Acetaminophen toxicity is caused when glucuronidation and sulfation become saturated after an acetaminophen overdose. The saturation of these major metabolic pathways cause the formation of excess NAPQI to be formed by CYP450-mediated N-hydroxylation (AAP, 2001). Two mechanisms can contribute to liver damage. The first of which occurs when NAPQI binds to hepatic cell macromolecules and can progress to necrotic cell death. The second mechanism is the depletion of glutathione which causes oxidative stress and subsequently liver damage and possibly death (AAP, 2001).
Acetaminophen is also one of the most widely used over-the-counter medications. Of particular concern is the ubiquitous statement about liver damage on Tylenol’s label is as follows: This product contains acetaminophen. Severe liver damage may occur if you take *more than 8 gelcaps in 24 hours, which is the maximum daily amount*with other drugs containing acetaminophen* 3 or more alcoholic drinks every day while using this product. The label does not mention that death may result as a consequence of the liver damage, nor how common overdose is associated with acetaminophen. Concurrently, the Tylenol brand has been synonymous with safety and universal applicability. This benign reputation is astounding in light of the 140,000 poisoning cases, 56,000 emergency room visits, 26,000 hospitalizations, and 150 deaths per annum (Bronstein et. al., 2006). These include accidental and intentional overdoses. The inclusion of a statement regarding the potential for death in addition to liver damage is warranted. In addition, encouraging physicians especially in primary care to address acetaminophen usage among their children and themselves would reinforce a cautionary message.
Reference:
American Academy of Pediatrics Committee on Drugs (2001) Acetaminophen toxicity in children. Pediatrics 108:1020–1024
Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. (2006) Annual Report of the American Association of Poison Control Centers National Poison Data System (NPDS). Clin Toxicol. 45, 815–917.
Schilling, A. (January 2010) Acetaminophen: Old drug, new warnings.Cleveland Clinic Journal of Medicine, 77 (1) 19-27
Saturday, April 30, 2011
Thursday, April 21, 2011
Cervical Cancer & HPV: Examining Gender-Based Vaccinations
Cervical cancer is an exemplary example of the conjunction between public health awareness, pharmaceutical influence, and women’s health. This cancer originates in the squamous cells of the cervix and is the third most common form of cancer to affect women worldwide (Kahn, 2009). This cancer has a slow progression and its precancerous condition known as dysplasia can be detected by routine Pap smear exams and is entirely treatable. Left untreated this condition can progress into cervical cancer, eventually affecting the bladder, intestines, lungs, and liver and may cause infertility and death.
The majority of cervical cancers have been determined to be caused by the Human Papilloma Virus (HPV). This virus is spread through sexual intercourse and has several risk factors including early onset of sexual activity, multiple sexual partners, and women whose mothers were prescribed diethylstilbestrol to prevent miscarriage. In June 2006, the FDA released the first vaccine to prevent cancer, Gardacil, which was specific to preventing HPV and subsequently cervical cancer (Kahn, 2009). The release of Gardacil into the market was coupled with widespread educational/marketing regarding the risks of HPV in the causation of cervical cancer (Merck, 2010). This coupling was unique not only in the revolutionary vaccine, but also in the level of awareness created about HPV by pharmaceutical promoters who lobbied for insurance companies and federal programs to routinize, subsidize, and cover the costs of vaccination in females aged 9-26 (Merck, 2010).
I understand why this vaccine targeted females as they are the only ones to suffer from cervical cancer. Yet, I was always perplexed why this vaccine was so heavily and exclusively promoted for females rather than including males as potential carriers of HPV. Recent studies have also examined the immunogenicity and safety of vaccinating males to prevent the spread of HPV and certain penile cancers associated with it (Petaja et. al., 2009). In Petaja et. al. (2009), males ages 10 to 18 years were randomized to receive HPV-16/18 AS04-adjuvanted vaccine (n = 181) or hepatitis B virus (HBV) control vaccine (n = 89) at 0, 1, and 6 months, and were followed for 7 months. Study research resulted in high antibody levels and seropositivity at the 7 month interval and concluded that the vaccine was well tolerated. The study did not specify recommendations regarding the vaccination of boys as they determined that the potential public health benefits required more data. Although I hesitate to conclude this for them, I am entirely supportive of the unilateral recommendation for vaccinating both male and females for HPV. The rationale that as predominantly carriers only, males should be excluded, is an affront to a basic public health tenant of prevention as integral and essential.
