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By: Daniel James George, MD

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The antibody screen is negative because no unusually drug related antibodies are present allergy treatment on the nhs purchase periactin 4mg on line. Hemolytic transfusion reactions the differential diagnosis of a positive direct antiglobulin test includes not just red cell autoantibodies but also alloantibodies-antibodies in the patient directed against foreign red cell antigens allergy treatment xanax 4mg periactin. These antibodies are either “naturally occurring allergy treatment calgary purchase generic periactin canada,” in that individuals acquire them without specific exposure to allergy forecast long island ny purchase genuine periactin the red cell antigen, or “immune,” form red cell transfusions. For example, a patient whose red cells are group O has anti-A and anti-B in his or her serum. Like many other IgM antibodies, these isoagglutinins are potent complement fixers. If inadvertently transfused with group A red cells, this patient’s anti-A would 296 Hematology immediately react with the donor cells. The direct Coombs test is positive due complement fixation, but may become negative within hours to days, depending on how rapidly the group a cells are destroyed. The presence of urine hemosiderin beginning 3 to 5 days after the transfusion attests to the recent presence of hemoglobinemia. If the patient then receives an antigen positive unit, an anamnestic rise in antibody occurs over the next 3 to 21 days. Here, red cell destruction is usually leisurely, since the cells are eliminated only after they are coated with sufficient antibody, which depends on the rapidity with which it is produced. The direct Coombs test on a posttransfusion blood specimen is positive due to IgG coated transfused red cells. The test becomes negative as the antibody-coated cells are removed from the circulation. The patient’s antibody screen, negative before the transfusion, becomes positive shortly 297 Hematology afterward. Hemolytic disease of the newborn this hemolytic process actually begins in utero to the baby of a mother with IgG red cell antibodies. IgG antibodies readily cross the placenta, as opposed to IgM antibodies, which cannot. In the past, many Rh(D) negative women became sensitized to the red cell antigen D at the time of birth of a first Rh-positive child, because at birth it is common for a small volume of fetal cells to enter the maternal circulation. Rh-positive fetuses carried by a sensitized Rh-negative mother can be severely affected by the IgG anti-D. Some babies develop profound in utero anemia with congestive heat failure (hydrops fetalis), leading to stillbirth. Over time, some patients develop hypochromic microcytic red cells due to progressive iron deficiency, resulting form hemoglobinuria and hemosiderinuria. The Ham test involves the addition of acidified serum from a normal volunteer to the patient’s red cells. The sucrose hemolysis (“sugar water”) test can be used as a simple 299 Hematology screening test. Here the patient’s blood is added to isotonic sucrose, which is a low ionic strength solution. Since occasional false positives occur, positive results require confirmation with the more complex and rigorous Ham test. Explain in brief microcytic anemia and the different forms included in this category 4. Leukemia the leukemias are a group of disorders characterized by the accumulation of abnormal white cells in the bone marrow. These abnormal cells may cause bone marrow failure, a raised circulating white cell count and infiltrate organs. Thus common but not essential features include abnormal white cells in the peripheral blood, a raise total white cell count, evidence of bone marrow failure. Other chronic types include hairy cell leukemia, prolymphocytic leukemia and various leukemia/lymphoma syndromes. In acute leukemia, in which there are over 50% myeloblasts or lymphoblasts in the bone marrow at clinical presentation, the blast cells fail to differentiate normally but are capable of further divisions. Their accumulation results in replacement of the normal hemopoietic precursor cells of the bone marrow by myeloblasts or lymphoblasts and, ultimately in bone marrow failure. The clinical condition of the patient