Category: Ailmemts & Remedies

Categories
Ailmemts & Remedies

Cytopenia

DEFINITION:

Cytopenia is a reduction in the number of blood cells. It takes a number of forms:
*Low red blood cell count: anemia.
*Low white blood cell count: leukopenia or neutropenia (because neutrophils make up at least half of all white cells, they are almost always low in leukopenia).
*Low platelet count: thrombocytopenia.
*Low granulocyte count: granulocytopenia
*Low red blood cell, white blood cell, and platelet counts: pancytopenia..

Click to see the picture

Blood cell development. A blood stem cell goes through several steps to become a red blood cell, platelet, or white blood cell.

CLICK & SEE THE PICTURES

Cancer patients may frequently develop cytopenia, a disorder in which the production of one or more blood cell types ceases or is greatly reduced. Cancer and chemotherapy used to treat cancer, and sometimes radiation therapy, may sometimes cause cytopenia.

TYPES:
A deficiency of red blood cells which  is called anemia; a deficiency of white blood cells, or leukocytes, leukopenia or neutropenia (neutrophils make up over half of all white blood cells); and deficiency of platelets is called  thrombocytopenia.

Pancytopenia is the deficiency of all three blood cell types and is characteristic of aplastic anemia, a potentially life-threatening disorder that requires a stem cell transplant.

Blood Cells
The blood consists of three different  types of cells: red blood cells (erythrocytes), white blood cells (leukocytes), and platelets. Erythrocytes contain hemoglobin, the protein that carries oxygen from the lungs to all cells in the body. Proper cell function depends on an adequate oxygen supply. When cells are oxygen deprived, organ function can be seriously impaired.

Leukocytes (white blood cells) protect the body against viral, bacterial, and parasitic infection and detect and remove damaged, dying, or dead tissues. Someone with a deficiency of white blood cells is extremely vulnerable to infection.

The term “leukocyte” refers to all six types of white blood cells; each plays a unique role in the immune system:

1. Basophils circulate in the blood and initiate the inflammatory response.
2.Eosinophils kill infecting parasites and produce allergic reactions.
3.Lymphocytes produce antibodies and regulate immune responses.
4. Mast cells are fixed in tissues and initiate the inflammatory response.
5. Monocytes capture infecting organisms for identification, ingest infecting organisms, and remove damaged or dying cells and cell debris. When monocytes become fixed in tissue, they are called macrophages.
6.Neutrophils identify and kill infecting organisms, and remove dead tissue.

Platelets are essential factors for blood clotting. Sudden blood loss triggers platelet activity at the site of the wound. Exposure to oxygen in the air causes platelets to break apart and combine with a substance called fibrinogen to form fibrin. Fibrin has a thread-like structure and forms a scab, or external clot, as it dries. Platelet deficiency causes one to bruise and bleed easily. Blood does not clot at an open wound, and there is greater risk for internal bleeding.

All blood cells have a lifespan: erythrocytes have a lifespan of about 120 days; leukocytes, 1 to 3 days; and platelets, approximately 10 days. The body continually replenishes the blood supply through a process called hematopoiesis.

Blood Cell Formation—Hematopoiesis, the formation and development of blood cells, occurs in bone marrow. Bone marrow is a nutrient-rich spongy tissue located mainly in the central portions of long flat bones (e.g., sternum, pelvic bones) in adults and all bones in infants.

All blood cells derive from blood-forming stem cells that reside in bone marrow. Stem cells replicate indefinitely and develop into mature, specialized cells. A hormone produced in the kidneys, erythropoietin, stimulates blood stem cells to produce all three types of blood cells.

CAUSES & RISK FACTORS:-

Chemotherapy and radiation therapy both reduce the number of blood-forming stem cells in cancer patients, but chemotherapeutic agents have a greater adverse effect because they suppress bone marrow function in several ways.The degree of damage is related to the particular drug(s) and the dose.

Chemotherapeutic agents can produce deficiencies in all blood cell types by

* damaging blood-forming stem cells,
* suppressing the kidneys? production of erythropoietin (hormone that stimulates blood cell production), and
* triggering red cell destruction (hemolysis) by inducing an immune response that causes the body to mistakenly identify erythrocytes as foreign bodies and destroy them.

Malignant tumors can cause anemia and other cytopenias when they directly invade bone marrow and suppress marrow function. Malignant cells also can migrate from tumors in other parts of the body to bone marrow. Tumors also can replace normal blood-forming stem cells with abnormal clones.

SIGN & SYMPTOMS:-

Anemia
A deficiency in erythrocytes reduces the amount of oxygen reaching all cells in the body, thus impairing all tissue and organ function. Severe fatigue is the most common symptom of anemia and is experienced by approximately 75% of chemotherapy patients. Patients find it more disabling than other treatment side effects, including nausea and depression.

Anemia also produces these symptoms:

* Confusion
* Dizziness
* Headache
* Lightheadedness
* Loss of concentration
* Pallor (pale skin, nail beds, gums, linings of eyelids)
* Rapid heart rate (tachycardia)
* Shortness of breath (dyspnea)

Neutropenia
Patients with a white blood cell deficiency experience frequent and/or severe bacterial, viral, and/or fungal infections; fever; and mouth and throat ulcers.

Complications—Bacteremia, the form of sepsis characterized by the presence of bacteria in the blood, can develop in immunocompromised patients who have neutropenia. Fever, rapid heart rate, and quick shallow breathing are signs of early sepsis, usually a reversible condition.

Untreated bacteremia can lead to severe sepsis, in which one or more organs become dysfunctional. Septic shock is severe sepsis with low blood pressure. The risk for death increases with the development of septic shock. Even aggressive treatment can fail to reverse the condition.

Thrombocytopenia
Platelet deficiency causes patients to bruise and bleed easily. Bleeding occurs most often in the mucous membranes lining the mouth, nose, colon, and vagina. Tiny reddish-purple skin lesions (petechiae), evidence of pinpoint hemorrhages, may appear on the skin or in the mouth.

Pancytopenia
Patients who are deficient in all blood cell types experience signs and symptoms associated with each, but bleeding from the nose and gums, and easy bruising usually appear first. Symptoms of anemia (e.g., fatigue, shortness of breath) are also common. Patients may look and feel well, otherwise, despite the seriousness of their condition.

Anemia
People with anemia (reduced red cell production) are advised to rest and eat foods high in iron (meat, fish, poultry, lentils, legumes, iron-enriched grains and flours).

If immediate remedy is necessary, treatment may include medication that helps restore the red blood supply and a transfusion of packed red blood cells.

Epoetin alpha (Epogen®, Procrit®)is a synthetic erythropoietin (normally produced by the kidneys) that stimulates stem cells to produce red blood cells. Restoration of the red blood cell supply with medication is gradual.

Darbepoetin alfa (Aranesp®) also stimulates red blood cell production but requires fewer doses and less disruption of daily living.

In March 2007, the Food and Drug Administration (FDA) issued a warning about these medications in response to studies indicating that they may increase the risk for blood clots, strokes, and heart attacks in some patients (e.g., patients who have kidney disease).

Thrombocytopenia
People with an abnormally low platelet count should avoid bruising or breaking the skin, and should carefully brush their teeth. A persistently decreased platelet count may be treated with a transfusion of platelets.

Neutropenia
The patient with a low white blood cell count is advised to  do the following:

*Avoid contact with people who are ill,
*Monitor closely for signs of infection (e.g., fever), and
*Take antibiotics when appropriate.

Medication, a colony-stimulating factor (CSF), may be prescribed to speed the development of white blood cells and shorten the period of susceptibility to infection.

Growth Factors
Growth factors are synthetic versions of substances involved in stimulating red and white blood cell production. Physicians exercise caution when prescribing these medications for people with tumors that involve the bone marrow, because growth factors might stimulate malignant cell growth.

