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What are some things hemophilic patients must know about hemophilia?

Hemophilia is a group of inherited blood disorders in which the blood does not clot properly. Hemophilia is the standard international spelling, also known as haemophilia in the UK, other translations include: hémophilie, hemofilie, hemofili, hemofilia, hämophilie, emofilia. We will use the standard international spelling for the purpose of this section .Bleeding disorders are due to defects in the blood vessels, the coagulation mechanism, or the blood platelets. An affected individual may bleed spontaneously or for longer than a healthy person after injury or surgery.The blood coagulation mechanism is a process which transforms the blood from a liquid into a solid, and involves several different clotting factors. The mechanism generates fibrin when it is activated, which together with the platelet plug, stops the bleeding.When coagulation factors are missing or deficient the blood does not clot properly and bleeding continues.Patients with Hemophilia A or B have a genetic defect which results in a deficiency in one of the blood clotting factors.Queen Victoria was a carrier and passed the mutation to her son Leopold, and through several of her daughters to members of the royal families of Spain, Russia, and Germany.Tsarevich Alexei Nikolaevich, son of Nicholas II (Russia) suffered from hemophilia and was a descendant of Queen Victoria - Rasputin was successful in treating his hemophilia, it was claimed .Types of hemophilia .Hemophilia A and Hemophilia BThere are two main types of hemophilia - Hemophilia A (due to factor VIII deficiency) and Hemophilia B (due to factor IX deficiency). They are clinically almost identical and are associated with spontaneous bleeding into joints and muscles and internal or external bleeding after injury or surgery.After repeated bleeding episodes permanent damage may be caused to the joints and muscles that have been affected, particularly the ankles, knees and elbows.Approximately 1 in 5,000 males is born with Hemophilia A, and 1 in 30,000 males is born with Hemophilia B. Hemophilia affects people of all races and ethnic origins globally. The conditions are both X-linked and virtually all sufferers of hemophilia are males. Female carriers may also bleed abnormally, because some have low levels of the relevant clotting factor.People with hemophilia have a genetic mutation in the affected gene on the X chromosome, which results in reduced production of Factor VIII or IX and creates a bleeding tendency, because coagulation takes much longer than normal, thus making the clot weak and unstableApproximately one third of patients with hemophilia have no family history of the disease, either because of new genetic mutations, or because previous affected generations either had daughters (who were carriers) or sons who died in early childhood from hemophilia or any other cause or who were not affected.Acquired hemophiliaThis is very rare. The patient develops the condition during his/her lifetime and it does not have a genetic or heritable cause. It occurs when the body forms antibodies that attack one or more blood clotting factors, (usually factor VIII), thus preventing the blood clotting mechanism from working properly. Patients may be male or female and the pattern of bleeding is rather different from that of classical hemophilia, the joints being rarely affected. The disorder is particularly associated with old age and occasionally complicates pregnancy.What Causes Hemophilia / Haemophilia?People with hemophilia are born with it. It is caused by a fault in one of the genes that determine how the body makes blood clotting factor VIII or IX. These genes are located on the X chromosome.To understand how hemophilia is inherited, it is important to learn about chromosomes.What are chromosomes?Chromosomes are blocks of DNA (deoxyribonucleic acid). They contain very detailed and specific instructions that determine:How the cells in a baby's body develop.What features the baby will have, including, for example, hair and eye color.Whether the baby is male or female.In humans there are 23 pairs of chromosomes, including the sex chromosome pair. There are two types of sex chromosome:The X chromosomeThe Y chromosomeAll humans have a pair of sex chromosomes:Males have an X + Y pairFemales have an X + X pairWhat chromosomes do we inherit from our parents?A Male inherits hisX chromosome from his motherY chromosome from his fatherA Female inheritsOne X chromosome from her motherOne X chromosome from her fatherShe does not inherit both X chromosomes from her mother. She has no Y chromosomes.How can we calculate the risk of hemophilia in offspring?(Before reading on, remember that the faulty gene is never on the Y chromosome. If it is present, it will be on the X chromosome.)Female (X + Xfaulty) is a carrier, but does not have hemophilia. The “good” X chromosome allows the production of enough clotting factor to prevent serious bleeding problems.Male (Y + Xfaulty) will develop hemophilia and can pass it on.If the father has hemophilia and the mother has no faulty gene (is not a carrier):Father (Y + Xfaulty). Mother (X + X).There is no risk of inherited hemophilia in their sons because boys will inherit their X chromosome from the mother, not the father (they inherit the father's Y chromosome only, which does not have the faulty gene).All the daughters will be carriers but will not develop hemophilia although they will inherit the father's X chromosome, which has the faulty gene. However, their maternal X chromosome, which does not have the faulty gene, usually allows the production of enough clotting factor to prevent serious bleeding problems.If the father does not have hemophilia and the mother has a faulty gene:Father (Y + X). Mother (X + Xfaulty).There is a 50% chance that sons will develop hemophilia because:There is a 50% risk that a son will inherit his mother's Xfaultychromosome, plus his father's Y chromosome - he will have hemophilia.There is a 50% chance he will inherit his mother's "good" X chromosome, plus his father's Y chromosome - he will not have hemophilia.There is a 50% chance that daughters will be carriers, (but no chance of developing hemophilia), because:There is a 50% chance she will inherit her mother's Xfaultychromosome, making her a carrier.There is a 50% chance she will inherit her mother's "good" X chromosome, which would mean she would not be a carrier.Approximately one third of patients with hemophilia have no family history of the disease, either because of new genetic mutations, or because previous affected generations either had daughters (who were carriers) or sons who died in early childhood from hemophilia or any other cause or who were not affected.What is Coagulation? How does our blood clot?Coagulation is a complex process by which the blood forms clots to block and then heal a lesion/wound/cut and stop the bleeding. It is a crucial part of hemostasis - stopping blood loss from damaged blood vessels. In hemostasis a damaged blood vessel wall is plugged by a platelet and a fibrin-containing clot to stop the bleeding, so that the damage can be repaired.Coagulation involves a cellular (platelet) and protein (coagulation factor) component.When the lining of a blood vessel (endothelium) is damaged, platelets immediately form a plug at the site of the injury, while at the same time proteins in the blood plasma respond in a complex chemical reaction, rather like a waterfall, to form fibrin strands which reinforce the platelet plug.Primary hemostasis - when the platelets gather at the site of an injury to plug (block) it.Secondary hemostasis - proteins (coagulation factors) act in a series of chemical reactions to strengthen the plug and allow healing to begin.What is a platelet?A platelet is a disc-shaped element in the blood that is involved in blood clotting. They aggregate (clump together) during normal blood clotting. They are classed as blood cells, but are in fact fragments of large bone marrow cells called megakaryocytes.What is fibrin?Fibrin is an insoluble protein involved in blood clotting. Fibrin is deposited around the wound in a form of mesh to strengthen the platelet plug. The whole thing dries and hardens (coagulates) so that the bleeding stops and the wound then heals. Fibrin is developed in the blood from a soluble protein, fibrinogen.When platelets come into contact with damaged tissue thrombin is formed as a result of a series of chemical processes (coagulation cascade) that culminate in the formation of fibrin from fibrinogen.Coagulation factors (clotting factors)Coagulation factors are proteins, mostly manufactured by the liver. They were originally numbered in the order of their discovery, traditionally using Roman numerals from I-XIII. Some of the numbers such as III and VI are not used any more and in recent years, many proteins that affect blood clotting have been discovered but have been given a name rather than a number. When a blood vessel wall is damaged, or any kind of wound occurs, a complex set of chemical reactions involving these coagulation factors (and acting rather like a waterfall) takes place.The final step of the cascade of chemical reactions is to convert fibrinogen - Factor I - into fibrin, forming a mesh which clumps platelets and blood cells into a solid clot, plugging the hole and stopping the bleeding. Patients with Hemophilia A have deficient levels of Factor VIII, while patients with Hemophilia B have deficient levels of Factor IX.What are the symptoms of hemophilia?Hemophilia symptoms vary, depending on the degree of blood clotting factor (coagulation factor) deficiency and they also depend on the nature of any injury.Three levels of hemophilia are recognized, according to the level of clotting factor amounts in the blood. These are often expressed as percentages of normal:Above 5% - mild hemophilia1% to 5% - moderate hemophiliaLess than 1% - severe