Citations

The evaluation of chronic wrist pain can be a diagnostic dilemma. Lidocaine injections combined with corticosteroids are often used for both diagnosis and therapy. The purpose of this study was to determine if a midcarpal injection of lidocaine could serve as a diagnostic tool in patients with chronic wrist pain. Specifically, the relationship of pain relief from the injection and improvement of grip strength were compared to the presence of intracarpal pathology as confirmed by wrist arthroscopy. Forty-five patients with chronic wrist pain underwent a midcarpal injection of lidocaine with or without corticosteroids. Forty of the 45 underwent comcomitant steroid injections; a majority of the 40 patients reported relief of pain for two or more weeks. Improvement of pain and improvement of grip strength were determined. Each of these patients subsequently underwent a radiocarpal and midcarpal arthroscopy, and the pathologic findings of arthroscopy were compared to the improvement of pain and grip strength. These data were compared to a cohort of six volunteers without history of wrist pain or trauma that underwent midcarpal injection of lidocaine. Statistical analysis was performed using Reciever-Operator-Characteristic analysis. The average age of patients with chronic pain was 30.3 years, with an average of 9.8 months of wrist pain. The ultimate diagnoses included 35 patients with carpal instability dissociative, two with nondissociative instability, seven with complex instability of the carpus, three with extensor carpi ulnaris tendonitis and one with deQuervain's tenosynovitis. After lidocaine injection, the normal cohort had a mean loss of 2 kg (-5.3%) ( p=0.02) in grip strength, whereas the experimental cohort had a mean improvement in grip strength of 5.73 kg (34.4%). Improvement of pain after injection did not correlate with pathologic arthroscopic findings ( p=0.92). Improvement in grip strength after midcarpal lidocaine injection of 6 kg or 28% had a 73% sensitivity and a 70% specificity ( p=0.02) of having intracarpal pathology at the time of arthroscopy. Of the chronic wrist pain patients, only four had a normal arthroscopy, and the remainder had at least one area of significant pathology attributing to their pain. We conclude that a midcarpal injection of lidocaine can serve as an effective diagnostic tool in the evaluation of the patient with chronic wrist pain. Improvement of grip of 28% with or without relief of pain is highly correlated with intracarpal pathology.

AbstractRecently, a new class of lipid lowering agents [3‐hydroxy‐3‐methylglutaryl (HMG)‐CoA reductase inhibitors] was introduced into clinical practice. The use of these agents could lead to a secondary deficiency in carnitine, which may manifest clinically as a myalgia/myositis—a side effect that is occasionally seen with this class of drugs. In the present study, we examined the effect of an HMG‐CoA reductase inhibitor (lovastatin) on serum and tissue levels of carnitine and carnitine acyltransferase activities in the rabbit. Rabbits (n=6) were fed chow containing lovastatin (30 mg/d) for 16 wk. Blood was collected and tissues (liver, heart, and skeletal muscle) harvested at sacrifice. Free and total carnitine were measured in serum and tissues by a radioenzymatic method. Carnitine acetyltransferase and carnitine palmitoyltransferase (CPT) activities were determined and expressed relative to DNA. Serum free (24.0±2.6 vs. 29.4±3.1 μM) and total (35.1±4.7 vs. 52.8±8.8 μM) carnitine levels increased significantly with 16 wk of treatment. This increase in total carnitine was mainly due to an increase in the levels of serum acylcarnitine (12.7±3.1 vs 26.5±5.7 μM). Tissue levels of total carnitine were significantly decreased by the treatment. Carnitine acetyltransferase was unaffected by the treatment, whereas there was a significant increase in the activity of CPT in the liver and heart.

Abstract Up to one fourth of women diagnosed with early breast cancer (EBC) have tumors that are human epidermal growth factor receptor 2 (HER-2) positive. This is associated with a high risk of relapse and death from meta-static disease. Trastuzumab, a monoclonal antibody directed against the extracellular domain of HER-2, improves survival and quality of life in women with HER-2-positive metastatic breast cancer receiving chemotherapy. Four major adjuvant trials—Herceptin® Adjuvant (HERA), National Surgical Adjuvant Breast and Bowel Project (NSABP) B-31, North Central Cancer Treatment Group (NCCTG) N9831, and Breast Cancer International Research Group (BCIRG) 006—including between them >13,000 women with HER-2-positive EBC, have investigated different adjuvant treatment approaches with trastuzumab. These trials have shown that trastuzumab reduces the 3-year risk of recurrence by about half in this population. The benefit was similar across the trials despite differences in patient populations, chemotherapy regimens, and sequencing of treatment. At a 2-year follow-up, interim results from the combined analysis of the NSABP B-31 and NCCTG N9831 trials showed a one third lower mortality for trastuzumab, and there was a trend toward an overall survival benefit in the HERA and BCIRG trials. A small Finnish trial, FinHer, investigating another regimen of trastuzumab, has also shown similarly positive results. Further follow-up of the major adjuvant trials will clarify the survival benefit for women receiving trastuzumab, as well as the optimal treatment duration (1 or 2 years). Notably, cardiac events in the trastuzumab-containing arms of these trials have remained within acceptable levels, with a slightly higher (0.6%–3.3%) incidence of congestive heart failure that mostly responded to treatment. Further follow-up will provide information on long-term cardiac safety. Overall, results from clinical trials are sufficiently compelling to consider 1 year of adjuvant trastuzumab treatment for women with HER-2-positive EBC based on the risk:benefit ratio demonstrated in these studies.