These medications include the following:

Epoetin alpha (Procrit®, Epogen®; stimulates red blood cell production)
G-CSF (granulocyte colony-stimulating factor; e.g., filgrastim [Neupogen®]; stimulates neutrophil production)
GM-CSF (granulocyte-macrophage colony-stimulating factor; stimulates production of several white blood cells, including macrophages)

Leukocytes and other cells that contain granules are also called granulocytes.

Side effects
Fever, fatigue, dizziness, diarrhea, nausea, vomiting, weakness, and paresthesia (prickling sensation) are side effects associated with epoetin alpha.

Bone pain, malaise, headache, flu-like symptoms, muscle ache, redness at the injection site, and skin rash may occur with GM-CSF.

G-CSF commonly produces bone pain.

MEDICATIONS:-

Medications used to treat bacterial infection and other illnesses also can contribute to immune system suppression.

Some of these are :

* Antacids: cimetidine (Tagamet®)
* Antibiotics: chloramphenical (Chloromycetin®), sulfonamide (Thiosulfil®, Gantanol®); cephalosporin (Cephalaxin®), vancomycin (Vancocin®)
* Anticonvulsants: phenytoin/hydantoin (Dilantin®), felbamate (Felbatol®), carbamazepine (Tegretol®)
* Antimalarials: chloroquine (Aralin®)
* Antivirals: ganciclovir (Vitrasert®), zidovudine (AZT®)
* Cardiac drugs: diltiazem (Cardizem®), nifedipine (Procardia®), verapamil (Calan®)
* Diabetes drugs: glipizide (Glucotrol®), glyburide (Micronase®)
* Hyperthyroid drug: propylthiouracil
* NSAIDs (nonsteroidal anti-inflammatory drugs): phenylbutazone (Butazolidine®), indomethacin (Indocin®, Indochron E-R®)—Due to potentially severe gastrointestinal and cardiovascular side effects, NSAIDs should only be used as instructed.
* Rheumatoid arthritis drugs: auranofin (Ridaura®), aurothioglucose (Solganal®), gold sodium thiomalate (Myochrisine®)

Bone Marrow and Stem Cell Transplantation:-
The treatment of choice for the pancytopenic patient with a matched bone marrow donor is stem cell transplantation. The goal of transplantation is to restore blood-forming stem cells to the marrow.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.oncologychannel.com/cytopenia/index.shtml
http://en.wikipedia.org/wiki/Cytopenia
http://www.cancer.umn.edu/cancerinfo/NCI/CDR378089.html

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Categories
Ailmemts & Remedies

Polycythemia

Definition:
Polycythemia is the increase of the RBC count, hemoglobin, and total RBC volume, accompanied by an increase in total blood volume. This must be distinguished from relative erythrocytosis secondary to fluid loss or decreased intake; this distinction can be made easily on a clinical basis. Polycythemia accompanies increased total blood volume, whereas relative erythrocytosis does not. Two basic categories of polycythemia are recognized:
...click to see…the picture..
* Primary polycythemias are due to factors intrinsic to red cell precursors and include the diagnoses of primary familial and congenital polycythemia (PFCP) and polycythemia vera (PV).
* Secondary polycythemias are caused by factors extrinsic to red cell precursors.

In normal hematopoiesis, myeloid stem cells give rise to erythrocytes, platelets, granulocytes, eosinophils, basophils, and monocytes. The production of each lineage is a function of cell proliferation, differentiation, and apoptosis. These various stages of differentiation rely on multiple interrelated processes. Protein growth factors, known as cytokines, stimulate proliferation of the multilineage cells (eg, interleukin [IL]-3, granulocyte-macrophage colony-stimulating activity [GM-CSF]). Other factors primarily stimulate the growth of committed progenitors (eg, GM-CSF, macrophage colony-stimulating factor [M-CSF], erythropoietin [Epo]).

Erythropoiesis is a carefully ordered sequence of events. Initially occurring in fetal hepatocytes, the process is taken over by the bone marrow in the child and adult. Although multiple cytokines and growth factors are dedicated to the proliferation of the RBC, the primary regulator is Epo. Red cell development is initially regulated by stem cell factor (SCF), which commits hematopoietic stem cells to develop into erythroid progenitors. Subsequently, Epo continues to stimulate the development and terminal differentiation of these progenitors. In the fetus, Epo is produced by monocytes and macrophages found in the liver. After birth, Epo is produced in the kidneys; however, Epo messenger RNA (mRNA) and Epo protein are also found in the brain and in RBCs, suggesting that some paracrine and autocrine function is present as well.  CLICK & SEE THE PICTURES

Erythropoiesis escalates as increased expression of the EPO gene produces higher levels of circulating Epo. EPO gene expression is known to be affected by multiple factors, including hypoxemia, transition metals (Co2+, Ni2+, Mn2+), and iron chelators. However, the major influence is hypoxia, including factors of decreased oxygen tension, RBC loss, and increased oxygen affinity of hemoglobin. In fact, Epo production has been observed to increase as much as 1000-fold in severe hypoxia.

Absolute polycythemia
The overproduction of red blood cells may be due to a primary process in the bone marrow (a so-called myeloproliferative syndrome), or it may be a reaction to chronically low oxygen levels or, rarely, a malignancy.

Primary polycythemia (Polycythemia vera)
Primary polycythemia, often called polycythemia vera (PCV), polycythemia rubra vera (PRV), or erythremia, occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow.  Often, excess white blood cells and platelets are also produced. Polycythemia vera is classified as a myeloproliferative disease. Symptoms include headaches, vertigo, and an abnormally enlarged spleen and/or liver. In some cases, affected individuals may have associated conditions including high blood pressure or the formation of blood clots. Transformation to acute leukemia is rare. Phlebotomy is the mainstay of treatment. A hallmark of polycythemia is an elevated hematocrit, with Hct > 55% seen in 83% of cases. Mutations in JAK2 are found in 95% of cases, though also present in other myeloproliferative disorders.

Secondary polycythemia
Secondary polycythemia is caused by either natural or artificial increases in the production of erythropoietin, hence an increased production of erythrocytes. In secondary polycythemia, there may be 6 to 8 million and occasionally 9 million erythrocytes per cubic millimeter (microliter) of blood. Secondary polycythemia resolves when the underlying cause is treated.

Secondary polycythemia in which the production of erythropoietin increases appropriately is called physiologic polycythemia. This physiologic (meaning normal) polycythemia is a normal adaptation to living at high altitudes (see altitude sickness). Many athletes train at high altitude to take advantage of this effect — a legal form of blood doping. Similarly, athletes with primary polycythemia may have a competitive advantage due to greater stamina.

Other causes of secondary polycythemia include smoking, renal or liver tumors, hemangioblastomas in the central nervous system, heart or lung diseases that result in hypoxia, and endocrine abnormalities including pheochromocytoma and adrenal adenoma with Cushing’s syndrome. People whose testosterone levels are high because of the use anabolic steroids, including athletes who abuse steroids and people whose doctors put them on doses that are too high, as well as people who take erythropoietin may develop secondary polycythemia.

Secondary polycythemia can be induced directly by phlebotomy to withdraw some blood, concentrate the erythrocytes, and return them to the body.

Chuvash polycythemia
Chuvash polycythemia refers to a familial form of erythrocytosis different from classical polycythemia vera. This involved patients from Chuvashia and is associated with a C598T mutation in the von Hippel-Lindau gene (VHL).[6] A cluster of patients with Chuvash polycythemia have been found in other populations, such as on the Italian island of Ischia, located in the Bay of Naples.

Relative polycythemia
Relative polycythemia is an apparent rise of the erythrocyte level in the blood; however, the underlying cause is reduced blood plasma. Relative polycythemia is often caused by loss of body fluids, such as through burns, dehydration and stress.

