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HICNet Medical News Digest Sun, 06 Feb 1994 Volume 07 : Issue 02 Today's Topics: [MMWR 4 Feb 94] Reported Vaccine-Preventable Disease [MMWR] Prevalence Adults No Risk Factors for Coronory Heart Disease [MMWR] Dracunculiasis Eradication [MMWR] State Cancer Registries Scientists Link Ancient Gene to Human Skull Deformity Scientists Use Fingerprints to Track Gum Disease Bacteria Multicenter Trial Confirms Pilocarpine Improves Dry Mouth +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-1165 Compilation Copyright 1994 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. E-Mail Address: Editor: Internet: david@stat.com FidoNet = 1:114/15 Bitnet = ATW1H@ASUACAD LISTSERV = MEDNEWS@ASUACAD.BITNET (or internet: mednews@asuvm.inre.asu.edu) anonymous ftp = vm1.nodak.edu Notification List = hicn-notify-request@stat.com FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- Date: Sun, 06 Feb 94 22:03:42 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR 4 Feb 94] Reported Vaccine-Preventable Disease Message-ID: <Vk3cHc1w165w@stat.com> Following is the final electronic text from the Morbidity and Mortality Weekly Report (MMWR), vol. 43, no. 4, dated February 4, 1994. The MMWR is published by the U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention (CDC). Inquiries about the MMWR Series, including material to be considered for publication, should be directed to: Editor, MMWR Series, Mailstop C-08, Centers for Disease Control and Prevention, Atlanta, GA 30333; telephone (404) 332-4555. All material in the MMWR Series is in the public domain and may be used and reprinted without special permission; citation as to source, however, is appreciated. ---------------- Current Trends Reported Vaccine-Preventable Diseases -- United States, 1993, and the Childhood Immunization Initiative In the United States, children are routinely vaccinated against nine diseases--diphtheria, Haemophilus influenzae type b (Hib), hepatitis B, measles, mumps, pertussis, poliomyelitis (paralytic), rubella, and tetanus (1). Based on public health surveillance and epidemiologic assessment of most of these diseases, the impact of childhood vaccination on reported occurrence has been substantial (2,3): provisional surveillance data for 1993 indicate that for five of these diseases and for congenital rubella syndrome (CRS), the number of reported cases is at or near the lowest levels ever, suggesting near interruption of transmission of these diseases. This report presents provisional data for December 1993 for these 10 diseases, compares provisional data for 1993 with final data for 1992, and describes the Childhood Immunization Initiative (CII). In December 1993, state health departments reported no cases of CRS, diphtheria, or poliomyelitis, and fewer than five cases each of measles and tetanus (Table 1). In addition, no cases of indigenously acquired measles were reported that could not be linked to chains of transmission from known imported cases during September-December, the longest such period since surveillance began in 1912. Provisional data for 1993 indicate that the numbers of reported cases of CRS, diphtheria, measles, poliomyelitis, rubella, and tetanus were at or near the lowest levels ever (Table 1). Marked differences were observed in the age- specific incidence of invasive H. influenzae disease,* acute hepatitis B, mumps, and pertussis; the number of persons with reported cases for whom age was known was 1211, 11,633, 1515, and 5793, respectively. For invasive H. influenzae disease, preschool-aged (aged less than 5 years) children constituted 399 (33%) cases; for acute hepatitis B, 142 (1%**); for mumps, 275 (18%); and for pertussis, 3753 (65%). Of preschool-aged children with pertussis, 2549 (68%) were aged less than 1 year (4). Reported by: National Immunization Program, CDC. Editorial Note: The findings in this report indicate that the incidences of most vaccine-preventable diseases during 1993 were at or near their lowest reported levels. However, decreases in disease burden and mortality can be sustained only by achieving and maintaining high vaccination levels among children aged 0-2 years. For example, although the incidence of measles was low during 1981-1988, during 1989-1991, a resurgence of measles--attributed primarily to a failure to vaccinate preschool-aged children on time (i.e., early during the second year of life) (5)--accounted for an estimated 55,000 measles cases, 11,000 hospitalizations, and 130 deaths (CDC, unpublished data, 1993). The national response to the resurgence of measles has improved vaccination coverage among children aged 0-2 years. However, because no system has been fully established to ensure that all children complete the recommended series of 11-15 doses of vaccine by their second birthday, vaccination coverage remains unacceptably low in many areas of the United States (1,6). In 1993, the President initiated CII, a more comprehensive national response to undervaccination. The goals of CII are to 1) eliminate indigenous cases of six vaccine-preventable diseases (i.e., diphtheria, Hib disease [among children aged less than 5 years], measles, poliomyelitis, rubella, and tetanus [among children aged less than 15 years] by 1996***; 2) increase vaccination coverage levels to at least 90% among 2-year-old children by 1996 for each of the vaccinations recommended routinely for children (for hepatitis B, the objective is set for 1998) (Table 2); and 3) establish a vaccination-delivery system that maintains and further improves high coverage levels. CII comprises six broad areas of activity that constitute the framework for meeting the nation's goals for 1996 and beyond: o Improve quality and quantity of vaccination-delivery services. State and local health agencies will use new federal resources to hire personnel, extend clinic hours, and encourage health-care providers to use all health-care contacts to administer needed vaccines and reduce obstacles parents encounter in obtaining vaccinations for children (7). Computerized state vaccination information systems are being developed to remind parents when vaccinations are due and to assist health-care providers in determining the vaccination needs of patients. o Increase