Jewish Hospital

About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.

Use of gabapentin for attenuation of symptoms following rapid opiate detoxification (ROD): -correlation with neurophysiological parameters-

Abstract: Rapid opiate detoxification (ROD) is a technique whereby the opiate-dependent patient is withdrawn acutely, under anesthesia, from the opioid. Following detoxification, patients experience severe back pain and restlessness often accompanied by a restless-leg-syndrome. We evaluated gabapentin given immediately following detoxification to attenuate these symptoms. In addition, we evaluated the use of the somatosensory-evoked potential (SEP) as a parameter to quantitate pain responses. Patients (n=21; mean age 32.5 +/- 7 SD; 12 males, 9 females) underwent ROD with naltrexone (2 x 50 mg) during propofol anesthesia and artificial ventilation (IPPV). Sympathetic overshoot was attenuated by clonidine, and increased bowl movement was managed by continuous i.v. somatostatin. Back pain, restlessness, and restless-leg-syndrome were treated with gabapentin (1200 mg) in the ICU. Efficacy was assessed by the patient's subjective ratings of restlessness (0-4). In addition, measurements of amplitude (microV), latency (ms) of late N100-peak of the somatosensory evoked potential (SEP), and tolerance to an increased electrical nociceptive stimulus (mA) to the forearm were performed. Data were compared to pre-treatment control and to the period shortly after detoxification. From a mean of 8.4 +/- 2.5 microV, N100-peak increased to a mean of 12.3 microV +/- 3.3 (p < 0.005) following opioid detoxification. Gabapentin reduced amplitude height to a mean of 3.5 +/- 1.5 microV. Also, tolerance to nociceptive stimulus, which had dropped to 4.4 mA, increased to 12.5 mA (p < 0.01), while intensity for restlessness and thrashing of limbs dropped from 3.2 to 1.2 (p < 0.05). The sudden displacement of the opiate from its receptor site induced by naltrexone, resulted in a post inhibitory SEP overshoot with an increase in nociceptive afferent volleys, and a lowering in pain threshold. This was associated with back pain, limb thrashing and a restless-leg-syndrome, all of which could be attenuated by gabapentin. The amplitude of late N100-peak parameter appears to be a potential candidate to quantify the increase of nociception in such patients.

An observational study of reduction of insulin resistance and prevention of development of type 2 diabetes mellitus in women with polycystic ovary syndrome treated with metformin and diet

Abstract: Our first specific aim in an observational study of 431 nondiabetic women with polycystic ovary syndrome (PCOS), aged >or=20 years and with >or=11 months follow-up on metformin diet, was to prospectively assess relationships between pretreatment glucose and insulin resistance (IR) and the development of type 2 diabetes mellitus (T2DM) or gestational diabetes (GD). Our second specific aim was to determine whether development of T2DM and GD was independently associated with lesser reduction of IR on metformin diet when compared with women who remained free of T2DM and GD. Women with body mass index or=25 kg/m(2) were, respectively, instructed in a 2000- or 1500-cal/d, high-protein (26% of calories), low-carbohydrate (44%) diet, with 30% of calories as fat and a polyunsaturate-saturate ratio of 2:1. Three groups of women with PCOS were categorized: (a) 17 with no previous GD, who developed T2DM on metformin diet (mean +/- SD follow-up, 49 +/- 33 months), (b) 401 with no previous GD and free of T2DM on metformin diet (follow-up, 38 +/- 25 months), and (c) 13 with either previous GD or GD on metformin diet (follow-up, 38 +/- 25 months). On metformin diet, women who developed T2DM vs those who remained free of T2DM had higher pretreatment glucose (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.03-1.16; P = .003) and homeostasis model assessment of insulin resistance (HOMA-IR) (OR, 1.22; 95% CI, 1.04-1.42; P = .01), and less reduction of HOMA-IR (OR, 0.82; 95% CI, 0.72-0.92; P = .0008). On metformin diet, women either with previous GD or who developed GD vs those who remained free of T2DM had less reduction of HOMA-IR (OR, 0.88; 95% CI, 0.78-0.99; P = .03). By repeated-measures analysis, on metformin diet, women who did not develop T2DM had reduction in HOMA-IR (P < .0001), with the slope of this curve different (P = .002) from the unchanged IR exhibited by women who developed T2DM and different (P = .017) from an increased IR slope (P = .049) in women who had GD. In women with PCOS, pretreatment glucose and IR, and lesser reduction in IR on metformin diet were associated with T2DM and GD.