Polycythemia vera
Earlier diagnostic criteria for polycythemia vera included the following (based on the Polycythemia Vera Study Group Diagnostic Criteria):1

* Red cell mass greater than 36 mL/kg for men and greater than 32 mL/kg for women
* Arterial oxygen saturation greater than 92%
* Splenomegaly or 2 of the following:
o Thrombocytosis greater than 400 X 109/L
o Leukocytosis greater than 12 X 109/L
o Leukocyte alkaline phosphatase activity greater than 100 U/L in adults (reference range, 30-120 U/L) without fever or infection
o Serum vitamin B-12 greater than 900 pg/mL (reference range, 130-785 pg/mL)
o Unsaturated vitamin B-12 binding capacity greater than 2200 pg/mL

The reference range for the clinician’s laboratory should be cross-correlated. The diagnostic criteria have undergone scrutiny and several revisions in recent years. In 2001, the World Health Organization (WHO) proposed a classification system for chronic myeloid neoplasms.2 The diagnosis of polycythemia vera fell under the broader category of chronic myeloproliferative diseases. This set of criteria quickly lost favor because of lack of validation3 and the discovery of JAK2 mutations in adult patients.4,5,6,7,8,9

Currently, the diagnosis of polycythemia vera is based on the 2008 WHO criteria, which has integrated molecular diagnostics into the evaluation and screening for polycythemia vera.10 A diagnosis of polycythemia vera is made when both major and one minor criterion are present or when the first major criterion is present with any two minor criteria.

The current criteria include the following:

* Major criteria
1. Hemoglobin level of more than 18.5 g/dL in men (>16.5 g/dL in women) or other evidence of increased red cell volume

or

Hemoglobin or hematocrit level higher than 99th percentile of method-specific reference range for age, sex, altitude, of residence

or

Hemoglobin level of more than 17 g/dL in men (>15 g/dL in women) if associated with a documented and sustained increase of at least 2 g/dL from an individual’s baseline value that can not be attributed to correction of iron deficiency

or

Elevated red cell mass greater than 25% above mean normal predicted value
2. Presence of JAK2V617F or similar mutation (eg, JAK2 exon 12 mutation)
* Minor criteria
1. Bone marrow trilineage myeloproliferation
2. Subnormal serum erythropoietin levels
3. Endogenous erythroid colony growth

Pathophysiology

Primary polycythemia

The disease is considered to be a form of the myeloproliferative syndromes that include polycythemia vera, essential thrombocythemia, agnogenic myeloid metaplasia, and myelofibrosis. The clonality of polycythemia vera is well established and was first demonstrated by Adamson et al in 1976.11 Subsequent studies suggest hypersensitivity of the myeloid progenitor cells to growth factors, including Epo, IL-3, SCF, GM-CSF, and insulinlike growth factor (IGF)–1, whereas other studies show defects in programmed cell death.

Until recently, the pathophysiology of polycythemia vera was unclear. In 2005, significant progress in the understanding of polycythemia vera was made with the discovery of an activating mutation in the tyrosine kinase JAK2 (JAK2V617F ), which now appears to cause most primary cases in adults.4,5,6,7,8 Several other mutations of JAK2 have since been described (eg, exon 12, JAK2H538-K539delinsI ).9,12 The JAK2 mutations are thought to possibly cause hypersensitivity to Epo via the Epo receptor, although the effects of this mutation remain to be fully characterized.

Familial clustering suggests a genetic predisposition. Whether these mutations are responsible for the development of polycythemia vera in pediatric patients is unclear. Some groups have reported lower rates of JAK2 mutations in children compared with adults,13,14,15 whereas other groups have seen similar rates with complete or near complete presence of JAK2V617F and other JAK2 mutations.12

PFCP is caused by a hypersensitivity of erythroid precursors to Epo. Several mutations (approximately 14) have been identified in the Epo receptor (EPOR) gene; however, EPOR mutations have not been identified in all PFCP kindreds. Most identified EPOR mutations (11) cause truncation of the c-terminal cytoplasmic receptor domain of the receptor. These truncated receptors have heightened sensitivity to circulating Epo due to a lack of negative feedback regulation.16

Secondary polycythemia

Secondary polycythemia may result from functional hypoxia induced by lung disease, heart disease, increased altitude (hemoglobin increase of 4% for each 1000-m increase in altitude), congenital methemoglobinemia, and other high–oxygen affinity hemoglobinopathies stimulating increased Epo production. Secondary polycythemia may also result from increased Epo production secondary to benign and malignant Epo-secreting lesions. Secondary polycythemia may also be a benign familial polycythemia.

Chuvash polycythemia, a congenital polycythemia first recognized in an endemic Russian population, has mutations in the von Hippel-Lindau (VHL) gene, which is associated with a perturbed oxygen dependent regulation of Epo synthesis.

Secondary polycythemia of the newborn is fairly common and is a result of either chronic or acute fetal hypoxia or delayed cord clamping and stripping of the umbilical cord.17
Frequency
United States

Primary polycythemia is rare; the overall prevalence of polycythemia vera is 2 cases per 100,000 people. The median age is 60 years. Only 0.1% of cases of polycythemia vera are observed in individuals younger than 20 years. Fewer than 50 cases of pediatric polycythemia vera have been reported in the literature. Secondary polycythemia is seen in 1-5% of all newborns in the United States.
International

Polycythemia vera has a similar incidence in Western Europe as in the United States, and occurrence rates are very low in Africa and Asia (as low as 2 cases per million per year in Japan).

Mortality/Morbidity
Death rates for children are unavailable. The complications found in polycythemia vera are related to 2 primary factors. The first includes complications related to hyperviscosity. The second involves bone marrow–related complications. Untreated, the median survival time for these patients is 18 months. However, if patients are treated, survival is greatly extended, as many as 10-15 years with phlebotomy alone. The causes of death in adults are as follows:

* Thrombosis/thromboembolism (30-40%)
* Acute myelogenous leukemia (19%)
* Other malignancies (15%)
* Hemorrhage (2-10%)
* Myelofibrosis/myeloid metaplasia (4%)
* Other (25%)

In the neonatal period, polycythemia-induced hyperviscosity can lead to altered blood flow and subsequently affect organ function. Infants with polycythemia are at increased risk for necrotizing enterocolitis, renal dysfunction, hypoglycemia, and increased pulmonary vascular resistance with resultant hypoxia and cyanosis. Although initially thought to cause neurologic dysfunction, the decrease in cerebral blood flow seen in newborns with polycythemia is a physiologic response and does not appear to cause cerebral ischemia.17
Race

In the United States, higher rates of polycythemia vera are observed in the Ashkenazi Jewish population, and lower rates are seen in blacks.
Sex

The male-to-female ratio is 1.2-2.2:1 in adults and 1:1 in children.
Age

The median age for polycythemia vera is 60 years. Only 0.1% of polycythemia cases occur in people younger than 20 years.
Clinical
History

The clinical features associated with polycythemia are a direct result of the increase in red cell mass, which causes an expansion of blood volume. Signs of hyperviscosity and increased metabolism accompany polycythemia. A thorough history must be obtained for a history of cardiac, pulmonary (including sleep apnea), hepatic or renal disease in the patient and a complete family history for evidence of familial polycythemia.

Symptoms include the following:

* Headache
* Weight loss
* Weakness or malaise
* Dizziness
* Pruritus
* Bruising
* Ruddy or red appearance of the skin
* Diaphoresis/dyspnea
* Visual disturbance
* Paresthesias
* Arthropathies
* GI – Fullness, thirst, abdominal discomfort, constipation

Physical

A thorough physical must be completed and include specific evaluation for signs and symptoms of underlying disease that may cause secondary polycythemia; it must include pulse oximetry, careful cardiac and pulmonary evaluation, and evaluation for signs of renal or hepatic disease.

