Caffeine-induced hypokalemia: a case report.

BACKGROUND: With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. CASE PRESENTATION: A 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6-2.9 mmol/L) and low urine osmolality (100-130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. CONCLUSIONS: An increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Elderly woman with subacute lower limb weakness and rapid systemic decline.

A 74-year-old woman developed bilateral leg weakness, with fluctuating cognitive and systemic symptoms that progressed despite treatment. Her diagnosis was confirmed at autopsy. Her case was discussed at the Edinburgh Clinical Neurology Course 2019 Clinicopathological Conference.

Strict Control of Blood Glucose With an Intravenous Insulin Infusion Decreases the Risk of Post-operative Lower Extremity Weakness After Complex Endovascular Aortic Aneurysm Repair.

OBJECTIVE/BACKGROUND: It has previously been shown that post-operative lower extremity weakness (LEW) is associated with elevated blood and cerebrospinal fluid (CSF) glucose levels after branched endovascular aneurysms repair (BEVAR) of extensive aortic aneurysms. The purpose of this study was to determine whether a post-operative insulin infusion protocol (IIP) to achieve tight blood glucose control decreases the rate of LEW. METHODS: From October 2013, blood and CSF samples were collected pre-operatively, immediately post-operatively, and on post-operative day one in asymptomatic patients undergoing BEVAR. In July 2016, an IIP was initiated to maintain post-operative blood glucose levels <120 mg/dL for 48 h. Data on demographics, operative repair, complications, and outcomes were collected prospectively. RESULTS: Between October 2013 and April 2018, 43 patients underwent BEVAR. Twenty-two (group A) underwent BEVAR before initiation of the IIP. Of these, seven (32%) developed LEW within 48 h of repair. This was temporary in five (23%) and permanent in two (9%) patients. Post-operative blood glucose levels were significantly higher in patients with LEW compared with those without LEW (140 ± 27 mg/dL vs. 117 ± 16 mg/dL; p = .02). Post-operative CSF glucose levels were significantly higher in patients with LEW compared with those without LEW (102 ± 15 mg/dL vs. 77 ± 15 mg/dL; p = .001). The subsequent 21 patients (group B) underwent BEVAR after initiation of the IIP. No patient in group B developed LEW while on the IIP, but one (5%) developed paraplegia on post-operative day four. The rate of early LEW (<48 h post-operatively) was significantly lower after initiation of the IIP (32% in group A vs. 0% in group B; p = .009). There was no difference in demographics, comorbidities, or operative time between the groups. CONCLUSION: An IIP to control blood glucose after BEVAR is associated with a decreased rate of post-operative LEW. Tight control of blood glucose should be considered after any extensive aortic reconstruction to minimise the risk of post-operative LEW.

Periostin and sclerostin levels in individuals with spinal cord injury and their relationship with bone mass, bone turnover, fracture and osteoporosis status.

BACKGROUND: Spinal cord injury (SCI) induces an acute alteration in bone metabolism. Although the aetiology of the bone disturbances is not precisely known, immobilisation reduces mechanical loading and the morphology of osteocytes, which are the primary mechanosensors. Periostin and sclerostin are secreted mostly by osteocytes and are involved in bone's mechanical response. OBJECTIVE: The present study was conducted to determine whether individuals with SCI present alterations in serum periostin and sclerostin and to assess their relationships with bone mineral density, bone turnover markers, fracture status, time since injury, densitometric osteoporosis and paraplegic vs. tetraplegic status. SUBJECTS AND METHODS: One hundred and thirty-one individuals with SCI (96 males and 35 females; 42.8 ±â€¯13.7 yr old) with a mean 14.2 ±â€¯12.1 years since the time of injury were evaluated and compared with 40 able-bodied controls in a cross-sectional study. Periostin and sclerostin were assayed by ELISA from Biomedica® (Vienna, Austria), and bone turnover markers and areal bone mineral density (aBMD) were concomitantly analysed. RESULTS: Compared with controls, individuals with SCI presented higher periostin (p < 0.01), lower sclerostin (p < 0.001), similar markers of bone turnover levels and lower aBMD at the hip. Compared with chronic individuals, bone turnover markers, sclerostin excepted, values were higher as well as aBMD at hip in individuals with acute SCI. Moreover, the aBMD differences were more marked in tetraplegic than paraplegic individuals. Bone mineral density, fracture status, densitometric osteoporosis and paraplegia vs. tetraplegia did not seem to substantially influence the values of biological markers, sclerostin excepted. CONCLUSION: This study showed for the first time that individuals with SCI presented higher periostin levels than healthy controls only during the acute phase. Conversely, sclerostin levels are lower whatever the post-injury time. Fractures and densitometric osteoporosis were not associated with differences in these two biological markers, whereas paraplegia vs. tetraplegia and fragility fracture status seemed to influence sclerostin levels only.

