an urban veteran spinal cord injured population.

The objective of this study was to determine the prevalence of viral hepatitis B (HBV) seropositivity in an urban veteran population with spinal cord injury (SCI) and the relationship of liver function test (LFT) values to HBV seropositivity. Eighty patients with chronic SCI (44 inpatients and 36 outpatients) had liver function tests (LFTs), hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBsAb) and hepatitis B core antibody (anti-HBcAb) evaluated. Seventy-seven able-bodied (non-SCI) outpatients without known viral hepatitis risk factors served as an urban veteran reference group. Results demonstrated a high prevalence of seropositivity for HBV in both veteran groups (SCI = 29 percent; non-SCI = 22 percent). Subdividing the SCI group by inpatients and outpatients, HBV positivity was found to be significantly higher in the SCI inpatients than in either the SCI outpatient (39 percent vs 17 percent, x2 = 4.67, p < 0.05) or non-SCI groups (39 percent vs 22 percent, x2 = 3.80, p = 0.05). For the whole group, the gamma-glutamyl transpeptidase (GGT) level was greater in the HBV seropositive (n = 40) compared with the HBV seronegative (n = 117) populations (82 +/- 17 vs 46 +/- 7 U/L, p = 0.019, respectively). In addition, the subgroup of spinal cord patients seropositive for hepatitis B (n = 23) had a higher mean GGT than their seronegative (n = 57) counterparts (101 +/- 26 vs 47 +/- 9 U/L, p = 0.018, respectively). We conclude that urban veterans in general, and especially those inpatients with SCI, may be at increased risk of HBV infection. An HBV vaccination program for veteran patients with SCI may be warranted.

Levels of plasma homocysteine in persons with spinal cord injury.

BACKGROUND: Premature coronary vascular disease is a leading cause of morbidity and mortality in persons with chronic spinal cord injury (SCI). Evidence indicates that an elevated plasma homocysteine level is an independent risk factor for vascular disease. METHODS: Plasma homocysteine levels were collected in 845 subjects with SCI and compared to those in a reference population. Differences in plasma homocysteine were determined for sex, race/ethnicity, neurological deficit, and age, as well as for serum creatinine concentration. RESULTS: Plasma homocysteine was significantly higher in men than in women. Men were more likely to have moderately or severely elevated plasma homocysteine levels. Stratifying by male sex, greater percentages of whites and African Americans had severely elevated plasma homocysteine levels (>20 micromol/L) compared with Latinos (12% and 14% versus 8%; P > .01). For the total group with SCI, plasma homocysteine levels were not significantly different by race/ethnicity or neurological deficit subgroup. For the total group (P < .05) and within each sex (men, P < .05; women, P < .01), the older age group with SCI (>50 years) had significantly higher mean plasma homocysteine levels than the younger age group. Age was positively related to plasma homocysteine levels in men (P < .05) and women (P < .01). Plasma homocysteine levels were higher among men for any given age than among women (P < .0001) by an average of 3.19 +/- 0.51 micromol/L. Regardless of age or sex, persons with SCI tended to have higher levels of plasma homocysteine than able-bodied persons matched for age and sex. CONCLUSION: Because the risk of a vascular event increases with age, elevated levels of plasma homocysteine place older persons with SCI at further increased risk for a vaso-occlusive event. Of note, there was a stepwise increase in plasma homocysteine concentration for each quartile of higher serum creatinine concentration. Patients who have elevated levels of plasma homocysteine should receive a trial course of daily supplementation with oral folic acid and vitamin B12. If that is ineffective, they should receive vitamin B6 supplementation to lower their plasma homocysteine levels.