垂体催乳素瘤的诊断和治疗指南

治疗的目的是PRL水平正常.然而,许多学者认为,最好是降低PRL水平到可能的最低值,因为这一策略能最大可能地缩小肿瘤体积甚至于肿瘤消失.为了避免不能耐受药物和药物不良反应,从低剂量开始治疗,并逐步加量.肿瘤缩小后假使PRL水平保持在正常范围,则可以慢慢减少DA剂量.     

Elevated visual motion detection thresholds in adults with acquired ophthalmoplegia

AIMS: To test the hypothesis that in patients with acquired chronic bilateral ophthalmoplegia, abnormal retinal image slippage during head movements would result in abnormal thresholds for visual perception of motion. METHODS: Five patients (two males and three females) with ophthalmoplegia were included in the study. The average age was 44 years (range 30-69 years). The aetiology of ophthalmoplegia was myasthenia gravis (MG; n=2), chronic progressive external ophthalmoplegia (CPEO; n=2), and chronic idiopathic orbital inflammation. Visual motion detection thresholds were assessed using horizontal and vertical gratings (spatial frequency) set at thresholds for visibility. The grating was then accelerated at 0.09 deg/s(2). The subject's task was to detect the drift direction of the stimulus. RESULTS: Visual motion detection thresholds were raised to a mean of 0.434 deg/s (SD 0.09) (mean normal value 0.287 deg/s (SD 0.08)) for horizontal motion; and to a mean of 0.425 deg/s (SD 0.1) (mean normal value 0.252 deg/s (SD 0.08)) for vertical motion. The difference in values for both horizontal and vertical motion detection were statistically significant when compared with age matched controls; p <0.023 for horizontal motion and p<0.07 for vertical motion (two tailed t test). CONCLUSION: Abnormally raised visual motion thresholds were found in patients with ophthalmoplegia. This may represent a centrally mediated adaptive mechanism to ignore excessive retinal slip and thus avoid oscillopsia during head movements.     

