Archives of Internal Medicine

doi: 10.1001/archinte.1996.00440050004001pmid: N/A

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doi: 10.1001/archinte.1996.00440050014002pmid: N/A

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Fennerty, M. Brian;Castell, Donald;Fendrick, A. Mark;Halpern, Michael;Johnson, Daniel;Kahrilas, Peter J.;Lieberman, David;Richter, Joel E.;Sampliner, Richard E.

doi: 10.1001/archinte.1996.00440050019003pmid: N/A

Abstract A group of experts from gastroenterology, internal medicine, health economics, medical outcomes, and managed care met in San Francisco, Calif, on September 27, 1994, in an effort to develop clinically and economically effective disease management guidelines to assist physicians in their treatment of gastroesophageal reflux disease in a managed care environment. This article represents a consensus opinion based on the evidence and expert interpretation at the time of that meeting. (Arch Intern Med. 1996;156:477-484) References 1. Hillman AL, Bloom BS, Fendrick AM, Schwartz JJ. Cost and quality effects of alternative treatments for persistent gastroesophageal reflux disease . Arch Intern Med. 1992;152:1467-1472.Crossref 2. Patrick DL, Erickson E. Health Status and Health Policy: Quality of Life in Health Care Evaluation and Resource Allocation . New York, NY: Oxford University Press Inc; 1993. 3. Pope CE. The quality of life following antireflux surgery . World J Surg. 1992;16:355-358.Crossref 4. Stewart AL, Greenfield S, Hays RD, et al. Functional status and well-being of patients with chronic conditions: results from the Medical Outcomes Study . JAMA. 1989;262:907-913.Crossref 5. Dimenas E. Methodological aspects of evaluation of quality of life in upper gastrointestinal diseases . Scand J Gastroenterol. 1993;28:18-21.Crossref 6. Dimenas E, Glise H, Hallerback B, et al. Quality of life in patients with upper gastrointestinal symptoms: an improved evaluation of treatment regimens? Scand J Gastroenterol. 1993;28:681-687.Crossref 7. Brand DL, Eastwood IR, Martin D, Carter WB, Pope CE. Esophageal symptoms, manometry, and histology before and after antireflux surgery . Gastroenterology. 1979;76:1393-1397. 8. Gallup Organization National Survey. Heartburn Across America . Princeton, NJ: Gallup Organization Inc; 1988. 9. Nebel OT, Fornes MF, Castell DO. Symptomatic gastroesophageal reflux: incidence and precipitating factors . Am J Dig Dis. 1976;21:953-956.Crossref 10. Richter JE, Bradley LA, Castel DO. Esophageal chest pain: current controversies in pathogenesis, diagnosis and therapy . Ann Intern Med. 1989; 110:66-78.Crossref 11. Irwin RS, Corrao WM, Pratter MR. Chronic persistent cough in the adult: the frequency and spectrum of causes and successful outcome of specific therapy . Am Rev Respir Dis. 1981;123:413-417. 12. Hewson EG, Sinclair JW, Dalton CB, Richter JE. Twenty-four-hour esophageal pH monitoring: the most useful test for evaluating noncardiac chest pain . Am J Med. 1991;90:576-583.Crossref 13. Sontag SJ, O'Connell S, Khandelwal S, et al. Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy . Gastroenterology. 1990;99:613-620. 14. Dakkak M, Hoare RC, Maslin SC, Bennett GR. Oesophagitis is as important as oesophageal stricture diameter in determining dysphagia . Gut. 1993; 34:152-155.Crossref 15. Winters C, Spurling TJ, Chobanian SJ, et al. Barrett's esophagus: a prevalent occult complication of gastroesophageal reflux disease . Gastroenterology. 1987;92:118-124. 16. Dent J, Dodds WJ, Friedman RH, et al. Mechanism of gastroesophageal reflux in recumbent asymptomatic human subjects . J Clin Invest. 1980; 65:256-267.Crossref 17. Wyman JB, Dent J, Heddle R, Dodds WJ, Toouli J, Downton J. Control of belching by the lower esophageal sphincter . Gut. 1990;31:639-646.Crossref 18. Mittal RK, Rochester DF, McCallum RW. Electrical and mechanical activity in the human lower esophageal sphincter during diaphragmatic contraction . J Clin Invest. 1988;81:1182-1189.Crossref 19. Sloan S, Rademaker AW, Kahrilas PJ. Determinants of gastroesophageal junction incompetence: hiatus hernia, lower esophageal sphincter, or both? Ann Intern Med. 1992:117:977-982.Crossref 20. Johnson LF. 24-hour pH monitoring in the study of gastroesophageal reflux . J Clin Gastroenterol. 1980;2:387-399.Crossref 21. Kahrilas PJ, Dodds WJ, Hogan WJ, Kern M, Arndorfer RC, Reece A. Esophageal peristaltic dysfunction in peptic esophagitis . Gastroenterology. 1986;91:897-904. 22. Mittal RK, Lange RC, McCallum RW. Identification and mechanism of delayed esophageal acid clearance in subjects with hiatus hernia . Gastroenterology. 1987;92:130-135. 23. Sloan S, Kahrilas PJ. Impairment of esophageal emptying with hiatal hernia . Gastroenterology. 1991;100:596-605. 24. Orr WC, Robinson MG, Johnson LF. Acid clearance during sleep in the pathogenesis of reflux esophagitis . Dig Dis Sci. 1981;26:423-427.Crossref 25. Powell DW. Barrier function of epithelia . Am J Physiol. 1981;241:G275-G288. 26. Cameron AJ, Zinsmeister AR, Ballard DJ, Carney JA. Prevalence of columnar-lined (Barrett's) esophagus: comparison of population-based clinical and autopsy findings . Gastroenterology. 1990;99:918-922. 27. Sampliner RF, Hixson LJ, Fennerty MB, Garewal HS. Regression of Barrett's esophagus by laser ablation in an antacid environment . Dig Dis Sci. 1993;38:365-368.Crossref 28. Sampliner RE, Garewal HS, Fennerty MB, Aickin M. Lack of impact of therapy on extent of Barrett's esophagus in 67 patients . Dig Dis Sci. 1990; 35:93-96.Crossref 29. Sampliner RE. Effect of up to 3 years of high-dose lansoprazole in Barrett's esophagus . Am J Gastroenterol. 