can be correlated with the total number of leukemic cells in the body. When the abnormal cell number approaches 1012 the patient is usually gravely ill with severe bone marrow failure. Peripheral blood involvement by the leukemic cells and infiltration of organs such as the spleen, liver and lymph nodes may not occur until the leukemic cell population comprised 60% or more of the marrow cell total. The clinical presentation and mortality in acute leukemia arises mainly from neutropenia, thrombocytopenia and anemia because of bone marrow failure and, less commonly, from organ infiltration. In over 95% of patients there is a replacement of normal bone marrow by cells with an abnormal chromosome the Philadelphia or Ph chromosome. This is an abnormal chromosome 22 due to the translocation of part of a long (q) arm of chromosome 22 to another chromosome, usually 9, with translocation of part of chromosome 9 to chromosome 22. It is an acquired abnormality of hemopoietic stem cells that is present in all dividing granulocytic, erythyroid and megakaryocytic cells in the marrow and also in some B and probably a minority of T lymphocytes. A great increase in total body granulocyte mass is responsible for most of the clinical features. In at least 70% of patients there is a terminal metamorphosis to 308 Hematology acute leukemia (myeloblastic or lymphoblastic) with an increase of blast cells n the marrow to 50% or more. It most cases there are no predisposing factors but the incidence was increased n survivors of the atom bomb exposures in Japan. The levels of neutrophils and myelocytes exceed those of blast cells and promyelocytes. The accumulation of large numbers of lymphocytes to 50-100 times the normal lymphoid mass in the blood, bone marrow, spleen, lymph nodes and liver may be related to immunological non-reactivity and excessive lifespan. Between 70% and 99% of white cells in the blood 310 Hematology film appear as small lymphocytes. It is an unusual disease of peak age 40-60 years and men are affected nearly four times as frequently as women. This disorder is characterized clinically by features due 311 Hematology to Pancytopenia. The is a monoclonal proliferation of cells with an irregular cytoplasmic outline (‘hairy’ cells, a type of B lymphocyte) in the peripheral blood, bone marrow, liver and other organs. The bone marrow trephine shows a characteristic appearance of mild fibrosis and a diffuse cellular infiltrate. A serum paraprotein may be present and the patients may have arthritis, serositis or vasculitis. There is a tendency to progress to acute myeloid leukemia, although death often occurs before this develops. In the acute leukemias the maturation defect leads to the accumulation of blast cells. Malignant Lymphomas 314 Hematology this group of diseases is divided into Hodgkin’s disease and non-Hodgkin’s lymphomas. In many patients, the disease is localized initially to a single peripheral lymph node region and its subsequent progression is by contiguity within the lymphatic system. After a variable period of containment within the lymph nodes, 315 Hematology the natural progression of the disease is to disseminate to involve non-lymphatic tissue. It has bimodal age incidence, one peak in young adults (age 20-30 years) and a second after the age of 50. In developed counties the ratio of young adults to child cases and of nodular sclerosing disease to other types is increased. With marrow infiltration, bone marrow failure may occur with a leuco-erythroblastic anemia. It may be demonstrated by trephine biopsy, usually in patients with disease at many sites. Tuberculosis may occur • Patients with bone disease may show hypercalcaemia, hypophosphataemia and increased levels of serum alkaline phosphatase. Laboratory findings • A Normochromic, normocytic anemia is usual but auto-immune hemolytic anemia may also occur. Paradoxically, bone marrow involvement is found more frequently in low-grade malignant lymphomas. Multiple Myeloma Multiple myeloma (myelomatosis) is a neoplastic monoclonal proliferation of bone marrow plasma cells, characterized by lytic bone lesions, plasma cell accumulation in the bone marrow, and the presence of monoclonal protein in the serum and urine. Ninety eight percent of cases occur over the age of 40 with a peak incidence in the seventh decade.