community participation and education. A long-term, national outreach campaign will be initiated in April 1994 to improve parent awareness of the need for timely childhood vaccination and to prompt health-care providers to use all health-care contacts to administer needed vaccines to children. At the national level, elements of this campaign will include widespread distribution of radio, television, and print public service announcements; dissemination of a national theme and call to action; and other activities designed to unify efforts throughout the country. At the state and community levels, the campaign will include a grass roots organizing effort to unite all sectors of the community (e.g. public and private health-care providers, business groups, community leaders, minority groups, voluntary and service organizations, religious institutions, and media affiliates). o Reduce vaccine cost for parents. To reduce vaccine cost as a barrier to vaccination, the U.S. Department of Health and Human Services will initiate the Vaccines for Children program on October 1, 1994. This program will purchase vaccines from manufacturers and provide them at no cost to participating public and private health-care providers for use in children aged 0-18 years who are eligible for Medicaid, are without health insurance, or are American Indian. Children with health insurance who are served by federally qualified health centers also will be able to receive free vaccine if their insurance does not cover vaccination. State vaccination programs will be permitted to purchase additional vaccines at reduced federal contract prices. o Improve surveillance for coverage and disease. An improved system for measuring vaccination coverage at the national, state, and local levels among infants and young children is being established to identify undervaccinated populations and to monitor progress in achieving coverage goals. Clinic or office-based assessments are being completed to assist health-care providers in increasing coverage among the populations they serve. Surveillance for vaccine-preventable diseases will be intensified by investigating each case of disease targeted for elimination to determine how that case might have been prevented and enable initiation of aggressive control measures when cases are detected. o Form and strengthen partnerships. Many federal agencies provide vaccinations to children, reimburse for vaccination services, or have access--through education, food, housing, or other assistance--to populations at high risk for undervaccination. Similarly, many private providers and organizations vaccinate children or otherwise serve or advocate for children. Coordination of these efforts will be strengthened and new partnerships formed to concentrate the efforts of these providers and organizations on improving the vaccination of children. o Improve vaccines. Emphasis will be placed on the development and licensure of new and safer or more effective vaccines. Existing vaccination schedules will be simplified, and development of combination vaccines will be promoted. To track progress toward achieving the goals of CII, CDC's National Immunization Program is initiating in this issue of MMWR monthly publication of a table that summarizes the number of cases of all diseases preventable by routine childhood vaccination reported during the previous month and year-to- date (provisional data) (Table 1). In addition, the table compares provisional data with final data for the previous year and highlights the number of reported cases among children aged less than 5 years--who are the primary focus of CII. Data in the table are derived from CDC's National Notifiable Diseases Surveillance System. References 1. CDC. General recommendations on immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1994;43(in press). 2. Orenstein WA, Atkinson W, Mason D, Bernier RH. Barriers to vaccinating preschool children. J Health Care Poor Underserved 1990;1:315-30. 3. Adams WG, Deaver KA, Cochi SL, et al. Decline of childhood Haemophilus influenzae type b (Hib) disease in the Hib vaccine era. JAMA 1993;269:221-6. 4. CDC. Resurgence of pertussis--United States, 1993. MMWR 1993;42:952-3,959- 60. 5. National Vaccine Advisory Committee. The measles epidemic: the problems, barriers, and recommendations. JAMA 1991;266:1547-52. 6. CDC. Vaccination coverage of 2-year-old children--United States, 1991-1992. MMWR 1993; 42:985-8. 7. CDC. Standards for pediatric immunization practices. JAMA 1993;269:1817-22. * H. influenzae serotype is not routinely reported to the National Notifiable Diseases Surveillance System. ** Because most hepatitis B virus infections among infants and children aged less than 5 years are asymptomatic (although more likely to become chronic), acute disease surveillance does not reflect the incidence of this problem in this age group or the effectiveness of hepatitis B vaccination in infants. *** Objectives to reduce cases of mumps, pertussis, and hepatitis B will be set during 1994. ------------------------------ Date: Sun, 06 Feb 94 22:04:36 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Prevalence Adults No Risk Factors for Coronory Heart Disease Message-ID: <Dm3cHc2w165w@stat.com> Current Trends Prevalence of Adults With No Known Major Risk Factors for Coronary Heart Disease -- Behavioral Risk Factor Surveillance System, 1992 Although the death rate for coronary heart disease (CHD) in the United States has declined approximately 50% since 1970, CHD remains the leading cause of death for both men and women and, in 1990, accounted for 489,340 deaths (1). National strategies and programs have targeted individual risk factors for death attributed to CHD. However, an alternative approach may be to measure the prevalence of adults who have no known risk factors for CHD. This report provides state-specific estimates of and characterizes adults who report having no known major risk factors for CHD. Data were analyzed from 91,428 persons aged greater than or equal to 18 years who resided in 48 states and the District of Columbia and participated in the 1992 Behavioral Risk Factor Surveillance System (BRFSS), a random- digit-dialed telephone survey. The analysis examined survey responses regarding the following risk factors: current cigarette smoking (smoked at least 100 cigarettes in their lifetime and now smoking), physical inactivity (no or irregular leisure-time physical activity), overweight (body mass index greater than or equal to 27.3 for women and greater than or equal to 27.8 for men), high blood pressure (told more than once by a health professional he/she has high blood pressure or is currently taking antihypertensive medications), high blood cholesterol (ever told by a health professional he/she has high blood cholesterol), and diabetes (ever told by a doctor he/she has diabetes). Persons who reported having none of these risk factors were defined as having no known risk factors for CHD. The results were weighted to account for the distribution of demographic characteristics in each state. To determine the actual prevalence of adults in each state with no known CHD risk factors, state-specific estimates were not standardized to a referent population. For data aggregated from all states, census data for the 1980 U.S. population were used to standardize comparisons by age, race, and educational status; aggregated analyses were restricted to black and white respondents for whom the age, race, and education distributions of the population were known. SESUDAAN was used to calculate the standard errors for the prevalence estimates (2). Of the 91,428 respondents, 18% reported having none of the six major CHD risk factors; 35% reported having one risk factor; 29%, two risk factors; 13%, three risk factors; and 5%, four to six risk factors. In every state, less than 30% of the population had no known risk factors. The state-specific proportion of respondents with no known risk factors varied minimally; in 45 (92%) of the states, the proportion ranged from 14% to 26% (Table 1). For both males and females, the percentage of respondents with no known risk factors was highest for 18-34-year-olds. Among males, the percentage was lowest for those aged 50-64 years, and among females, the percentage varied inversely with age (Table 2). The prevalence of no known risk factors for CHD increased directly with increasing level of education. Reported by the following BRFSS coordinators: M Scott, Alabama; P Owen, Alaska; R Porter, Arizona; L Lund, California; M Leff, Colorado; M Adams, Connecticut; F Breukelman, Delaware; C Mitchell, District of Columbia; D McTague, Florida; E Pledger, Georgia; F Newfield, Hawaii; G Louis, Idaho; B Steiner, Illinois; R Guest, Indiana; P Busick, Iowa; K Pippert, Kansas; K Bramblett, Kentucky; D Hargrove-Roberson, Louisiana; D Maines, Maine; A Weinstein, Maryland; R Lederman, Massachusetts; H McGee, Michigan; N Salem, Minnesota; E Jones, Mississippi; J Jackson-Thompson, Missouri; P Smith, Montana; S Huffman, Nebraska; M Atherton, Nevada; K Zaso, New Hampshire; G Boeselager, New Jersey; E Plunkett, New Mexico; C Baker, New York; C Washington, North Carolina; B Burgum-Lee, North Dakota; E Capwell, Ohio; N Hann, Oklahoma; J Grant-Worley, Oregon; C Becker, Pennsylvania; J Buechner, Rhode Island; M Lane, South Carolina; B Miller, South Dakota; D Ridings, Tennessee; R Diamond, Texas; R Giles, Utah; P Brozicevic, Vermont; R Schaeffer, Virginia; T Jennings, Washington; F King, West Virginia; E Cautley, Wisconsin. P Remington, Bur of Public Health, Wisconsin Div of Health. Cardiovascular Health Studies Br, Div of Chronic Disease Control and Community Intervention, National Center for Chronic Disease Prevention and Health Promotion, CDC. Editorial Note: The finding in this report that, in 1992, only 18% of adults reported having no known risk factors for CHD indicates that, despite improvements in the treatment and control of CHD-related conditions, a substantial percentage of adults continue to be at risk for CHD. This low prevalence underscores the need for primary prevention efforts that focus on achieving behavioral changes that prevent the occurrence of risk factors. Several of the year 2000 national health objectives target the primary prevention of specific risk factors for CHD, including overweight (objective 15.10), physical inactivity (objective 15.11), high blood cholesterol (objective 15.7), and cigarette smoking (objective 15.12) (3). Achievement of these objectives should substantially increase the number of U.S. adults who have no known major risk factors for CHD and should further reduce CHD- associated mortality. The prevalences of two risk factors--cigarette smoking and high blood cholesterol--have decreased substantially. In 1965, approximately 40% of U.S. adults smoked cigarettes; in comparison, by 1991, 26% smoked cigarettes (4). In addition, from the second National Health and Nutrition Examination Survey (NHANES II) (1976-1980) to NHANES III (1988-1991), the proportion of adults with high blood cholesterol levels (greater than or equal to 240 mg/dL) decreased from 26% to 20% (5). For other risk factors, however, prevalences have remained constant or increased. For example, when compared with 1987, the proportion of adults who engaged in no leisure-time physical activity (24%) in 1991 was unchanged, and the proportion who engaged in moderate physical activity five or more times per week increased only slightly (22% in 1987 and 24% in 1991) (6). From 1987 through 1991, the proportion of U.S. adults who were overweight increased from 26% to 28%, respectively (6). Finally, despite substantial improvements in the awareness, treatment, and control of hypertension, hypertension continues to affect an estimated 50 million persons in the United States (7). Although the findings in this report assist in targeting efforts to reduce specific risk factors for CHD, these findings are subject to at least two limitations. First, because BRFSS estimates are based on self-reports, the prevalence of most risk factors, especially overweight and current smoking status, are likely to be underreported. Second, risk factors for which awareness is low are underreported; for example, only an estimated 29% of adults know their cholesterol level (8). Therefore, this report most likely overestimates the proportion of adults without CHD risk factors. To assist in reducing the prevalence of CHD risk factors, health programs and organizations have intensified advocacy of primary prevention strategies. For example, the National High Blood Pressure Education Program has developed policy recommendations for implementing primary prevention interventions for hypertension (9), and the National Cholesterol Education Program has made dietary recommendations to reduce cholesterol levels (10). The need for the primary prevention of CHD risk factors also is important because education or treatment of persons with established risk factors may not reduce their risk to the level of persons who never have the risk factor; for example, persons who effectively control their hypertension remain at higher risk for CHD than do persons who never develop hypertension (9). References 1. American Heart Association. 