1994;89:1844-1848. 30. Smith PM, Kerr GD, Cockel R, et al. A comparison of omeprazole and ranitidine in the prevention and recurrence of benign oesophageal stricture . Gastroenterology. 1994;107:1312-1318.Crossref 31. Katzka DA, Castell DO. Successful elimination of reflux symptoms does not insure adequate control of acid reflux in patients with Barrett's esophagus . Am J Gastroenterol. 1994;89:989-991. 32. Hacker JF, Chobanian SJ, Johnson DA, Winters C, Cattau EL. Patient acceptability of upper GI radiography versus endoscopy . South J Med. 1987;80:1091-1093.Crossref 33. Waring JP, Hunter JG, Oddsdottir M, Wo J, Katz E. The preoperative evaluation of patients considered for laparoscopic antireflux surgery . Am J Gastroenterol. 1995;90:35-38. 34. Shindlebeck NE, Klauser AG, Berghammer G, Londong W, Muller-Lissner SA. Three-year follow-up with patients with gastroesophageal reflux disease . Gut. 1992;33:1016-1019.Crossref 35. McDougall NI, Johnston BT, Kee F, et al. Three-year follow-up of reflux oesophagitis: do patients still require acid suppression therapy? Gut. 1994;35( (suppl 4) ):A175. Abstract. 36. Hetzel DJ, Dent J, Reed WD, et al. Healing and relapse of severe peptic esophagitis after treatment with omeprazole . Gastroenterology. 1988; 95:903-912. 37. Johnson DA. Medical therapy of gastroesophageal reflux disease . Am J Med. 1992;92( (suppl 5A) ):88-97.Crossref 38. Thomson ABR, Babiuk L, Kirdeikis P, et al. A dose ranging study of ranitidine in its effect on intragastric and intra-oesophageal acidity in subjects with gastro-oesophageal reflux disease . Aliment Pharmacol Ther. 1994;8:443-451.Crossref 39. Johnson NJ, Boyd EJS, Mills JG, Wood JR. A key treatment of reflux oesophagitis: a multi-centered trial to compare 150 mgs ranitidine b.d. with 300 mgs. ranitidine q.d.s . Aliment Pharmacol Ther. 1989;3:259-266.Crossref 40. Bate CM, Keeling PW, O'Morain C, et al. Comparison of omeprazole and cimetidine in reflux oesophagitis: symptomatic endoscopic and histologic evaluations . Gut. 1990;31:968-972.Crossref 41. Bardhaan, KD, Morris P, Tompson M, et al. Omeprazole in the treatment of erosive oesophagitis refractory to high dose of cimetidine and ranitidine . Gut. 1990;31:745-759.Crossref 42. Lundell L, Backkman L, Ekstrom P, et al. Omeprazole or high-dose ranitidine in the treatment of patients with reflux oesophagitis not responding to 'standard doses' of H2 receptor antagonists . Aliment Pharmacol Ther. 1990;4:145-156.Crossref 43. Rianchai, Porro G, Pace F, Peracchia A. Short-term treatment of refractory reflux oesophagitis with different doses of omeprazole or ranitidine . J Clin Gastroenterol. 1992;15:192-198.Crossref 44. Havelund T, Laursen LS, Lauritsen K. Efficacy of omeprazole in lower grades of gastrooesophageal reflux disease . Scand J Gastroenterol. 1994;29( (suppl 201) ):69-73.Crossref 45. Spencer CM, Faulds D. Lansoprazole: a reappraisal of its pharmacodynamic and pharmacokinetic properties, and its therapeutic efficacy in acid related disease . Drugs. 1994; 48:404-430.Crossref 46. Klinkenberg-Krol EC, Festen HP, Jansen JB, et al. Efficacy and safety of long-term treatment with omeprazole for refractory reflux esophagitis . Ann Intern Med. 1994;121:161-167.Crossref 47. Maton PN. Omeprazole . N Engl J Med. 1991; 324:965-975.Crossref 48. Ramirez B, Richter JE. Review article: promotility drugs and the treatment of gastrooesophageal reflux disease . Aliment Pharmacol Ther. 1993;7:5-20.Crossref 49. Geldof H, Hazelhoff B, Otten MH. Two different dose regimens of cisapride in the treatment of reflux oesophagitis: a double-blind comparison with ranitidine . Aliment Pharmacol Ther. 1993; 7:409-415.Crossref 50. Robinson M, Deckator DL, Maton PN, et al. Omeprazole is superior to ranitidine plus metoclopramide in the short-term treatment of erosive oesophagitis . Aliment Pharmacol Ther. 1993; 7:67-73.Crossref 51. Mundo F, Felix R, Aguilar J, et al. Omeprazole vs ranitidine plus cisapride in the treatment of reflux oesophagitis: comparative endoscopic study . Am J Gastroenterol. 1992;87:1254. 52. Swarbrick ET, Gough AL, Christian J, et al. Prevention of recurrence of oesophageal stricture: a comparative study of lansoprazole and high-dose ranitidine . Gut. 1994;35( (suppl 4) ):A175. Abstract. 53. Dent K, Yeomans ND, Mackinoon M, et al. Omeprazole vs ranitidine for prevention of relapse in reflux oesophagitis: a double-blind trial of their efficacy and safety . Gut. 1994;35:590-598.Crossref 54. Hallerback B, Unge P, Carling L, et al. Omeprazole and ranitidine in long-term treatment of reflux oesophagitis . Gastroenterology. 1994;107:1305-1311.Crossref 55. Lundell L. Long-term treatment of gastrooesophageal reflux disease with omeprazole . Scand J Gastroenterol. 1994;29( (suppl 201) ):74-78.Crossref 56. Marks R, Richter JE, Rizzo J, et al. Omeprazole vs. H2 receptor antagonists in treating patients with peptic stricture and oesophagitis . Gastroenterology. 1994;106:907-915. 57. Lieberman DA. Medical therapy for chronic reflux esophagitis . Arch Intern Med. 1987;147:1717-1720.Crossref 58. Just R, Katzka DA, Castell DO. Omeprazole failure in a patient with gastroesophageal reflux disease . Ann Intern Med. 1994;121:899.Crossref 59. Kasapidis P, Xynos E, Mantides A, et al. Differences in manometry in 24-hour ambulatory pH-metry between patients with and without endoscopic or histologic esophagitis and gastroesophageal reflux disease . Am J Gastroenterol. 1993;88:1893-1899.