Kahn JA. (2009) HPV vaccination for the prevention of cervical intraepithelial neoplasia. New England Journal of Medicine. 16,361(3),271-278.
Merck & Co. (2010) Gardacil. Accessed April 21, 2011 from http://www.gardasil.com/
NCCN Clinical Practical Guidelines in Oncology: Cervical cancer. V.1.2010. National Comprehensive Cancer Network, Inc. Available at www.NCCN. org. Accessed December 28, 2009.
Petäjä T, Keränen H, Karppa T, Kawa A, Lantela S, Siitari-Mattila M, Levänen H, Tocklin T, Godeaux O, Lehtinen M, Dubin G. (2009) Immunogenicity and safety of human papillomavirus (HPV)-16/18 AS04-adjuvanted vaccine in healthy boys aged 10-18 years. J Adolesc Health. 44(1):33-40.
The majority of cervical cancers have been determined to be caused by the Human Papilloma Virus (HPV). This virus is spread through sexual intercourse and has several risk factors including early onset of sexual activity, multiple sexual partners, and women whose mothers were prescribed diethylstilbestrol to prevent miscarriage. In June 2006, the FDA released the first vaccine to prevent cancer, Gardacil, which was specific to preventing HPV and subsequently cervical cancer (Kahn, 2009). The release of Gardacil into the market was coupled with widespread educational/marketing regarding the risks of HPV in the causation of cervical cancer (Merck, 2010). This coupling was unique not only in the revolutionary vaccine, but also in the level of awareness created about HPV by pharmaceutical promoters who lobbied for insurance companies and federal programs to routinize, subsidize, and cover the costs of vaccination in females aged 9-26 (Merck, 2010).
I understand why this vaccine targeted females as they are the only ones to suffer from cervical cancer. Yet, I was always perplexed why this vaccine was so heavily and exclusively promoted for females rather than including males as potential carriers of HPV. Recent studies have also examined the immunogenicity and safety of vaccinating males to prevent the spread of HPV and certain penile cancers associated with it (Petaja et. al., 2009). In Petaja et. al. (2009), males ages 10 to 18 years were randomized to receive HPV-16/18 AS04-adjuvanted vaccine (n = 181) or hepatitis B virus (HBV) control vaccine (n = 89) at 0, 1, and 6 months, and were followed for 7 months. Study research resulted in high antibody levels and seropositivity at the 7 month interval and concluded that the vaccine was well tolerated. The study did not specify recommendations regarding the vaccination of boys as they determined that the potential public health benefits required more data. Although I hesitate to conclude this for them, I am entirely supportive of the unilateral recommendation for vaccinating both male and females for HPV. The rationale that as predominantly carriers only, males should be excluded, is an affront to a basic public health tenant of prevention as integral and essential.
Kahn JA. (2009) HPV vaccination for the prevention of cervical intraepithelial neoplasia. New England Journal of Medicine. 16,361(3),271-278.
Merck & Co. (2010) Gardacil. Accessed April 21, 2011 from http://www.gardasil.com/
NCCN Clinical Practical Guidelines in Oncology: Cervical cancer. V.1.2010. National Comprehensive Cancer Network, Inc. Available at www.NCCN. org. Accessed December 28, 2009.
Petäjä T, Keränen H, Karppa T, Kawa A, Lantela S, Siitari-Mattila M, Levänen H, Tocklin T, Godeaux O, Lehtinen M, Dubin G. (2009) Immunogenicity and safety of human papillomavirus (HPV)-16/18 AS04-adjuvanted vaccine in healthy boys aged 10-18 years. J Adolesc Health. 44(1):33-40.
