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Leg Cramps (leg + cramp)
Selected AbstractsOutpatient Intravenous Dihydroergotamine for Refractory Cluster HeadacheHEADACHE, Issue 3 2004E. Magnoux MD Objective.,To evaluate the efficacy and safety of outpatient intravenous dihydroergotamine (DHE) for treatment of refractory cluster headache. Method.,Medical records were retrospectively reviewed of all patients with cluster headache who received outpatient intravenous DHE for treatment of refractory cluster headache between January 1992 and May 2000. Results.,One hundred four treatments were identified in 70 patients. There were 7 dropouts. Of the 97 completed treatments, 60 were for episodic cluster headache and 37 were for chronic cluster headache. Results for all treatments showed complete resolution of pain during the intravenous phase at 1 month in 61 (63%) of 97 cases, partial resolution in 13 cases (15%), and failure in 23 cases (24%). For the treatment of episodic cluster headache, there was complete resolution in 44 (73%) of 60 cases, partial resolution in 9 cases (13%), and failure in 7 cases (12%). For treatment of chronic cluster headache, there was complete resolution in 17 (46%) of the 37 cases, partial resolution in 4 cases (11%), and 16 failures (43%). As regards side effects and safety, the treatment triggered chest pain suspected of being vasospastic angina in 1 patient on day 7 of the treatment, when she was in the subcutaneous phase. Two patients dropped out due to fear of the injection, 1 because of palpitations, 1 because of chest tightness, and 2 others because of leg cramps, nausea, and diarrhea. Conclusions.,Outpatient intravenous DHE is a safe treatment. It is useful for refractory cluster headache, is more effective for the episodic form than the chronic form, and has a rapid onset of action. It did not change the evolution of the episodic form, but it did appear to induce remission in the chronic form or transform it to the episodic form. We advance a hypothesis to explain this. [source] Hemodynamic and Volume Changes during HemodialysisHEMODIALYSIS INTERNATIONAL, Issue 3 2003Robert M. Lindsay Background:,Volume overload is a factor in the hypertension of hemodialysis (HD) patients. Fluid removal is therefore integral to the hemodialysis treatment. Fluid removal by hemodialysis ultrafiltration (UF) may cause intradialytic hypotension and leg cramps. Understanding blood pressure (BP) and volume changes during UF may eliminate intradialytic hypotension and cramps. Studies (S1, S2, and S3) were carried out to determine the amount and direction of changes in body fluid compartments following UF and to determine the relationships between BP, changes in blood volume (,BV), central blood volume (CBV), cardiac output (CO), peripheral vascular resistance (PVR) plus total body water (TBW), and intra- and extracellular fluid volumes (ICF, ECF) in both the whole body and body segments (arms, legs, trunk). Methods:,Indicator dilution technology (Transonic) was used for CBV, CO, and PVR; hematocrit monitoring (Crit-Line) was used for ,BV segmental bioimpedance (Xitron) for TBW, ICF, and ECF. Results:,S1 (n = 21) showed UF sufficient to cause ,BV of ,7% and lead to minor changes (same direction) in CBV and CO, and with cessation of UF, vascular refilling was preferential to CBV. S2 (n = 20) showed that predialysis HD patients are ECF-expanded (ECF/ICF ratio = 0.96, controls = 0.74 [P < 0.0001]) and BP correlates with ECF (r = 0.47, P = 0.35). UF to cause ,BV of ,7% was associated with a decrease in ECF (P < 0.0001) and BP directly (r = 0.46, P = 0.04) plus ,BV indirectly (r = ,0.5, P = 0.024) correlated with PVR, while CBV and CO were maintained. S3 (n = 11) showed that following UF, total-body ECF changes were correlated with leg ECF (r = 0.94) and arm ECF (r = 0.72) but not trunk ECF. Absolute ECF reduction was greatest from the legs. Conclusions:,Predialysis ECF influences BP and UF reduces ,BV and ECF, but CBV and BP are conserved by increasing PVR. ECF reduction is mainly from the legs, hence may cause cramps. Intradialytic hypotension is caused by failure of PVR response. [source] Effect of Teriparatide {rhPTH(1-34)} on BMD When Given to Postmenopausal Women Receiving Hormone Replacement TherapyJOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2006Louis G Ste-Marie Abstract The effects of teriparatide when given in combination with HRT were studied in postmenopausal women with low bone mass or osteoporosis. The data provide evidence that the adverse event profile for combination therapy with teriparatide + HRT together is consistent with that expected for each treatment alone and that the BMD response is greater than for HRT alone. Introduction: Teriparatide {rhPTH(1-34)}, given as a once-daily injection, activates new bone formation in patients with osteoporosis. Hormone replacement therapy (HRT) prevents osteoporosis by reducing bone resorption and formation. Combination therapy with these two compounds, in small clinical trials, increased BMD and reduced vertebral fracture burden. The purpose of this study was