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Internal interferences result from abnormal physiologic states interfer ing with the test measurement allergy treatment vivite vibrance therapy by allergan order periactin 4 mg on-line. For example allergy testing unitedhealthcare generic 4 mg periactin with amex, patients with gross lipemia may have spuriously low serum sodium levels if the test methodology includes a step in which serum is diluted before sodium is measured allergy testing yeovil purchase 4mg periactin mastercard, and patients with endogenous antibodies (eg allergy medicine 18 month old discount periactin uk, human anti-mouse antibodies) may have falsely 8 Pocket Guide to Diagnostic Tests high or low results in automated immunoassays. Because of the potential for test interference, clinicians should be wary of unexpected test results and should investigate reasons other than disease that may explain abnor mal results, including pre-analytical and analytical laboratory error. Sensitivity and Specicity Clinicians should use measures of test performance such as sensitivity and specicity to judge the quality of a diagnostic test for a particular disease. Test sensitivity is the ability of a test to detect disease and is expressed as the percentage of patients with disease in whom the test is positive. Thus, a test that is 90% sensitive gives positive results in 90% of diseased patients and negative results in 10% of diseased patients (false negatives). Gener ally, a test with high sensitivity is useful to exclude a diagnosis because a highly sensitive test renders fewer results that are falsely negative. A test’s specicity is the ability to detect absence of disease and is expressed as the percentage of patients without disease in whom the test is negative. Thus, a test that is 90% specic gives negative results in 90% of patients without disease and positive results in 10% of patients without disease (false positives). A test with high specicity is useful to conrm a diagnosis, because a highly specic test has fewer results that are falsely positive. For instance, to make the diagnosis of gouty arthritis, a clinician might choose a highly specic test, such as the presence of negatively birefringent needle-shaped crystals within leukocytes on microscopic eval uation of joint uid. To determine test sensitivity and specicity for a particular disease, the test must be compared against an independent “gold standard” test or established standard diagnostic criteria that dene the true disease state of the patient. For instance, the sensitivity and specicity of rapid antigen detection testing in diagnosing group A -hemolytic streptococcal phar yngitis are obtained by comparing the results of rapid antigen testing with the gold standard test, throat swab culture. Application of the gold standard test to patients with positive rapid antigen tests establishes specicity. Fail ure to apply the gold standard test to patients with negative rapid antigen tests will result in an overestimation of sensitivity, since false negatives will not be identied. However, for many disease states (eg, pancreatitis), an independent gold standard test either does not exist or is very difcult or expensive to apply—and in such cases reliable estimates of test sensitivity and specicity are sometimes difcult to obtain. Sensitivity and specicity can also be affected by the population from which these values are derived. For instance, many diagnostic tests are evaluated rst using patients who have severe disease and control groups Diagnostic Testing and Medical Decision Making 9 who are young and well. Compared with the general population, these study groups will have more results that are truly positive (because patients have more advanced disease) and more results that are truly negative (because the control group is healthy). Thus, test sensitivity and specicity will be higher than would be expected in the general population, where more of a spectrum of health and disease is found. Clinicians should be aware of this spectrum bias when generalizing published test results to their own practice. To minimize spectrum bias, the control group should include indi viduals who have diseases related to the disease in question, but who lack this principal disease. For example, to establish the sensitivity and specic ity of the anti-cyclic citrullinated peptide test for rheumatoid arthritis, the control group should include patients with rheumatic diseases other than rheumatoid arthritis. Other biases, including spectrum composition, popu lation recruitment, absent or inappropriate reference standard, and verica tion bias, are discussed in the references. It is important to remember that the reported sensitivity and specicity of a test depend on the analyte level (threshold) used to distinguish a nor mal from an abnormal test result. If the threshold is lowered, sensitivity is increased at the expense of decreased specicity. If the threshold is raised, sensitivity is decreased while specicity is increased (Figure 1–3). Figure 1–4 shows how test sensitivity and specicity can be calculated using test results from patients previously classied by the gold standard test as diseased or nondiseased. The resulting curves, obtained by plotting sensitivity against No disease Disease A Test results