hemophiliaMild hemophiliaPeople with inherited mild hemophilia may not have any symptoms until an event occurs which wounds the skin or tissue, such as a dental procedure or surgery, and results in prolonged bleeding. In societies where male circumcision is carried out soon after birth, mild hemophilia will be detected earlier. Joint bleeding is uncommon.Moderate hemophiliaThose with inherited moderate hemophilia will be noticeable early on. The child will bruise easily and may also experience internal bleeding symptoms, especially around the joints, and after a blow or a fall. Bleeding that occurs inside a joint is usually referred to as a joint bleed.Symptoms of a joint bleed:Tingling sensation in the jointPain in the jointIrritation in the jointIf left untreated, the patient may eventually experience:More severe pain in the jointJoint stiffnessThe affected area becomes swollen, tender and hotJoint bleeds most commonly affect the:AnklesKneesElbowsAny surgical intervention, circumcision, dental procedure or injury will result in prolonged bleeding in a person with hemophilia.Severe hemophiliaSymptoms are similar to those found in moderate hemophilia, but occur more frequently and are usually more severe.A child with severe hemophilia will often bleed for no apparent reason, often referred to as spontaneous bleeding. Most commonly, in early childhood from about 18 months of age, the nose or mouth start to bleed or apparently spontaneous bruises appear, particularly on the legs. Parents are sometimes suspected of causing non-accidental injury (deliberate harm) to their children.Symptoms of hemophilia type bleeding may include:Several large or deep bruisesJoint pain or swellingUnexplained bleeding or bruisingBlood in feces (stools)Blood in urineUnexplained nosebleedsUnexplained gum bleedingTightness in the jointsIntracranial hemorrhage (bleeding inside the skull)About 1 in every 30 patients with hemophilia will have intracranial hemorrhage at least once during their lives. This should be treated as a medical emergency. Spontaneous intracranial hemorrhage is rare and in many cases bleeding inside the skull will be the result of a blow to the head.Symptoms of intracranial hemorrhage include:A bad headacheVomitingConfusionFitting (Convulsion)Loss of balanceSlurred speech, or other speaking difficultiesStiff neckVision problemsLoss of coordinationSome of the facial muscles do not work (sometimes all of them)How is hemophilia diagnosed?Prenatal testing - if a pregnant woman has a history of hemophilia, a hemophilia gene test can be done during pregnancy. A sample of placenta is removed from the uterus and tested. This test is known as a CVS (chorionic villus sampling) test.Blood test - if a doctor suspects a child may have hemophilia a blood test can determine whether the patient has hemophilia A or B, and how severe it is. Blood tests can be performed from the time of birth onwards.Treatment for Hemophilia / Haemophilia .Up to a few decades ago a considerable proportion of patients with hemophilia died prematurely because of hemophilia. Tragically, many deaths were the result of childhood injury or surgery. Over the last forty years treatment has advanced so much that the vast majority of patients today are expected to live long and active lives.The main breakthrough in treatment occurred when coagulation factor deficiencies linked to hemophilia could be identified and then replaced, using products derived from human blood.In the past patients used to receive whole blood or plasma infusions to control episodes of bleeding. Even though this helped, levels of clotting factors, especially factors VIII and IX, never reached the levels required for really effective blood coagulation, nor could these levels be sustained - in other words, serious bleeding was only partly treated.Cryoprecipitate, made through the cold precipitation of frozen plasma from1965 onwards, was the first really effective treatment for hemophilia A. Freeze-dried concentrates made from human plasma containing the right levels of Factors VIII and IX became available in the late 1960s and early 1970s. Being able to keep the treatment at home and use it as required meant that patients could travel, leave the home, go to work, and enjoy a level of independence. However, a large number of patients subsequently became infected with blood-borne pathogens, such as hepatitis B, hepatitis C and HIV.From the mid 1980s rigorous donor selection and viral inactivation procedures reduced the risk of blood-borne viral transmission to nearly zero. During the 1990s it became possible to prepare synthetic (recombinant) factors, using specially prepared mammalian cells and these recombinant concentrates are now widely used.Hemophilia treatment will mainly depend on its severity and for patients with Hemophilia A or B involves clotting factor replacement therapy. There are two approaches:On demand - giving treatment to stop prolonged bleeding when it occurs. This is more common in the management of patients with mild hemophilia.Preventative treatment (prophylaxis)- medication to prevent bleeding episodes, and subsequent complications, such as joint and/or muscle damage. More commonly used for patients with moderate or severe hemophilia.Clotting factor concentratesClotting factor concentrates can be made in two different ways:Plasma-derived clotting factors - prepared from the plasma of donated human blood.Recombinant clotting factors - the first generation of recombinant products use animal products in the culture medium and had human albumin (a human blood product) added as a stabiliser. Second generation products use animal-derived materials in the culture medium but do not have added albumin and instead use sucrose or other non-human derived material as a stabiliser. Third generation clotting factors have no albumin present at any stage of their preparation. Mouse monoclonal antibodies have been routinely used in the purification of coagulation factors for many years but a recently licensed recombinant factor VIII employs a synthetic ligand for this step. This has resulted in the production of the first factor VIII concentrate to be free of all exogenous human and animal protein, a goal which was reached for hemophilia B when the first recombinant factor IX was licensed in 1997.Desmopressin (DDAVP)(for mild hemophilia A)This medication is a synthetic hormone which encourages the body to produce more of its own Factor VIII. It is unsuitable for patients with hemophilia B and those with severe hemophilia A. In patients with milder forms of hemophilia A, factor VIII replacement therapy may be necessary, especially for severe bleeds, or after serious injury or major surgery.RICE (Rest, Ice, Compression, Elevation)RICE is a treatment many health care professionals recommend for joint bleeds. It also reduces swelling and tissue damage when used together with clotting factor concentrates.Administering clotting factor concentratesThe medication is injected into a vein - generally in the back of the hand or at the crook of the elbow. Initial treatments are usually administered by a doctor or nurse at a hospital or clinic. Most adults can learn how to do this themselves, which means they can stop bleeding rapidly and effectively wherever they are.If the patient is a child the parents or caregivers (UK/Ireland/Australia: carers) can learn how to administer treatment. The majority of very young patients can receive most of their treatment at home.If a patient is finding it hard to access a suitable vein, or if intensive treatment is required, a port-a-cath, or an external catheter called a Broviac or Hickman line can be placed surgically into a vein, allowing factor replacement therapies to be given, and blood to be drawn easily for routine emergency tests. The use of such catheters can be complicated by infection and blockage and they have to be used with great care.Treating bleedsBleeding episodes (bleeds) are an inevitable complication for patients with hemophilia A and B, even for patients with mild forms. As the underlying problem is one of prolonged bleeding, rather than rapid bleeding, they often appear not to be medical emergencies.If a person with hemophilia experiences any of the following he should seek immediate skilled medical help:There is an injury to the neck, mouth, tongue, face or eye.There is a severe blow to the head.Bleeding is heavy or persistent.There is severe pain or swelling in any part of the body.An open wound requires stitching.Most other bleeds, such as joint/muscle bleeds, small injuries and cuts that do not require stitches, and nosebleeds are generally treated at home, but patients should always seek the advice of a healthcare professional when in doubt. Any treatment will be more effective if it is started early.Storing treatmentFactor concentrates should usually be stored in a refrigerator but are stable at room temperature for quite long periods. They should not be frozen as this may damage the vials or syringes. Some may be taken out for travel but should ideally be kept in a cool bag. Read instructions on product storage. If you are unsure, check with a health care professional or qualified pharmacist.InhibitorsApproximately 30% of people with severe hemophilia A develop antibodies to transfused factor VIII, usually shortly after their first few treatments. These antibodies (also called inhibitors) prevent the factor VIIII treatment working properly. It is often the case that, after a while, the inhibitors disappear and only about 10% or less of people with severe hemophilia A will suffer from long term inhibitors. In recent years it has become possible to prevent inhibitors becoming persistent through immune tolerance induction therapy. Where inhibitors do not respond to this approach alternative treatments are available.Inhibitors rarely develop in mild hemophilia A or in hemophilia B of any severity.

What are the risks and benefits of silver amalgams? Why is there so much controversy surrounding it?