Effects of upper-body resistance exercise training on serum nesfatin-1 level, insulin resistance, and body composition in obese paraplegic men.

BACKGROUND: As a recently discovered adipokine, nesfatin-1 is conducive to insulin sensitivity, lipid profile, energy balance, and probably obesity. OBJECTIVE: The aim of the present study was to investigate the effect of upper-body resistance exercise training (RET) on nesfatin-1 levels, insulin resistance, lipid profile, and body composition in obese paraplegic men. METHODS: Twenty obese paraplegic men were randomly assigned into control and upper-body RET groups. Upper-body RET was performed for 8 weeks, 3 sessions per week at an intensity corresponding to 60-80% maximum amount of force that can be generated in one maximal contraction in 5 stations (bench press, seated rows, sitting lat pulldown, arm extension, and arm curls). Body fat percentage was determined according to 4-sites skinfold protocol of Durnin and Womersley and Siri equation. Obesity for spinal cord injury patients in the current study was set at BMI >22 kg/m2. Data were statistically analyzed by paired and independent t-test (P < 0.05). RESULTS: We found significant improvements in serum levels of nesfatin-1 (21.13%), insulin sensitivity (8.95%), and high-density lipoprotein (10.87%). Other lipid profile markers, i.e. low-density lipoprotein (4.32%), cholesterol (8.20%), and triglyceride (15.10%) reduced significantly after upper-body RET. Moreover, upper-body RET led to a significant reduction in body mass index (2.36%), body fat percentage (2.79%), and waist-to-hip ratio (2.40%). CONCLUSION: Upper-body RET improved insulin sensitivity, lipid profile, and body composition in paraplegic men. Serum nefastin-1 may be a potential marker of success in weight management in this population.

Differences in Glucose Metabolism Among Women With Spinal Cord Injury May Not Be Fully Explained by Variations in Body Composition.

OBJECTIVE: To investigate the differences in glucose metabolism among women with paraplegic, and tetraplegic spinal cord injury (SCI) in comparison to their able-bodied (AB) counterparts after adjusting for differences in body composition. DESIGN: Cross-sectional study. After an overnight fast, each participant consumed a 75-g glucose solution for oral glucose tolerance test (OGTT). Blood glucose, insulin, and C-peptide concentrations were analyzed before and 30, 60, 90, and 120 minutes after ingesting glucose solution. Insulin sensitivity index (ISI) was estimated using the Matsuda index. Percentage fat mass (%FM) and total body lean mass (TBLM) were estimated using data from dual-energy x-ray absorptiometry. Visceral fat (VF) was quantified using computed tomography. Outcome measures were compared among groups using analysis of covariance with %FM (or VF) and TBLM as covariates. SETTING: Research university. PARTICIPANTS: Women (N=42) with SCI (tetraplegia: n=8; paraplegia: n=14) and their race-, body mass index-, and age-matched AB counterparts (n=20). INTERVENTIONS: Not applicable. RESULTS: At fasting, there was no difference in glucose homeostasis (glucose, insulin, C-peptide concentrations) among 3 groups of women. In contrast, glucose, insulin, and C-peptide concentrations at minute 120 during OGTT were higher in women with tetraplegia versus women with paraplegia and AB women (P<.05, adjusted for TBLM and %FM). In addition, women with tetraplegia had lower ISI (P<.05, adjusted for TBLM and %FM) versus AB women. These differences remained after adjusting for VF and TBLM. CONCLUSION: Our study confirms that impaired glucose metabolism among women with tetraplegia may not be fully explained by changes in their body composition. Future studies exploring additional factors involved in glucose metabolism are warranted.

Spinal Cord Injury Level Influences Acute Plasma Caffeine Responses.