Figure 1–3. If point A is the cutoff point, the test would have 100% sensitivity but low specicity. If point C is the cutoff point, the test would have 100% specicity but low sensitivity. In some situations, the cutoff is altered to enhance either sensitivity or specicity. Calculation of sensitivity, specicity, and probability of disease after a positive test (posttest probability). This is located at the point closest to the upper-left corner of the Diagnostic Testing and Medical Decision Making 11 1 1 0. Routine acid phosphatase testing for screening and monitoring prostate cancer no longer justied. The optimal clinical cutoff value, however, depends on the condition being detected and the relative importance of false-positive versus false negative results. The results of a useful test substantially change the probability that the patient has the disease (posttest probability). Figure 1–4 shows how posttest probability can be calculated from the known sensitivity and specicity of the test and the estimated pretest probability of disease (or disease prevalence), based on Bayes theorem. As demonstrated in Table 1–4, when a test with 90% sensitivity and specicity is used, the posttest probability can vary from 8% to 99%, depending on the pretest probability of disease. Furthermore, as the pretest probability of disease decreases, it becomes more likely that a positive test result represents a false positive. The clinician estimates the pretest probability of disease given all the evi dence and then calculates the posttest probability using the approach shown in Figure 1–4. The pretest probability that an otherwise healthy 50-year-old man has prostate cancer is the prevalence of prostate cancer in that age group (10%) and the posttest probability after a positive test is 20%. Even though the test is positive, there is still an 80% chance that the patient does not have prostate cancer (Figure 1–6A). If the clinician nds a prostate nodule on rec tal examination, the pretest probability of prostate cancer rises to 50% and the posttest probability using the same test is 69% (Figure 1–6B). This example illustrates that pretest probability has a profound effect on posttest probability and that tests provide more information when the diagnosis is truly uncertain (pretest probability about 50%) than when the diagnosis is either unlikely or nearly certain. Effect of pretest probability and test sensitivity and specicity on the posttest probability of disease. The pretest probability, or prevalence, of the disease has a profound effect on the posttest probability of the disease. Diagnostic tests provide more information when the diagnosis is truly uncertain (pretest probability about 50%, as in Part B) than when the diagnosis is either unlikely (Part A) or nearly certain (Part C). For continuous measures, multiple likelihood ratios can be dened to cor respond to ranges or intervals of test results. They can also be found in some textbooks, journal articles, and online programs (see Table 1–6 for sample values). Likelihood ratios provide an estimation of whether there will be signicant change in pretest to posttest probabil ity of a disease given the test result, and thus can be used to make quick estimates of the usefulness of contemplated diagnostic tests in particular situations. A likelihood ratio of 1 implies that there will be no difference between pretest and posttest probabilities. The simplest method for calculating posttest probability from pretest probability and likelihood ratios is to use a nomogram (Figure 1–7). Nomogram for determining posttest probability from pretest probability and likelihood ratios. To gure the posttest probability, place a straightedge between the pretest probability and the likelihood ratio for the particular test. The posttest probability will be where the straightedge crosses the posttest probability line. A more formal way of calculating posttest probabilities uses the likeli hood ratio as follows: Pretest odds Likelihood ratio = Posttest odds To use this formulation, probabilities must be converted to odds, where the odds of having a disease are expressed as the chance of having the disease divided by the chance of not having the disease. To estimate the potential benet of a diagnostic test, the clinician rst estimates the pretest odds of disease given all available clinical information and then multiplies the pretest odds by the positive and negative likelihood ratios. The results are the posttest odds, or the odds that the patient has the disease if the test is positive or negative.