Signs of polycythemia include the following:

* Rubor, especially facial rubor
* Skin plethora
* Hypertension, both systolic and diastolic
* Hepatomegaly
* Splenomegaly
* Conjunctival plethora (engorged vessels in the bulbar conjunctiva)
* Ecchymosis
* Cardiac hypertrophy (rarely observed)

Causes

* Primary polycythemia
o In the past, the pathophysiology was unclear, and primary polycythemias were thought to be due to both inherited and acquired mutations in erythroid progenitors, leading to abnormal red cell proliferation. However, in 2005, an activating mutation found in the tyrosine kinase JAK2 was implicated as the causative factor in polycythemia vera (PV). Five separate groups identified this mutation in approximately 80% (56-97% reported) of patients with polycythemia vera.
o This acquired V617F mutation in JAK2 leads to constitutively activated JAK2. Activated JAK2 induces erythropoietin (Epo) hypersensitivity; although not yet completely delineated, it is thought to act through an activating EPOR.
o Additional JAK2 mutations have been identified in exon 12,9 JAK2H538-K539delinsI ,18 and others.19
o Primary familial and congenital polycythemia (PFCP), which is commonly found to have mutations in the Epo receptor (EPOR) gene. Approximately 14 mutations have been identified.
* Secondary polycythemia
o Congenital causes include high affinity hemoglobin and 2,3-Bisphosphoglycerate (2,3-BPG) deficiency.
o Chuvash polycythemia, a congenital polycythemia first recognized in an endemic Russian population, has mutations in the von Hippel-Lindau (VHL) gene, which is associated with a perturbed oxygen-dependent regulation of Epo synthesis.
o Acquired causes included hypoxemia and Epo-secreting tumors.
o Polycythemia of the newborn usually results from a poor intrauterine environment or hypoxic insult during labor or delivery.

Treatment
Medical Care

* Primary polycythemia: The goals of therapy are to maximize survival while minimizing the complications of therapy as well as of the disease itself.
o Phlebotomy and myelosuppressive chemotherapy are the cornerstones of therapy and have produced a median survival time of 9-14 years after the beginning of treatment. The goal of phlebotomy is to maintain normal red cell mass and blood volume, with a target hematocrit of 45%. The mean survival time of adult patients treated solely with phlebotomy is 13.9 years; however, a high risk of thromboembolic complications is observed.
o In the past, patients have been treated with chlorambucil and other alkylating agents such as pipobroman and busulfan. However, these patients exhibited the highest rates of secondary malignancy including acute leukemia, lymphocytic lymphomas, and skin and GI carcinomas. The rates of malignancy appear lower with busulfan than with the other alkylating agents. Currently, these agents are rarely used.
o Patients treated with phosphorus-32 (32 P) tolerate treatment well and have prolonged periods of remission. However, these patients also exhibit increased rates of acute leukemias (10-15%). The mean survival time with32 P treatment is 10.9 years.
o Studies suggest that the use of interferon alfa decreases the need for phlebotomy and decreases the risk of thrombotic events. Its use is limited by side effects, cost, and route of administration.
o Recent studies using hydroxyurea as a myelosuppressive agent also show promise, reducing the need for phlebotomy. However, similarly to those treated with chlorambucil, these patients also experience higher rates of malignancy. Early clinical studies using imatinib are currently underway and are thus far inconclusive.
o Current recommendations for treatment of young patients rely primarily on phlebotomy because the thrombosis is far less likely to occur in children and the long-term risks of leukemia over a longer life span are increased.
o In the past, the use of anticoagulants, including antiplatelet drugs such as aspirin and dipyridamole (Persantine) had demonstrated increased risk of bleeding without an associated decrease in thrombotic events; therefore, anticoagulants have not previously been recommended. However, a large European study, results of which were published in the New England Journal of Medicine by Landolfi et al (2004),20 showed a decrease in thrombotic events in those patients receiving low-dose aspirin therapy and recommended aspirin therapy for those patients for whom no contraindications existed. This issue continues to remain under debate in the field of polycythemia treatment.
* Secondary polycythemia: Phlebotomy is used for symptomatic hyperviscosity. The goal is to treat the underlying cause of polycythemia.

Surgical Care
Surgery is not typically indicated. Occasionally, splenectomy is performed late in the course of the disease if massive splenomegaly causes adverse effects such as early satiety, anemia, or thrombocytopenia from sequestration.

Please note that these patients have a high risk of complications during surgical procedures.
Consultations

Consult a neurologist and neurosurgeon if evidence of a stroke is present.
Diet

Diet is unrestricted.
Activity

Contact sports and other activities should be limited for individuals in hypercoagulable and hypocoagulable states.
Medication

Current recommendations for treatment of young patients rely primarily on phlebotomy.
Antineoplastic agents

The following medications are not approved for pediatric polycythemia but are extrapolated from other pediatric treatment regimens, including leukemia and myelodysplastic syndrome.

Interferon alfa 2a and 2b (Roferon-A [alfa-2a], Intron A [alfa-2b])

A recombinant purified protein used IV for CML, hairy cell leukemia, and Kaposi sarcoma. Inhibits cellular growth and alters cell differentiation.

Dosing
Adult
CML: 9 million U/d IM/SC; initiate with 3 million U/d, increase by 3 million U every third day; not to exceed 9 million U/d
Pediatric: 2.5-5 million U/d IM/SC

Interactions:Theophylline may increase toxicity; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity.

Contraindictions : Documented hypersensitivity.

Precautions:
Pregnancy
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus.

Precautions
Caution in brain metastases, severe hepatic or renal insufficiencies, seizure disorders, multiple sclerosis, or compromised CNS; use has been associated with depression, suicidal ideation and suicide attempts, and GI hemorrhage

Chlorambucil (Leukeran)
Antineoplastic alkylating agent of nitrogen mustard type used for CLL, giant follicular lymphoma, Hodgkin lymphoma, and lymphosarcoma.

Dosing:
Adult
0.1-0.2 mg/kg/d PO; adjust dose according to blood count

Pediatric
Not established; limited data available

Intractions:Live virus vaccines (eg, MMR) may result in severe or fatal infection when used in immunosuppressed patients

Contraindictions :Documented hypersensitivity; previous resistance to medication

Precautions:
Pregnancy
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions
Caution in history of seizure disorders or current bone marrow suppression

Busulfan (Myleran)
Potent cytotoxic drug that, at recommended dosage, causes profound myelosuppression. As alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Dosing:
Adult
4-8 mg/d PO; may administer up to 12 mg/d; maintenance dosing range is 1-4 mg/d to 2 mg/wk; discontinue regimen when WBC reaches 10,000-20,000 cells/mL; resume therapy when WBC reaches 50,000/mL

Pediatric
0.06-0.12 mg/kg/d or 1.8-4.6 mg/m2/d PO; titrate dose to maintain WBC >40,000/mL; reduce dose by 50% if WBC is 30,000-40,000/mL; discontinue if WBC <20,000/mL

Pipobroman (Vercyte, Vercite)
The mechanism of action is not fully understood; however, the drug is considered to be an alkylating agent. Pipobroman has been used with some success for treatment of polycythemia vera and chronic granulocytic leukemia. The product was discontinued by the manufacturer in the United States in 1996 but is available in Europe.

Dosing
Adult
1 mg/kg/d PO initially for at least 30 d; if refractory, may increase to 1.5-3 mg/kg/d
Maintenance: 0.1-0.2 mg/kg/d PO; typically initiated when hematocrit has decrease by 50-55%
Pediatric

<15 years: Not established
>15 years: Administer as in adults

Follow-up
Inpatient & Outpatient Medications

* Allopurinol for hyperuricemia or gout
* Iron supplementation to manage the increased red cell production that may produce a functional iron deficiency that can cause red cell rigidity and increase the risk of stroke
* Folate
* Cimetidine for pruritus and upper GI distress

Complications

* Vascular occlusive events – Splenic infarcts, thrombosis (cerebral, portal vein, pulmonary embolus)
* Hemorrhage
* Marrow fibrosis resulting in pancytopenia
* Malignancy – Acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), lymphoma
* Hyperuricemia – Renal stones, nephropathy, gout
* Budd-Chiari syndrome

Prognosis

* The median survival time for patients with polycythemia vera (PV) is 18 months for untreated patients and 9-14 years for treated patients.