to determine whether teriparatide provided additional effect on BMD when given in combination with HRT. Materials and Methods: A randomized, double-blind, placebo-controlled study was conducted in postmenopausal women with either low bone mass or osteoporosis. Patients were randomized to placebo subcutaneous plus HRT (n = 125) or teriparatide 40 ,g/day (SC) plus HRT (TPTD40 + HRT; n = 122) for a median treatment exposure of 13.8 months. Approximately one-half of the patients in each group were pretreated with HRT for at least 12 months before randomization. Patients received 1000 mg calcium and 400,1200 IU of vitamin D daily as oral supplementation. BMD was measured by DXA. Results: Compared with HRT alone, TPTD40 + HRT produced significant (p < 0.001) increases in spine BMD (14% versus 3%), total hip (5.2% versus 1.6%), and femoral neck (5.2% versus 2%) at study endpoint. BMD, in whole body and ultradistal radius, was higher, and in the one-third distal radius was lower, in the combination therapy but not in the HRT group. Serum bone-specific alkaline phosphatase and urinary N-telopeptide/Cr were increased significantly (p < 0.01) in the women receiving TPTD40 + HRT compared with HRT. A similar profile of BMD and bone markers was evident in both randomized patients as well as in subgroups of patients not pretreated or pretreated with HRT. Patients tolerated both the treatments well. Nausea and leg cramps were more frequently reported in the TPTD40 + HRT group. Conclusions: Adding teriparatide, a bone formation agent, to HRT, an antiresorptive agent, provides additional increases in BMD beyond that provided by HRT alone. The adverse effects of teriparatide when added to HRT were similar to the adverse effects described for teriparatide administered alone. Whether teriparatide was initiated at the same time as HRT or after at least 1 year on HRT, the incremental increases over HRT alone were similar. [source] Teriparatide (Biosynthetic Human Parathyroid Hormone 1,34): A New Paradigm in the Treatment of OsteoporosisBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2004Kim T. Brixen Biosynthetic human parathyroid hormone 1,34 (teriparatide) was recently approved in the EU and the USA as the first anabolic treatment of osteoporosis. The effects of teriparatide are mediated by the G-protein-dependent, parathyroid hormone receptor-1 in the cell membrane. The binding of the ligand to the receptor activates adenylate cyclase and a number of phospholipases (A, C, and D) and increases intracellular levels of cAMP and calcium. Intermittent teriparatide increases the number of osteoblasts and bone formation by activation of pre-existing osteoblasts, increased differentiation of lining cells, and reduced osteoblast apoptosis. Anabolic effects of teriparatide on bone have been demonstrated in several species. It increases bone mass, structural integrity, bone diameter, and bone strength. Clinical efficacy was demonstrated in a randomized study comprising 1637 post-menopausal women with osteoporosis showing a 65% and 35% reduction of the relative risk of vertebral and appendicular fractures, respectively, during 18 months of treatment. Moreover, bone mineral density in the lumbar spine and hip increased by 9.7% and 2.6%, respectively. Similar effects on bone mineral density have been reported in men with osteoporosis and in glucocorticoid-induced osteoporosis, however, fracture data are limited in these groups. Direct comparison with alendronate revealed that teriparatide has a more pronounced effect on bone mineral density. Teriparatide should be used in combination with calcium plus vitamin D, and may be combined with hormonal replacement therapy. In contrast, alendronate attenuates the effect of teriparatide. The efficacy of other combinations remains uncertain. After termination of teriparatide, bone mineral density of the lumbar spine is reduced by approximately 2,3% after 2 1/2 years. This decrease is prevented by treatment with bisphosphonates. The most frequent adverse effects with teriparatide are nausea, headache, dizziness, and leg cramps, however, only the latter two differed significantly between the groups receiving teriparatide 20 ,g/day and placebo. In the pivotal clinical study, reduced dosage or termination of therapy due to hypercalcaemia was necessary in 3% and 0.2%, respectively. In a rat toxicology study, in which teriparatide was administered in high dosages for an extended period of time, osteosarcoma was seen in a significant number of animals. However, none of the approximately 2800 patients in clinical trials has developed osteosarcoma. Teriparatide constitutes a break-through in the treatment of severe osteoporosis, although a number of issues about the optimal use of teriparatide remains unsettled. The published data provide proof of concept on anabolic therapy which changes several paradigms of bone physiology. Other parathyroid hormone analogues are being investigated in clinical trials and the development of non-peptide, small molecules targeted at the parathyroid hormone receptor may be envisaged. [source] | ||||||||||