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Ultrasound Low-grade dysplasia (choice D) is incorrect because the dys examination of the liver shows multiple lesions allergy forecast lincoln ne 4mg periactin for sale. A ne plastic cells shown here have minimal cytoplasm and a very needle aspiration is performed under ultrasound guidance allergy eye drops contacts periactin 4 mg amex. Herpes simplex virus infec the smear discloses numerous round cells allergy symptoms order generic periactin on line, with poorly dened tion (choice A) shows multinucleation and “ground glass” cytoplasm allergy forecast delaware purchase generic periactin on line, eccentric nuclei, and prominent nucleoli. Human papillomavirus infection (choice C) features cytoplasm of these cells contains pigmented granules (shown perinuclear vacuoles. In inva sive squamous cell carcinoma, the neoplastic cells are usually pleomorphic, with caudate and elongate forms, and coarsely granular or pyknotic chromatin. Choices A, B, and C represent morphologic characteristics of cellular adaptation to chronic persistent stress. Diagnosis: Squamous cell carcinoma of the cervix 4 the answer is B: Herpes simplex virus infection. Multinucleated giant cells with “ground glass” appearance of the nuclei are typical. Diagnosis: Genital herpes (A) Hepatic adenoma (B) Hepatocellular carcinoma 5 the answer is C: B-cell lymphoma. Lymphomas are malignant (C) Metastatic adenocarcinoma proliferations of lymphocytes or lymphoblasts. The World (D) Metastatic melanoma Health Organization classication distinguishes between (E) Metastatic squamous cell carcinoma Hodgkin lymphoma and B-cell and T-cell lymphomas (non Hodgkin lymphomas). Cell clusters may form papil oles, combined with alterations in the chromatin pattern of lary congurations. Transitional cell carcino nuclear membranes and abnormally distributed chromatin. Invasive squamous cell carcinoma (choice E) is characterized by pleomorphic elon Diagnosis: Transitional cell carcinoma of the urothelium gate squamous cells, with enlarged, irregular, and hyperchro matic nuclei. The clinical features of this case Diagnosis: Human papillomavirus are most consistent with neuroblastoma. This malignant neural crest tumor is composed of neuroblasts and originates in the adrenal medulla or sympathetic ganglia. Lymphoid inltrates are not features of the other for 30% of all invasive lung cancers in the United States. Well-differentiated tumors display keratin “pearls,” which appear as small, rounded nests of brightly eosino 13 the answer is C: Mesothelioma. The sputum sample philic aggregates of keratin surrounded by concentric layers shows a ferruginous body, which appears as a yellow, of squamous epithelial cells. The other choices are bodies, they are formed by the precipitation of iron and unlikely to exhibit keratinization. Asbestos exposure is Diagnosis: Squamous cell carcinoma of the lung a well-known risk factor for the development of mesothe lioma. Mucin secretion is rarely, if ever, encountered in of the other choices display a foamy appearance shown in the the other choices. Diagnosis: Adenocarcinoma of the lung Diagnosis: Pneumocystis pneumonia 15 the answer is A: Adenocarcinoma of the ovary. Microscopically, thyroid nodules are lined by hyperplas (“peritoneal carcinomatosis”). Monoclonal antibody to a tumor tic follicular epithelial cells and are distended with colloid. The neoplastic cells shown here exhibit nuclear atypia, and E) or chronic inammatory cells (choice A). Diagnosis: Adenocarcinoma of the ovary 11 the answer is B: Follicular confguration. Follicular thyroid carcinoma does not contain papillae or other architectural ele ments. On cytologic examination, the tumor cells form small 16 the answer is D: Metastatic melanoma. Kera in the cytoplasm is composed of ne melanin granules, which tin pearls (choice C) or mucin secretion (choice D) are not is characteristic of malignant melanoma. Intracellular pigment Diagnosis: Follicular carcinoma of the thyroid is not encountered in the other choices. Chronic, autoim mune thyroiditis displays a conspicuous inltrate of lym phocytes and plasma cells. Rubin’s Pathology: Clinicopatho Q3-6: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinicopatho Q9-24: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinicopatho Q9-26: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q9-33: Image from Rubin E, Gorstein F, Rubin R, et al. Davis, Department of Pathology, University of ogy: Clinicopathologic Foundations of Medicine. Davis, Department of Pathology, University of Q9-46: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Williams & Q9-61: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinicopatho Q10-1: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinicopatho Q10-3: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathol Q8-2: Image from Courtesy of the Armed Forces Institute of Pathology. Rubin’s Pathology: Clinico Q12-10: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q12-14: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q12-38: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Wil Q14-34: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Wil Q14-38: Image from Rubin E, Gorstein F, Rubin R, et al. Figure Credits 347 Chapter 16 Q17-7: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Wil Q16-23: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Wil Q16-27: Image from Rubin E, Gorstein F, Rubin R, et al. Baltimore: Lippincott Wil Q16-28: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q20-22: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q20-33: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q20-34: Image from Rubin E, Gorstein F, Rubin R, et al. Rubin’s Pathology: Clinico Q24-11: Image from Rubin E, Gorstein F, Rubin R, et al. Synopsis and Atlas of Lever’s Histopathology of ogy: Clinicopathologic Foundations of Medicine. Synopsis and Atlas of Lever’s Histopathology of Q21-33: Image from Rubin E, Gorstein F, Rubin R, et al. Synopsis and Atlas of Lever’s Histopathology of Lippincott Williams & Wilkins, 2005.