Wednesday, April 20, 2011
What's on your plate? Examining genetic modification.
Having been raised in the developing world, food shortage is a critically important ethical and humanitarian issue and one that I am personally invested in. Food shortage may be less of an issue with production and more of an issue of redistribution (Pollan, 2006). The role of genetic modification and differing agricultural practices such as organic farming, aquaponics, hydroponics, etc. are all important components to this multi-faceted issue. Genetically modified organisms are not the whole answer to the complex problem of food scarcity especially when balancing high yield crops with the extensive pesticide use and expense. In light of the mass suicides in India due in part to GMO and hybrid seeds (Sengupta, 2006), one needs to examine not only the agricultural impact of such technology, but also the environmental and socio-economic issues and consequences as well. Similarly touted as agriculture’s messiah, organic farming is also considered an irresponsible venture. These alternatives may have long-term consequences that we are just beginning to understand such as potential allergencity of genetically modified foods (Goodman et. al., 2011).
Genetic modification is fundamentally a natural process. Cross-pollination, selective-breeding, genetic recombination, and hybridization all occur as natural processes in our biological system. Genetic modification differs in the rate at which these genetic recombinations occur (Weale, 2010). For example, in may take a millennia or more for a plant to develop a certain genetic trait whereas genetic modification allows for it instantaneously. This precious power is coupled with a deep responsibility that may at times be neglected in the eagerness to provide sustenance for our burgeoning world population.
References
Goodman, R.E., Tetteh, A.O. (2011) Suggested Improvements for the Allergenicity Assessment of Genetically Modified Plants Used in Foods. Current Allergy Asthma Report.
Pollan, Michael. (2006) The Omnivore’s Dilleama: A Natural History of Four Meals. Penguin Press: New York.
Sengupta, Someni, (2006) On India’s Farms, a Plague of Suicide. New York Times Accessed April 11, 2011 from http://www.nytimes.com/2006/09/19/world/asia/19india.html
Weale, Albert. (2010) Ethical arguments relevant to the use of GM crops. New Biotechnology, 27, 5.
Genetic modification is fundamentally a natural process. Cross-pollination, selective-breeding, genetic recombination, and hybridization all occur as natural processes in our biological system. Genetic modification differs in the rate at which these genetic recombinations occur (Weale, 2010). For example, in may take a millennia or more for a plant to develop a certain genetic trait whereas genetic modification allows for it instantaneously. This precious power is coupled with a deep responsibility that may at times be neglected in the eagerness to provide sustenance for our burgeoning world population.
References
Goodman, R.E., Tetteh, A.O. (2011) Suggested Improvements for the Allergenicity Assessment of Genetically Modified Plants Used in Foods. Current Allergy Asthma Report.
Pollan, Michael. (2006) The Omnivore’s Dilleama: A Natural History of Four Meals. Penguin Press: New York.
Sengupta, Someni, (2006) On India’s Farms, a Plague of Suicide. New York Times Accessed April 11, 2011 from http://www.nytimes.com/2006/09/19/world/asia/19india.html
Weale, Albert. (2010) Ethical arguments relevant to the use of GM crops. New Biotechnology, 27, 5.
Tuesday, April 12, 2011
Asthma, Allergy, and Medication Exposure in Early Childhood: A Catch-22 of Care
Living on the Island of Hawai'i has certain considerations concerning asthma as we have the highest prevalence among children in the United States.
Biological Basis
Asthma is a chronic disorder that is characterized by lung airway inflammation. This inflammation is caused and perpetuated by an inappropriate immune response, an increase in airway responsiveness, and airflow obstruction. Asthma symptoms can be mild, moderate, and severe and may include wheezing, cough, and chest tightness, among other life-threatening implications. Asthma and the closely associated allergic diseases of atopic dermatitis, allergic rhinitis, and immunoglobulin E-medicated food allergy are characterized by inflammatory T-helper cell responses of the T-helper 2 phenotype initiating and perpetuating symptoms (Devereux, 2006). Further mediators in the process include cytokines secreted by T-helper 2 cells, interleukin-4 and interleukin-13, which contribute to elevated immunoglobulin E, mast-cell regulation, and eosinophilic inflammation.