2005 Annual Report of the American Association of Poison Control Centers' national poisoning and exposure database

BACKGROUND: The American Association of Poison Control Centers (AAPCC; http://www.aapcc.org) maintains the national database of information logged by the country's 61 Poison Control Centers (PCCs). Case records in this database are from self-reported calls: they reflect only information provided when the public or healthcare professionals report an actual or potential exposure to a substance (e.g., an ingestion, inhalation, or topical exposure.), or request information/educational materials. Exposures do not necessarily represent a poisoning or overdose. The AAPCC is not able to completely verify the accuracy of every report made to member centers. Additional exposures may go unreported to PCCs, and data referenced from the AAPCC should not be construed to represent the complete incidence of national exposures to any substance(s). U.S. Poison Centers make possible the compilation and reporting of this report through their staffs' meticulous documentation of each case using standardized definitions and compatible computer systems. The 61 participating poison centers in 2005 are: Regional Poison Control Center, Birmingham, AL; Alabama Poison Center, Tuscaloosa, AL; Arizona Poison and Drug Information Center, Tucson, AZ; Banner Poison Control Center, Phoenix, AZ; Arkansas Poison and Drug Information Center, Little Rock, AK; California Poison Control System-Fresno/Madera Division, CA; California Poison Control System-Sacramento Division, CA; California Poison Control System-San Diego Division, CA; California Poison Control System-San Francisco Division, CA; Rocky Mountain Poison and Drug Center, Denver, CO; Connecticut Poison Control Center, Farmington, CT; National Capital Poison Center, Washington, DC; Florida Poison Information Center, Tampa, FL; Florida Poison Information Center, Jacksonville, FL; Florida Poison Information Center, Miami, FL; Georgia Poison Center, Atlanta, GA; Illinois Poison Center, Chicago, IL; Indiana Poison Center, Indianapolis, IN; Iowa Statewide Poison Control Center, Sioux City, IA; Mid-America Poison Control Center, Kansas City, KA; Kentucky Regional Poison Center, Louisville, KY; Louisiana Drug and Poison Information Center, Monroe, LA; Northern New England Poison Center, Portland, ME; Maryland Poison Center, Baltimore, MD; Regional Center for Poison Control and Prevention Serving Massachusetts and Rhode Island, Boston, MA; Children's Hospital of Michigan Regional Poison Control Center, Detroit, MI; DeVos Children's Hospital Regional Poison Center, Grand Rapids, MI; Hennepin Regional Poison Center, Minneapolis, MN; Mississippi Regional Poison Control Center, Jackson, MS; Missouri Regional Poison Center, St Louis, MO; Nebraska Regional Poison Center, Omaha, NE; New Jersey Poison Information and Education System, Newark, NJ; New Mexico Poison and Drug Information Center, Albuquerque, NM; New York City Poison Control Center, New York, NY; Long Island Regional Poison and Drug Information Center, Mineola, NY; Ruth A. Lawrence Poison and Drug Information Center, Rochester, NY; Upstate (formerly Central) New York Poison Center, Syracuse, NY; Western New York Poison Center, Buffalo, NY; Carolinas Poison Center, Charlotte, NC; Cincinnati Drug and Poison Information Center, Cincinnati, OH; Central Ohio Poison Center, Columbus, OH; Greater Cleveland Poison Control Center, Cleveland, OH; Oklahoma Poison Control Center, Oklahoma City, OK; Oregon Poison Center, Portland, OR; Pittsburgh Poison Center, Pittsburgh, PA; The Poison Control Center, Philadelphia, PA; Puerto Rico Poison Center, San Juan, PR; Palmetto Poison Center, Columbia, SC; Tennessee Poison Center, Nashville, TN; Central Texas Poison Center, Temple, TX; North Texas Poison Center, Dallas, TX; Southeast Texas Poison Center, Galveston, TX; Texas Panhandle Poison Center, Amarillo, TX; West Texas Regional Poison Center, El Paso, TX; South Texas Poison Center, San Antonio, TX; Utah Poison Control Center, Salt Lake City, UT; Virginia Poison Center, Richmond, VA; Blue Ridge Poison Center, Charlottesville, VA; Washington Poison Center, Seattle, WA; West Virginia Poison Center, Charleston, WV; Wisconsin Poison Center, Milwaukee, WI.     

Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas

In June 2005, an ad hoc Expert Committee formed by the Pituitary Society convened during the 9th International Pituitary Congress in San Diego, California. Members of this committee consisted of invited international experts in the field, and included endocrinologists and neurosurgeons with recognized expertise in the management of prolactinomas. Discussions were held that included all interested participants to the Congress and resulted in formulation of these guidelines, which represent the current recommendations on the diagnosis and management of prolactinomas based upon comprehensive analysis and synthesis of all available data.     

Imparied cyclic-AMP response to thyrotrophin in congenital hypothyroidism with thyroglobulin deficiency.

A 19 year old man had congenital hypothyroidism and severely retarded development. His thyroid gland was not enlarged and laboratory findings included low serum concentration of T4 (2.8 microgram/100 ml) and T3 (16 ng/100 ml) with a high level of TSH (52 microU/ml) that rose to 192 microU/ml after TRH. 131I uptake by the thyroid was normal (41.5% at 24 h) and did not show a normal increase after exogenous TSH administration (49.5% at 24 h). The perchlorate discharge test was negative and no antibodies against thyroid antigens were found. Studies on the biopsy specimen revealed low iodide trapping by the thyroid slices and no formation of cyclic AMP after TSH was added to the medium. The endogenous TSH of the patient was biologically active increasing cyclic adenosine monophosphate c-AMP concentration in normal thyroid slices. No thyroglobulin was found in the thyroid tissue either by immunological or ultracentrifugational methods. An increased proportion of iodoalbumin was present in the serum. We postulate that the fundamental defect in this gland is an impaired generation of c-AMP by the defective thyroid cell and deficiency of thyroglobulin formation resulting in inadequate thyroxine and triiodothyronine synthesis.