Patient Education

* Inform patients that they are prone to surgical complications and are at high risk in trauma situations secondary to coagulopathies.

Miscellaneous
Medicolegal Pitfalls<%2

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Ailmemts & Remedies

Swine Flu

Other Names: Pig influenza, hog flu and pig flu.

Description:
Swine flu (also swine influenza) refers to influenza caused by any strain of the influenza virus endemic in pigs (swine). Strains endemic in swine are called swine influenza virus (SIV).

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Swine flu is common in swine and rare in humans. People who work with swine, especially people with intense exposures, are at risk of catching swine influenza if the swine carry a strain able to infect humans. However, these strains rarely are able to pass from human to human. Rarely, SIV mutates into a form able to pass easily from human to human. The strain responsible for the 2009 swine flu outbreak is believed to have undergone such a mutation. This virus is named swine flu because one of its surface proteins is similar to viruses that usually infects pigs, but this strain is spreading in people and it is unknown if it infects pigs.

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It is an infection caused by any one of several types of swine influenza viruses. Swine influenza virus (SIV) or swine-origin influenza virus (S-OIV) is any strain of the influenza family of viruses that is endemic in pigs.As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3.

In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort. The strain responsible for the 2009 swine flu outbreak in most cases causes only mild symptoms and the infected person makes a full recovery without  requiring medical attention and without the use of antiviral medicines.

Of the three genera of human flu, two are endemic also in swine: Influenzavirus A (common) and Influenzavirus C (rare). Influenzavirus B has not been reported in swine. Within Influenzavirus A and Influenzavirus C, the strains endemic to swine and humans are largely distinct.

History:
The swine flu is likely a descendant of the infamous “Spanish flu” that caused a devastating pandemic in humans in 1918–1919. In less than a year, that pandemic killed more an estimated 50 million people worldwide. Descendants of this virus have persisted in pigs; they probably circulated in humans until the appearance of the Asian flu in 1957, and reemerged in 1977. Direct transmission from pigs to humans is rare, with 12 cases in the U.S. since 2005.

The flu virus is perhaps the trickiest known to medical science; it constantly changes form to elude the protective antibodies that the body has developed in response to previous exposures to influenza or to influenza vaccines. Every two or three years the virus undergoes minor changes. Then, at intervals of roughly a decade, after the bulk of the world’s population has developed some level of resistance to these minor changes, it undergoes a major shift that enables it to tear off on yet another pandemic sweep around the world, infecting hundreds of millions of people who suddenly find their antibody defenses outflanked. Even during the Spanish flu pandemic, the initial wave of the disease was relatively mild and the second wave was highly lethal.In 1957, an Asian flu pandemic infected some 45 million Americans and killed 70,000. Eleven years later, lasting from 1968 to

1969, the Hong Kong flu pandemic afflicted 50 million Americans and caused 33,000 deaths, costing approximately $3.9 billion.

In 1976, about 500 soldiers became infected with swine flu over a period of a few weeks. However, by the end of the month investigators found that the virus had “mysteriously disappeared” and there were no more signs of swine flu anywhere on the post.  There were isolated cases around the U.S. but those cases were supposedly to individuals who caught the virus from pigs.

Medical researchers worldwide, recognizing that the swine flu virus might again mutate into something as deadly as the Spanish flu, were carefully watching the latest 2009 outbreak of swine flu and making contingency plans for a possible global pandemic.

Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human flu, often resulting only in the production of antibodies in the blood. If transmission does cause human flu, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection.

Around the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.

In August 2010, the World Health Organization declared the swine flu pandemic officially over.

Cases of swine flu have been reported in India, with over 31,156 positive test cases and 1,841 deaths till March 2015.

Signs and symptoms:
According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting.

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Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person’s recent history. For example, during the 2009 swine flu outbreak in the United States, CDC advised physicians to “consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset.” A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab)……click & see

Pathophysiology
Influenza viruses bind through hemagglutinin onto sialic acid sugars on the surfaces of epithelial cells; typically in the nose, throat and lungs of mammals and intestines of birds (Stage 1 in infection figure).

Swine flu in humans:
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. The 2009 swine flu outbreak is an apparent reassortment of several strains of influenza A virus subtype H1N1, including a strain endemic in humans and two strains endemic in pigs, as well as an avian influenza.

The CDC reports that the symptoms and transmission of the swine flu from human to human is much like that of seasonal flu. Common symptoms include fever, lethargy, lack of appetite and coughing, while runny nose, sore throat, nausea, vomiting and diarrhea have also been reported. It is believed to be spread between humans through coughing or sneezing of infected people and touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days, to the CDC for analysis.

The swine flu is susceptible to four drugs licensed in the United States, amantadine, rimantadine, oseltamivir and zanamivir; however, for the 2009 outbreak it is recommended it be treated under medical advice only with oseltamivir and zanamivir to avoid drug resistance. The vaccine for the human seasonal H1N1 flu does not protect against the swine H1N1 flu, as they are antigenically very different.

Causes:
The cause of the 2009 swine flu was an influenza A virus type designated as H1N1. In 2011, a new swine flu virus was detected. The new strain was named influenza A (H3N2)v. Only a few people (mainly children) were first infected, but officials from the U.S. Centers for Disease Control and Prevention (CDC) reported increased numbers of people infected in the 2012-2013 flu season. Currently, there are not large numbers of people infected with H3N2v. Unfortunately, another virus termed H3N2 (note no “v” in its name) has been detected and caused flu, but this strain is different from H3N2v. In general, all of the influenza A viruses have a structure similar to the H1N1 virus; each type has a somewhat different H and/or N structure.

Complications Of Swine Flu And Higher Risk Individuals:-

Those at higher risk include those with the following:
*Age of 65 years or older
*Chronic health problems (such as asthma, diabetes, heart disease)
*Pregnant women
*Young children

Complications (for all patients but especially for those at higher risk) can include:
*Pneumonia
*Bronchitis
*Sinus infections
*Ear infections
*Death

Diagnosis :-
1. A respiratory sample collected within the first five days of illness will be collected.

2. The sample is sent to the CDC for laboratory analysis and confirmation.

At this time the CDC is recommending the use of oseltamivir (Tamiflu) or zanamivir (Relenza) for treatment and/or prevention of Swine flu.

Why is swine flu now infecting humans?

Many researchers now consider that two main series of events can lead to swine flu (and also avian or bird flu) becoming a major cause for influenza illness in humans.

First, the influenza viruses (types A, B, C) are enveloped RNA viruses with a segmented genome; this means the viral RNA genetic code is not a single strand of RNA but exists as eight different RNA segments in the influenza viruses. A human (or bird) influenza virus can infect a pig respiratory cell at the same time as a swine influenza virus; some of the replicating RNA strands from the human virus can get mistakenly enclosed inside the enveloped swine influenza virus. For example, one cell could contain eight swine flu and eight human flu RNA segments. The total number of RNA types in one cell would be 16; four swine and four human flu RNA segments could be incorporated into one particle, making a viable eight RNA-segmented flu virus from the 16 available segment types. Various combinations of RNA segments can result in a new subtype of virus (this process is known as antigenic shift) that may have the ability to preferentially infect humans but still show characteristics unique to the swine influenza virus . It is even possible to include RNA strands from birds, swine, and human influenza viruses into one virus if a single cell becomes infected with all three types of influenza (for example, two bird flu, three swine flu, and three human flu RNA segments to produce a viable eight-segment new type of flu viral genome). Formation of a new viral type is considered to be antigenic shift; small changes within an individual RNA segment in flu viruses are termed antigenic drift   and result in minor changes in the virus. However, these small genetic changes can accumulate over time to produce enough minor changes that cumulatively alter the virus’ makeup over time (usually years).