The prevalence of asthma as the world’s most common chronic disorder (Devereux, 2006) has encouraged a plethora of studies examining prenatal and postnatal exposures, environment, family history, and has resulted in an increase in awareness and subsequent diagnosis. The following discourse examines three such studies that pertain to medication exposure among infants and the association and subsequent development of asthma and allergies. Asthma predominates as a Western disease and the possible correlation between high medication usage and antibiotic usage, in particular, may depict the pitfalls of easy access and excess usage. As the following studies suggest, use of such common over-the-counter medications such as paracetamol and prescribed medications such as antibiotics in early childhood may result in a debilitating asthmatic disease requiring additional medications and/or medical attention. This seeming paradox, when adequately examined, illustrated, and exposed may result in the reduction of unintentional parentally and/or physician-induced asthma and allergies.
Research Findings
Bakkeheim et. al. (2010) examined the role of paracetamol in early infancy and the associated risk of developing childhood allergies and asthma. Paracetamol or acetaminophen is a common analgesic and antipyretic that is readily used on infants and children for fever, teething, and to alleviate general pain and discomfort. Commonly known as Tylenol, its label specifies, “Give your child Infants' Tylenol products to reduce fever and for the temporary relief of minor aches and pains associated with:Cold. Flu. Headache. Sore throat. Toothache and teething.” Its usage was examined in this prospective cohort study that included 1019 children at birth who were then reexamined at 10 years of age. Their prenatal exposure through maternal paracetamol use or postnatal exposure during the first 6 months of life were documented. Subsequent outcomes at the 10 year reexamination period included existing asthma diagnosis, a history of asthma, allergic sensitization, and/or allergic rhinitis.
Bakkeheim’s research resulted in the finding that maternal paracetomol use in the first trimester only increased the risk for allergic rhinitis with an odds ratio of 2.30 for both male and female children. The significant findings of the study related to paracetamol use until 6 months of age in girls, resulting in an increased risk of allergic sensitization (odds ratio of 2.20) and a history of asthma (odds ratio of 2.20 as well) in 10 year olds.
Further research by Risnes et. al. (2010) also examined the role of medication exposure in regards to antibiotic exposure within the first 6 months of life and the development of asthma and allergy at 6 years of age. This study included a cohort of 1401 children whose hospital records and physician records were examined to document antibiotic exposure. At 6 years of age, maternal interviews were conducted to determine whether the child had experienced an allergic reaction, if blood immunoglobulin E or a skin prink had been conducted, and the results of such testing. Those children who experienced an allergic reaction and had a positive blood or skin prick test were classified as allergy positive. Children diagnosed with asthma and who had a positive allergy test were determined to have allergic asthma.
The research findings included an increased risk of asthma (odds ratio of 1.52) among those children who had been prescribed antibiotics in infancy. The adverse effect of antibiotics use was particularly evident in children who had no family history of asthma (odds ratio 1.89). In addition, the odds ratio of a positive blood immunoglobulin E or skin prink test was 1.59 among those with early antibiotic exposure.
Sobko et. al. (2010) examined the role that neonatal sepsis and early antibiotic therapy have on bacterial colonization and immune activation in infancy and childhood. These were investigated for their implications in allergy and asthma development. This cohort study utilized a validated questionnaire by the International Study of Asthma and Allergies in Children. The three cohorts in this study that were screened examined different perinatal exposures of infection and medication exposure to antibiotics.
The research findings concluded that asthma was more prevalent after neonatal sepsis and antibiotic therapy with an adjusted odds ratio 1.63 as compared with a control group. Also documented was increased atopic eczema after neonatal sepsis (odds ratio 1.39). These findings resulted in the conclusion that neonatal sepsis is associated with an increased risk for later development of asthma and that early antibiotic exposure may be the contributing factor in this association. This study also examined the confounding bias that may occur in regards to infection and subsequent antibiotic use. Infection without the subsequent use of antibiotics did not result in the associated increase.