Kalra, Sanjay;Bergeron, Catherine;Lang, Anthony E.

doi: 10.1001/archinte.1996.00440050031004pmid: N/A

Abstract Lewy bodies (LBs) are intracytoplasmic neuronal inclusions sometimes found in the brain stem, diencephalon, basal ganglia, and cerebral cortex. Cases designated as diffuse Lewy body disease (DLBD) demonstrate widespread cortical and subcortical Lewy body formation. The fact that DLBD is possibly the second most common cause of dementia after Alzheimer's disease is not generally recognized. We hope to emphasize the importance of this common neurodegenerative disorder by reviewing the literature and our own experience with DLBD. The English-language literature dealing with the clinical and pathological features of DLBD was reviewed. Pathological material from the Canadian Brain Tissue Bank, Toronto, Ontario, was reviewed over a 2-year period from 1991 through 1993. Prominent LB pathology may occur in isolation or mixed with pathological changes seen in Alzheimer's disease. Lewy body diseases include Parkinson's disease that presents with a classic movement disorder and sometimes dementia, and DLBD where LBs occur in a widespread distribution in the cortex in addition to the usual subcortical sites. Diffuse LB disease usually presents with a neurobehavioral syndrome that may include hallucinations, delusions, and psychosis; all patients eventually become demented. A day-to-day fluctuating mental state may be an important distinguishing clinical feature. Parkinsonism may follow the psychiatric disturbance although occasionally it is a presenting feature. Serious life-threatening side effects may occur with the use of standard neuroleptics. The variable clinical features and additional presence of Alzheimer-type pathological changes in many cases of DLBD has led to a confusing and inconsistent classification of LB disease and, together with little awareness of its existence, its misdiagnosis. Although DLBD may be the second most common cause of dementia, the terminology and classification of LB disorders and their relationship to Alzheimer's disease remain sources of intense debate. Further research is needed to resolve these issues and to provide insight into the pathogenesis of LB formation and accompanying neuronal degeneration. (Arch Intern Med. 1996;156:487-493) References 1. Larson EB, Kukull WA, Katzman RL. Cognitive impairment: dementia and Alzheimer's disease . Annu Rev Public Health. 1992;13:431-449.Crossref 2. Aronson MK, Ooi WL, Geva DL, Masur D. Dementia: age-dependent incidence, prevalence, and mortality in the old . Arch Intern Med. 1991;151:989-992.Crossref 3. Canadian Study of Health and Aging Working Group. Canadian study of health and aging: study methods and prevalence of dementia . Can Med Assoc J. 1994;150:899-913. 4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders , Fourth Edition. 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Deposition of detergent-resistant neurofilaments into Lewy body fibrils . Brain Res. 1993;603:121-124.Crossref 12. Dickson DW, Crystal H, Mattiace LA, et al. Diffuse Lewy body disease: light and electron microscopic immunocytochemistry of senile plaques . Acta Neuropathol. 1989;78:572-584.Crossref 13. Kuzuhara S, Mori H, Izumiyama N, Yashimura M, lhara Y. Lewy bodies are ubiquitinated . Acta Neuropathol (Berl) . 1988;75:345-353.Crossref 14. Forno LS. The Lewy body in Parkinson's disease . Adv Neurol. 1986;45:35-43. 15. Pollanen MS, Dickson DW, Bergeron C. Pathology and biology of the Lewy body . J Neuropathol Exp Neurol. 1993;52:183-191.Crossref 16. Kosaka K, Yoshimura M, Ikeda K, Budka H. Diffuse type of Lewy body disease: progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree: a new disease? Clin Neuropathol. 1984;3:185-192. 17. Yoshimura M. 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Senile dementia of Lewy body type: a clinically and neuropathologically distinct form of Lewy body dementia in the elderly . J Neurol Sci. 1990; 95:119-139.Crossref 23. Hansen L, Salmon D, Galasko D, et al. The Lewy body variant of Alzheimer's disease: a clinical and pathologic entity . Neurology . 1990;40:1-8.Crossref 24. De la Monte SM, Wells SE, Hedley-Whyte ET, Growdon JH. Neuropathological distinction between Parkinson's dementia and Parkinson's plus Alzheimer's disease . Ann Neurol. 1989;26:309-320.Crossref 25. Lennox G, Lowe J, Landon M, Byrne EJ, Mayer RJ, Godwin-Austen RB. Diffuse Lewy body disease: correlative neuropathology using anti-ubiquitin immunocytochemistry . J Neurol Neurosurg Psychiatry . 1989;52:1236-1247.Crossref 26. Dickson DW, Ruan D, Crystal H, et al. Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer's disease: light and electron microscopic immunocytochemistry of CA2-3 neurites specific to DLBD . 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Saunders AM, Strittmatter WJ, Schmechel D, et al. Association of apolipoprotein E allele ε4 with late-onset familial and sporadic Alzheimer's disease . Neurology. 1993;43:1467-1472.Crossref 51. Poirier J, Davignon J, Bouthillier D, Kogan S, Bertrand P, Gauthier S. Apolipoprotein E polymorphism and Alzheimer's disease . Lancet. 1993; 342:697-699.Crossref 52. Mayeux R, Stern Y, Ottman R, et al. The apolipoprotein ε4 allele in patients with Alzheimer's disease . Ann Neurol. 1993;34:752-754.Crossref 53. Brousseau T, Legrain S, Berr C, Groulet V, Vidal O, Amouyel P. Confirmation of the ε4 allele of the apolipoprotein E gene as a risk factor for late-onset Alzheimer's disease . Neurology. 1994;44:342-344.Crossref 54. Galasko D, Saitoh T, Xia Y, et al. The apolipoprotein E allele ε4 is overrepresented in patients with the Lewy body variant of Alzheimer's disease . Neurology. 1994;44:1950-1951.Crossref 55. Arai H, Higuchi S, Muramatsu T, Iwatsubo T, Sasaki H, Trojanowski JQ. 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Kim, Chee Jeong;Ryu, Wang Seong;Kwak, Ju Won;Park, Chong Taik;Ryoo, Un Ho

