The Effect of Surgical Weight Reduction on Functional Status in Morbidly Obese Patients with Low Back Pain

Background: Although low back (LBP) pain is not a lifethreatening disease, it is a source of significant discomfort and disability and accounts for work absences. It has been shown previously that morbid obesity is associated with increased frequency of LBP and that surgical weight loss improves the symptomatology. However, there are no studies to quantitatively assess the exact degree of functional disability caused by severe obesity and the degree of improvement of LBP that follows weight loss from bariatric surgery. Methods: 29 morbidly obese candidates for bariatric surgery with LBP, weight 132.5±27 (mean±SD) kg and BMI 47.2±8.8 kg/m² were examined for their functional status using psychometric instruments specifically designed to objectively assess the patients' complaints. The preoperative scores were measured by a) visual analogue scales (VAS1, VAS2, VAS3), b) Roland-Morris disability questionnaire, c) Oswestry LBP disability questionnaire, and d) Waddell disability index, and were compared with the scores obtained by the same instruments 2 years after vertical banded gastroplasty. Results: The postoperative weight (92.3±19 kg) and BMI (32.9±6.3 kg/m²) of the 29 patients were significantly reduced (P<0.001). The improved functional disability scores were statistically significant: a) VAS1 1.59±1.86 (mean±SD) vs 0.32±0.64, P<0.001; b) VAS2 5.5±1.97 vs 2.14±1.88, P<0.001; c) VAS3 0.77±1.11 vs 0.09±0.29, P=0.006, d) Roland-Morris 7.89±5.11 vs 1.89±2.13, P<0.001; e) Oswestry 21.22±15.63 vs 5.61±7.51, P<0.001; f) Waddell 2.81±1.37 vs 0.56±0.72, P<0.001. Conclusions: Surgical weight loss significantly improves the degree of functional disability of morbidly obese patients suffering from LBP.     

Parkinson disease among patients treated for benign prostatic hyperplasia with α1 adrenergic receptor antagonists

BACKGROUNDRecently the α₁ adrenergic receptor antagonist terazosin was shown to activate PGK1, a possible target for the mitochondrial deficits in Parkinson disease related to its function as the initial enzyme in ATP synthesis during glycolysis. An epidemiological study of terazosin users showed a lower incidence of Parkinson disease when compared with users of tamsulosin, an α₁ adrenergic receptor antagonist of a different class that does not activate PGK1. However, prior research on tamsulosin has suggested that it may in fact potentiate neurodegeneration, raising the question of whether it is an appropriate control group.METHODSTo address this question, we undertook an epidemiological study on Parkinson disease occurrence rate in 113,450 individuals from the United States with 5 or more years of follow-up. Patients were classified as tamsulosin users (n = 45,380), terazosin/alfuzosin/doxazosin users (n = 22,690), or controls matched for age, sex, and Charlson comorbidity index score (n = 45,380).RESULTSIncidence of Parkinson disease in tamsulosin users was 1.53%, which was significantly higher than that in both terazosin/alfuzosin/doxazosin users (1.10%, P < 0.0001) and matched controls (1.01%, P < 0.0001). Terazosin/alfuzosin/doxazosin users did not differ in Parkinson disease risk from matched controls (P = 0.29).CONCLUSIONThese results suggest that zosins may not confer a protective effect against Parkinson disease, but rather that tamsulosin may in some way potentiate Parkinson disease progression.FUNDINGThis work was supported by Cerevel Therapeutics.