Public Health Application
All three studies addressed the development of childhood asthma as a result of medications (either paracetamol or antibiotics) given to children prior to 6 months of age. Collectively, they suggest that paracetamol and antibiotic usage may contribute to asthma and allergies. The public health application should pertain to preventing exposure to these medications during the 6 month infancy time-period and curbing exposure throughout early childhood. While public education efforts regarding the use of these medications in infancy is essential to curbing usage and limiting exposure, the particulars of paracetamol and antibiotics usage are unique in the way that these medications are distributed and can possibly be managed more effectively.
For example, in the use of paracetamol, the Tylenol Concentrated Infant Drops’ label specifies that its use for children under the age of 2 should be done with a doctor’s consultation. While this labeling may be intended to provide a caregiver with encouragement in contacting a child’s physician when a child is ill, this may not always occur. Therefore, specific dosing and age parameters are more efficient and useful guidelines. The label guidelines should specify that use in children less than 6 months of age has been associated with the development of asthma and allergy. Albeit this association was gender specific (Bakkenheim et. al., 2010), such considerations would need to be further researched prior to possibly ever attaching a gender-specific label to medication. In the event that a physician is contacted regarding use, the physician should adequately inform and encourage proper and limited usage.
Similar to paracetamol in that there are avenues to curbing usage, antibiotics have an additional barrier to usage, the physicians themselves. The distribution of prescriptions for antibiotic medications are limited to physicians and in some states, physicians’ assistants and registered nurses. Regardless of the persistence of parents/ caregivers, physician should address the issue of antibiotic over-prescription, especially among infants who may suffer the additional consequences of asthma and allergies. Patient awareness and education is a key contributing factor to reducing parental demand for antibiotics, but ultimately, it is a physician’s determination whether or not to prescribe antibiotics and to determine at what age they believe it is beneficial or detrimental to the current and future health status of their patients. Further physician education and awareness may also be a key component in reducing usage of antibiotics among infants.
References
Bakkehaim, E. , Mowincckel, P., Carlsen, K. H., Haland, G., Carlsen, K. (2010). Paracetamol in early infancy: the risk of childhood allergy and asthma. Acta Paediatricia, 100, 90-96.
Devereux, G. (2006). The increase in the prevalence of asthma and allergy: Food for thought. Nature Reviews Immunology, 6 (11), 869-874.
Johnson, M.D. (2010). Human Biology: Concepts and current issues. San Francisco. CA: Pearson Benjamin Cummings.
Risnes, K., Belanger, K., Murk, W., Bracken, M. (2010) Antibiotic Exposure by 6 Months and Asthma and Allergy at 6 Years: Findings in a Cohort of 1,401 US Children. American Journal of Epidemiology, 173, 3, 310-318.
.Sobko T, Schiött J, Ehlin A, Lundberg J, Montgomery S, Norman M. (2010). Neonatal sepsis, antibiotic therapy and later risk of asthma and allergy. Paediatr Perinat Epidemiol. 24(1):88-92.
Tantisira, K.G., & Weiss, S.T. (2006). The pharmacogenetics of asthma therapy. Current Drug Targets, 7 (12), 1697-1708.
Umetsu, D.T. & DeKruyff, R.H. (2006). The regulation of allergy and asthma. Immunological Reviews, 212 (1), 238-255.
Biological Basis
Asthma is a chronic disorder that is characterized by lung airway inflammation. This inflammation is caused and perpetuated by an inappropriate immune response, an increase in airway responsiveness, and airflow obstruction. Asthma symptoms can be mild, moderate, and severe and may include wheezing, cough, and chest tightness, among other life-threatening implications. Asthma and the closely associated allergic diseases of atopic dermatitis, allergic rhinitis, and immunoglobulin E-medicated food allergy are characterized by inflammatory T-helper cell responses of the T-helper 2 phenotype initiating and perpetuating symptoms (Devereux, 2006). Further mediators in the process include cytokines secreted by T-helper 2 cells, interleukin-4 and interleukin-13, which contribute to elevated immunoglobulin E, mast-cell regulation, and eosinophilic inflammation.