We describe two adults with stroke-like migraine attacks after radiation therapy (SMART syndrome), propose revised diagnostic criteria, and review the previously reported patients. ‘SMART’ is an acronym for a newly recognized syndrome which occurs as a delayed consequence of cerebral irradiation and consists of prolonged, unilateral, migrainous neurological symptoms with transient, dramatic cortical gadolinium enhancement of the affected cerebral hemisphere and is sometimes punctuated by generalized seizures and ipsilateral EEG slowing. Although the neurological symptoms can last for weeks, full recovery occurs. An appropriate evaluation should exclude alternative explanations.

Abstract Studies were performed to determine if the nonsteroidal anti-inflammatory drug ibuprofen alters bone and mineral metabolism in female rats. In experiment 1, four groups of growing rats underwent either sham operation or ovariectomy (OVX). One week later, controlled-release pellets with ibuprofen or placebo were implanted subcutaneously at the back of the neck. Following 3 weeks of treatment, rats were sacrificed and blood and bone samples were removed for serum assays and histomorphometric analysis. Body growth rate and the static cortical bone measurements made at the tibial diaphysis did not change in response to OVX. OVX, however, did increase radial bone growth, lowered serum 17β-estradiol, reduced uterine weight, and decreased the cancellous bone area of the tibial metaphysis in the rats. Ibuprofen did not alter serum 17β-estradiol or uterine weight but reduced radial bone growth as well as cancellous bone area of the tibial metaphysis in both sham-operated and OVX animals. In experiments 2 and 3, we tested the influence of ibuprofen on the effects of the tissue-selective estrogen agonist tamoxifen and of exogenous 17β-estradiol in the OVX rat. Ibuprofen completely blocked the effects of tamoxifen and partially blocked the effects of 17β-estradiol to prevent cancellous osteopenia. In contrast, ibuprofen did not influence the effects of tamoxifen and 17β-estradiol to reduce radial bone growth. Besides the skeletal effects, ibuprofen suppressed estrogen-induced uterine growth. Our data suggest that ibuprofen blocks selective estrogen receptor-mediated activities in the rat.

Research in genomics is producing new testing and treatments that are altering the way that mental health care is provided. To respond to questions and requests for information from patients and to provide comprehensive care, psychiatric nurses are seeking education on genomics. The planning process, content, and general outcomes of a regional psychiatric conference with the purpose of increasing participants’ knowledge related to genomics are described. Outcomes of learning from the participant’s assessment of knowledge gained and from correct responses to conference content were assessed. Data indicated positive learning occurred following participation in the conference.

Although interleukin 1 (IL-1) receptor signaling events in T helper lymphocytes are incompletely characterized, events associated with translocation of the transcription factor NF-kappa B are receptor-proximal assays of ligand-initiated responses. In this report we demonstrate that the transient nature of IL-1-induced NF-kappa B nuclear translocation occurs as a consequence of ligand-induced receptor desensitization. Other receptor-initiated events including induction of I kappa B alpha phosphorylation, expression of c-jun and junB mRNA, and costimulatory effects on IL-2 synthesis also are altered by IL-1 receptor desensitization. IL-1 receptor desensitization is not initiated by tumor necrosis factor, which also stimulates NF-kappa B translocation, and is not a consequence of alterations in either IL-1 receptor expression or binding affinity. In the absence of IL-1, the effects of desensitization are completely reversed within 18 h. Since IL-1 desensitization is initiated under conditions of low receptor occupancy, it is likely that receptor desensitization results from alterations to a receptor-proximal transducer, rather than from direct modification of the IL-1 receptor. These results suggest that the cyclic nature of the events in the T helper lymphocyte activation program can be controlled, in part, by the reversible desensitization of cell surface IL-1 receptors.