PURPOSE: This study aimed to investigate the absorption curve and acute effects of caffeine at rest in individuals with no spinal cord injury (SCI), paraplegia (PARA), and tetraplegia (TETRA). METHODS: Twenty-four healthy males (eight able-bodied [AB], eight PARA, and eight TETRA) consumed 3 mg·kg caffeine anhydrous (CAF) in a fasted state. Plasma caffeine [CAF], glucose, lactate, free fatty acid, and catecholamine concentrations were measured during a 150-min rest period. RESULTS: Peak [CAF] was greater in TETRA (21.5 µM) compared with AB (12.2 µM) and PARA (15.1 µM), and mean peak [CAF] occurred at 70, 80, and 80 min, respectively. Moderate and large effect sizes were revealed for TETRA compared with PARA and AB (-0.55 and -1.14, respectively) for the total area under the [CAF] versus time curve. Large interindividual responses were apparent in SCI groups. The change in plasma catecholamine concentrations after CAF did not reach significance (P > 0.05); however, both adrenaline and noradrenaline concentrations were lowest in TETRA. Significant increases in free fatty acid were seen over time (P < 0.0005), but there was no significant influence of SCI level. Blood lactate concentration reduced over time (P = 0.022), whereas blood glucose concentration decreased modestly (P = 0.695), and no difference between groups was seen (P > 0.05). CONCLUSION: The level of SCI influenced the caffeine absorption curve, and there was large interindividual variation within and between groups. Individual curves should be considered when using caffeine as an ergogenic aid in athletes with an SCI. The results indicate TETRA should trial low doses in training and PARA may consider consuming caffeine greater than 60 min before exercise performance. The study also supports caffeine's direct effect on adipose tissue, which is not secondary to catecholamine release.

Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes.

STUDY DESIGN: Experimental study. OBJECTIVES: Exercise improves functional capacity in spinal cord injury (SCI). However, exhaustive exercise, especially when sporadic, is linked to the production of reactive oxygen species that may have a detrimental effect on SCI. We aimed to study the effect of a single bout of exhaustive exercise on systemic oxidative stress parameters and on the expression of antioxidant enzymes in individuals with paraplegia. SETTING: The study was conducted in the Physical Therapy department and the Physical Education and Sports department of the University of Valencia. METHODS: Sixteen paraplegic subjects were submitted to a graded exercise test (GET) until volitional exhaustion. They were divided into active or non-active groups. Blood samples were drawn immediately, 1 and 2 h after the GET. We determined plasma malondialdehyde (MDA) and protein carbonylation as markers of oxidative damage. Antioxidant gene expression (catalase and glutathione peroxidase-GPx) was determined in peripheral blood mononuclear cells. RESULTS: We found a significant increase in plasma MDA and protein carbonyls immediately after the GET (P<0.05). This increment correlated significantly with the lactate levels. Active paraplegics showed lower levels of exercise-induced oxidative damage (P<0.05) and higher exercise-induced catalase (P<0.01) and GPx (P<0.05) gene expression after the GET. CONCLUSIONS: These results suggest that exercise training may be useful in SCI patients to develop systemic antioxidant defenses that may protect them against exercise-induced oxidative damage.

Preliminary results of using ALAnerv® in subacute motor incomplete paraplegics.

RATIONALE: To assess whether using ALAnerv® contributes to improvements of outcomes obtained in post SCI patients. OBJECTIVE: A prospective controlled clinical survey also to evaluate the safety and efficacy of ALAnerv® (2cps/ day for 28 days) in motor incomplete (AIS/ Frankel C) paraplegic subacute patients. METHODS AND RESULTS: 59 patients divided in study (treated with ALAnerv®) and control, groups. This survey's follow-up duration was of 28 days. Most of the studied patients were mid-aged (mean 43.75 years old) and respectively, men (64,29% in the study group; 58,06% in controls). We used descriptive statistics (functions: minimum, maximum, mean, median, standard deviation) and for related comparisons, parametric (Student t) and non-parametric (Mann-Whitney, Fisher's exact, chi-square) tests. The primary end-point: AIS motor values' evolution (P= 0.015 - Mann-Whitney), showed that patients treated with ALAnerv® - vs. controls - had a statistically significant better increase of such scores at discharge. Paraclinical parameters, mainly exploring systemic inflammatory status (secondary end-point): ESR dynamics (P=0.13) had no statistical significance; the plasma leucocytes number (P=0.018), the neutrophils' percentage (P=0.001) and fibrinogenemia (P= 0,017) proved in the treated group to have a statistically significant better evolution. We used "Statistical Package for Social Sciences" (SPSS). DISCUSSION: As there is actually no effective curative solution for the devastating pathology following SCI, any medical approach susceptible to bring even limited improvements, such as treatment with ALAnerv® seemed to have proven, is worth being surveyed, under strict circumstances of ethics and research methodology. Considering the necessity for more statistical power concerning primary, secondary end-points, and safety issues, as well, continuing this research is needed. ABBREVIATIONS: SCI = spinal cord injury, TSCI = traumatic spinal cord injury, BBB = blood brain barrier, CNS = central nervous system, SC = spinal cord, NSAIDs = non-steroidal anti-inflammatory drugs, SAIDs = steroidal anti-inflammatory drugs, AIS = American Spinal Injury Association Impairment Scale, SPSS = Statistical Package for Social Sciences, BATEH = Bagdasar-Arseni Teaching Emergency Hospital.