1993 Heart and stroke facts statistics. Dallas: American Heart Association, 1992. 2. Shah BV. SESUDAAN: standard errors program for computing of standardized rates from sample survey data. Research Triangle Park, North Carolina: Research Triangle Institute, 1981. 3. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives--full report, with commentary. Washington, DC: US Department of Health and Human Services, Public Health Service, 1991; DHHS publication no. (PHS)91-50212. 4. CDC. Cigarette smoking among adults--United States, 1991. MMWR 1993;42:230- 3. 5. Sempos CT, Cleeman JI, Carroll MD, et al. Prevalence of high blood cholesterol among US adults: an update based on guidelines from the second report of the National Cholesterol Education Program Adult Treatment Panel. JAMA 1993;269:3009-14. 6. CDC. Health, United States, 1992, and healthy people 2000 review. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, 1993; DHHS publication no. (PHS)93-1232. 7. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med 1993;153:154-83. 8. CDC. Cholesterol screening and awareness--Behavioral Risk Factor Surveillance System, 1990. MMWR 1992;41:669,675-8. 9. National High Blood Pressure Education Program Working Group. National High Blood Pressure Education Program Working Group report on primary prevention of hypertension. Arch Intern Med 1993;153:186-208. 10. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA 1993;269:3015-23. ------------------------------ Date: Sun, 06 Feb 94 22:05:06 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Dracunculiasis Eradication Message-ID: <8m3cHc3w165w@stat.com> International Notes Update: Dracunculiasis Eradication -- Mali and Niger, 1993 Mali and Niger, countries in West Africa, ranked sixth and eighth in the number of reported cases of dracunculiasis (i.e., Guinea worm disease) in 1992 (1). In March 1993, Global 2000, Inc., and the World Health Organization (WHO) Collaborating Center for Research, Training, and Eradication of Dracunculiasis at CDC began providing direct assistance for the eradication of dracunculiasis in both countries by assigning a resident public health advisor to each country. This report summarizes surveillance data for the two countries during 1991-1993 and describes their progress toward eradication of dracunculiasis. Mali In 1990, Mali (population: 8.5 million) reported 884 cases of dracunculiasis to WHO (1). During that year, health officials in Mali initiated a pilot project to control dracunculiasis in 68 villages with endemic disease within Douentza District of Mopti Region. This effort employed trained village-based health workers to conduct health education, undertake active surveillance, and distribute nylon cloth to families for filtering drinking water. From December 1991 through March 1992, national village-by-village searches for cases detected 16,060 cases of dracunculiasis in 1264 villages in five of seven regions of the country (Table 1). Approximately 95% of cases were enumerated in two regions (Mopti and Kayes). By December 1993, Mali's Guinea Worm Eradication Program (GWEP) had trained one village-based health worker in each of 1100 (87%) villages with endemic dracunculiasis and had begun monthly reporting of cases from 433 (34%) such villages. In addition, health education had been initiated in 68% of villages with endemic disease in Mali and use of cloth filters in 34%; improved water supplies already existed or were scheduled to be available by 1994 in 60%. A provisional total of 5779 cases was reported for 1993. Niger In 1989 (the most recent year for which passive data were available), Niger (population: 8 million) reported 288 cases of dracunculiasis to WHO. In 1991, the Ministry of Health initiated a pilot project to control dracunculiasis in Boubon, Niger (population: approximately 4500), a village in which 2700 cases had been reported that year. Elements of this project included trained village-based health workers, health education, improved water supplies, and use of nylon filters. By 1993, the incidence of dracunculiasis in Boubon had declined to 108 cases. From October through November 1991, national village-by-village searches detected 32,831 cases of dracunculiasis in 1690 villages. Nearly two thirds of persons with dracunculiasis (21,057) resided in Zinder, one of the country's seven departments; of these, 85% resided in one district (Mirriah). By December 1993, Niger's GWEP had initiated at least one intervention in 928 (55%) villages with endemic dracunculiasis and had trained health workers for dracunculiasis eradication activities at national, regional, and district levels and in 298 (18%) villages with endemic disease. In addition, health education had been initiated in 49% of villages with endemic disease in Niger and use of cloth filters in 31%; improved water supplies already existed or were scheduled to be available by 1994 in 63%. Completion of training of village-based health workers for all villages in Niger with endemic disease is projected in early 1994. Niger has not yet begun monthly reporting of cases but has recorded a provisional total of 16,231 cases for 1993. Reported by: AT Toure, President, National Intersectorial Committee for Dracunculiasis Eradication; I Degoga, MD, National Program Coordinator, Guinea Worm Eradication Program, Ministry of Public Health, Mali. S Moussa, National Program Coordinator, Guinea Worm Eradication Program, Ministry of Public Health, Niger. Global 2000, Inc, The Carter Center, Atlanta. World Health Organization Collaborating Center for Research, Training, and Eradication