The prevalence of asthma as the world’s most common chronic disorder (Devereux, 2006) has encouraged a plethora of studies examining prenatal and postnatal exposures, environment, family history, and has resulted in an increase in awareness and subsequent diagnosis. The following discourse examines three such studies that pertain to medication exposure among infants and the association and subsequent development of asthma and allergies. Asthma predominates as a Western disease and the possible correlation between high medication usage and antibiotic usage, in particular, may depict the pitfalls of easy access and excess usage. As the following studies suggest, use of such common over-the-counter medications such as paracetamol and prescribed medications such as antibiotics in early childhood may result in a debilitating asthmatic disease requiring additional medications and/or medical attention. This seeming paradox, when adequately examined, illustrated, and exposed may result in the reduction of unintentional parentally and/or physician-induced asthma and allergies.
Research Findings
Bakkeheim et. al. (2010) examined the role of paracetamol in early infancy and the associated risk of developing childhood allergies and asthma. Paracetamol or acetaminophen is a common analgesic and antipyretic that is readily used on infants and children for fever, teething, and to alleviate general pain and discomfort. Commonly known as Tylenol, its label specifies, “Give your child Infants' Tylenol products to reduce fever and for the temporary relief of minor aches and pains associated with:Cold. Flu. Headache. Sore throat. Toothache and teething.” Its usage was examined in this prospective cohort study that included 1019 children at birth who were then reexamined at 10 years of age. Their prenatal exposure through maternal paracetamol use or postnatal exposure during the first 6 months of life were documented. Subsequent outcomes at the 10 year reexamination period included existing asthma diagnosis, a history of asthma, allergic sensitization, and/or allergic rhinitis.
Bakkeheim’s research resulted in the finding that maternal paracetomol use in the first trimester only increased the risk for allergic rhinitis with an odds ratio of 2.30 for both male and female children. The significant findings of the study related to paracetamol use until 6 months of age in girls, resulting in an increased risk of allergic sensitization (odds ratio of 2.20) and a history of asthma (odds ratio of 2.20 as well) in 10 year olds.
Further research by Risnes et. al. (2010) also examined the role of medication exposure in regards to antibiotic exposure within the first 6 months of life and the development of asthma and allergy at 6 years of age. This study included a cohort of 1401 children whose hospital records and physician records were examined to document antibiotic exposure. At 6 years of age, maternal interviews were conducted to determine whether the child had experienced an allergic reaction, if blood immunoglobulin E or a skin prink had been conducted, and the results of such testing. Those children who experienced an allergic reaction and had a positive blood or skin prick test were classified as allergy positive. Children diagnosed with asthma and who had a positive allergy test were determined to have allergic asthma.
The research findings included an increased risk of asthma (odds ratio of 1.52) among those children who had been prescribed antibiotics in infancy. The adverse effect of antibiotics use was particularly evident in children who had no family history of asthma (odds ratio 1.89). In addition, the odds ratio of a positive blood immunoglobulin E or skin prink test was 1.59 among those with early antibiotic exposure.
Sobko et. al. (2010) examined the role that neonatal sepsis and early antibiotic therapy have on bacterial colonization and immune activation in infancy and childhood. These were investigated for their implications in allergy and asthma development. This cohort study utilized a validated questionnaire by the International Study of Asthma and Allergies in Children. The three cohorts in this study that were screened examined different perinatal exposures of infection and medication exposure to antibiotics.
The research findings concluded that asthma was more prevalent after neonatal sepsis and antibiotic therapy with an adjusted odds ratio 1.63 as compared with a control group. Also documented was increased atopic eczema after neonatal sepsis (odds ratio 1.39). These findings resulted in the conclusion that neonatal sepsis is associated with an increased risk for later development of asthma and that early antibiotic exposure may be the contributing factor in this association. This study also examined the confounding bias that may occur in regards to infection and subsequent antibiotic use. Infection without the subsequent use of antibiotics did not result in the associated increase.