A 7-month-old male with Allan-Herndon-Dudley syndrome and the power of T3.

Allan-Herndon-Dudley syndrome (AHDS, MIM 300523) is an X-linked neurodegenerative disorder characterized by intellectual disability, severe hypotonia, diminished muscle mass, and progressive spastic paraplegia. All affected males have pathognomonic thyroid profiles with an elevated T3 , low-normal free T4 , and normal TSH. Mutations in the monocarboxylate transporter 8 (MCT8) gene, SLC16A2, have been found to be causative. Here, we describe a proband whose extensive evaluation and ultimate diagnosis of AHDS unmasked three previously undiagnosed generations of affected individuals in one family. This case illustrates the need for clinicians to consider obtaining full thyroid studies on individuals with the non-specific findings of severe hypotonia, failure to thrive, and gross motor delay.

Bone mass and hormone analysis in patients with spinal cord injury: evidence for a gonadal axis disruption.

CONTEXT: Bone loss is a constant finding in patients with spinal cord injury (SCI). OBJECTIVE: We sought to evaluate potential modifiable factors that could lead to bone loss in complete motor paraplegia by examining gonadal axis hormones, vitamin D status, and bone markers. DESIGN: This is a cross sectional. SETTING: It includes SCI Outpatient. PATIENTS AND OTHER PARTICIPANTS: Twenty-nine chronic male patients with SCI were compared with 17 age-matched, able-bodied men. MAIN OUTCOME MEASURE: The bone mineral density (BMD) of lower limbs and lumbar spine were measured using dual x-ray absorptiometry. Parathormone, 25-hydroxyvitamin D [25(OH)D], collagen type I C-terminal telopeptide (CTX), and sexual hormone were measured. RESULTS: Patients with SCI had lower BMD at the inferior limbs sites. CTX showed an inverse relationship with the time since injury. Patients had lower free T levels (SCI, 12.00 ± 2.91 vs controls, 19.51 ± 5.72; P ≤ .001), and the majority (72%) had normal/low levels of gonadotropins. Low T, however, was not related to low bone mass in patients with SCI. In the controls, the 25(OH)D level was positively correlated with the T and with the lumbar spine BMD, but these correlations were not observed in the SCI. CONCLUSIONS: Impairment of testicular function after SCI was indicated by the low levels of T and the loss of correlation between T and 25(OH)D levels; this correlation was present in the able-bodied controls. Inappropriate levels of gonadotropins were identified in most patients, featuring a hypogonadotropic hypogonadism and suggesting a disruption of the pituitary-gonadal axis. T concentrations might not be an effective target for bone loss therapy.

Inflammation-mediating cytokine response to acute handcycling exercise with/without functional electrical stimulation-evoked lower-limb cycling.

This feasibility study compared the plasma inflammation-mediating cytokine response to an acute bout of handcycling (HC) with and without the addition of functional electrical stimulation (FES)-evoked lower-limb cycling. On two separate occasions, five recreationally active, community-based participants with motor complete paraplegia (thoracic 5- 7) performed 30 min HC and hybrid exercise (HYB) at a fixed power output. Venous blood samples were collected at rest, immediately postexercise, 1 h postexercise (post+1) and 2 h postexercise (post+2). Plasma interleukin (IL)-6, IL-10, IL-1 receptor antagonist (IL-1ra), adrenaline, and cortisol concentrations were determined via enzyme-linked immunoassay. Plasma IL-6 concentrations were significantly (p < 0.04) elevated (~2.5-fold) at post+1 and post+2 in HYB only. A small (0.5-fold), nonsignificant (p > 0.05) increase in IL-6 was observed at post+1 in HC, with concentrations significantly higher in HYB at post+2 (p < 0.02). Plasma IL-1ra was unaffected in both trials. Although not reaching statistical significance (p = 0.15), a ~1-fold increase in IL-10 concentration was seen in HYB at post+2. In contrast, increases in adrenaline (p < 0.04) and cortisol (p = 0.08) were observed immediately postexercise in HC and HYB. Initial findings suggest paralyzed skeletal muscle releases IL-6 in response to FES-evoked contractions. HYB may provide a greater anti-inflammatory potential in individuals with a thoracic spinal cord injury compared with HC alone.