doi: 10.1001/archinte.1996.00440050046005pmid: N/A

Abstract Objective: To investigate the serial changes in Lp(a) lipoprotein levels with the loss of female sex hormones by surgical menopause and with estrogen replacement therapy in the same women. Patients and Methods: Forty-four premenopausal women who underwent a transabdominal hysterectomy (TAH) because of benign gynecological disorders were divided into two groups: women who underwent a TAH and unilateral salpingo-oophorectomy (n=31) and women who underwent a TAH and bilateral salpingo-oophorectomy (n=13). In the group of women who underwent a TAH and bilateral salpingo-oophorectomy, 0.625 mg of conjugated equine estrogen was given daily 2 months after the operation. The levels of Lp(a) lipoprotein and lipids were measured before and at 2 and 4 months after the operation. Results: In the group of women who underwent a TAH and bilateral salpingo-oophorectomy, the mean (±SD) concentration of Lp(a) lipoprotein was increased by 24.5% from 0.48±0.47 mmol/L (18.4± 18.3 mg/dL) to 0.59±0.54 mmol/L (22.9±21.0 mg/dL) after 2 months (P<.05), and it was reduced by 30.6% to 0.41±0.51 mmol/L (15.9±20.1 mg/dL) (P<.005) with therapy with conjugated equine estrogen (Premarin). The Lp(a) lipoprotein levels were not changed in the group of women who underwent a TAH and unilateral salpingooophorectomy. In the group of women who underwent a TAH and bilateral salpingo-oophorectomy, the high-density lipoprotein cholesterol level showed a trend of increase after 2 months from 1.45±0.48 mmol/L (56.1 ±18.5 mg/dL) to 1.58±0.39 mmol/L (61.2±15.1 mg/dL) without statistical significance, and it revealed a significant elevation to 1.76±0.43 mmol/L (68.2± 16.8 mg/dL) with therapy with conjugated equine estrogen (Premarin) compared with that of the basal level (P<.05). Conclusions: The Lp(a) lipoprotein levels appear to be closely associated with female sex hormones. This association might play a pivotal role in postmenopausal increases of atherosclerotic diseases and cardioprotective effect of estrogen in postmenopausal women.(Arch Intern Med. 1996;156:500-504) References 1. Berg K, Dahlen G, Frick MH. Lp(a) lipoprotein and pre-beta 1-lipoprotein in patients with coronary heart disease . Clin Genet. 1974;6:230-235.Crossref 2. Dahlen GH, Guyton JR, Attar M, Farmer JA, Kautz JA, Gotto AM. Association of levels of lipoprotein Lp(a), plasma lipids, and other lipoproteins with coronary artery disease documented by angiography . Circulation. 1986;74:758-765.Crossref 3. Genest J Jr, McNamara JR, Ordovas JM, et al. Lipoprotein cholesterol, apolipoprotein A-1 and B and lipoprotein(a) abnormalities in men with premature coronary artery disease . J Am Coll Cardiol. 1992;19:792-802.Crossref 4. Murai A, Miyahara T, Fujimoto N, Matzuda M. Kameyama M. Lp(a) lipoprotein as a risk factor for coronary heart disease and cerebral infarction . Atherosclerosis. 1986;59:199-204.Crossref 5. Zenker G, Koeltringer P, Bone G, Niederkorn G, Pfeiffer K, Juergens G. Lipoprotein(a) as a strong indicator for cerebrovascular disease . Stroke. 1986;17:942-945.Crossref 6. Utermann G. The mysteries of lipoprotein(a) . Science. 1989;246:904-910.Crossref 7. Brewer HB Jr. Effectiveness of diet and drugs in the treatment patients with elevated Lp(a) levels . In: Scanu AM, ed. Lipoprotein(a) . Orlando, Fla: Academic Press Inc; 1990:211-220. 8. Berg K, Leren TP. Unchanged serum lipoprotein(a) concentrations with lovastatin . Lancet. 1989;2:812.Crossref 9. Vessby B, Kostner G, Lithell H, Thomis J. Diverging effects of cholestyramine on apolipoprotein B and lipoprotein(a) . Atherosclerosis. 1982;44:61-71.Crossref 10. Gurakar A, Hoeg JM, Kostner G, Papadopoulos NM, Brewer HB Jr. Levels of lipoprotein Lp(a) decline with neomycin and niacin treatment . Atherosclerosis. 1985;57:293-301.Crossref 11. Lepre F, Campbell B, Crane S, Hickman P. Low-dose sustained release nicotinic acid (Tri-B3) and lipoprotein(a) . Am J Cardiol. 1992;70:133.Crossref 12. Brown SA, Hutchinson R, Morrisett J, Boerwinkle E, Davis CE, Gotto AM. Plasma lipid, lipoprotein cholesterol, and apoprotein distributions in selected US communities: The Atherosclerosis Risk in Communities (ARIC) Study . Arterioscler Thromb Vase Biol. 1993;13:1139-1158.Crossref 13. Nabulsi AA, Folsom AR, White A, et al. Association of hormone-replacement therapy with various cardiovascular risk factors in postmenopausal women . N Engl J Med. 1993;15:1069-1075.Crossref 14. Soma M, Fumagalli R, Paoletti R, et al. Plasma Lp(a) concentration after oestrogen and progestagen in postmenopausal women . Lancet. 1991;1:612.Crossref 15. Kim CJ, Jang HC, Cho DH, Min YK. Effects of hormone replacement therapy on lipoprotein(a) and lipids in postmenopausal women . Arterioscler Thromb Vasc Biol. 1994;14:275-281.Crossref 16. Naito HK. Reliability of lipid, lipoprotein, and apolipoprotein measurements . Clin Chem. 1988;34:B84-B94. 17. Jauhiainen M, Koskinen P, Ehnhorm C, et al. Lipoprotein(a) and coronary heart disease risk: a nested case-control study of the Helsinki Heart Study participants . Atherosclerosis. 1991;89:59-67.Crossref 18. Ridker PM, Hennekens CH, Stampfer MJ. A prospective study of lipoprotein(a) and the risk of myocardial infarction . JAMA. 1993;270:2159-2199.Crossref 19. Schaefer EJ, Lamon-Fava S, Jenner JL, et al. Lipoprotein(a) levels and the risk of coronary heart disease in men: The Lipid Research Clinics Coronary Primary Prevention Trial . JAMA. 1994;271:999-1003.Crossref 20. Moliterno DJ, Leffert CC, Lange RA, et al. Plasma lipoprotein(a) is not a risk factor for coronary atherosclerosis in blacks . Circulation. 1992;86( (suppl 1) ): 337. Abstract.Crossref 21. Marcovina SM, Alber JJ, Jacobs DR Jr, et al. Lipoprotein(a) concentrations and apolipoprotein(a) phenotypes in Caucasians and African Americans: The CARDIA Study . Arterioscler Thromb Vase Biol. 1993;13:1037-1045.Crossref 22. Meilahn EN. Kuller LH, Matthews KA, Stein EA. Lp(a) concentrations among pre- and postmenopausal women over time : The Healthy Women Study. Circulation. 1991;84( (suppl 2) ):546. Abstract. 23. Kannel WB, Hjortland MC, McNamara PM, Gordon T. Menopause and risk of cardiovascular disease . Ann Intern Med. 1976;85:447-452.Crossref 24. Knopp RH. The effect of postmenopausal estrogen therapy on the incidence of arteriosclerotic vascular disease . Obstet Gynecol. 1988;72:23S-30S. 25. Matthews KA, Meilahn E, Kuller LH, Kelsey SF, Caggiula AW, Wing RR. Menopause and risk factors for coronary artery disease . N Engl J Med. 1989;321:641-646.Crossref