Public Health Application
All three studies addressed the development of childhood asthma as a result of medications (either paracetamol or antibiotics) given to children prior to 6 months of age. Collectively, they suggest that paracetamol and antibiotic usage may contribute to asthma and allergies. The public health application should pertain to preventing exposure to these medications during the 6 month infancy time-period and curbing exposure throughout early childhood. While public education efforts regarding the use of these medications in infancy is essential to curbing usage and limiting exposure, the particulars of paracetamol and antibiotics usage are unique in the way that these medications are distributed and can possibly be managed more effectively.
For example, in the use of paracetamol, the Tylenol Concentrated Infant Drops’ label specifies that its use for children under the age of 2 should be done with a doctor’s consultation. While this labeling may be intended to provide a caregiver with encouragement in contacting a child’s physician when a child is ill, this may not always occur. Therefore, specific dosing and age parameters are more efficient and useful guidelines. The label guidelines should specify that use in children less than 6 months of age has been associated with the development of asthma and allergy. Albeit this association was gender specific (Bakkenheim et. al., 2010), such considerations would need to be further researched prior to possibly ever attaching a gender-specific label to medication. In the event that a physician is contacted regarding use, the physician should adequately inform and encourage proper and limited usage.
Similar to paracetamol in that there are avenues to curbing usage, antibiotics have an additional barrier to usage, the physicians themselves. The distribution of prescriptions for antibiotic medications are limited to physicians and in some states, physicians’ assistants and registered nurses. Regardless of the persistence of parents/ caregivers, physician should address the issue of antibiotic over-prescription, especially among infants who may suffer the additional consequences of asthma and allergies. Patient awareness and education is a key contributing factor to reducing parental demand for antibiotics, but ultimately, it is a physician’s determination whether or not to prescribe antibiotics and to determine at what age they believe it is beneficial or detrimental to the current and future health status of their patients. Further physician education and awareness may also be a key component in reducing usage of antibiotics among infants.
References
Bakkehaim, E. , Mowincckel, P., Carlsen, K. H., Haland, G., Carlsen, K. (2010). Paracetamol in early infancy: the risk of childhood allergy and asthma. Acta Paediatricia, 100, 90-96.
Devereux, G. (2006). The increase in the prevalence of asthma and allergy: Food for thought. Nature Reviews Immunology, 6 (11), 869-874.
Johnson, M.D. (2010). Human Biology: Concepts and current issues. San Francisco. CA: Pearson Benjamin Cummings.
Risnes, K., Belanger, K., Murk, W., Bracken, M. (2010) Antibiotic Exposure by 6 Months and Asthma and Allergy at 6 Years: Findings in a Cohort of 1,401 US Children. American Journal of Epidemiology, 173, 3, 310-318.
.Sobko T, Schiött J, Ehlin A, Lundberg J, Montgomery S, Norman M. (2010). Neonatal sepsis, antibiotic therapy and later risk of asthma and allergy. Paediatr Perinat Epidemiol. 24(1):88-92.
Tantisira, K.G., & Weiss, S.T. (2006). The pharmacogenetics of asthma therapy. Current Drug Targets, 7 (12), 1697-1708.
Umetsu, D.T. & DeKruyff, R.H. (2006). The regulation of allergy and asthma. Immunological Reviews, 212 (1), 238-255.
Friday, April 8, 2011
Gattaca in Africa: The Unique Qualities of Sickle Cell Anemia
Sickle cell anemia (homozygous Hb SS) constitutes 60-70% of sickle cell disease in the United States (Bender et. al, 2009) affecting 90,000 -100,000 individuals (CDC, 2010) and is a fascinating example of the dynamic nature of genetic distribution, adaptation, and disorders. The term sickle cell disease encompasses a group of symptomatic disorders associated with mutations in the HBB gene (Bender et. al., 2009). The disease is defined by the presence of hemoglobin S which is a result of a point mutation in the HBB gene in which the sixth amino acid in the hemoglobin chain is changed from glutamic acid to valine. Sickle cell prevalence is also a result of natural selection in regions of endemic malaria. This condition is attributed with high survival rates for those infected with acute malaria and depicts how a genetic disorder can gain momentum.