Peripheral and central venous blood glucose concentrations in dogs and cats with acute arterial thromboembolism.

BACKGROUND: Acute limb paralysis because of arterial thromboembolism (ATE) occurs in cats and less commonly in dogs. ATE is diagnosed based on physical examination findings and, occasionally, advanced imaging. HYPOTHESIS/OBJECTIVES: Peripheral, affected limb venous glucose concentration is decreased in ATE, whereas its systemic concentration is within or above reference interval. ANIMALS: Client-owned cats and dogs were divided into 3 respective groups: acute limb paralysis because of ATE (22 cats and 9 dogs); acute limb paralysis secondary to orthopedic or neurologic conditions (nonambulatory controls; 10 cats and 11 dogs); ambulatory animals presented because of various diseases (ambulatory controls; 10 cats and 9 dogs). METHODS: Prospective observational, clinical study. Systemic and local (affected limb) blood glucose concentrations were measured. Their absolute and relative differences (ΔGlu and %ΔGlu, respectively) were compared among groups. RESULTS: ΔGlu and %ΔGlu were significantly higher in the ATE cats and dogs groups, compared to both of their respective controls (P < .0001 and P < .001, respectively). No significant differences were observed between the control groups. Receiver operator characteristics analysis of ΔGlu and %ΔGlu as predictors of ATE had area under the curve of 0.96 and 0.99 in cats, respectively, and 1.00 and 1.00, in dogs, respectively. ΔGlu cutoffs of 30 mg/dL and 16 mg/dL, in cats and dogs, respectively, corresponded to sensitivity and specificity of 100% and 90% in cats, respectively, and 100% in dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: ΔGlu and %ΔGlu are accurate, readily available, diagnostic markers of acute ATE in paralyzed cats and dogs.

Adiponectin is associated with bone strength and fracture history in paralyzed men with spinal cord injury.

UNLABELLED: We explored the association between adiponectin levels and bone strength in paralyzed men with spinal cord injury. We found that bone strength was inversely associated with circulating adiponectin levels. Thus, strength estimates and adiponectin levels may improve fracture risk prediction and detection of response to osteogenic therapies following spinal cord injury. PURPOSE: Previous research has demonstrated an inverse relationship between circulating adiponectin and bone mineral density, suggesting that adiponectin may be used as a biomarker for bone health. However, this relationship may reflect indirect effects on bone metabolism via adipose-mediated mechanical pathways rather than the direct effects of adipokines on bone metabolism. Thus, we explored the association between circulating adiponectin levels and bone strength in 27 men with spinal cord injury. METHODS: Plasma adiponectin levels were quantified by ELISA assay. Axial stiffness and maximal load to fracture of the distal femur were quantified via finite element analysis using reconstructed 3D models of volumetric CT scans. We also collected information on timing, location, and cause of previous fractures. RESULTS: Axial stiffness and maximal load were inversely associated with circulating adiponectin levels (R (2) = 0.44, p = 0.01; R (2) = 0.58, p = 0.05) after adjusting for injury duration and lower extremity lean mass. In individuals with post-SCI osteoporotic fractures, distal femur stiffness (p = 0.01) and maximal load (p = 0.005) were lower, and adiponectin was higher (p = 0.04) than those with no fracture history. CONCLUSIONS: Based on these findings, strength estimates may improve fracture risk prediction and detection of response to osteogenic therapies following spinal cord injury. Furthermore, our findings suggest that circulating adiponectin may indeed be a feasible biomarker for bone health and osteoporotic fracture risk in paralyzed individuals with spinal cord injury.

Oxidized low-density lipoprotein, matrix-metalloproteinase-8 and carotid atherosclerosis in spinal cord injured subjects.