The controversy centres on the fact that amalgams contain mercury. In high enough concentrations, mercury is toxic.Some make the point that amalgams make people sick from allergies to neurotoxicity to a whole host of other systemic alimentsThere has been a great deal of bunk science done on amalgam.I will simply post some key concensus documents which also reference reputable science with respect to the use of dental amalgam.the overall consensus is that amalgam has been used for more than 200 years and except for a small number of patients who might have sensitivities to it, it is safe.Another key point made across the documents is that wholsesale removal of amalgam filling from patient is not indicated.Statement on Dental AmalgamStatement on Dental AmalgamFor dental patients: Please visit the ADA’s MouthHealthy website for information about amalgam and silver-colored fillings.Dental amalgam is considered a safe, affordable and durable material that has been used to restore the teeth of more than 100 million Americans. It contains a mixture of metals such as silver, copper and tin, in addition to mercury, which binds these components into a hard, stable and safe substance. Dental amalgam has been studied and reviewed extensively, and has established a record of safety and effectiveness.The FDI World Dental Federation and the World Health Organization concluded in a 1997 consensus statementi: “No controlled studies have been published demonstrating systemic adverse effects from amalgam restorations.” Another conclusion of the report stated that, aside from rare instances of local side effects of allergic reactions, “the small amount of mercury released from amalgam restorations, especially during placement and removal, has not been shown to cause any … adverse health effects.”In 1998, the ADA’s Council on Scientific Affairsii published its first major review of the scientific literature on dental amalgam which concluded that “based on available scientific information, amalgam continues to be a safe and effective restorative material.” The Council’s report also stated, “There currently appears to be no justification for discontinuing the use of dental amalgam.”In an articleiii published in the February 1999 issue of the Journal of the American Dental Association, researchers report finding “no significant association of Alzheimer’s Disease with the number, surface area or history of having dental amalgam restorations” and “no statistically significant differences in brain mercury levels between subjects with Alzheimer’s Disease and control subjects.”A 2003 paper published in the New England Journal of Medicineiv states, “Patients who have questions about the potential relation between mercury and degenerative diseases can be assured that the available evidence shows no connection.”In 2004, an expert panel reviewed the peer-reviewed, scientific literature published from 1996 to December 2003 on potential adverse human health effects caused by dental amalgam and published a report. The review was conducted by the Life Sciences Research Office (LSRO) and funded by the National Institutes of Dental and Craniofacial Research, National Institutes of Health and the Centers for Devices and Radiological Health, U.S. Food and Drug Administration (FDA). The resulting report states that, “The current data are insufficient to support an association between mercury release from dental amalgam and the various complaints that have been attributed to this restoration material. These complaints are broad and nonspecific compared to the well-defined set of effects that have been documented for occupational and accidental elemental mercury exposures. Individuals with dental amalgam-attributed complaints had neither elevated urinary mercury nor increased prevalence of hypersensitivity to dental amalgam or mercury when compared with controls.” The full report is available from LSRO (The Life Sciences Research Office (LSRO)). A summary of the review is published in Toxicological Reviews.vIn 2006, the Journal of the American Medical Association (JAMA) and Environmental Health Perspectives published the results of two independent clinical trials designed to examine the effects of mercury release from amalgam on the central and peripheral nervous systems and kidney function. The authors concluded that “there were no statistically significant differences in adverse neuropsychological or renal effects observed over the 5-year period in children whose caries are restored using dental amalgam or composite materials”;vi,vii and “children who received dental restorative treatment with amalgam did not, on average, have statistically significant differences in neurobehavioral assessments or in nerve conduction velocity when compared with children who received resin composite materials without amalgam. These findings, combined with the trend of higher treatment need later among those receiving composite, suggest that amalgam should remain a viable dental restorative option for children.”viiiIn May 2008, a Scientific Committee of the European Commission addressed safety concerns for patients, professionals and the use of alternative restorative materials.ix The committee concluded that dental amalgams are effective and safe, both for patients and dental personnel and also noted that alternative materials are not without clinical limitations and toxicological hazards.The ADA Council on Scientific Affairs prepared a comprehensive literature review (PDF) on amalgam safety that summarized the state of the evidence for amalgam safety (from January 2004 to June 2010). Based on the results of this review, the Council reaffirmed at its July 2009 meeting that the scientific evidence supports the position that amalgam is a valuable, viable and safe choice for dental patients.On July 28, 2009, the U.S. Food and Drug Administration (FDA) issued its final rule on encapsulated dental amalgam classifying amalgam and its component parts, elemental mercury and powder alloy, as a class II medical device. Previously there was no classification for encapsulated amalgam, and dental mercury (class I) and alloy (class II) were classified separately. This new regulation places encapsulated amalgam in the same class of devices as most other restorative materials, including composite and gold fillings. At the same time, the FDA also reaffirmed the agency’s position that the material is a safe and effective restorative option for patients.The CSA supports ongoing research on the safety of existing dental materials and in the development of new materials, and continues to believe that amalgam is a valuable, viable and safe choice for dental patients.Referencesi. FDI Policy Statement/WHO Consensus Statement on Dental Amalgam. September 1997. Accessed October 9, 2013.ii. ADA Council on Scientific Affairs. Dental Amalgam: Update on Safety Concerns. J Am Dent Assoc. 1998;129:494-503. Accessed October 9, 2013.iii. Saxe SR, Wekstein MW, Kryscio RJ, et al. Alzheimer’s disease, dental amalgam and mercury. J Am Dent Assoc. 1999;130(2):191-9. Accessed October 9, 2013. (Abstract)iv. Clarkson TW, Magos L, Myers GJ. The toxicology of mercury – Current exposures and clinical manifestations. N Engl J Med. 2003;349:1731-7.v. Brownawell AM, Berent S, Brent RL, et al. The potential adverse health effects of dental amalgam. Toxicol Rev 2005;24(1):1-10. Accessed October 9, 2013. (Abstract)vi. Bellinger DC, Trachtenberg F, Barregard L, et al. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. JAMA 2006;295(15):1775-83. Accessed October 9, 2013. (Abstract)vii. Bellinger DC, Daniel D, Trachtenberg F, Tavares M, McKinlay S. Dental amalgam restorations and children’s neuropsychological function: the New England Children’s Amalgam Trial. Environ Health Perspect 2007;115(3):443-6. Accessed October 9, 2013.viii. DeRouen TA, Martin MD, Leroux BG, et al. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. JAMA 2006;295(15):1784-92. Accessed October 9, 2013.ix. European Commission: Scientific Committee on Emerging and Newly Identified Health Risks. The Safety of Dental Amalgam and Alternative Dental Restoration Materials for Patients and Users May 6, 2008. Accessed October 9, 2013.Another link from the Government of Canada which looks at amalgam safety and delves into amalgam policies from other countries:The Safety of Dental AmalgamStatement from the Canadian Dental Association on amalgam: paper on this controversy:The Dental Amalgam Toxicity Fear: A Myth or ActualityToxicology InternationalMedknow PublicationsThe Dental Amalgam Toxicity Fear: A Myth or ActualityMonika Rathore, Archana Singh, and Vandana A. PantAdditional article informationAbstractAmalgam has been used in dentistry since about 150 years and is still being used due to its low cost, ease of application, strength, durability, and bacteriostatic effect. When aesthetics is not a concern it can be used in individuals of all ages, in stress bearing areas, foundation for cast-metal and ceramic restorations and poor oral hygiene conditions. Besides all, it has other advantages like if placed under ideal conditions, it is more durable and long lasting and least technique sensitive of all restorative materials, but, concern has been raised that amalgam causes mercury toxicity. Mercury is found in the earth's crust and is ubiquitous in the environment, so even without amalgam restorations everyone is exposed to small but measurable amount of mercury in blood and urine. Dental amalgam restorations may raise these levels slightly, but this has no practical or clinical significance. The main exposure to mercury from dental amalgam occurs during placement or removal of restoration in the tooth. Once the reaction is complete less amount of mercury is released, and that is far below the current health standard. Though amalgam is capable of producing delayed hypersensitivity reactions in some individuals, if the recommended mercury hygiene procedures are followed the risks of adverse health effects could be minimized. For this review the electronic databases and PubMed were used as data sources and have been evaluated to produce the facts regarding amalgam's safety and toxicity.Keywords: Amalgam, mercury, myth, restoration, safety, tooth, toxicityINTRODUCTIONAmalgam, an alloy of mercury (Hg), is an excellent and versatile dental restorative material. It has been used in dentistry since 150 years due to its low cost, ease of application, strength, durability, and bacteriostatic effects.