Second, pigs can play a unique role as an intermediary host to new flu types because pig respiratory cells can be infected directly with bird, human, and other mammalian flu viruses. Consequently, pig respiratory cells are able to be infected with many types of flu and can function as a “mixing pot” for flu RNA segments . Bird flu viruses, which usually infect the gastrointestinal cells of many bird species, are shed in bird feces. Pigs can pick these viruses up from the environment, and this seems to be the major way that bird flu virus RNA segments enter the mammalian flu virus population.

Present vaccination strategies for SIV control and prevention in swine farms, typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses.

swine_flu_h1_n1

Treatment
In response to requests from the U.S. Centers for Disease Control and Prevention, on April 27, 2009 the FDA issued Emergency Use Authorizations to make available diagnostic and therapeutic tools to identify and respond to the swine influenza virus under certain circumstances. The agency issued these EUAs for the use of certain Relenza and Tamiflu antiviral drugs, and for the rRT-PCR Swine Flu Panel diagnostic test.

The CDC recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses, however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs The virus isolates that have been tested from the US and Mexico are however resistant to amantadine and rimantadine. If a person gets sick, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms).

Antiviral Stockpiles:
Some countries have issued orders to stockpile antivirals . These typically have an expiry date of five years after manufacturing.

Preparedness
To maintain a secure household during a pandemic flu, the Water Quality & Health Council recommends keeping as supplies food and bottled water, portable power sources and chlorine bleach as an emergency water purifier and surface sanitizer.

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Prevention.

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Prevention of swine influenza has three components:-(1) prevention in swine, (2) prevention of transmission to humans, and (3)  prevention of its spread among humans.

(1)Prevention in swine
Swine influenza has become a greater problem in recent decades as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases.

(2) Prevention of transmission to humans
There are antiviral medicines you can take to prevent or treat swine flu. There is no vaccine available right now to protect against swine flu. You can help prevent the spread of germs that cause respiratory illnesses like influenza by

*Covering your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.
*Washing your hands often with soap and water, especially after you cough or sneeze. You can also use alcohol-based hand cleaners.
*Avoiding touching your eyes, nose or mouth. Germs spread this way.
*Trying to avoid close contact with sick people.
*Staying home from work or school if you are sick.

(3) Prevention of spread in humans
Recommendations to prevent spread of the virus among humans include using standard infection control against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public. Vaccines against the H1N1 strain in the 2009 human outbreak are being developed and could be ready as early as June 2009.

Experts agree that hand-washing can help prevent viral infections, a surprisingly effective way to prevent all sorts of diseases, including ordinary influenza and the new swine flu virus. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows little particles of virus can linger on tabletops, telephones and other surfaces and be transferred via the fingers to the mouth, nose or eyes. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms such as a sudden fever, cough or muscle aches should stay away from work or public transportation and should see a doctor to be tested.

Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community.

You may click to see the latest information & instruction from WHO about the spread of swine flu

Click to see:-:>Critical Alert: The Swine Flu Pandemic – Fact or Fiction?

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Swine_influenza

http://diseases-viruses.suite101.com/article.cfm/swine_flu_symptoms_treatment_and_prevention

http://www.nlm.nih.gov/medlineplus/swineflu.html

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Food Allergy

Definition:
Food allergy is an immune system reaction that occurs soon after eating a certain food. Even a tiny amount of the allergy-causing food can trigger signs and symptoms such as digestive problems, hives or swollen airways. In some people, a food allergy can cause severe symptoms or even a life-threatening reaction known as anaphylaxis

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Food allergy affects an estimated 6 to 8 percent of children under age 3, and about 4 percent of adults. While there’s no cure, some children outgrow their food allergy as they get older. It’s easy to confuse a food allergy with a much more common reaction known as food intolerance. While bothersome, food intolerance is a less serious condition that does not involve the immune system.

Food allergy is distinct from other adverse responses to food, such as food intolerance, pharmacologic reactions, and toxin-mediated reactions.

Food allergy :Adverse immune response to a food protein

Pharmacologic: Caffeine tremors, cheese/wine (tyramine) migraine, scombroid (histamine) fish poisoning

Toxins:Bacterial food poisoning, staphylotoxin

Intolerance: lactose intolerance (lactase deficiency)

The food protein triggering the allergic response is termed a food allergen. It is estimated that up to 12 million Americans have food allergies, and the prevalence is rising. Six to eight percent of children under the age of three have food allergies and nearly four percent of adults have them. Food allergies cause roughly 30,000 emergency room visits and 100 to 200 deaths per year in the United States. The most common food allergies in adults are shellfish, peanuts, tree nuts, fish, and eggs, and the most common food allergies in children are milk, eggs, peanuts, and tree nuts.

Treatment consists of avoidance diets, in which the allergic person avoids all forms of the food to which they are allergic. For people who are extremely sensitive, this may involve the total avoidance of any exposure with the allergen, including touching or inhaling the problematic food as well as touching any surfaces that may have come into contact with it. Areas of research include anti-IgE antibody (omalizumab, or Xolair) and specific oral tolerance induction (SOTI), which have shown some promise for treatment of certain food allergies. People diagnosed with a food allergy may carry an autoinjector of epinephrine such as an EpiPen or Twinject, wear some form of medical alert jewelry, or develop an emergency action plan, in accordance with their doctor.

Signs and symptoms:–
Classic immunoglobulin-E (IgE)-mediated food allergies are classified as type-I immediate hypersensitivity reactions. These allergic reactions have an acute onset (from seconds to one hour) and may include:

*Angioedema: soft tissue swelling, usually involving the eyelids, face, lips, and tongue. Angioedema may result in severe swelling of the tongue as well as the larynx (voice box) and trachea, resulting in upper airway obstruction and difficulty breathing.

*Hives

*Itching of the mouth, throat, eyes, skin

*Nausea, vomiting, diarrhea, stomach cramps, and/or abdominal pain. This group of symptoms is termed gastrointestinal hypersensitivity or anaphylaxis.

*Rhinorrhea, nasal congestion

*Wheezing, scratchy throat, shortness of breath, or difficulty swallowing

*Anaphylaxis: a severe, whole-body allergic reaction that can result in death (see below)

The reaction may progress to anaphylactic shock: A systemic reaction involving several different bodily systems including hypotension (low blood pressure),loss of consciousness, and possibly death. Allergens most frequently associated with this type of reaction are peanuts, nuts, milk, egg, and seafood, though many food allergens have been reported as triggers for anaphylaxis.

Food allergy is thought to develop more easily in patients with the atopic syndrome, a very common combination of diseases: allergic rhinitis and conjunctivitis, eczema and asthma.[8] The syndrome has a strong inherited component; a family history of allergic diseases can be indicative of the atopic syndrome.

Conditions caused by food allergies are classified into 3 groups according to the mechanism of the allergic response:

1. IgE-mediated (classic):

Type-I immediate hypersensitivity reaction (symptoms described above)
Oral allergy syndrome
2. IgE and/or non-IgE-mediated:

*Allergic eosinophilic esophagitis
*Allergic eosinophilic gastritis
*Allergic eosinophilic gastroenteritis

3. Non-IgE mediated:

*Food protein-induced Enterocolitis syndrome (FPIES)

*Food protein proctocolitis/proctitis

*Food protein-induced enteropathy. An important example is Coeliac disease, which is an adverse immune response to the protein gluten.