OBJECTIVE: Previous reports have indicated that subjects with chronic spinal cord injury (SCI) exhibit increased cardiovascular risk compared to able-bodied individuals. This study investigated the relationship between plasmatic oxidized low-density lipoprotein (OxLDL), matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) levels and vascular remodeling in SCI subjects and the role of physical activity in this regard. METHODS: We studied 42 men with chronic (≥2 years) SCI [18 sedentary (S-SCI) and 24 physically active (PA-SCI)] and 16 able-bodied men by clinical, anthropometric, laboratory, and carotid intima-media thickness (IMT) analysis. All enrolled subjects were normotensive, non-diabetics, non-smokers and normolipemic. Plasmatic OxLDL, MMP-2, MMP-8, MMP-9, TIMP-1 and TIMP-2 levels were determined by enzyme-linked immunosorbent assay. RESULTS: Carotid IMT, IMT/diameter ratio and OxLDL levels of PA-SCI and able-bodied subjects were statistically similar. Conversely, S-SCI subjects exhibited higher IMT, IMT/diameter ratio and OxLDL levels compared to PA-SCI (p < 0.01, p < 0.001 and p = 0.01, respectively) and able-bodied (p < 0.001 for all) individuals. Results of bivariate correlation analysis including all injured subjects showed that carotid IMT and IMT/diameter ratio only correlated with OxLDL, MMP-8 and MMP-8/TIMP-1 ratio. Further stepwise regression analysis adjusted for the presence or not of physical activity and age showed that OxLDL was associated with carotid IMT and IMT/diameter ratio, while MMP-8 was associated with IMT/diameter ratio in SCI individuals. CONCLUSIONS: Plasmatic OxLDL and MMP-8 levels are associated with carotid atherosclerosis and there is an interaction among physical inactivity, atherosclerosis and OxLDL in SCI individuals.

Cardiometabolic risk factors in Iranians with spinal cord injury: analysis by injury-related variables.

Persons with spinal cord injury (SCI) have a high prevalence of abnormalities in carbohydrate and lipid metabolism. These abnormalities cause adverse coronary heart disease (CHD) in patients with SCI. In this study, we performed a detailed analysis of the level-specific cardiometabolic risk factors in individuals with SCI and analyzed the association of injury level on these risk factors. This was a cross-sectional study of 162 patients with SCI, assessing the prevalence of diabetes mellitus, dyslipidemia, hypertension, obesity, and smoking. Fasting blood sugar (>100) was diagnosed in 27 patients (16.7%). Of the total patients, 36 (22.2%) had a total cholesterol (TC) level of >200. A triglyceride level of >150 was present in 56 patients (34.6%). Hypertension was present in 2.5% of the entire patient group. Body mass index (BMI), TC, and low-density lipoprotein cholesterol (LDL-C) were significantly higher in the paraplegia group than the tetraplegia group (24.44 +/- 4.23 vs 22.65 +/- 4.27, p = 0.01; 185.71 +/- 40.69 vs 163.28 +/- 37.92, p < 0.001; and 102.51 +/- 28.20 vs 89.15 +/- 22.35, p = 0.01, respectively). Patients with paraplegia may have increased hypertension, higher BMI, and increasing levels of serum LDL-C and TC than those with tetraplegia. Conventional risk factors for CHD should be identified and treated in individuals with SCI.

Low-dose baclofen therapy raised plasma insulin-like growth factor-1 concentrations, but not into the normal range in a predictable and sustained manner in men with chronic spinal cord injury.

OBJECTIVE: To evaluate, whether once-daily oral baclofen administration increases and/or sustains plasma insulin-like growth factor-1 (IGF-1) concentration in 11 men with chronic spinal cord injury (SCI) and IGF-1 deficiency (i.e. <250 ng/ml). DESIGN: Prospective, open-label, dose titration study. Baclofen was administered at 20 mg/day for 8 weeks; then increased to 40 mg/day for another 8 weeks. Plasma IGF-1 and self-reported side effects were measured at baseline and every other week for the duration of the study. RESULTS: The subjects were 43 ± 12 years old, had duration of injury of 20 ± 12 years; eight subjects had a complete motor injury, and eight had paraplegia. Nine of 11 subjects completed the 20 mg/day treatment and 5 subjects completed the 40 mg/day treatment. Plasma IGF-1 levels improved with each baclofen dose; however, only one subject increased from baseline and remained above the targeted physiological range of 250 ng/ml throughout treatment. A significant increase in IGF-1concentration was observed between baseline and week 2 (154 ± 63 vs. 217 ± 69 ng/ml; P < 0.05), weeks 8 and 10 (188 ± 95 vs. 228 ± 93 ng/ml; P < 0.05), and weeks 8 and 16 (188 ± 95 vs. 259 ± 92 ng/ml; P < 0.05). No serious side effects were observed at 20 mg/day; the 40 mg/day dose was less well tolerated. CONCLUSION: Baclofen was not effective at sustaining plasma IGF-1 concentrations in the physiological range in men with chronic SCI.