of Dracunculiasis, Div of Parasitic Diseases, National Center for Infectious Diseases, CDC. Editorial Note: Mali and Niger are part of the core area of West Africa where dracunculiasis is endemic. Although Mali and Niger joined the campaign to eradicate dracunculiasis when fewer than 3 years remained until the target date for eradication (December 1995), both countries were successful in rapidly establishing GWEPs. However, implementation of the interventions described in this report (i.e., health education, cloth filters, and improved supplies of safe drinking water) will probably be insufficient alone to eradicate dracunculiasis before December 1995. To complete eradication of dracunculiasis, in 1994 health officials in Mali and Niger are planning to implement more stringent measures for case containment and begin selective use of temephos (Abate[Registered])* to kill the copepod intermediate host of the parasite in unsafe drinking water sources of selected villages (2). References 1. World Health Organization. Dracunculiasis: global surveillance summary, 1992. Wkly Epidemiol Rec 1993;68:125-31. 2. Hopkins DR, Ruiz-Tiben E. Strategies for dracunculiasis eradication. Bull World Health Organ 1991;69:533-40. * Use of trade names and commercial sources is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services. ------------------------------ Date: Sun, 06 Feb 94 22:05:43 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] State Cancer Registries Message-ID: <9N3cHc4w165w@stat.com> Current Trends State Cancer Registries: Status of Authorizing Legislation and Enabling Regulations -- United States, October 1993 Population-based cancer registries have identified cancer incidence rates indicating that the burden of cancer in the United States is substantial and varies widely by geographic location and ethnicity. However, for most existing state cancer registries, resources are inadequate for insuring minimum standards for quality and for completeness of case information. In October 1992, Congress enacted the Cancer Registries Amendment Act* that authorized CDC to establish a national program in support of cancer registries. The goal of this program is to enhance existing state cancer registries and to help establish statewide cancer registries so that all states have population-based cancer registries meeting minimum standards for completeness, timeliness, and quality. To ensure complete and timely reporting of newly diagnosed cases of cancer, the federal statute requires authorization of cancer registries under state-specific laws and promulgation of regulations that ensure case reporting and use of data for research. This report extends efforts by the National Cancer Institute (1) to assess existing state laws and regulations to determine how they compare to state-specific legislation required in the cancer registries act. In August and September 1993, all 50 states provided CDC with copies of state laws, statutes, regulations, and rules related to cancer registries in effect as of October 1, 1993. State law was defined as legislation enacted by the state legislature. Regulations were defined as measures promulgated by agencies such as state health departments and, although enforceable as law, can be modified by administrative action. In addition to enacting an authorizing law, each state is required to promulgate eight categories of regulations regarding the collection and use of cancer data; these regulations are intended to 1) require reporting of newly diagnosed cancer cases by hospitals and other health-care facilities; 2) require reporting of cancer cases by physicians and other health-care practitioners; 3) guarantee access by the statewide cancer registry to all records of medical status of persons with cancer; 4) require the use of standardized reporting formats; 5) ensure confidentiality of cancer case data; 6) allow use of confidential case data by certain researchers; 7) authorize the conduct of studies using cancer registry data; and 8) ensure protection of persons complying with the law from liability. On October 1, 1993, nine states had a law authorizing state cancer registries and had all essential regulations in place (Table 1). Twenty-nine states had laws authorizing state cancer registries but did not have all essential regulations (Table 1). Seven states had only regulations authorizing cancer registries. Four states had no law or regulation authorizing cancer registries and had none of the essential regulations. Of the other 46 states, 38 required reporting on cancer cases by health-care facilities, and 44 required protection of the confidentiality of case information. Reported by: Epidemiology and Statistics Br, Div of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, CDC. Editorial Note: Comprehensive, timely, and accurate information regarding cancer incidence and stage at diagnosis is essential for monitoring cancer trends and identifying variations in incidence by factors such as age, race/ethnicity, and geographic region. Cancer incidence rates vary by ethnicity, but whether these variations reflect differences in factors such as socioeconomic status, access to medical care, prevalence of specific risks, or misclassification of ethnicity is not known. Registries provide a means for collecting such information and may assist in conducting population-based epidemiologic and biologic research, allocating of health resources, and evaluating cancer-control and cancer-prevention programs. At the state level, both authorizing legislation and enabling regulations are necessary to establish and maintain statewide, population-based cancer registries. The findings in this report indicate that legislation and regulations related to cancer registries vary widely among states. For states seeking federal funding, the cancer registries act can provide an incentive to enact needed legislation or regulations. In fiscal year 1994, CDC will offer support to states, the District of Columbia, and Puerto Rico to enhance existing cancer registries and to plan and implement statewide cancer registries in states and territories that do not have registries. This support is intended to ensure that state cancer registries are population-based and meet minimum standards of completeness, timeliness, and quality. In addition, CDC will assist states in the development of model state legislation. These efforts also should enable evaluation of progress toward cancer control and national health objectives for the year 2000 (2). References 1. Fisher R, Haenlein M. Legislative authorizations for cancer registries. In: National Cancer Institute, National Institutes of Health. State Cancer Legislative Database Update. Bethesda, Maryland: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, April 1991:8-15. 2. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives--full report, with commentary. Washington, DC: US Department of Health and Human Services, Public Health Service, 1991; DHHS publication no. (PHS)91-50212. * Copies of the Cancer Registries Amendment Act, Public Law 102-515, section(c)(2)(D), October 24, 1992, are available from CDC's Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, 4770 Buford Highway, NE, Mailstop K-55, Atlanta, GA 30341-3724; telephone (404) 488-4682. ------------------------------ Date: Sun, 06 Feb 94 22:06:24 MST From: mednews (HICNet Medical News) To: hicnews Subject: Scientists Link Ancient Gene to Human Skull Deformity Message-ID: <DP3cHc5w165w@stat.com> SCIENTISTS LINK ANCIENT GENE TO HUMAN SKULL DEFORMITY A 600 million-year-old gene is responsible for a human birth defect, according to a report released today. The gene, called MSX2, belongs to a group of genes that are crucial to the embryological development of most forms of animal life. A defective version of the gene has been discovered in members of a New England family who were born with skull deformity known as craniosynostosis, It is possible that mutations of MSX2 or similar genes are involved in other developmental abnormalities of the head and face, according to the researchers. The research was supported by the National Institute of Dental Research, the National Institute of Child Health and Human Development, and the National Center for Research Resources, all of which are components of the National Institutes of Health. The study appears in the November 5 issue of the journal Cell. Craniosynostosis is the term that refers to a spectrum of skull malformations that result from premature joining of the separate bones that make up human skull. Normal development of the fetal skull requires coordinated growth and fusion of these bones along boundaries called sutures, in part to accommodate the enlarging brain. In the United States, approximately 1 infant in 3,000 is born with premature closure of one or more of these sutures, resulting in an abnormally shaped skull. Approximately 90 forms of craniosynostosis have been reported in all ethnic and racial groups, with more than 50 having a genetic cause. Severe cases of the skull deformity require surgery to relieve increased pressure within the skull and the problems it can lead to, such as seizures, breathing difficulty, and loss of vision and hearing. Scientists have thought for some time that the genetic cause of craniosynostosis lies within so-called homeobox family of genes. These genes control basic processes of embryo development that are common to both primitive and advanced forms of aminal life, and their structure has remained relatively constant throughout evolutionary history. The report in Cell has produced a clear link between a homeobox gene, MSX2, and a form of craniosynostosis. Historically, an MSX-like gene was first discovered in the fruit fly, and similar genes have since been found in a variety of animals, including sea urchins, fish, amphibians, birds, and mammals. The discovery of a analogous gene in sea urchins dates the MSX2 lineage to animals that were present on the earth 600 million years ago. Today, several laboratories have thoroughly studied MSX2 in the mouse and associated it with development of the skull, limbs, and heart. It was a family in New England, however, that ultimately provided a crucial link between MSX2 and a form of human craniosynostosis, known as "Boston type." This therapeutic particular syndrome was first observed by members of the research team in a large three generation family. The trait first appeared in the grandmother, and was passed to some members of two succeeding generations. The syndrome appeared in a pattern of autosomal dominant inheritance, in which individuals who inherited one defective gene and one normal gene, exhibited varying degrees of skull deformity. This classic pattern of gene inheritance and expression provided the researchers with the ideal situation for establishing a cause-effect relationship between a particular gene and a form of craniosynostosis. By following the inheritance pattern of known genetic markers, the researchers linked the appearance of skull abnormalities with a region of chromosome 5. The researchers the mapped the human MSX2 gene to the same region of chromosome 5 that is associated with the Boston type of craniosynostosis. Comparison of the MSX2 gene in normal and affected family members revealed a single DNA nucleotide base mutation in individuals with the syndrome. The mutation was found in a part of the MSX2 gene known as the homeodomain. This is the first report of a human craniofacial disorder that is due to a mutation in the critical region of a homeobox gene that is believed to regulate other genes during embryo development. The MSX2 mutation was observed at a site within the homeodomain that has remained unchanged for millions of years. This study, which has linked the MSX2 gene to the Boston type of craniosynostosis, has opened the door to tracking the genetic cause of other forms of craniosynostosis. Researchers believe that future studies may provide additional insights into improved therapeutic approaches to this serious craniofacial disorder. The investigators were Drs. Ethylin Jabs and Xiang Li of The John Hopkins University, Baltimore, MD; Dr. Ulrich Muller of the Institut fur Humangenetik, Giessen, Germany; Drs. Liang Ma and Rob Maxson of the USC/Norris Comprehensive Cancer Center, Los Angeles, CA; Drs. Wen Luo and Malcolm Snead of the Center for Craniofacial Molecular Biology, University of Southern California School of Dentistry, Los Angeles, CA; Dr. Ian Haworth of the University of Southern California School of Pharmacy, Los