[1] Popularity of amalgam as restorative material is decreasing these days due to concerns about detrimental health effects, environmental pollution, and aesthetics.[2] The metallic colour of amalgam does not blend with the natural tooth colour so patients and professionals preferred tooth-coloured restorative material for cavity filling in carious teeth for better aesthetics. Researchers agree that amalgam restorations leach mercury into the mouth, but consistent findings are not available to report whether it has any significant health risk.[3] In this review, an attempt has been made to summarize that there is no convincing evidences pointed out to adverse health effects due to dental amalgam restorations and can be used as a preferred restorative material where aesthetics is not a concern.Amalgam composition and historical backgroundAmalgam consists of an alloy of silver, copper, tin, and zinc combined with mercury. Unreacted alloy particles of silver-tin are considered as gamma phase. These particles combine with mercury and form a matrix consisting of gamma-1(Ag2Hg3) and gamma-2 phases. (Sn7-8Hg). The gamma-2 phase is responsible for early fracture and failure of amalgam restorations. Hence, copper was introduced to avoid gamma-2 phase, replacing the tin-mercury phase with a copper-tin phase (Cu5Sn5).[4] Louis Regnart, known as the ‘Father of Amalgam’, improved on boiled mineral cement by adding mercury, which greatly reduced the high temperature originally needed to pour the cement on to a tooth. In 1890s GV Black gave a formula for dental amalgam that provided clinically acceptable performance and remained unchanged virtually for 70 years. In 1959, Dr Wilmer Eames[5] promoted low mercury-to-alloy mixing ratio. The mercury-to-amalgam ratio, dropped from 8:5 to 1:1. The formula was again changed in 1963, when amalgam consisting of a high-copper dispersion alloy was introduced.[6] It was later discovered that the improved strength of the amalgam was a result of the additional copper forming a copper–tin phase that was less susceptible to corrosion than the tin–mercury phase in the earlier amalgam.[7]Modern amalgams are produced from precapsulated (preproportioned) alloy consisting of 42% to 45% mercury by weight. These are convenient to use and provide some degree of assurance that the material has not been not contaminated before use or spilled before mixing.[8]Amalgam controversy and amalgam warIn the year 1843, the American Society of Dental Surgeons (ASDS), founded in New York City, declared use of amalgam to be malpractice because of the fear of mercury poisoning in patients and dentists and forced all its members to sign a pledge to abstain from using it.[9] It was the beginning of the amalgam war.[10] Because of its stance against amalgam, membership in the American Society of Dental Surgeons declined, and due to the loss of members, the organization was disbanded in 1856 thus resulting in the end of the amalgam war. In 1859, the American Dental Association (ADA) was founded and it did not forbid use of amalgam.[11] The ADA position on the safety of amalgam has remained consistent since its foundation. In 1920s inferences were made that mercury was not tightly bound in amalgam so its use was discouraged. In 1991, National Institute of Health-National Institute for Dental Research (NIH-NIDR) and FDA concluded that there was no basis for claims that amalgam was a significant health hazard,[12] but claims of amalgam hazards continued to be published in non-scientific journals, and occasionally in scientific journals.Mercury exposure from amalgam restorationsMercury is ubiquitous in environment and humans are routinely exposed via air, water, and food.[8] Exposure to mercury in human individuals with amalgam restoration occurs during the placement or removal of dental restorations. Once the reaction is complete, less amount of mercury is released, that is far below the current health standard.[8] The exposure to mercury from restoration depends on the number and size of restoration, composition, chewing habits, food texture, grinding, brushing of teeth, and many other physiological factors. As a vapour, metallic mercury could be inhaled and absorbed through the alveoli in the lungs at 80% efficiency. It is the main route of entry of mercury into the human body, whereas the absorption of metallic mercury through skin or via the gastrointestinal tract is very poor.[8] The organic compounds of mercury such as methyl mercury are readily absorbed by many organisms and accumulate as it passes into food chain. Research on monkeys had shown that mercury released from amalgam restorations is absorbed and accumulated in various organs such as kidney, brain, lung, liver, gastro-intestinal tract, and the exocrine glands.[13] The organic form of mercury was also found to have crossed the placental barrier in pregnant rats[14] and proven to cross the gastrointestinal mucosa when amalgam particles are swallowed at the time of amalgam insertion or during removal of old amalgam fillings,[15] whereas the inorganic form of Mercury ions (Hg+2) circulate into the blood stream but hardly cross the blood–brain barrier and placental barrier.Mercury does not collect irreversibly in human tissues. The average half life of mercury is 55 days for transport through the body to the point of excretion. Thus mercury that came into the body years ago may no longer be present in the body.[8]Diagnostic methods to detect levels of mercury in bodyToxicity from mercury could occur through exposure to organic, inorganic, and elemental forms of mercury. According to decreasing toxicity of mercury it is classified as organomercury (methyl and ethyl mercury), mercury vapour, and inorganic mercury. Various diagnostic methods exist to detect the level of mercury in body, including tests for blood, urine, stool, saliva, hair analysis, and others. These tests may determine if mercury is in the body and/or if it is being excreted. A study[16] conducted by measuring the intraoral vapour levels over a 24-h period in patients with at least nine amalgam restorations showed that the average daily dose of inhaled mercury vapour was 1.7 μg (range from 0.4 to 4.4 μg), which is approximately 1% of the threshold limit value of 300 to 500 μg/day established by WHO, based on a maximum allowable environmental level of 50 μg/day in the workplace. According to Berdouses et al.[17] mercury exposure from amalgam can be greatly increased by personal habits such as, chewing and brushing.Berglund,[18] in 1993, determined the daily release of mercury vapour from amalgam restorations made of alloys of the same types and batches as those used in the in vitro part of the study. He carried out a series of measurements on each of eight subjects before and after amalgam therapy and found that none of the subjects were occupationally exposed to mercury. The amalgam therapy, that is, from 3 to 6 occlusal amalgam surfaces and from 3 to 10 surfaces in total-had very little influence on the intraoral release of mercury vapour, regardless of amalgam type used, effects was not found on mercury levels in urine and saliva. Rapid and reliable detection of mercury in blood and urine resulting from environmental and occupational exposure may be carried out by using atomic fluorescence spectrophotometry.[19] Measurements of total mercury in the urine tend to reflect inorganic mercury exposure and total mercury levels in whole blood are more indicative of methyl mercury exposure. Commonly two types of urine tests have been used in which one is the unprovoked mercury test that does not use a pharmaceutical mercury chelator and only reflects the amount of mercury the body naturally removes via the urine. The other is the urine mercury challenge (provoked) test, which uses a pharmaceutical chelator to remove the mercury captured via the kidneys/urine pathway. Both methylmercury and inorganic mercury can also be measured in breast milk. The relative proportions of these species depend on the frequency of fish consumption, dental amalgam status, and occupational exposures. In a study for comparison of hair, nails, and urine for biological monitoring of low level inorganic mercury exposure in dental workers, the data suggested that urine mercury remains the most practical and sensitive means of monitoring low level occupational exposure to inorganic mercury.[20]Various related studiesIn this review electronic databases and PubMed have been used for data sources and articles from peer reviewed journals and various organizations including WHO (1991), the Agency for Toxic Substances and Disease Registry (ATSDR) (1999), US Environmental Protection Agency (EPA,1997), the National Research Council (NRC) (2000), the Institute of Medicine (2001; 2004) and Life Science Research Office (LSRO) (2004) have been evaluated to investigate the biochemical, behavioural, and/or toxicological effects resulting from exposure to amalgam, mercury vapour (HgO), inorganic mercury (Hg2+), or organic mercury (methyl and ethyl mercury). The LSRO search was limited to in vivo studies on humans relevant to amalgam and biochemical, behavioural and/or toxicological effects as health effects in laboratory animals do not reliably predict health effects in humans.Effects of prenatal mercury exposureNonionized mercury is capable of crossing through lipid layers at membrane barriers of the brain and placenta, is oxidised within these tissues and is slowly removed. This fact has become the basis for claims of neuromuscular problems in patients with amalgam restorations.