Goldberg, Robert J.;Larson, Martin;Levy, Daniel

doi: 10.1001/archinte.1996.00440050051006pmid: N/A

Abstract Background: Whereas a variety of epidemiological stud-ies ies have examined factors associated with overall and cause-specific morbidity and mortality, limited data exist about factors associated with longevity, particularly in middle-aged men and women. The present study examined factors associated with survival to 75 years of age in middle-aged men and women from the community-based Framingham Study. Methods: After excluding persons with cancer, cardiovascular disease, or diabetes, 747 men and 973 women from the Framingham Study, who were 50 years of age at the time of a routine clinical examination and who could potentially reach 75 years of age during follow-up, were studied. Logistic regression modeling was used to examine factors associated with survival to 75 years of age. Results: Fewer cigarettes smoked per day, lower systolic blood pressure, and higher forced vital capacity were associated with longevity in both sexes. Lower heart rate in men and parental survival to 75 years of age in women were additionally associated with survival to 75 years of age. Conclusions: The results of this long-term, prospective study suggest a number of lifestyle characteristics and one familial factor associated with increased life expectancy. These data lend further support to the positive impact on life expectancy of health promotional efforts directed at smoking cessation and control of hypertension in middle-aged men and women.(Arch Intern Med. 1996;156:505-509) References 1. The Pooling Project Research Group. Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events: final report of the Pooling Project . J Chronic Dis. 1978;31:201-306.Crossref 2. Keys A, Aravanis C, Blackburn HW, et al. Epidemiological studies related to coronary heart disease: characteristics of men aged 40-59 in seven countries . Acta Med Scand. 1967;180( (suppl 460) ):1-392. 3. Stamler J, Lindberg HA, Berkson DM, et al. Prevalence and incidence of coronary heart disease in strata of the labor force of a Chicago industrial corporation . J Chronic Dis. 1960;11:405-420.Crossref 4. Epstein FH, Ostrander LD Jr, Johnson BC, et al. Epidemiological studies of cardiovascular disease in a total community— Michigan . Ann Intern Med. 1965;62:1170-1187.Crossref 5. Kagan A, Gordon T, Rhoads GG, Schiffman JC. Some factors related to coronary heart disease incidence in Honolulu Japanese men: the Honolulu Heart Study . Int J Epidemiol. 1975;4:271-279.Crossref 6. Crimmins EM. The changing pattern of American mortality decline, 1940-77, and its implications for the future . Popul Dev Rev. 1986;7:229-254.Crossref 7. Devesa SS, Schneiderman MA. Increase in the number of cancer deaths in the United States . Am J Epidemiol. 1977;106:1-5. 8. Doll R. Major epidemics of the 20th century: from coronary thrombosis to AIDS . J R Stat Soc Am. 1987;150:373-395.Crossref 9. Rothenberg RB, Koplan JP. Chronic disease in the 1990's . Annu Rev Public Health. 1990;11:267-296.Crossref 10. Hahn RA, Teutsch SM, Rothenberg RB, Marks JS. Excess deaths from nine chronic diseases in the United States, 1986 . JAMA. 1990;264:2654-2659.Crossref 11. Vital and Health Statistics for selected years . Bethesda, Md: US Dept of Health and Human Services. 12. Dawber TR, Meadors GF, Moore FE Jr. Epidemiological approaches to heart disease: the Framingham Study . Am J Public Health. 1951;41:279-286.Crossref 13. Gordon T, Kannel WB. Premature mortality from coronary heart disease: the Framingham Study . JAMA. 1971;215:1617-1625.Crossref 14. Shurtleff D. Some characteristics related to the incidence of cardiovascular disease and death: Framingham Study, 16-year follow-up. In: Kannel WB, Gordon T, eds. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease. Washington, DC: US Government Printing Office; 1971: section 26. No. 0-414-297. 15. Gordon T, Sorlie P, Kannel WB. Coronary heart disease, atherothrombotic brain infarction, intermittent claudication: a multivariate analysis of some factors related to their incidence: Framingham Study, 16-year follow-up. In: Kannel WB, Gordon T, eds. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease. Washington, DC: US Government Printing Office; 1971: section 27. No. 426-1301/1345. 16. Hosmer DW Jr, Lemeshow S. Applied Logistic Regression. New York, NY: John Wiley & Sons; 1989. 17. Statistical Analysis System. SAS/STAT User's Guide, Version 6, Fourth Edition, Volume 2: The Logistic Procedure, 1071-1126. Cary, NC: SAS Institute Inc; 1989. 18. Havlik RJ, Feinleib M, eds. Proceedings of the Conference on the Decline in Coronary Heart Disease Mortality. Washington, DC: US Government Printing Office; 1979. No. USDHEW (NIH) 79-1610. 19. Higgins MW, Leupker RV, eds. Trends in Coronary Heart Disease Mortality: The Influence of Medical Care . New York, NY: Oxford University Press; 1988. 20. Stern MP. The recent decline in ischemic heart disease mortality . Ann Intern Med. 1979;91:630-640.Crossref 21. Goldman L, Cook EF. The decline in schemic heart disease mortality rates: an analysis of the comparative effects of medical interventions and changes in lifestyle . Ann Intern Med. 1984;101:825-836.Crossref 22. Goldberg RJ. Temporal trends and declining mortality rates from coronary heart disease in the United States . In: Ockene, Ockene J, eds. Prevention of Coronary Heart Disease . Boston, Mass: Little Brown & Co; 1992:41-68. 23. Menotti A, Keys A, Kromhout D, et al. All cause mortality and its determinants in middle aged men in Finland, the Netherlands, and Italy in a 25 year follow-up . J Epidemiol Community Health. 1991;45:125-130.Crossref 24. Hames CG, Rose K, Knowles M, Davis CE, Tyroler HA. Black-white comparisons of 20-year coronary heart disease mortality in the Evans County Heart Study . Cardiology. 1993;82:122-136.Crossref 25. Goldbourt U, Yaari S, Medalie JH. Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees: a 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study . Cardiology. 1993;82:100-121.Crossref 26. Stamler J. Dyer AR, Shekelle RB, Neaton J. Stamler R. Relationship of baseline major risk factors to coronary and all-cause mortality, and to longevity: findings from long-term follow-up of Chicago cohorts . Cardiology. 1993;82:191-222.Crossref 27. Marmot MG, Smith GD. Why are the Japanese living longer? BMJ. 1989;299:1547-1551.Crossref 28. Curb JD, Reed DM, Miller FD, Yano K. Health status and lifestyle in elderly Japanese men with a long life expectancy . J Gerontol. 1990;45( (suppl) ):S206-S211.Crossref 29. Simons LA, McCallum J, Simons J, Friedlander Y. Health status and lifestyle in elderly Hawaiian Japanese and Australian men: exploring known differences in longevity . Med J Aust. 1992;157:188-190. 30. Brand FN, Kiely DK, Kannel WB, Myers RH. Family patterns of coronary heart disease mortality: the Framingham Longevity Study . J Clin Epidemiol. 1992; 45:169-174.Crossref 31. Harris T, Cook EF, Kannel WB, Goldman L. Proportional hazards analysis of risk factors for coronary heart disease in individuals aged 65 or older: the Framingham Heart Study . J Am Geriatr Soc. 1988;36:1023-1028. 32. Harris T, Cook EF, Garrison R, Higgins M. Kannel W, Goldman L. Body mass index and mortality among nonsmoking older persons: the Framingham Heart Study . JAMA. 1988;259:1520-1524.Crossref

Lockhart, Peter B.