Angeles, CA; Drs. Ivana Klisak and Robert Sparkes of the UCLA School of Medicine; and Drs. Matthew Warman and John Mulliken of Children's Hospital, Boston, MA. ------------------------------ Date: Sun, 06 Feb 94 22:07:03 MST From: mednews (HICNet Medical News) To: hicnews Subject: Scientists Use Fingerprints to Track Gum Disease Bacteria Message-ID: <gq3cHc6w165w@stat.com> SCIENTISTS USE FINGERPRINTS TO TRACK GUM DISEASE BACTERIA Dental researchers can now identify the bacteria that cause gum disease as precisely as fingerprint experts can identify people. NIDR grantee Dr. Joseph Zambon, at the State University of New York at Buffalo, recently reported on a technique that produces a 'DNA fingerprint' so unique it can be used to track these disease-causing bacteria from one individual to another. "The ability to identify periodontal bacteria with this degree of precision is a technological advance that can provide important clues for preventing and treating gum disease," said Dr. Zambon. In addition to examining person-to-person transmission, the new fingerprinting technique can detect subtle differences in the bacterial distribution within an individual's mouth or among human populations scattered throughout the world. The technique can be also used to follow changes in bacterial populations during disease progression or in response to different types of treatment. "The applications are far-reaching," says Dr. Zambon. "We've just begun to apply this technique to study how to stop the initial infection by periodontal bacteria and how to eliminate existing infections." The procedure, developed independently at the California Institute of Biological Research and the E.I. du Pont Company, was adapted by Dr. Zambon to track periodontal bacteria--the microorganisms that live deep below the gum line and contribute to soft tissue destruction, bone degradation, and, finally, tooth loss. The new technique holds great promise for unraveling the mystery of how these fragile bacteria, which are readily killed by oxygen in the air, initially gain access to the human mouth. In the past, studies attempting to answer questions about the source of an infection or person-to- person transmission of periodontal bacteria were hampered by the inability to distinguish between bacteria within the same species. These so-called 'strains' can look essentially the same, even when analyzed in great detail. In recent years, DNA fingerprinting technology has made it easier to discriminate between strains. The classic approach to DNA fingerprinting relies on enzymes that digest, or break apart, DNA. In this way the single bacterial chromosome, which is made up of two complimentary strands of DNA containing millions of nucleotide bases, is broken into many smaller fragments. The actual number and size of the DNA fragments depends on the structure of the bacterial chromosome. The DNA fragments can be separated on electrophoresis gels according to the molecular size of the DNA pieces. The fragments appear in the gel as a pattern of bands, referred to as the DNA fingerprint, which visually resembles the "bar codes" used by stores to identify merchandise. It is now known that each bacterial species can be separated into a finite number of strains based on differences in fingerprint patterns. However, the number of strains is highly variable among the different species of periodontal bacteria. For example, 29 different fingerprints have been reported for one species, Porphyromonas gingivalis, while only 3 fingerprints have been identified for another species, Actinobacillus actinomycetemcomitans (A.a.). Even with this kind of DNA fingerprinting, it is difficult to do transmission studies on species like A.a., in which there are a small number of detectable strains. Moreover, fingerprint patterns produced by DNA digestion can consist of several hundred bands, making it difficult to discriminate subtle strain differences. To get around these shortcomings, Dr. Zambon and his colleagues used a modified version called the arbitrarily primed polymerase chain reaction, or AP-PCR. This technique is based on the polymerase chain reaction (PCR), a method that is widely used to copy sections of DNA for identifying gene structure or matching tissue specimens. PCR uses two small, synthetic strips of DNA called primers to amplify a larger region of DNA. The primers bind to specific sites on opposing strands of the double-stranded DNA, and make millions of copies of the intervening stretch of DNA. The primers usually have specific nucleotide sequences that bind to previously identified segments of DNA. However, in the case of AP-PCR, no knowledge of the DNA sequence is required. A single primer, consisting of an arbitrary sequence of 10 or 12 bases, binds at random sites along the bacterial chromosome. The amplified segments vary in number and size depending on the unique structure of each bacterial chromosome. AP-PCR generates fewer bands and more unique patterns than does conventional fingerprinting, thereby increasing the ability to discriminate between similar strains. Although the work is still in the early stages, Dr. Zambon's group has successfully used AP-PCR to fingerprint several species of periodontal bacteria. In the case of A.a., 14 different fingerprints were produced from 20 isolates examined, compared to only three distinct genetic patterns from a large number of strains evaluated in studies using conventional fingerprinting. When AP-PCR was used to study A.a. from different families, it was observed that in 6 of 7 cases husband and wife harbored different strains. The children, however, carried strains identical to those found in one of the parents. These findings support the hypothesis that periodontal bacteria are transmitted from parent to child. Such information could eventually be useful in determining how and when a child is infected with A.a. or other periodontal bacteria, and what preventive measures may be effective. The study, funded by the National Institute of Dental Research and the Norwegian Research Council, appeared in the October issue of the Journal of Clinical Microbiology. The investigators were Dr. Hans Preus of the Department of Periodontology, Dental Faculty, University of Oslo, Oslo, Norway; and Drs. Violet