[8] Removing these restorations do not eliminate exposure to mercury. Maternal amalgam restoration results in in utero exposure to low levels of elemental mercury. There is no evidence that exposure to mercury has been associated with any adverse pregnancy outcomes or health effects in the newborn and infants. In a prospective study consisting of 72 pregnant women, it was found that the number and surface areas of amalgam restorations positively influenced the concentration of mercury in amniotic fluid. The levels of mercury detected in amniotic fluid were low and no adverse outcomes were observed during the pregnancy or in the newborns.[21] Blood samples obtained from umbilical cord had no significant mercury levels considered to be hazardous for neurodevelopmental effects in children using the EPA reference dose (5.8 μg/L in cord blood).[22] To find co-relation between mercury exposure from amalgam restorations placed during pregnancy and low-birth weight 1,117 women with low birth weight infants were compared with random sample of 4,468 women who gave birth to infants with normal birth weight. Women (4.9%) had at least one amalgam restoration placed during pregnancy. These women were not at greater risk for a low birth weight infant and neither were women who had 4 to 11 amalgam restorations placed.[23] In a study conducted by Daniels[24] 90% of the women received dental care during pregnancy. Having more restorations placed at time of conception did not negatively affect pregnancy or birth outcome. Mean umbilical cord mercury concentration was slightly higher in women who had dental care. However, cord mercury concentrations did not differ significantly among mothers in relation to amalgam restoration during pregnancy or by the number of amalgams in place prior to pregnancy. Overall, amalgam restorations were not associated with negative birth outcomes or delayed language development. They stated that amalgam restorations in girls and women of reproductive age should be used with caution to avoid prenatal mercury exposure, although there were no adverse effects seen.Health effects of amalgam in childrenThe Children's Amalgam Trial is a randomized trial, to address potential impact of mercury from amalgam restorations on neuropsychological and renal function in children. Bellinger et al.[25] conducted a study on 534 New England children, aged 6–10 years for 5 years. All subjects were in need of at least two posterior occlusal restorations. Participants were randomized to receive either amalgam or composite restoration at baseline and at subsequent visits. The primary endpoint was to assess the 5-year change in IQ scores. Secondary endpoints included measures of other neuropsychological assessments and renal functioning. In the 5-year follow-up period the investigators conducted multiple assessments of IQ score, memory index, and urinary albumin. No statistically significant differences were reported in neuropsychological or renal effects observed in the children who had amalgam restorations compared to those with composite restorations.In another study, authors have concluded that there was no difference in the neuropsychological function of the children who received amalgam restorations compared to the children with composite restorations.[26] A dose-effect analysis of children's exposure to amalgam and neuropsychological function was also evaluated in the children's amalgam trial. The authors examined a sample of children with substantial unmet dental needs using a dose–effect analysis. There was no significant association between neuropsychological outcomes and mercury exposure. The authors concluded that there appeared to be no detectable adverse neuropsychological outcomes in children attributable to the use of amalgam restorations.[27] The relation between amalgam and the psychosocial status of children was also assessed as a part of the New England Children's Amalgam Trial (NECAT). The two groups of children were examined for psychosocial outcomes. It was carried out using both a parent-completed “Child Behaviour Checklist” and children's self-reports and concluded that there was no evidence associated with adverse psychosocial outcomes in the 5-year period following amalgam placement.[28]Kingman et al.[29] studied correlation between exposure to amalgam and neurological functions. No significant associations between amalgam exposure and clinical neurological signs of abnormal tremor, coordination, gait, strength, sensation or muscle stretch reflexes or for any level of peripheral neuropathy in the subjects have been observed. A significant association was detected between amalgam exposure and the continuous vibro-tactile sensation response. The study reported that this association was a subclinical finding that was not associated with symptoms, clinically evident signs of neuropathy or any functional impairment.In the Children's Amalgam Trial, one of the secondary endpoints included renal functioning. The investigators assessed changes on markers of glomerular and tubular kidney function and urinary mercury levels. They found no significant differences between the treatment groups and no significant effects related to the number of dental amalgam restorations on the markers. Children in both treatment groups experienced micro albuminuria, but the prevalence was higher in amalgam group. The authors concluded that the increase in micro albuminuria may be random, but should be further evaluated.[30] The other safety trial was conducted in Lisbon, Portugal[27] in which a randomized controlled clinical trial carried out in 507 children 8- to 10-years old at baseline. They were evaluated for several years thereafter to determine if any health changes occurred following restorations with amalgam or composites. On carrying out annual standardized tests of memory, attention, physical coordination, and velocity of nerve conduction, the scientists did not detect a pattern of decline in the test scores of individual children who received amalgam restorations. They found a trend of higher treatment need in children receiving composite, thus suggesting that amalgam should remain a viable dental restorative option for children. The investigators performed annual clinical neurological examinations to assess neurobehavioral and neurological effects. The authors concluded that amalgam exposure had no adverse neurological outcomes.[31]The 7 years of longitudinal data provide extensive evidence about relative safety of amalgam in dental treatment. Substantial amalgam exposure did lead to creatinine adjusted urinary mercury levels that were higher in the amalgam group. Children with amalgam restorations had slightly elevated levels of mercury in their urine, measuring on average 1.5 μg/L of urine for the first two years and levelling off to 1.0 μg/L or less thereafter. However, these values fall within the background level of 0–4 μg/L, which is usual for an average person not exposed to industrial or other known sources of mercury.[32] Thus, the longitudinal studies on the use of amalgam in children did not suggest any negative effects on neuropsychological function or renal function within the 5-year follow-up period. It was reported that urinary mercury concentrations were highly correlated with both the number of amalgam restorations and the time since placement in children. The finding suggested that there may be sex-related differences in mercury excretion. They found that females have significant increase in the rate of mercury excreted in urine than males. Thus, this association might confer a lower mercury toxicity risks in females.[33] Dunn et al.[34] evaluated scalp, hair, and urine mercury content of children collected over the 5-year period, mean hair mercury level was 0.3–0.4 μg/g and mean urinary mercury level was 0.7–0.9 μg/g creatinine. The authors reported that use of chewing gum in the presence of amalgam restoration was a predictor of higher urinary mercury levels. Data suggested that amalgam-associated mercury exposure might be reduced by avoidance of gum-chewing in the presence of amalgam restorations.Sixty children were studied to assess urinary mercury excretion and its relation to amalgam restoration and fish consumption. Children with amalgam restorations had significantly higher urinary mercury levels compared to children with non-amalgam restorations. The urinary mercury levels in the amalgam group were well below levels that are known to cause adverse health effects.[35]Health effects related to mercury exposure in adultsAn investigation on 20,000 people in the New Zealand Defence Force between years 1977–1997 was done to find out association between amalgam restorations and disorders related with nervous system and kidney. No significant correlation between amalgam restorations and chronic fatigue syndrome or kidney disease was observed. A slightly elevated risk for multiple sclerosis was reported, but may have been due to confounding variables.[36] In another study, where few patients believed that their amalgam restoration made them ill, medical examination including physical examination, electrocardiogram, abdominal sonography, and blood chemistry was done. The study concluded that symptoms of the patients were due to psychological factors. There was no connection between the mercury levels in the patient's blood, urine, and saliva and their symptoms.