doi: 10.1001/archinte.1996.00440050059007pmid: N/A

Abstract Background: The literature is unclear concerning the nature and incidence of bacteremias from oral surgical procedures, the relationship of these bacteremias to dental disease, and the preventive benefit of antibacterial mouth rinses. Objective: To determine the incidence and nature of bacteremias during single-tooth extractions in adults. Methods: A double-blind, randomized placebo-controlled study of 70 patients in which the status of dental disease was compared with the incidence and nature of aerobic and anaerobic bacteremias following a singletooth extraction and the antibacterial effect of rinses with chlorhexidine hydrochloride. Multiple indicators of dental disease were evaluated and recorded before the surgical procedure. Timing of the mouth rinses, the steps in the surgical procedure, and the two blood drawings were controlled for. Results: Thirty-one (94%) of 34 control patients and 62 (89%) of 70 patients overall had blood cultures positive for organisms at either the l-minute and/or 3-minute mark following the initiation of surgery. The majority of cultures yielded gram-positive cocci. Cultures yielded polymicrobial organisms in 17 patients (24%). Although there was a wide range of severity of odontogenic disease, this did not correlate with results of blood cultures. However, there was a statistically significant difference in the incidence of blood cultures positive for organisms at both shorter (<3 minutes, P=.04) and longer (>6 minutes, P=.04) surgery times. There was no statistically significant difference in either the incidence of blood cultures positive for organisms or in the nature of organisms identified between the chlorhexidine and placebo groups. Conclusions: Single-tooth extraction should be expected to cause a bacteremia regardless of the status of the dentition or periodontium. Mouth rinses with chlorhexidine did not significantly alter the number of positive blood cultures or the nature of the organisms at either of the two blood drawings.(Arch Intern Med. 1996;156:513-520) References 1. Horder TJ. Infective endocarditis with an analysis of 150 cases and with special reference to the chronic form of the disease . Q J Med. 1909;2:289-324. 2. Case records of the Massachusetts General Hospital: weekly clinicopathological exercises . N Engl J Med. 1977;297:546-551. Case 36-1977.Crossref 3. Wohl TA, Kattah JC, Kolsky MP, Alper MA, Horton JC. Hemianopsia from occipital lobe abscess after dental care . Am J Ophthalmol. 1991;112:689-694. 4. Case records of the Massachusetts General Hospital: weekly clinicopathological exercises . N Engl J Med. 1993;328:717-725. Case 10-1993.Crossref 5. Case records of the Massachusetts General Hospital: weekly clinicopathological exercises . N Engl J Med. 1993;329:1335-1341. Case 43-1993.Crossref 6. Lockhart PB, Schmidtke MA. Antibiotic considerations in medically compromised patients . Dent Clin North Am. 1994;38:381-402. 7. Durack DT. Prevention of infective endocarditis . N Engl J Med. 1995;332:38-44.Crossref 8. Guntheroth WG. How important are dental procedures as a cause of infective endocarditis? Am J Cardiol. 1984;54:797-801.Crossref 9. Wahl MJ. Myths of dental-induced endocarditis . Arch Intern Med. 1994;154:137-144.Crossref 10. Van der Meer JTM, van Wijk W, Thompson J, Vandenbroucke JP, Valkenburg HA, Michel MF. Efficacy of antibiotic prophylaxis for prevention of native-valve endocarditis . Lancet. 1992;339:135-139.Crossref 11. Durack DT, Kaplan EL, Bisno AL. Apparent failures of endocarditis prophylaxis: analysis of 52 cases submitted to a national registry . JAMA. 1983;250:2318-2322.Crossref 12. Imperiale TF, Horwitz RI. Does prophylaxis prevent postdental infective endocarditis? a controlled evaluation of protective efficacy . Am J Med. 1990;88:131-136.Crossref 13. Jokinen MA. Prevention of postextraction bacteremia by local prophylaxis . Int J Oral Surg. 1978;7:450-452.Crossref 14. MacFarlane TW, Ferguson MM, Mulgrew CJ. Post-extraction bacteremia: role of antiseptics and antibiotics . Br Dent J. 1984;196:179-181.Crossref 15. Scopp IW, Orvietto LD. Gingival degerming by povidine-iodine irrigation: bacteremia reduction in extraction procedures . J Am Dent Assoc. 1971;83:1294-1296. 16. Brenman HS, Randall E. Local degerming with povidone-iodine, II: prior to gingivectomy . J Periodontol. 1974;45:870-872.Crossref 17. Rise E, Smith JF, Bell J. Reduction of bacteremia after oral manipulations . Arch Otolaryngol. 1969;90:106-109. 18. Francis LE, deVries J, Lang D. An oral antiseptic for the control of postextraction bacteraemia . J Can Dent Assoc. 1973;39:55-57 19. Winslow MB. Millstone SH. Bacteremia after prophylaxis II . J Periodontol. 1965; 36:371-374. 20. Jones JC, Cutcher JL, Goldberg JR, Lilly GE. 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Jolkovsky DL, Otomo-Corgel J, et al. Effects of subgingival irrigation on bacteremia following scaling and root planing . J Periodontol. 1990; 61:405-411.Crossref 32. Dajani AS, Bisno AL, Chung KJ, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association . JAMA. 1990;264:2919-2922.Crossref 33. Ross AF, Tinker JH. Anesthesia risk . In: Miller RD, ed. Anesthesia . 3rd ed. New York, NY: Churchill Livingstone Inc; 1990:723. 34. Facklam RR, Washington JA II. Streptococcus and related catalase-negative gram-positive cocci . In: Balows A, Hausler WJ, Herrmann KL, Isenberg HD, Shadomy HI, eds. Manual of Clinical Microbiology. 5th ed. Washington, DC: American Society for Microbiology; 1991:238-257. 35. Brown LJ, Oliver RC, Loe H. Evaluating periodontal status of US employed adults . J Am Dent Assoc. 1990;121:226-232. 36. Saglie FR, Smith CT, Newman MG, et al. The presence of bacteria in the oral epithelium in periodontal disease . J Periodontol. 1986;57:492-500.Crossref 37. Baltch AL. Pressman HL, Schaffer C, et al. Bacteremia in patients undergoing oral procedures: study following parenteral antimicrobial prophylaxis as recommended by the American Heart Association . Arch Intern Med. 1988;148:1084-1088.Crossref 38. Hall G, Hedström SA, Heimdahl A, Nord CE. Prophylactic administration of penicillins for endocarditis does not reduce the incidence of postextraction bacteremia . Clin Infect Dis. 1993;17:188-194.Crossref 39. Morello JA, Matushek SM, Dunne WM, Hinds DB. Performance of a BACTEC nonradiometric medium for pediatric blood cultures . J Clin Microbiol. 1991; 29:359-362. 40. Roberts GJ, Gardner P, Simmons NA. Optimum sampling time for detection of dental bacteraemia in children . Int J Cardiol. 1992;35:311-315.Crossref 41. Heimdahl A, Hall G, Hedberg M, et al. Detection and quantitaion by lysisfiltration of bacteremia after different oral surgical procedures . J Clin Microbiol 1990;28:2205-2209. 42. Elliott SD. Bacteriaemia and oral sepsis . Proc R Soc Med. 1939;32:747-754. 43. Moreillon P. Overholser CD, Malinverni R, Bille J, Glauser MP. Predictors of endocarditis in isolates from cultures of blood following dental extractions in rats with periodontal disease . J Infect Dis. 1988;157:990-995.Crossref 44. Speck WT, Hurwitz GA, Keller G. Transient bacteremia in pediatric patients following dental manipulation . AJDC. 1971;121:286-288. 45. Strand CL, Wajsbort RR, Sturmann K. Effect of iodophor vs iodine tincture skin preparation on blood culture contamination rate . JAMA. 1993;269:1004-1006.Crossref 46. Greenstein G. Effects of subgingival irrigation on periodontal status . J Periodontol. 1987;58:827-836.Crossref 47. Pitcher GR, Newman HN, Strahan JD. Access to subgingival plaque by disclosing agents using mouthrinsing and direct irrigation . J Clin Periodontol 1980;7:300-308Crossref 48. Hardy JH, Newman HN, Strahan JD. Direct irrigation and subgingival plaque . J Clin Periodontol. 1982;9:57-65.Crossref 49. Randall E, Brenman HS. Local degerming with povidone-iodine, I: prior to dental prophylaxis . J Periodontol. 1974;45:866-869.Crossref 50. Witzenberger T, O'Leary TJ, Gillette WB. Effect of a local germicide on the occurrence of bacteremia during subgingival scaling . J Periodontol. 1982;53:172-179.Crossref 51. Eldirini A. Effectiveness of epinephrine in local anesthetic solutions on the bacteremia following dental extraction . J Oral Ther Pharmacol. 1968;4:317-326. 52. Weisdorf DJ, Bostrom B, Raether D, et al. Oropharyngeal mucositis complicating bone marrow transplantation: prognostic factors and the effect of chlorhexidine mouth rinse . Bone Marrow Transplant. 1989;4:89-95. 53. Epstein JB, Vickars L, Spinelli J, Reece D. Efficacy of chlorhexidene and nystatin rinses in prevention of oral complications in leukemia and bone marrow transplantation . Oral Surg Oral Med Oral Pathol. 1992;73:682-689.Crossref 54. Brown AT, Shupe JA. Sims RE, et al. In vitro effect of chlorhexidine and amikacin on oral gram-negative bacilli from bone marrow transplant recipients . Oral Surg Oral Med Oral Pathol 1990;70:715-719.Crossref 55. Hall G, Heimdahl A. New trends in antibiotic prophylaxis of infective endocarditis in patients undergoing surgery in the oral cavity . Swed Dent J. 1989;13:193-200. 56. Lockhart PB, Crist D, Stone PH. The reliability of the medical history in the identification of patients at risk for infective endocarditis . J Am Dent Assoc. 1989;119:417-422. 57. Thayer W. Studies on bacterial (infective) endocarditis . Hopkins Hosp Rep. 1926;22:1-185. 58. Starkebaum M, Durack D, Beeson P. The 'incubation period' of subacute bacterial endocarditis . Yale J Biol Med. 1977;50:49-58. 59. Kaplan EL, Rich H, Gersony W, Manning J. A collaborative study of infective endocarditis in the 1970s . Circulation. 1979;59:327-335.Crossref 60. Prophylaxis of bacterial endocarditis: faith, hope, and charitable interpretations . 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Kawachi, Ichiro;Willett, Walter C.;Colditz, Graham A.;Stampfer, Meir J.;Speizer, Frank E.