Sickle cell anemia is a debilitating disease characterized by intermittent vaso-occlusive events and chronic hemolytic anemia. Common symptoms include attacks of acute and chronic abdominal pain, bone pain, breathlessness, delayed growth and puberty, fatigue, fever, rapid heart rate, ulcers, and jaundice. Current treatment consists of symptom management as the condition is chronic and life-threatening and may include folic acid supplementation to encourage red blood cell production, pain medication during crises, and routine blood transfusions. Bone marrow or stem cell transplants are considered risky, yet viable options to cure the disease.
Currently, transfusions are readily utilized to treat sickle cell patients in order to improve blood flow by reducing the proportion of red cells capable of forming the sickle hemoglobin polymer (Raghypathy, 2010). However, a major and unavoidable complication of transfusions in sickle cell disease is iron overload. Iron overload can damage organs and cause other severe symptoms. The risks associated with such treatment are not easily quantified as there is no national database for sickle cell anemia (CDC, 2010). Prevalence rates, health outcomes, and impact on quality of life are not documented. Although every newborn is screened for sickle cell anemia, a national registry has not been established. From a public health perspective the establishment of such a center and service would enable additional documentation and dissemination of information such as the risks associated with iron overload. Surveillance is a key public health tool that allows health professionals to monitor and address health issues, sickle cell anemia should not be immune to such ongoing examination.
References
Bender, MA, Hobbs, W. (2009) Sickle Cell Anemia, Gene Reviews.
Centers for Disease Control and Prevention. Sickle Cell Disease. Retrieved on April 6, 2011 from www.cdc.gov/ncbddd/blooddisorders/documents/BBV_PNV_C0_1159_Sickle_Cell_R1mtr.pdf.
Raghupathy, R., Manwani, D., Little, J. (2010) Iron Overload in Sickle Cell Disease. Adv. Hematol. 272940. doi: 10.1155/2010/272940
Sickle cell anemia is a debilitating disease characterized by intermittent vaso-occlusive events and chronic hemolytic anemia. Common symptoms include attacks of acute and chronic abdominal pain, bone pain, breathlessness, delayed growth and puberty, fatigue, fever, rapid heart rate, ulcers, and jaundice. Current treatment consists of symptom management as the condition is chronic and life-threatening and may include folic acid supplementation to encourage red blood cell production, pain medication during crises, and routine blood transfusions. Bone marrow or stem cell transplants are considered risky, yet viable options to cure the disease.
Currently, transfusions are readily utilized to treat sickle cell patients in order to improve blood flow by reducing the proportion of red cells capable of forming the sickle hemoglobin polymer (Raghypathy, 2010). However, a major and unavoidable complication of transfusions in sickle cell disease is iron overload. Iron overload can damage organs and cause other severe symptoms. The risks associated with such treatment are not easily quantified as there is no national database for sickle cell anemia (CDC, 2010). Prevalence rates, health outcomes, and impact on quality of life are not documented. Although every newborn is screened for sickle cell anemia, a national registry has not been established. From a public health perspective the establishment of such a center and service would enable additional documentation and dissemination of information such as the risks associated with iron overload. Surveillance is a key public health tool that allows health professionals to monitor and address health issues, sickle cell anemia should not be immune to such ongoing examination.
References
Bender, MA, Hobbs, W. (2009) Sickle Cell Anemia, Gene Reviews.
Centers for Disease Control and Prevention. Sickle Cell Disease. Retrieved on April 6, 2011 from www.cdc.gov/ncbddd/blooddisorders/documents/BBV_PNV_C0_1159_Sickle_Cell_R1mtr.pdf.
Raghupathy, R., Manwani, D., Little, J. (2010) Iron Overload in Sickle Cell Disease. Adv. Hematol. 272940. doi: 10.1155/2010/272940
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