[37] The association between amalgam and multiple sclerosis was assessed via a systematic review and meta-analysis. Three case control studies and one cohort study met their inclusion criteria. The meta-analysis revealed a slight nonstatistically significant increase between the presence of amalgam restorations and multiple sclerosis. The study does not provide evidence for or against an association.[38]Halbach et al.[39] evaluated the internal exposure to amalgam-related mercury and estimated the amalgam-related absorbed dose of mercury. The integrated mercury absorbed from amalgam restorations was estimated at up to 3 μg per day for an average number of restorations and 7.4 μg per day for a high amalgam load. The authors concluded that these estimates are below the tolerable dose of 30 μg per day established by WHO.Hypersensitivity reactions by amalgam restorationsAmalgam is capable of producing delayed hypersensitivity reactions in some individuals. These reactions usually present with dermatological or oral symptoms. The constant exposure to mercury in amalgam restorations may sensitize some individuals, making them more susceptible to oral lichenoid lesions. These oral lesions are rarely noticed by the affected individuals and cause no discomfort. There is evidence that a certain percentage of lichenoid lesions are caused by amalgam restorations,[40] but other restorative materials can also cause lichenoid lesions. It was also noted that the restorations associated with lichenoid lesions are poorly contoured, corroded and old. Hence corrosion of amalgam restoration or perhaps the biofilm present on such restorations may contribute to the development of hypersensitive reaction rather than material itself.[41] Symptoms of an amalgam allergy include skin rashes in the oral, head and neck area, itching, swollen lips, localized eczema-like lesions in the oral cavity. These clinical signs usually require no treatment and will disappear on their own within a few days of exposure. However, in some instances, an amalgam restoration will have to be removed and replaced with alternate restorative material. The replacements have led to significant improvements.[42] Although mercury allergy is rare but sometimes hypersensitivity to it may lead to dermatitis or type IV delayed hypersensitivity reactions most often affecting the skin as a rash.[43]Mercury exposure in dental professionalsDentists and dental nurses are at risk of potential exposure to inorganic mercury through their handling of amalgam, although now days their exposure has reduced due to low mercury to alloy ratio and through mercury management. One hundred and eighty dentists were evaluated in West Scotland for mercury exposure and its effects on their health and cognitive function. Dentists were found to have, on an average, over four times the level of urinary mercury compared to age and education-matched control subjects. The authors reported that based on their questionnaire, dentists were more likely to report having a disorder of the kidney, although the effect was not significantly associated with their urinary mercury level. An age effect was found for memory disturbances in dentists but not in the control subjects. There was no significant association between urinary mercury concentrations and self-reported memory disturbance.[44] A study on 43 dental nurses, with an average age of 52, were exposed to copper amalgam with a 30-year follow-up; were compared with 32 matched controls. It was concluded that the dental nurses did not appear to be neurobehavioraly compromised. Seven symptoms of mercury poisoning that were reported at a higher rate by exposed group than by the control group (arthritis, bloating, dry skin, headache, metallic taste, sleep disturbances, and unsteadiness). It did not appear that the investigators performed post-hoc testing to compensate for multiple comparisons.[45] The possible health risk of occupational exposure to mercury vapour in the dental office was assessed by evaluating the cytogenetic examination of leukocytes and blood mercury levels of dentists.[46] Genotoxicity of occupational exposure to mercury vapour in ten dentists was evaluated. The authors concluded that mercury vapour concentration in blood was below 0.1 mg/m3 and did not exhibit cytogenetic damage to leukocytes.Mercury management in dental operatoryIn 1999, the ADA Council on Scientific Affairs adopted mercury hygiene recommendations to provide guidance to dentists and their staff members for safe handling of mercury and minimizing the release of mercury into the dental office environment. These were updated in 2003 and are as follows: work in well-ventilated areas, remove professional clothing before leaving the workplace, periodically check the dental operatory atmosphere for mercury vapour, (use dosimeter badges or use of mercury vapour analysers for rapid assessment after any mercury spill or clean-up procedure). The current Occupational Safety and Health Administration (OSHA), standard for mercury is 0.1 mg per cubic meter of air averaged over 8-h work shift. The National Institute for Occupational Safety and Health has recommended the permissible exposure limit to be changed to 0.05 mg/m3 averaged over 8-h work shift over a 40-h workweek.[47] During preparation and placement of amalgam only precapsulated amalgam alloys should be used. If possible, recap single-use capsules after use, store them in a closed container and recycle them. Avoid skin contact with mercury or freshly mixed amalgam. Use high-volume evacuation systems when finishing or removing amalgam. Floor coverings should be non absorbent, seamless and easy to clean. Use of carpet in operatory is not recommended where an accidental mercury spill might occur. Chemical decontamination of carpeting may not be effective, as mercury droplets can seep through the carpet and remain inaccessible to the decontaminant. In case of accidental mercury spill a vacuum cleaner should never be used to clean up the mercury. Small spills (less than 10 g of mercury present) can be cleaned safely using commercially available mercury cleanup kits.Amalgam substitutesIn the recent year's composites, glass ionomer cements and a variety of hybrid structures have been used due to increased demand for aesthetic restorations. Composite serves better than amalgam when conservative preparation is recommended like small occlusal restorations, in which amalgam require removal of more sound tooth structure.[48] Composites have different setting reaction mechanisms and it interacts with the patient's tissues in different ways . The small organic molecules (monomers) react to form polymers. Some of the monomers may not have reacted during placement and therefore low levels remain in the set restoration, which are known to be toxic to cells and others may cause allergic reactions. The effects they cause vary depending on the substance and on the type of body tissue with which they come into contact. Concerns have been raised about the endocrine disrupting (in particular, oestrogen-mimicking) effects of plastic chemicals such as “Bisphenol A” used in composite resins.[49]Amalgam possesses greater longevity than composite.[50] However, this difference has decreased with continued development of composite resins.[51] Amalgam is moderately tolerant to the presence of moisture during placement. In contrast, technique for composite resin placement is more sensitive and require “extreme care” and “considerably greater number of steps”.[51] Mercury acts as bacteriostatic agent whereas TEGMA (constituting some older resin-based composites) “encourages the growth of microorganisms”.[51] The New England Children's Amalgam Trial suggested that the longevity of amalgam is higher than that of resin-based compomer placed in primary teeth and composites in permanent teeth.[50,52] Compomers and composites were seven times likely to require replacement than amalgam.[52] “Recurrent marginal decay” is the main reason for failure in both, amalgam and composite restorations, accounting for 66% (32/48) and 88% (113/129), respectively.[53] “Christensen[50] quoted Amalgam restorations are and will continue to be the mainstay of posterior tooth restorations for many years to come.” Though use of amalgam has decreased during the past few years, more studies on safety of composites or other aesthetic materials with long-term follow-up of are necessary before they can be considered a definitive alternative for amalgam.CONCLUSIONThe current use of amalgam has not posed a health risk apart from allergic reactions in few patients. Clinical justifications have not been available for removing clinically satisfactory amalgam restorations, except in patients allergic to amalgam constituents. Mercury hypersensitivity is an immune response to very low levels of mercury. There is no evidence that mercury released from amalgams results in adverse health effects in the general population. If the recommended mercury hygiene procedures are followed, the risks of adverse health effects in the dental office could be minimized. Amalgam is safe and effective restorative material and its replacement by nonamalgam restorations is not indicated. Also a recent review by the American Dental Association Council on Scientific Affairs states that: “Studies continue to support the position that dental amalgam is a safe restorative option for both children and adults. When responding to safety concerns it is important to make the distinction between known and hypothetical risks.”

Do any vaccinations have long-term side effects?