doi: 10.1001/archinte.1996.00440050067008pmid: N/A

Abstract Background: Among the many reported central nervous system effects of long-term caffeine use is improvement in mood. Objective: To examine prospectively the relationship of coffee and caffeine intake to risk of death from suicide. Methods: We conducted a 10-year follow-up study (1980 to 1990) in an ongoing cohort of 86 626 US female registered nurses aged 34 to 59 years in 1980, who were free of diagnosed coronary heart disease, stroke, or cancer. Information on coffee and caffeine intake was collected by a semiquantitative food frequency questionnaire in 1980. Deaths from suicide were determined by physician review of death certificates. Results: Fifty-six cases of suicide occurred during 832 704 person-years of observation. Compared with non-drinkers of coffee, the age-adjusted relative risk of suicide in women who consumed two to three cups per day was 0.34 (95% confidence interval [CI], 0.17 to 0.68) and 0.42 (95% CI, 0.21 to 0.86) in women who consumed four or more cups per day (P for linear trend=.002). These findings remained essentially unchanged after adjusting for a broad range of potential confounding factors, including smoking habit, alcohol intake, medication use (diazepam and phenothiazine), history of comorbid disease (hypertension, hypercholesterolemia, or diabetes), marital status, and self-reported stress. A strong inverse relationship was similarly found for caffeine intake from all sources and risk of suicide. Conclusions: The data suggest a strong inverse association between coffee intake and risk of suicide. Whether regular intake of coffee or caffeine has clinically significant effects on the maintenance of affect or the prevention of depression merits further investigation in clinical trials and population-based prospective studies.(Arch Intern Med. 1996;156:521-525) References 1. Chou T. Wake up and smell the coffee: caffeine, coffee, and the medical consequences . West J Med. 1992;1657:544-553. 2. Goldstein A, Kaizer S. Psychotropic effects of caffeine in man, II: alertness, psychomotor coordination, and mood . J Pharmacol Exp Ther. 1965;150:146-151. 3. Goldstein A, Kaizer S, Whitby O. Psychotropic effects of coffee in man, IV: quantitative differences associated with habituation to coffee . Clin Pharmacol Ther. 1978;24:243-252. 4. Griffiths RR, Evans SM, Heishman SJ, et al. Low-dose caffeine discrimination in humans . J Pharmacol Exp Ther. 1990;2556:1123-1132. 5. Klatsky AL, Armstrong MA, Friedman GD. Coffee, tea, and mortality . Ann Epidemiol. 1993;3:375-381.Crossref 6. 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Perrier, Arnaud;Bounameaux, Henri;Morabia, Alfredo;de Moerloose, Philippe;Slosman, Daniel;Didier, Dominique;Unger, Pierre-Francois;Junod, Alain