*Milk-soy protein intolerance (MSPI) is a non-medical term used to describe a non-IgE mediated allergic response to milk and/or soy protein during infancy and early childhood. Symptoms of MSPI are usually attributable to food protein proctocolitis or FPIES.

*Heiner syndrome – lung disease due to formation of milk protein/IgG antibody immune complexes (milk precipitins) in the blood stream after it is absorbed from the GI tract. The lung disease commonly causes bleeding into the lungs and results in pulmonary hemosiderosis.

Pathophysiology:-
For more details on this topic, see allergy.
Generally, introduction of allergens through the digestive tract is thought to induce immune tolerance. In individuals who are predisposed to developing allergies (atopic syndrome), the immune system produces IgE antibodies against protein epitopes on non-pathogenic substances, including dietary components.[citation needed] The IgE molecules are coated onto mast cells, which inhabit the mucosal lining of the digestive tract.

Upon ingesting an allergen, the IgE reacts with its protein epitopes and release (degranulate) a number of chemicals (including histamine), which lead to oedema of the intestinal wall, loss of fluid and altered motility. The product is diarrhea.

Any food allergy has the potential to cause a fatal reaction.

Causes:-
The immune system’s Eosinophils, once activated in a histamine reaction, will register any foreign proteins they see. One theory regarding the causes of food allergies focuses on proteins presented in the blood along with vaccines, which are designed to provoke an immune response. Influenza vaccines and the Yellow Fever vaccine are still egg-based, but the Measles-Mumps-Rubella vaccine stopped using eggs in 1994. However large scientific studies do not support this theory, especially as it applies to autoimmune disease.

Another theory focuses on whether an infant’s immune system is ready for complex proteins in a new food when it is first introduced.

One hypothesis at this time is the Hygiene hypothesis. While there is no proof for the hygiene hypothesis, people speculate that in modern, industrialized nations, such as the United States, food allergies are more common due to the lack of early exposure to dirt and germs, in part due to the over use of antibiotics and antibiotic cleansers. This hypothesis is based partly on studies showing less allergy in third world countries. Some research suggests[citation needed] that the body, with less dirt and germs to fight off, turns on itself and attacks food proteins as if they were foreign invaders.

Antibiotics have also been implicated in Leaky Gut Syndrome which is another possible cause of food allergies

A lower incidence of food allergies in the developing world could also be due to differences in diet from the West and less exposure to food allergens.

Others have found that food allergies are due to widespread usage of baby skin care products that contain allergens, such as lotions based upon peanut’s oil. These skin care products are cheaper to manufacture than non-allergenic ones and using them sensitizes the baby, which later develops into a food allergy. This theory has yet to come with sufficient explanation as to why occurrence of allergies are on a steady rise in the last two decades.

Prevention:-
According to a report issued by the American Academy of Pediatrics, “There is evidence that breastfeeding for at least 4 months, compared with feeding infants formula made with intact cow milk protein, prevents or delays the occurrence of atopic dermatitis, cow milk allergy, and wheezing in early childhood.”[23]

Treatment:-
The mainstay of treatment for food allergy is avoidance of the foods that have been identified as allergens.

If the food is accidentally ingested and a systemic reaction occurs, then epinephrine (best delivered with an autoinjector of epinephrine such as an Epipen or Twinject) should be used. It is possible that a second dose of epinephrine may be required for severe reactions. The patient should also seek medical care immediately.

At this time, there is no cure for food allergies. There are no allergy desensitization or allergy “shots” available for food allergies. Some doctors feel they do not work in food allergies because even minute amounts of the food in question or even food extracts (as in the case of allergy shots) can cause an allergic response in many sufferers.

Ronald van Ree of Amsterdam University expects that vaccines can in theory be created using genetic engineering to cure allergies. If this can be done, food allergies could be eradicated in about ten years.
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Statistics:-
For reasons that are not entirely understood, the diagnosis of food allergies has apparently become more common in Western nations in recent times. In the United States food allergy affects as many as 5% of infants less than three years of age and 3% to 4% of adults. There is a similar prevalence in Canada.

The most common food allergens include peanuts, milk, eggs, tree nuts, fish, shellfish, soy, and wheat – these foods account for about 90% of all allergic reactions.

Differing views:-
Various medical practitioners have a differing views on food allergies. Irritable Bowel Syndrome (IBS) patients have been studied with regards to food allergies. Some studies have reported on the role of food allergy in IBS; only one epidemiological study on functional dyspepsia and food allergy has been published. However, since 2005 several studies have demonstrated strong correlation between IgG and/or IgE food allergy and IBS symptoms The mechanisms by which food activates mucosal immune system are incompletely understood, but food specific IgE and IgG4 appeared to mediate the hypersensitivity reaction in a subgroup of IBS patients. Specific chemicals and receptors have been demonstrated to be critical in food allergy development in murine models. Exclusion diets based on skin prick test, RAST for IgE or IgG4, hypoallergic diet and clinical trials with oral disodium cromoglycate have been conducted, and some success has been reported in a subset of IBS patients.

Studies comparing skin prick testing and ELISA blood testing have found that the results of skin prick testing correlate poorly with symptoms of irritable bowel syndrome that correlate with food allergies demonstrated through ELISA testing and dietary challenge.

Extensive clinical experience has demonstrated significant improvement of patients with IBS whose ELISA-based food allergy testing is positive and where treatment includes a careful exclusion diet.

In addition, many practitioners of alternative medicine ascribe symptoms to food allergy where other doctors do not. The causal relationships between some of these conditions and food allergies have not been studied extensively enough to provide sufficient evidence to become authoritative. The interaction of histamine with the nervous system receptors has been demonstrated, but more study is needed.[36] Other immune response effects are commonly known (swelling, irritation, etc.), but their relationships to some conditions has not been extensively studied. Examples are arthritis, fatigue, headaches, and hyperactivity. Nevertheless, hypoallergenic diets reportedly can be of benefit in these conditions, indicating that the current medical views on food allergy may be too narrow. Holford and Brady (2005) suggest three levels of response; classical immediate-onset allergy (IgE), delayed-onset allergy (giving a positive response on an ELISA IgG test but rarely on an IgE skin prick test), and food intolerance (non-allergic), and claim the last two to be more common. It is important to note that IgG is present in the body and is known to respond to foods. So some medical practitioners, especially allergists, claim that there is no predictive value to these types of tests, despite the studies cited above.

In children:-
Milk and soy allergies in children can often go undiagnosed for many months, causing much worry for parents and health risks for infants and children. Many infants with milk and soy allergies can show signs of colic, blood in the stool, mucous in the stool, reflux, rashes and other harmful medical conditions. These conditions are often misdiagnosed as viruses or colic.

Some children who are allergic to cow’s milk protein also show a cross sensitivity to soy-based products.[ There are infant formulas in which the milk and soy proteins are degraded so when taken by an infant, their immune system does not recognize the allergen and they can safely consume the product. Hypoallergenic infant formulas can be based on hydrolyzed proteins, which are proteins partially predigested in a less antigenic form. Other formulas, based on free amino acids, are the least antigenic and provide complete nutrition support in severe forms of milk allergy.

Seventy-fice percent of children who have allergies to milk protein are able to tolerate baked-in milk products, ie., muffins, cookies, cake.

About 50% of children with allergies to milk, egg, soy, and wheat will outgrow their allergy by the age of 6. Those that don’t, and those that are still allergic by the age of 12 or so, have less than an 8% chance of outgrowing the allergy.

Peanut and tree nut allergies are less likely to be outgrown, although evidence now shows[40] that about 20% of those with peanut allergies and 9% of those with tree nut allergies will outgrow their allergies. In such a case, they need to consume nuts in some regular fashion to maintain the non-allergic status.[citation needed] This should be discussed with a doctor.

Those with other food allergies may or may not outgrow their allergies.

Labeling laws
In response to the risk that certain foods pose to those with food allergies, countries have responded by instituting labeling laws that require food products to clearly inform consumers if their products contain major allergens or by-products of major allergens.