I would say that we are experienceing the long term side effects as we speak, “long term” meaning that we are finally, after 60+ years of exposure, recognizing those effects in our children. Medical science now has the means to detect many neurological disorders that they once simply considered mental or neurological defects. Before the technology became available various disorders were simply grouped together. Epilepsy, for instance. Anyone having a siezure disorder was simply diagnosed as epileptic, with not much in the way of cause. Now medical science knows that there are many disorders that can cause siezures. The same goes for vaccine side effects, but that is one area that no one wants to admit to. However, the numbers alone can tell a story. In 2007 the vaccine “schedule” for children and infants accelerated…and so did the incidences of Autism.~Although this is a very long list it is in no way complete:“February 5, 2019CDC released the 2019 U.S. recommended immunization schedules for children/adolescents as well as for adults on its website.January 23, 2019FDA approved use of the 0.5 mL dose of Sanofi's Fluzone Quadrivalent influenza vaccine to include children age 6 through 35 months.January 14, 2019FDA approved expanded use of Sanofi's Adacel Tdap vaccine for a second dose in people ages 10 through 64 years of age.December 21, 2018FDA licensed pediatric hexavalent vaccine (DTaP, IPV, HepB, and Hib) developed by Sanofi and Merck; not available in the U.S. until 2020 or later.November 7, 2018ACIP published updated recommendations on use of hepatitis A vaccine for pre- and post-exposure prophylaxis for international travel.October 25, 2018The American Dental Association adopted a policy to support the use and administration of HPV vaccine for the prevention of oral HPV infection.October 8, 2018FDA approved expanded age indication for Seqirus’s Afluria influenza vaccine to include children age 6 months through 59 months.October 5, 2018FDA announced approval of expanded use of Merck’s Gardasil 9 (HPV9, Human papillomavirus) vaccine to include adults 27 through 45 years old.August 24, 2018CDC published ACIP's 2018–19 influenza vaccination recommendations.June 8, 2018CDC published ACIP's recommendations for the use of quadrivalent live attenuated influenza vaccine (LAIV4) in the 2018–19 influenza season.June 2018The American College of Obstetricians and Gynecologists issued a committee opinion on maternal immunization.May 16, 2018CDC released information about a new rapid rabies test that could save lives and lead to fewer unnecessary rabies shots.April 27, 2018CDC published a comprehensive summary of previously published ACIP recommendations for prevention of tetanus, diphtheria, and pertussis in the U.S.April 20, 2018CDC published ACIP recommendations for use of hepatitis B vaccine with a novel adjuvant [Heplisav-B].April 2018The American College of Obstetricians and Gynecologists released a committee opinion on influenza vaccination in pregnancy.February 6, 2018CDC published the 2018 U.S. recommended immunization schedule for 0 through 18 years.February 6, 2018CDC published the 2018 U.S. recommended adult immunization schedule.January 26, 2018CDC published ACIP recommendations for use of herpes zoster vaccines.January 12, 2018CDC published updated ACIP recommendations for prevention of hepatitis B virus infection.January 12, 2018CDC published ACIP recommendations on use of a third dose of MMR during a mumps outbreak.January 11, 2018FDA approved expanded pediatric age indication for Fluarix Quadrivalent influenza vaccine.November 9, 2017FDA licensed Heplisav-B, the new hepatitis B vaccine from Dynavax, for use in adults age 18 and older.October 20, 2017FDA licensed Shingrix, the new shingles vaccine from GlaxoSmithKline, for use in adults age 50 and older.September 15, 2017CDC published updated dosing instructions for hepatitis A prophylaxis with immune globulin.August 31, 2017FDA expanded licensure of Afluria quadrivalent (Seqirus) to include people age 5 years and older.August 25, 2017CDC published ACIP 2017–18 influenza vaccination recommendations.August 2017AAP issued policy stating that newborns should routinely receive hepatitis B vaccine within 24 hours of birth.July 6, 2017CDC published a Vaccine Information Statement for cholera.June 30, 2017CDC and FDA announced new Vaccine Adverse Event Reporting website and reporting form.May 19, 2017CDC published ACIP's updated recommendations on use of Trumenba meningococcal serogroup B vaccine.May 12, 2017CDC published ACIP recommendations for use of cholera vaccine.April 20, 2017CDC published ACIP recommendations titled "General Best Practice Guidelines for Immunization" to replace the 2011 "General Recommendations on Immunization."February 7, 2017CDC published the 2017 U.S. recommended immunization schedules for 0 through 18 years; includes new “16-year-old vaccination" column.February 7, 2017CDC published the 2017 U.S. recommended adult immunization schedule.December 16, 2016CDC published ACIP's recommendations on 2-dose HPV vaccine series for younger adolescents.November 18, 2016FDA approved extending the age range for use of FluLaval Quadrivalent to include children 6 to 35 months of age.November 4, 2016CDC published ACIP recommendations for use of meningococcal conjugate vaccines in HIV-infected persons.September 27, 2016PAHO/WHO announced measles elimination in the Americas.August 26, 2016CDC published 2016–17 influenza vaccination recommendations.August 2016AAP released new policy statement that urges states to eliminate all non-medical exemptions to vaccine requirements.July 11, 2016FDA extended the age indication for PCV13 (Prevnar 13) to include adults age 18 through 49 years.June 22, 2016ACIP voted that live attenuated influenza vaccine (LAIV) should not be used during the 2016–2017 flu season.June 15, 2016FDA approved revisions in the package insert for YF-Vax to reflect changes to International Health Regulations and WHO/ACIP recommendations.June 10, 2016FDA approved Vaxchora for the prevention of cholera.April 14, 2016FDA approved changes to vaccine administration schedule for Trumenba vaccine.February 5, 2016National Vaccine Program Office released an National Adult Immunization Plan.February 1, 20162016 U.S. recommended immunization schedules for 0 through 18 years and "catch up" published in MMWR.January 14, 2016FDA approved Hiberix for full Hib vaccine series.December 14, 2015FDA expanded Gardasil 9 licensure to include males age 16–26 years.November 24, 2015FDA approved new injectable influenza vaccine, Fluad, for use in people age 65 years and olderOctober 23, 2015ACIP published recommendations for the use of serogroup B meningococcal vaccines in adolescents and young adults.September 4, 2015CDC published updated ACIP recommendations regarding the intervals between PCV13 and PPSV23 vaccines for use in immunocompetent adults age 65 years and olderAugust 14, 2015WHO published "Recommendations on Vaccine Hesitancy" in special issue of the journal Vaccine.June 19, 2015ACIP published recommendations for yellow fever booster doses.June 12, 2015ACIP published recommendations for use of serogroup B meningococcal vaccines in people age ten years and older at increased risk for serogroup B meningococcal disease.June 8, 2015American Medical Association adopted a new policy that supports ending non-medical vaccine exemptions, including those for healthcare professionals.April 29, 2015The Pan American Health Organization declared rubella eliminated in the Americas.March 27, 2015CDC published ACIP recommendations for use of 9-valent HPV vaccine.March 27, 2015CDC published new ACIP recommendations for typhoid vaccination.March 24, 2015FDA approved Quadracel, a new combination DTaP+IPV vaccine for use in children age 4–6 years.January 23, 2015CDC's Health Alert Network issued a health advisory about a multi-state outbreak of measles linked to Disneyland.January 23, 2015FDA approved the use of Bexsero, the second vaccine licensed in the U.S. to prevent serogroup B meningococcal disease.December 19, 2014FDA approved Rapivab to treat influenza infection.December 11, 2014FDA approved quadrivalent formulation of Fluzone Intradermal inactivated influenza vaccine.December 10, 2014FDA approved the use of Gardasil 9 (Merck) 9-valent HPV vaccine in the U.S.October 29, 2014FDA approved the use of Trumenba in the U.S. to prevent serogroup B meningococcal disease.September 19, 2014CDC published ACIP recommendations for use of PCV13 and PPSV23 vaccines in adults age 65 and older.June 20, 2014CDC published ACIP's recommendations for use of MenACWY-CRM vaccine in children age 2–23 months at increased risk for meningococcal disease.May 5, 2014WHO Director-General declared the international spread of wild poliovirus in 2014 a Public Health Emergency of International Concern.April 25, 2014CDC report showed 20-year U.S. immunization program spares millions of children from diseases.March 24, 2014FDA lowered age of licensure for Adacel vaccine administration from age 11 years to 10 years.February 28, 2014CDC published ACIP recommendations for prevention and control of Haemophilus influenzae type b (Hib) disease.December 20, 2013CDC published guidance for HBV protection and postexposure management of healthcare personnel.November 15, 2013CDC published new recommendations for use of Japanese encephalitisvaccine in children.September 10, 2013National Vaccine Advisory Committee released revised "Standards for Adult Immunization Practice."August 16, 2013FDA extended FluLaval IIV (GlaxoSmithKline) age range to include children and teens age 3–17 years; licenses quadrivalent FluLaval product.August 1, 2013FDA expanded age indication for Menveo (Novartis) to include infants and toddlers age 2 through 23 months.July 19, 2013CDC issued updated recommendations for use of VariZIG immune globulin for varicella postexposure prophylaxis.June 28, 2013CDC issued recommendations for PCV and PPSV vaccination of children with immunocompromising conditions.June 20, 2013ACIP voted to recommend FluBlok influenza vaccine for people age 18 through 49 with egg allergy.June 14, 2013CDC published