Haraszthy, Joseph Zambon, and Robert Genco, representing the Departments of Oral Biology and Periodontology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, New York. ------------------------------ Date: Sun, 06 Feb 94 22:07:44 MST From: mednews (HICNet Medical News) To: hicnews Subject: Multicenter Trial Confirms Pilocarpine Improves Dry Mouth Message-ID: <LR3cHc7w165w@stat.com> MULTICENTER TRIAL CONFIRMS PILOCARPINE IMPROVES DRY MOUTH Results of a large clinical trial using pilocarpine to treat dry mouth in patients who received radiation therapy to the head and neck show that the drug improved saliva productions and oral dryness in more than half of the participants. The finding is welcome news, since until now, there has been no widely accepted or effective treatment for the dry mouth experienced by these patients. The results of the study, in which NIDR's Clinical Investigations and Patient Care Branch participated, were reported in the August 5 issue of the New England Journal of Medicine. Each year, 43,000 Americans are diagnosed with head and neck cancer. Many of these patients undergo radiation therapy to the head and neck area, which often damages nearby salivary glands and causes them to produce little or no saliva. Post-irradiation xerostomia, or dry mouth, is permanent. It results in oral discomfort and pain, a greatly increased risk of tooth decay, frequent oral infections, and difficulty in speaking, chewing and swallowing. Stimulation of Salivary Gland Cells The collaborating researchers tested pilocarpine in more than 200 patients at 39 centers who had received radiation therapy for head and neck cancer. They found that pilocarpine increased saliva production and improved patients subjective feelings of oral dryness and discomfort, as well as their ability to speak. The investigators believe that the drug works by stimulating what salivary gland tissue remains functional in these patients. Pilocarpine binds to receptors on salivary gland cells, triggering them to secrete fluid. Only a very low dose of pilocarpine is needed to achieve this effect. One hundred and sixty-six patients completed the 12-week study. All had at least one parotid salivary gland and some evidence of residual salivary function. Patients were assigned randomly to receive tablets containing either 5 mg. of pilocarpine, 10 mg. of pilocarpine, or placebo. The tablets were taken three times a day at mealtimes. Evaluation of salivary function was conducted at the beginning of the study and every four weeks thereafter by measuring salivary flow rate. Patients also responded to questions about their perception of oral dryness and other symptoms. Benefits of Lowest Dose Fifty-four percent of those receiving 5 mg. of pilocarpine reported improvement in their overall condition of xerostomia, compared to 44 percent of those receiving 10 mg. and 25 percent of those receiving placebo. Some patients experienced minor side effects, usually limited to an increase in sweating. Interestingly, patients whose symptoms improved continued to experience even more improvement as the study progressed. The best responses generally occurred at 12 weeks. The reason for the time-related improvement may be linked to favorable changes in the oral mucosa as the pilocarpine treatment stimulated saliva production. "This study is an excellent example of the many benefits of increasing normal salivary secretions inpatients with salivary hypofunction," said Dr. Philip C. Fox, chief of the NIDR Clinical Investigations Section. "Saliva does more than just wet the mouth. It helps preserve and protect oral hard and soft tissues, as well as support other important oral functions such as chewing, swallowing, and speaking." Patients who participated in the research protocol are currently enrolled in a follow up study. According to Dr. Jonas T. Johnson, lead author of the article published in the New England Journal of Medicine and director of the Center for Head and Neck Oncology at the Pittsburgh Cancer Institute, University of Pittsburgh Medical Center, "The new study seeks to better define the dose of pilocarpine and schedule of administration that is ideally suited to relieving symptoms while minimizing any unpleasant side effects. Clinicians everywhere have expressed the desire that oral pilocarpine be made available for clinical use in an expeditious manner." Past Use of Pilocarpine The approach to using pilocarpine to treat xerostomia actually had its origins in 19th century South America. Missionaries there observed that the local people chewed the leaves of a shrub of the genus pilocarpus to increase their saliva while they worked outside in the heat. The alkaloid pilocarpine, which was isolated from this plant 100 years ago, was found to stimulate not just salivary glands, but also sweat glands. >From the 1890s through the 1950s, based on anecdotal evidence, dentists used pilocarpine to treat dry mouth. In the 1960s pilocarpine was used in studies that tested the effects of a number of different medications on salivary secretion in normal volunteers. The data showed that while pilocarpine could stimulate human saliva production and other gland secretions, it also could increase heart rate and blood pressure. In 1985, Dr. Fox received approval from the Food and Drug Administration to conduct a pilot study at the NIDR using pilocarpine to treat patients with diminished salivary function. He found that in small doses, the drug was safe and effective in stimulating saliva production. In 1991, he published the results of a larger study that examined in greater detail the stimulating effects and potential side effects of pilocarpine. In addition to Dr. Johnson and Dr. Fox co-authors of the paper were Dr. Gerald a. Ferretti, University of Kentucky; Dr. W. James Nethery, Loma Linda University; Dr. Ingrid N. Valdez, NIDR; Dr. David Ng, Phamarco Dynamics Research; and Dr. Charles C. Muscoplat and Ms. Susan C. Gallagher, MGI Pharma. ------------------------------ End of HICNet Medical News Digest V07 Issue #02 *********************************************** --- Editor, HICNet Medical Newsletter Internet: david@stat.com FAX: +1 (602) 451-1165 Bitnet : ATW1H@ASUACAD -------------------------------------------------------------------------------