doi: 10.1001/archinte.1996.00440050079009pmid: N/A

Abstract Background: Assessment of the clinical probability of pulmonary embolism, plasma D-dimer measurement, and lower-limb venous compression ultrasonography have all been advocated in the workup of suspected pulmonary embolism, to minimize the requirement for pulmonary angiography in patients with nondiagnostic lung scans. However, their contribution has not been assessed prospectively. Methods: Three hundred eight consecutive patients who came to the emergency department with suspected pulmonary embolism were managed according to a diagnostic protocol that included clinical probability assessment, lung scan, and sequential noninvasive tests: plasma D-dimer measurement by enzyme-linked immunosorbent assay (a concentration <500 μg/L ruled out pulmonary embolism) and lower-limb B-mode venous compression ultrasonography (a positive finding was diagnostic of venous thromboembolism). Patients without pulmonary embolism according to the diagnostic workup did not receive anticoagulant treatment. The safety of this approach was assessed by a 6-month follow-up. Results: Of the 308 patients, 106 (34%) had a diagnostic lung scan (normal in 43 and high probability in 63). For the remaining 202 patients, noninvasive workup was diagnostic in 125 (62%). Pulmonary embolism was ruled out by a low clinical probability and a nondiagnostic scan in 48 patients and a D-dimer level less than 500 μg/L in 53; pulmonary embolism was established by a high clinical probability and a nondiagnostic scan in seven patients and by a finding of a deep vein thrombosis on ultrasonography in 17. Therefore, only 77 of these 202 patients underwent pulmonary angiography (negative in 55; positive in 22). At 6-month follow-up (completed for 99.4% of the study population), only two of the 199 patients in whom the diagnostic protocol had ruled out pulmonary embolism (1.0% [95% confidence interval, 0.1 to 3.6]) had a thromboembolic event (pulmonary embolism, one; deep vein thrombosis, one). Conclusions: This decision analysis strategy yielded a definitive noninvasive diagnosis in 62% of patients with a nondiagnostic scan and appears to be safe.(Arch Intern Med. 1996;156:531-536) References 1. The PIOPED Investigators. Value of the ventilation-perfusion scan in acute pulmonary embolism . JAMA. 1990;263:2753-2759.Crossref 2. Moser KM. Venous thromboembolism . Am Rev Respir Dis. 1990;141:235249. 3. Stein PD, Athanasoulis C, Alavi A, et al. Complications and validity of pulmonary angiography in acute pulmonary embolism . Circulation. 1992;85:462468.Crossref 4. Sostman HD, Ravin CE, Sullivan DC, Mills SR, Glickman MG, Dorfman GS. Use of pulmonary angiography for suspected pulmonary embolism: influence of scintigraphic diagnosis . AJR Am J Roentgenol. 1982;139:673-677.Crossref 5. Kelley MA, Carson JL, Palevsky HJ, Schwartz JS. Diagnosing pulmonary embolism: new facts and strategies . Ann Intern Med. 1991;114:300-306.Crossref 6. Moser KM. Diagnosing pulmonary embolism: D-dimer needs rigorous evaluation . BMJ. 1994;309:1525-1526.Crossref 7. Stein PD, Hull RH, Saltzmann HA, Pineo G. Strategy for diagnosis of patients with suspected acute pulmonary embolism . Chest. 1993;103:1553-1559.Crossref 8. Bell WR, Simon TL, DeMets DL. The clinical features of submassive and massive pulmonary emboli . Am J Med. 1977;62:355-360.Crossref 9. Hull RD, Raskob GE, Carter CJ, et al. Pulmonary embolism in outpatients with pleuritic chest pain . Arch Intern Med. 1988;148:838-844.Crossref 10. Patil S, Henry JW, Rubenfire M, Stein PD. Neural network in the clinical diagnosis of acute pulmonary embolism . Chest. 1993;104:1685-1689.Crossref 11. Bounameaux H, Cirafici P, de Moerloose P, et al. Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism . Lancet 1991; 337:196-200.Crossref 12. Bounameaux H, de Moerloose P, Perrier A, Reber G. Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview . Thromb Haemost 1994;71:1-6. 13. Goldhaber SZ, Simons GR, Elliott CG, et al. Quantitative D-dimer levels among patients undergoing pulmonary angiography for suspected pulmonary embolism . JAMA. 1993;270:2819-2822.Crossref 14. Becker DM, Philbrick JT, Abbitt PL. Real-time ultrasonography for the diagnosis of lower extremity deep venous thrombosis: the wave of the future? Arch Intern Med. 1989;149:1731-1734.Crossref 15. Lensing AWA, Prandoni P, Brandjes D, et al. Detection of deep vein thrombosis by real-time B-mode ultrasonography . N Engl J Med. 1989;320:342-345.Crossref 16. Perrier A, Bounameaux H, Morabia A, et al. Contribution of D-dimer plasma measurement and lower-limb venous ultrasound to the diagnosis of pulmonary embolism: a decision analysis model . Am Heart J. 1994;127:624-635.Crossref 17. Barritt DW, Jordan SC. Anticoagulant drugs in the treatment of pulmonary embolism . Lancet. 1960;1:1309-1312.Crossref 18. Hull RD, Delmore T, Genton E, et al. Warfarin sodium vs low-dose heparin in the long-term treatment of venous thrombosis . N Engl J Med. 1979;301:855-858.Crossref 19. Morabia A, Steinig-Stamm M, Unger PF, et al. Applicability of decision analysis to everyday practice: a controlled feasibility trial . J Gen Intern Med. 1994; 9:496-502.Crossref 20. Worsley DF, Palevsky HI, Alavi A. A detailed evaluation of patients with acute pulmonary embolism and low- or very-low-probability lung scan interpretations . Arch Intern Med. 1994;154:2737-2741.Crossref 21. Rabinov K, Paulin S. Roentgen diagnosis of venous thrombosis in the leg . Arch Surg. 1972;104:134-144.Crossref 22. Sox HC, Blatt MA, Higgins MC, Marton Kl. Medical Decision Making . Boston, Mass: Butterworths Inc; 1988. 23. StatXact-Turbo: Statistical Software for Exact Nonparametric Inference . Cambridge, Mass: CYTEL Software Corp; 1992. 24. De Moerloose P, Minazio P. Reber G, Perrier A, Bounameaux H. D-dimer determination to exclude pulmonary embolism: a two-step approach using latex as a screening tool . Thromb Haemost. 1994;72:89-91. 25. Hull RD, Raskob GE, Coates G, Panju AA, Gill JG. A new noninvasive management strategy for patients with suspected pulmonary embolism . Arch Intern Med. 1989;149:2549-2555.Crossref 26. Hull RD, Raskob GE, Ginsberg JS, et al. A noninvasive strategy for the treatment of patients with suspected pulmonary embolism . Arch Intern Med. 1994; 154:289-297.Crossref 27. Girard P, Mathieu M, Simonneau G, et al. Recurrence of pulmonary embolism during anticoagulant treatment; a prospective study . Thorax. 1987;42:481486.Crossref 28. Carson JL, Kelley MA, Duff A, Palevitch M. The clinical course of pulmonary embolism . N Engl J Med. 1992;326:1240-1245.Crossref 29. Alpert JS, Smith R, Carlson CJ, Ockene IS, Dexter L, Dalen JE. Mortality in patients treated for pulmonary embolism . JAMA. 1976;236:1477-1480.Crossref 30. Levine MN, Hirsh J, Landefeld S, Raskob G. Hemorrhagic complications of anticoagulant therapy . Chest. 1992;102( (suppl) ):352S-363S.Crossref 31. Oudkerk M, van Beek JR, van Putten WLJ, Büller HR. Cost-effectiveness analysis of various strategies in the diagnostic management of pulmonary embolism . Arch Intern Med. 1993;153:947-954.Crossref

Gillum, Richard F.;Mussolino, Michael E.;Madans, Jennifer H.

doi: 10.1001/archinte.1996.00440050091010pmid: N/A

Abstract Objective: To assess the level of fish consumption as a risk factor for stroke. Methods: Participants were members of the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study, a longitudinal cohort study of a national sample. Included in this analysis were white and black women and men aged 45 to 74 years when examined in 1971 through 1975 who did not report a history of stroke at that time. Av-erage follow-up for survivors was 12 years (maximum, 16 years). The main outcome measure was incident stroke (fatal and nonfatal). Fish consumption at baseline was obtained from a 3-month food frequency questionnaire. Results: White women aged 45 to 74 years who consumed fish more than once a week had an age-adjusted risk of stroke incidence only about half that of women who never consumed fish. This effect persisted after controlling for multiple stroke risk variables (relative risk, 0.55; 95% confidence interval [ CI], 0.32 to 0.93). Fish consumption more than once a week compared with never was not associated with age-adjusted stroke risk in white men aged 45 to 74 years (relative risk, 0.85; 95% CI, 0.49 to 1.46). In black women and men combined aged 45 to 74 years, any fish consumption compared with never was significantly associated with reduced adjusted stroke risk (relative risk, 0.51; 95% CI, 0.30 to 0.88). Conclusions: White women who consumed fish more than once a week had significantly lower stroke incidence than those who never consumed fish. A similar protective effect was seen in black women and men combined. Further studies are needed to confirm these findings and to elucidate mechanisms for the effect of fish consumption on stroke incidence.(Arch Intern Med. 1996;156:537-542) References 1. Kromhout D. Epidemiological aspects of fish in the diet . Proc Nutr Soc. 1993; 52:437-439.Crossref 2. Kromhout D, Bosschieter EB, de Lezenne Coulander C. 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