United States law
Under the Food Allergen Labeling and Consumer Protection Act of 2004 (Public Law 108-282), companies are required to disclose on the label whether the product contains a major food allergen in clear, plain language. The allergens have to clearly be called out in the ingredient statement. Most companies list allergens in a statement separate from the ingredient statement

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IT IS ADVISED TO DO  YOGA & MEDITATION  (BREATHING EXERCISE) DAILY  TO GET RID OF ALLERGY 

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Food_allergy
http://www.mayoclinic.com/health/food-allergy/DS00082/DSECTION=symptoms

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Insect Allergy

Definition:
Insect  allergy from its venom is a harmful reaction to insect stings that occurs in people who have an abnormally high sensitivity to insect venom. It is an acquired trait, which is not present at the first exposure to the venom, but sensitization can occur after the first or subsequent exposures. Animals classified as insects usually have three main body segments (head, thorax and abdomen), six legs and a pair of sensory antennae. Winged insect species have two sets of wings, such as mosquitoes, bees, and wasps. Other biting or stinging insects include fleas, lice, and ants. Many other related animals that are frequently mistaken for insects such as ticks, spiders and mites also bite human beings. They can transmit infectious diseases or cause poisoning but generally do not cause allergic reactions. Allergic reactions to the venom of some stinging insects, such as honey bee, yellow jacket, hornet, wasp or fire ant can be life threatening.

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Who gets it?
While not everyone is allergic to insect venom, reactions in the skin such as mild pain, swelling, and redness may occur with an insect sting. Anyone can experience an allergic reaction to an insect bite or sting. However, only a small number of people with insect bite or sting allergies suffer fatal reactions.

Who is at risk for insect sting allergies?
Over 2 million Americans are allergic to stinging insects. The degree of allergy varies widely. Most people are not allergic to insect stings, and most insect stings result in only local itching and swelling. Many, however, will have severe allergic reactions. Severe allergic reactions to insect stings are responsible for at least 50 deaths each year in the U.S.

If you are known to be allergic to insect stings, then the next sting is 60% likely to be similar or worse than the previous sting. Since most stings occur in the summer and fall, you are at greatest risk during these months. Males under the age of 20 are the most common victims of serious insect-sting allergic reactions, but this may reflect a greater exposure to insects of males, rather than a true predisposition.

Causes:
An allergic reaction occurs when the immune system produces antibodies and other disease fighting cells in response to an allergen, in this case the insect venom. The antibodies release chemicals that actually injure the surrounding cells and cause the physical symptoms of an allergic reaction. Certain antibodies release histamines, which affect the skin, mucous membrane, mucous gland, and smooth muscle cells. Life-threatening allergic reactions can occur without any previous symptoms of allergy. In fact, most people with insect bite or sting allergies do not experience a severe reaction with their first bite. Multiple bites or stings increase the risk of an allergic reaction, but just one bite will cause serious symptoms for someone who is severely allergic.

What insects are usually involved?
Most serious allergic reactions to insect venom are caused by stinging insects, such as bees, yellow jackets, hornets, wasps and imported fire ants. As natives of the tropics, fire ants can live only in the warmer climate of the southern states and cannot survive in the north. They are extremely aggressive and sting exposed parts of the skin when they feel threatened. Bites or stings from other insects usually do not cause allergic reaction.

Symptoms:
Symptoms of insect venom allergy often begin within 15 to 30 minutes and arise distant from the site of sting. The first symptom is often itchiness that can affect all or any part of the skin, the eyes and the nose. As symptoms progress, the patient begins to sneeze, cough and wheeze, feel congested, and develop hives or swelling. These symptoms may be warning signs of a dangerous condition called anaphylaxis. Symptoms of anaphylaxis include sudden anxiety and weakness, difficulty breathing, tightness in the chest, lightheadedness and palpitation, and loss of consciousness. Anaphylactic shock can occur within minutes and result in death. Anaphylaxis is a medical emergency that needs immediate medical treatment, and any delay may reduce the chance of survival.

Diagnosis:
Insect venom allergy is suspected based on a constellation of suggestive symptoms that follow an insect sting. The diagnosis is confirmed by performing a skin test with the venom of specific insects, such as honey bee, yellow jacket, hornet, wasp or fire ant that may be the culprit of the allergic reaction.

Treatment:
If you have been bitten or stung by an insect, carefully remove the stinger, if it is left behind. Wash the bite/sting area gently with soap and water. Apply ice to the site of sting. People who are allergic to insect bites should, of course, avoid situations in which they are likely to get stung or bitten. Mild reactions, such as pain, itching, and swelling, can be treated with an over-the counter antihistamine, pain reliever and topical corticosteroid creams. Anaphylactic shock is treated with an injection of epinephrine, a hormone that stimulates the heart and relaxes the airways. This may be combined with an injection of an antihistamine, which counteracts the histamine produced by the immune cells during an allergic reaction. Those who are known to have severe insect venom allergies should carry a self-injection kit, including antihistamine tablets, for emergency treatment. However, they should still seek emergency medical care after any type of reaction to an insect bite or sting.

People who are severely allergic to the venom of stinging insects, such as bees, yellow jackets, hornets, wasps or fire ants may, undergo a desensitization. First, skin testing is performed by an allergy specialist to determine the type of insect that responsible for the venom allergy. Then the patient receives a series of injections of the venom from the same insect(s). Starting dose is minute but increasingly larger doses are given until the venom doses several times larger than a single insect sting can be tolerated. This type of program must be administered by an allergy specialist, and it usually takes 20 weekly injections to eliminate this abnormal and exaggerated sensitivity. These are followed up with monthly booster shots and continued for 3 to 5 years to consolidate the cure.
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Alternative Treatments For Insect Bite Allergy

Alternative therapy for insect bites

Are There Any Ways To Treat Insect Sting Allergies Using Alternative Medicine?

Self-care tips
There are many ways you can help prevent insect bites and stings. Don’t use flowery colognes, soaps, or lotions, or wear brightly colored clothing, which attract insects. Do not keep open garbage or food that attract stinging insects when you are outdoors. Avoid drinking sweet beverages especially from open cans that have been left unattended and may harbor insects. Wear light, protective clothing such as long sleeves top and long pants whenever you will be outside for longer periods of time. Wear work gloves when you are gardening. Do not walk barefoot on the grass where insects are difficult to detect and can be stepped on. If an insect is near you, move away. Do not swat at the insect, which may awaken its defensive instincts and trigger aggressive behavior. Make sure any insect nests around your home are removed and destroyed.

Stinging Insect Allergies At A Glance:-
*Severity of reactions to stings varies greatly.

*Most insect stings do not produce allergic reactions.

*Anaphylactic reactions are the most serious reactions and can be fatal.

*Avoidance and prompt treatment are essential.

*Epinephrine (available in portable, self-injectable form) is the treatment of choice for anaphylactic reactions.

*In selected people, allergy injection therapy is highly effective in preventing future reactions.

*The three “A’s” of insect allergy are adrenaline, avoidance, and allergist.


The U.S. Department of Agriculture recommends the following:–

*Avoid disturbing likely beehive sites, such as large trees, tree stumps, logs, and large rocks.

*If a colony is disturbed, run and find cover as soon as possible. Running in a zigzag pattern may be helpful.

*Never stand still or crawl into a hole or other space with no way out.

*Do not slap at the bees.

*Cover as much of the head and face as possible, without obscuring vision, while running.

*Once clear of the bees, remove stingers and seek medical care if necessary, especially if there is a history of allergy to bee venom.

For more knowledge you may click to see:->Insect Allergy Reminders

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:–
http://www.hmc.psu.edu/healthinfo/i/insectallergy.htm
http://www.medicinenet.com/insect_sting_allergies/article.htm

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