Spinal cord injury level and the circulating cytokine response to strenuous exercise.

PURPOSE: A complete spinal cord injury (SCI) above the sixth thoracic vertebra (T6) results in the loss of sympathetic innervation of the adrenal medulla. This study examined the effect of a complete SCI above and below T6 on plasma concentrations of epinephrine, circulating interleukin 6 (IL-6) and other inflammatory cytokines in response to acute strenuous exercise. METHODS: Twenty-six elite male wheelchair athletes (8 = C6-C7 tetraplegic [TETRA], 10 = T6-L1 paraplegic [PARA], and 8 = non-spinal-cord-injured controls [NON-SCI]) performed a submaximal exercise test followed by a graded exercise to exhaustion on a motorized treadmill. Blood samples were taken preexercise, postexercise, and 30 min postexercise and analyzed for concentrations of IL-6, IL-10, IL-1 receptor antagonist (IL-1ra), tumor necrosis factor α (TNF-α), epinephrine, and cortisol. RESULTS: The circulating IL-6 concentration was significantly elevated at postexercise and 30 min postexercise (post30; approximately fivefold) in NON-SCI and PARA (P = 0.003), whereas concentrations in TETRA did not change significantly from preexercise values. IL-10, IL-1ra, and TNF-α were unaffected by exercise in all groups; however, both SCI groups presented elevated concentrations of IL-10 compared with NON-SCI (P = 0.001). At postexercise, epinephrine concentrations were significantly higher than preexercise and post30 concentrations in NON-SCI (approximately threefold) and PARA (approximately twofold) (P = 0.02). Plasma epinephrine concentrations were unchanged in TETRA throughout exercise; concentrations were significantly lower than NON-SCI and PARA at all time points. Plasma cortisol concentrations were significantly elevated in all groups at postexercise and post30 compared with preexercise (P < 0.001). Total exercise time was similar between groups (NON-SCI = 38 ± 6; PARA = 35 ± 5; TETRA = 36 ± 5 min). CONCLUSIONS: These findings suggest that the sympathetic nervous system plays an important regulatory role in the circulating IL-6 response to exercise and has implications for the metabolic and inflammatory responses to exercise in individuals with injuries above T6.

Exercise significantly increases plasma adrenaline and oxidized low-density lipoprotein in normal healthy subjects but not in persons with spinal cord injury.

OBJECTIVES: To compare plasma concentrations of oxidized low-density lipoprotein (oxLDL) and adrenaline during exercise between persons with spinal cord injury (SCI) and able-bodied (AB) individuals. DESIGN: Randomized controlled study. SETTING: Human laboratory at a medical university. PARTICIPANTS: Persons with SCI (n=7) and AB individuals (n=9). INTERVENTION: Two-hour arm crank ergometer exercise at 60% maximum oxygen consumption. MAIN OUTCOME MEASURES: Plasma oxLDL and adrenaline levels. RESULTS: Exercise significantly increased plasma adrenaline levels in AB persons (mean ± SD: rest, 45.4±32.2 pg/mL; exercise, 200.9±113.7 pg/mL; P<.05) and persons with SCI; however; the magnitude of the increase in those with SCI was attenuated (mean ± SD: rest, 45.4±14.0 pg/mL; exercise, 83.0±55.8 pg/mL; P<.05). Exercise also significantly increased plasma oxLDL levels in AB persons (mean ± SD: rest, 102.2±30.2 U/L; exercise, 179.7±60.0 U/L; P<.05), but not in persons with SCI (mean ± SD: rest, 124.3±66.0 U/L; exercise, 138.9±59.5 U/L). CONCLUSIONS: The results suggest that increases in plasma adrenaline levels during exercise contribute to the increase in plasma oxLDL levels.