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The 2018-2019 flu vaccine predicted to allergy treatment for adults buy cheap periactin 4mg online be only 20% effective the Journal of Clinical Infectious Diseases predicts another miserable success rate for the flu vaccine allergy forecast waco texas generic 4mg periactin otc. In an article published April 17 allergy medicine 93\/12 order genuine periactin on line, 2018 titled allergy testing bakersfield ca purchase 4mg periactin visa, Predicting Influenza H3N2 Vaccine Efficacy From Evolution of the Dominant Epitope. An estimated 20% efficacy against H3N2, as published in Clinical Infectious Diseases. Maybe that is why more and more people feel that the risk of the flu shot outweighs the stated benefits. The prestigious Cochrane Collaboration finds the flu vaccine only protects 1 of every 100 people A 2013 comprehensive review of 50 published papers of over 70,000 people titled, Vaccines for preventing influenza in healthy adults, by the world-renowned Cochrane Collaboration finds the effectiveness of the flu vaccine to be pitiful. At best, vaccines might be effective against only influenza A and B, which represent about 10% of all circulating viruses. Each year, the World Health Organization recommends which viral strains should be included in vaccinations for the forthcoming season. The combined results of these trials showed that under ideal conditions (vaccine completely matching circulating viral configuration) 33 healthy adults need to be vaccinated to avoid one set of influenza symptoms. In average conditions (partially matching vaccine by far the most common scenario) 100 439 people need to be vaccinated to avoid one set of influenza symptoms. Vaccine use did not affect the number of people hospitalised or working days lost but caused one case of Guillian-Barre syndrome (a major neurological condition leading to paralysis) for every one million vaccinations. Fifteen of the 36 trials were funded by vaccine companies and four had no funding declaration. Our results may be an optimistic estimate because company-sponsored influenza vaccines trials tend to produce results favorable to their products and some of the evidence comes from trials carried out in ideal viral circulation and matching conditions and because the harms evidence base is limited. Flu marketing continues the fear mongering Despite all the false alarms in the past, the media continues the steady drum beat in their annual hype of impending doom. Like the boy that cried wolf, the continual overhype is likely to fall on deaf ears. When it happens, they tell us, it will probably have a greater impact on humanity than anything else currently happening in the world. The article goes on to identify certain key players and their conflicts of interest between seemingly independent and unbiased public health agencies and the pharmaceutical industry. This article drew a critical review from the editor of Nature, to which the editor of the British Medical Journal strongly countered in this rebuttal. The effectiveness was highest among children aged six months to 17 at 26 per cent. Effectiveness fell to about 12 per cent among people aged 18 to 49 and 14 per cent for those aged 50 and older. In Canada, the flu vaccine could be working even more poorly, with "little or no protection. Risk vs Reward At what point does the risk of the toxic soup in the vaccine become greater than the perceived benefit And, at what point of ineffectiveness should there be public push back against the mantra, that “X% is better than zero” The flu vaccine causes other health risks the Trivalent Influenza Vaccine, caused a higher rate of the flu cases in those receiving it the following year A study looking at 4 other studies on the subject published in 2010 titled, Association between the 2008–09 Seasonal Influenza Vaccine and Pandemic H1N1 Illness during Spring– Summer 2009: Four Observational Studies from Canada, shows that those who were vaccinated for the flu with the Trivalent Influenza Vaccine (against three strains), were approximately twice as likely to contract the pH1N1 illness during the spring–summer 2009 in Canada. Risk of pH1N1 hospitalization was not further increased among vaccinated people when comparing hospitalized to community cases. The reality is that vaccination against the flu appears to increase the rates of other non-influenza upper respiratory infections by greater than 400%! The hazard of influenza in individuals during the 14-day post-vaccination period was similar to unvaccinated individuals during the same period (this indicates that non-vaccinated people had no higher incidence of the flu). The hazard of non-influenza respiratory pathogens was higher during the same period when stratified by age the hazard remained higher for children but not for adults. If the mother has tested positive or if the mother’s status in unknown for Hep B, the preemie should still receive the dose at birth. I say minor victory because, the slight delay of 1 month in administering