recommendations for preventing measles, rubella, congenital rubella syndrome, and mumps.June 7, 2013FDA approved Fluzone (Sanofi Pasteur) as the third quadrivalent influenza vaccine licensed for U.S. use.May 17, 2013Booster dose of yellow fever vaccine not needed, according to WHO. A single dose of vaccine is effective in providing long-term protection from yellow fever.January 25, 2013FDA approved use of Prevnar 13 vaccine in older children and teens (6-17 years).December 18, 2012Institute for Safe Medication Practices (ISMP) launched new Vaccine Error Reporting Program.December 12, 2012FDA approved quadrivalent formulation of Fluarix (inactivated influenza vaccine; GlaxoSmithKline).November 20, 2012FDA approved first seasonal influenza vaccine manufactured using cell culture technology (Flucelvax, Novartis).October 24, 2012ACIP voted to recommend use of HibMenCY (Menhibrix, GlaxoSmithKline), a new combination (meningococcal and Hib) vaccine, in infants at increased risk for meningococcal disease.October 24, 2012ACIP voted to recommend that pregnant women receive a dose of Tdap during each pregnancy irrespective of the patient's prior history of receiving Tdap.June 24, 2012FDA approved HibMenCY (Menhibrix, GlaxoSmithKline), a new combination (meningococcal and Hib) vaccine for infants.June 7, 2012FDA expanded licensure of PCV13 to include adults ages 50 years and older.June 5, 2012U.S. Department of Health and Human Services (HHS) Office of the Inspector General (OIG) released a report titled "Vaccines for Children (VFC) Program: Vulnerabilities in Vaccine Management."April 1, 2012United Nations Foundation launched Shot@Life campaign.December 30, 2011FDA expanded use of Prevnar 13 (PCV13, Pfizer) vaccine to include people ages 50 and older.October 25, 2011ACIP recommended all 11 to 12 year-old males get vaccinated against HPV.October 21, 2011Addition of history of intussusception as a contraindication for rotavirus vaccination.August 25, 2011National survey indicated HPV vaccine rates trail other teen vaccines.August 25, 2011Institute of Medicine issued the report titled "Review of Adverse Effects of Vaccines." Overall, the committee concludes that few health problems are caused by or clearly associated with vaccines.July 8, 2011FDA approved Boostrix (Tdap, GlaxoSmithKline) to prevent tetanus, diphtheria, and pertussis in older people.May 19, 2011CDC hailed vaccinations as one of 10 public health achievements of first decade of 21st century in Morbidity and Mortality Weekly Report (MMWR).April 22, 2011FDA approved the first vaccine (Menactra, meningococcal conjugate vaccine, Sanofi Pasteur) to prevent meningococcal disease in infants and toddlers.February 15, 2011HHS releases U.S. National Vaccine Plan, covers activities, goals, and priorities for 2010-2015.December 22, 2010FDA approved Gardasil HPV vaccine to include the indication for the prevention of anal cancer.August 11, 2010WHO declared end to 2009 H1N1 influenza pandemic.July 10, 2010First smallpox vaccine for certain immune-compromised populations delivered under Project BioShield.March 19, 2010ACIP recommended use of a reduced (4-dose) vaccine schedule for PEP to prevent human rabies.February 24, 2010FDA approved licensure of Pneumococcal 13-valent conjugate vaccine (PCV13), which offers broader protections against Steptococcus pneumoniae infections.February 19, 2010FDA approved licensure of Menveo (Novartis), meningococcal conjugate vaccine for people ages 11 through 55 years.January 29, 2010WHO hailed new Gates Foundation support ($10 billion) as the "Decade of Vaccines."February 24, 2010ACIP recommended universal Influenza vaccination for those 6 months of age and older.February 24, 2010FDA approved pneumococcal 13-valent conjugate vaccine (Prevnar 13), which offers broader protection against Streptococcus pneumoniae.December 23, 2009FDA approved high-dose inactivated influenza vaccine (Fluzone High-Dose) for people ages 65 years and older.November 16, 2009CDC issued Health Advisory 2009 H1N1 Pandemic Update: Pneumococcal vaccination recommended to help prevent secondary infections.October 21, 2009Merck issued announcement that the company will not resume production of monovalent measles, mumps, and rubella vaccines.October 16, 2009FDA approved new vaccine (Cervarix, GlaxoSmithKline) for the prevention of cervical cancer.October 16, 2009FDA approved new indication for gardasil to prevent genital warts in men and boys.September 15, 2009FDA approved four vaccines against the 2009 H1N1 influenza virus.July 1, 2009WHO and ACIP issued recommendations on the use of H1N1 influenza vaccines.June 23, 2009HHS announced advanced development contract for new way to make flu vaccine.June 11, 2009Dr Margaret Chan, Director-General WHO, declared world now at the start of 2009 influenza pandemic.May 22, 2009HHS directed $1 billion toward development of vaccine for novel influenza A (H1N1).March 16, 2009ACIP voted to recommend hepatitis A vaccination for close contacts of international adoptees from countries with high and intermediate endemicity.February 12, 2009Vaccine Court ruled that MMR vaccine, when administered with thimerosal-containing vaccines, does not cause autism.January 15, 2009HHS awarded a $487 million contract to Novartis Vaccines and Diagnostics, Inc to build a facility to manufacture cell-based influenza vaccine.December 11, 2008FDA approved changes in the schedule for administering anthrax vaccine (BioThrax, manufactured by Emergent BioSolutions) and in the route of administration.December 4, 2008FDA approved expanded indication for use of Boostrix Tdap vaccine in people ages 10-64 years.October 27, 2008National Quality Forum included the hepatitis B birth dose among its consensus standards for improving health care for mothers and newborns.June 24, 2008FDA approved new DTaP-IPV vaccine (Kinrix) for use in children ages 4-6 years.June 5, 2008FDA approved the use of Sanofi Pasteur's Tenivac tetanus and diphtheria toxoids adsorbed for adults age 60 years and older. In the original licensure, the age indication was for persons ages 7-59 years.April 3, 2008FDA approved new rotavirus vaccine (Rotarix) for use in U.S. Rotarix is a liquid and given in a two-dose series to infants from 6 to 24 weeks of age.April 2, 2008CDC issued Health Advisory in response to widespread measles outbreaks in U.S.March 14, 2008CDC updated its recommendations for administering combination MMRV vaccine.February 29, 2008CDC announced it had begun distribution of a new-generation smallpox vaccine, ACAM2000 (Acambis, Inc., Cambridge, Massachusetts), to civilian laboratory personnel, the military, and state public health preparedness programs.February 27, 2008ACIP voted to expand influenza recommendation to include vaccination for children ages 6 months-18 years.December 7, 2007CDC published updated recommendation for meningococcal vaccination of at-risk children age 2-10 years in MMWR.October 26, 2007ACIP voted to recommend the use of FluMist, the live attenuated influenza vaccine (LAIV; nasal-spray formulation) to include children age 2-5 years.October 19, 2007CDC published updated recommendations for prevention of hepatitis A virus infection after exposure and before international travel in MMWR.October 18, 2007FDA approved use of Menactra, a bacterial meningitis vaccine, in children age 2-10 years.September 28, 2007FDA approved Afluria, a new inactivated influenza vaccine for use in people age 18 years and older.September 19, 2007FDA approved use of FluMist nasal-spray influenza vaccine in children age 2-5 years.August 10, 2007CDC notified MMWR readers of revised recommendations to vaccinate all persons ages 11-18 with MCV4 at earliest opportunity.July 20, 2007MMWR notified readers that revised International Health Regulations have gone into effect for the United States.July 17, 2007HHS announced a plan to provide $175 million to assist states in pandemic influenza preparedness efforts.June 27-28, 2007ACIP voted to recommend routine use of meningococcal conjugate vaccine in adolescents ages 11-18 years.June 15, 2007HHS awarded $132.5 million to Sanofi Pasteur and MedImmune over five years to retrofit existing domestic vaccine manufacturing facilities on a cost-sharing basis and to provide warm-base operations for manufacturing pandemic influenza vaccines.March 28, 2007FDA approved an accelerated dosing schedule for Twinrix (hepatitis A and B vaccine). The schedule consists of three doses given within three weeks followed by a booster dose at 12 months (0, 7, 21–30 days, 12 months).” Historic Dates and Events Related to Vaccines and Immunization~Compared to this:“This is the sixth report by the ADDM Network, which has used the same surveillance methods for more than a decade. Estimated prevalence rates of ASD (Autism Spectrum Disorder) in the U.S. reported by previous data were:one in 68 children in the 2016 report that looked at 2012 dataone in 68 children in the 2014 report that looked at 2010 dataone in 88 children in the 2012 report that looked at 2008 dataone in 110 children in the 2009 report that looked at 2006 dataone in 150 children in the 2007 report that looked at 2000 and 2002 dataThe estimated overall prevalence rates reported by ADDM at the monitoring sites have more than doubled since the report was first published in 2007," says Dr. Li-Ching Lee, PhD, ScM, a psychiatric epidemiologist with the Bloomberg School's departments of Epidemiology and Mental Health and the principal investigator for Maryland-ADDM. "Although we continue to see disparities among racial and ethnic groups, the gap is closing," Lee says.”” U.S. autism rate up 15 percent over two-year period: Researchers say racial and ethnic disparities are narrowing~So, can anyone really look at the timeframes of the increase in infant/childhood vaccinations and the increase in childhood neurological disorders and still say there is no link? Again, I believe we are experiencing the long term negative side effects of vaccines as is evidenced by the increase in the vaccination schedule coinciding with the ever increasing incidence of Autism.

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