the vaccine will make very little difference as it relates to reducing risk to the baby. Additionally, the Hep B virus can only be contracted by sexual activity, dirty needles or from a Hepatitis B positive mother during the birth process. The fact that infants should require this vaccine makes no sense whatsoever, especially to Hepatitis B negative mothers. Why not just test the mothers and at least give the babies born from mothers that have tested negatively a pass In addition, the schedule calls for pregnant women to receive the Hep B vaccine with the tiny fetus in utero. It is based on poor scientific methodology (including studies that are too small, too short, and too limited in populations represented), which is, moreover, insulated from independent criticism. The evidence is far too poor to warrant overriding the independent judgments of patients, parents, and attending physicians, even if this were ethically or legally acceptable. The evidence is far too poor to warrant overriding the independent judgments of patients and parents! The current 2016 report includes 248 listings of agents, substances, mixtures, and exposure circumstances that are known or reasonably anticipated to cause cancer in humans. The hepatitis b virus is one that is categorized as a known human carcinogen as it can cause liver cancer. It is not known whether the surface antigen itself has the same carcinogenic properties or potential as the virus itself. As we know from many other instances of compounds that have made their way into the human population through consumer products and medicines, the recognition of the hazards of those substances often takes a very long time. It would be a tragedy to find out many years later that the same vaccine that was designed to prevent liver cancer, was actually causing that same cancer that it was designed to prevent. The association between hepatitis B vaccination of male neonates and parental report of autism diagnosis was determined. This cross-sectional study used weighted probability samples obtained from National Health Interview Survey 1997-2002 data sets. Logistic regression was used to estimate the odds for autism diagnosis associated with neonatal hepatitis B vaccination among boys age 3-17 years, born before 1999, adjusted for race, maternal education, and two-parent household. Boys vaccinated as neonates had threefold greater odds for autism diagnosis compared to boys never vaccinated or vaccinated after the first month of life. Non-Hispanic white boys were 64% less likely to have autism diagnosis relative to nonwhite boys. Packer is an internationally recognized clinical investigator who has made many seminal contributions to the field of heart failure, both in understanding its mechanisms and defining its rational management. Packer, “In the trial, an acute myocardial infarction occurred in 14 people in the Dynavax group, but in only one person receiving the conventional vaccine. Since the Dynavax group was twice as large, the risk of acute myocardial infarction in the trial was seven times greater with the new vaccine. The new adjuvant in the vaccine caused an inflammatory response (of uncertain duration), and inflammation is an important cause of rupture of atherosclerotic plaques. But a post-marketing trial was possible only if the vaccine was approved for public use. There’s got to be a better way to determine safety and effectiveness, than put thousands of people’s life at risk. If 50,000 people get the Dynavax vaccine and the initial numbers are proved out, that means 125 people will have suffered a heart attack as a result. Cases then peaked in 1985 at around 27,000 and have been declining steadily ever since. The second graph shows the death rate for every year since 1979, when 260 people died from Hepatitis B. Deaths then reached a peak in 1994, thirteen years after the introduction of the Hep B Vaccine at 1,120 deaths (a 431% increase from 1979). Even so, a 431% increase in deaths with only a 29% increase in population doesn’t speak to any degree of success in mortality rates from the vaccine. Even as of 2010 (the last reported year on the chart), the death rate was still 588 annually, more than double the rate two years before the vaccine was first introduced. The third graph shows the rates of vaccination coverage of children under 3 years old. Those rates have been consistently over 90% since 2002, yet as just mentioned the death rate in 2010 was still more than double what it was 31 years prior in 1979. The point of showing you all of these statistics, is to demonstrate that after over 37 years of injecting adults and tens of millions of babies on their first day of birth and two more doses by their first birthday with the Hepatitis B vaccine, containing aluminum, formaldehyde, polysorbate 80 and other chemicals and biological compounds, the statistics are still worse than they were 15 years before the vaccine was ever introduced! And, at what cost financially and to the health of our children, and now our adult population