Guest guest Posted November 5, 2008 Report Share Posted November 5, 2008 --- Yes. Low IG's and low or no response to vaccinations is CVID. valarie In , Suz Blokzyl <ryanthomas04@...> wrote: > > Hello all- > > I am very new to this and still tryign to figure out my son.. So if he gets an immunization (tetanus and diptheria) and his titers come back very low for that. Are you definetly considered to have a CVID? > > thanks, > suzanne > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 5, 2008 Report Share Posted November 5, 2008 --- Yes. Low IG's and low or no response to vaccinations is CVID. valarie In , Suz Blokzyl <ryanthomas04@...> wrote: > > Hello all- > > I am very new to this and still tryign to figure out my son.. So if he gets an immunization (tetanus and diptheria) and his titers come back very low for that. Are you definetly considered to have a CVID? > > thanks, > suzanne > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 5, 2008 Report Share Posted November 5, 2008 I Found this....Hope it helps My son Blake was first DX'ed with Hypogammaglobulinemia with hypocomplementemia(T-Cell Dysfunction) That was age 3. At age 6 we were sent to DUKE. His DX'ed was Changed to CommonVariabe Immunodeficiency with hypocomplementemia(T-Cell Dysfunction) They then thought Blake had OMEN SYNDROME....Total T-Cell Depletion. Blake still had a lot of break through infections and was STILL spending most of his days in a hospital. He started IVIG at age 6. The increased the doasage on a regular basis. Blake wound up with & losing 7 ports, thousands of PICC Lines and 4 Broviac. We finally removed his last line in July last yr. because of a resistant Pseudomonas infection that would NOT clear. We Started Sub-Q in August last yr. and have not looked back.....he has not been in the hospital (for infections) since then!!!! Getting that DX is very hard. What deterred the Drs. from giving Blake the DX was he was born a Micro Preemie. The Preemie part was a catch all....since he was not gestationaly up to age....he would out grow this problem...Transient(Our Immune Dr, told us that Hyopgammaglobulinemia is often used for Transient....will eventually out grow) But his status was changed when they found he would NOT out grow and definitely NEEDED IgG Therapy. Blake does have a Total T-Cell Dysfunction.....He has no function of what is made by his body. His Titers for all vaccines and Pneumovaxes & anything that tested his T-Cells....everything came back as NON existant!!! at age 9 his DX was changed to Severe Combined Immunodeficiency...he is IgG Threapy dependant!!! Mom to Blake age 16, SCID with Complete T-Cell Dysfuntion http://www3.caringbridge.org/sc/blakester Come & see why I call him: The Greatest Adventure of MY Lifetime " Children are like butterflies in the wind. Some fly higher than others, BUT each one flies the best they can!!!! " Hope this helps with the CVID understanding: Common variable immunodeficiency From Wikipedia, the free encyclopedia Jump to: navigation, search Common variable immunodeficiency Classification and external resources ICD-10 D83. ICD-9 279.06 OMIM 240500 DiseasesDB 3274 eMedicine ped/444 derm/870 MeSH D017074 Common variable immunodeficiency (CVID) is a group of 20-30 primary immunodeficiencies (PIDs) which have a common set of symptoms (including hypogammaglobulinemia)[1] but with different underlying causes. Common variable immunodeficiency is the most commonly encountered primary immunodeficiency.[2] Contents[hide] 1 Causes and types 2 Clinical Features 3 Diagnosis 4 Associated conditions 5 Treatment 5.1 Reactions 6 Research 7 Epidemiology 8 History 9 References 10 External links // [edit] Causes and types CVID is believed to be a genetically determined primary immune defect; however, the underlying causes are different. The result of these defects is that the patient doesn't produce sufficient antibodies in response to exposure to pathogens. As a result, the patient's immune system fails to protect them against common bacterial and viral (and occasionally parasitic and protozoan) infections. The net result is that the patient is susceptible to illness. In CVID, the B cells are affected. In combined severe immunodeficiency, a more severe condition than CVID, diagnosed in infancy, both parts of the immune system (the cellular and humoral system) are affected, hence its classified as combined immunodeficiency. CVID appears to include a number of defects, some of which have been identified. For the majority, the genetic causes are still unknown. ICOS, TACI and CD19 have been identified as candidates.[3][4] It is possible that environmental agents provoke the immune defect, due to genetic predisposition, but this has not been clarified. [/] [edit] Clinical Features Signs and Symptoms of CVID include: hypogammaglobulinemia, or low levels of immunoglobulin G (IgG), immunoglobulin A (IgA) and/or immunoglobulin M (IgM). lack of normal levels of antibody in the serum is part of the diagnosis Chronic swelling of the lymph glands Enlarged spleen atrophic gastritis with pernicious anemia nodular lymphoid hyperplasia of the intestine. This finding can be mistaken for intestinal lymphoma bacterial overgrowth of the intestine. increased intestinal permeability (i.e. leaky gut) villous atrophy in the small intestine, which can resemble coeliac disease and cause diarrhoea and malabsorption increased incidence of inflammatory bowel disease bronchiectasis (lung tissue damage as a result of repeated chest infections) leading to shortness of breath poor titer levels in response to vaccination. Responsiveness may be tested after administration of polysaccharide and non-polysaccharide coated pathogens (e.g. streptococci and tetanus respectively) polyarthritis, or joint pain, spread across most joints, but specifically fingers, wrists, elbows, toes, ankles and knees chronic infections. (most common symptom) Specifically: upper respiratory tract infection - e.g. bronchitis, sinusitis which respond to antibiotics but return or recur. Viral infections that usually respond to antivirals, sinusitis, tonsilitis, epiglottitis, dermatological abscesses/boils (often, but not exclusively, facial and axillary), pneumonia, bronchitis, pleurisy, stomach/intestinal infections, colds, influenza, shingles, conjunctivitis Tiredness chronic diarrhoea (often arises as a result of " minor " intestinal infections, including protozoan and parasitic infections) children may show a " failure to thrive " - they may be underweight and underdeveloped compared with " normal " peers patients may lose weight [edit] Diagnosis Diagnosis is often delayed; and diagnosis is often made in the second or third decade of life after referral to an immunologist. It is a diagnosis of exclusion,[5] and sometimes considered a wastebasket diagnosis.[6] It presents similar to X-linked agammaglobulinemia, but the conditions can be distinguished with flow cytometry.[7] [edit] Associated conditions As with several other immune cell disorders, CVID may predispose to lymphoma or possibly stomach cancer.[8] There also appears to be a predilection for autoimmune diseases, with a risk of up to 25%. Autoimmune destruction of platelets or red blood cells are the most common of these. [edit] Treatment Treatment usually consists of immunoglobulin therapy, which is an injection of human antibodies harvested from blood donations: intravenous immunoglobulin (IVIG, most common treatment in the US)[9] subcutaneous immunoglobulin G (SCIG, relatively new treatment in the US) intramuscular immunglobulin (IMIG, less effective, painful) This is not a cure, but it strengthens immunity by ensuring that the patient has " normal " levels of antibodies, which helps to prevent recurrent upper respiratory infections. IG therapy can't be used if the patient has anti-IgA antibodies but in this case, products low in IgA can be used; subcutaneous delivery also is a means of permitting such patients to have adequate antibody replacement. IVIG treatment can be received by patients with a complete IgA deficiency if the IgA is completely removed from the treatment. [edit] Reactions Some CVID patients may experience reactions to IG therapies; reactions may include: anaphylactic shock (very rare) hives (rare) difficulty breathing headache (relatively common, may be relieved by an antihistamine, paracetamol/acetaminophen, or an anti-inflammatory (naproxen, advil, aspirin) nausea (common in IVIG) fever (common in IVIG and rare in SCIG) aseptic meningitis (rare) severe fatigue (common in IVIG) muscle aches and pain, or joint pain thrombotic events (rare) swelling at the insertion site (common in SCIG) Patients should not receive therapy if they are fighting an active infection as this increases the risk of reaction. Also, patients changing from one brand of product to another may be at higher risk of reaction for the first couple of treatments on the new brand. Reactions can be minimised by taking an antihistamine and/or hydrocortisone and some paracetamol/acetaminophen/anti-inflammatory (naproxen, advil, aspirin) prior to treatment; patients should also be thoroughly hydrated and continue to drink water before, after and during treatment (if possible). [edit] Research Research is currently focussing on genetic analysis, and in differentiating between the various different disorders in order to allow a cure to be developed. Cures are likely to be genetic in nature, repairing faulty genes and allowing the individual to start producing antibodies. Funding for research in the US is provided by the National Institutes of Health. Key research in the UK is funded by the Primary Immunodeficiency Association (PiA), and funding is raised through the annual Jeans for Genes campaign. [edit] Epidemiology CVID has an estimated prevalence is about 1:50,000.[10] The typical patient is between 20 and 40, and males and females are equally affected. About 20% of patients are diagnosed in childhood. [edit] History Janeway et al (1953) is generally credited with the description of the first case of CVID.[11] [edit] References ^ common variable immunodeficiency at Dorland's Medical Dictionary ^ Park MA, Li JT, Hagan JB, Maddox DE, Abraham RS (August 2008). " Common variable immunodeficiency: a new look at an old disease " . Lancet 372 (9637): 489–502. doi:10.1016/S0140-6736(08)61199-X. PMID 18692715. ^ Salzer U, Neumann C, Thiel J, et al (2008). " Screening of functional and positional candidate genes in families with common variable immunodeficiency " . BMC Immunol. 9 (1): 3. doi:10.1186/1471-2172-9-3. PMID 18254984. ^ Blanco-Quirós A, Solís-Sánchez P, Garrote-Adrados JA, Arranz-Sanz E (2006). " Common variable immunodeficiency. Old questions are getting clearer " . Allergol Immunopathol (Madr) 34 (6): 263–75. PMID 17173844. ^ Common Variable Immunodeficiency : Article by C Lucy Park at eMedicine ^ Online 'Mendelian Inheritance in Man' (OMIM) COMMON VARIABLE IMMUNODEFICIENCY; CVID -240500 ^ Common Variable Immunodeficiency at Merck Manual of Diagnosis and Therapy Professional Edition ^ Mellemkjaer L, Hammarstrom L, Andersen V, et al (2002). " Cancer risk among patients with IgA deficiency or common variable immunodeficiency and their relatives: a combined Danish and Swedish study " . Clin. Exp. Immunol. 130 (3): 495–500. doi:10.1046/j.1365-2249.2002.02004.x. PMID 12452841. ^ Pourpak Z, Aghamohammadi A, Sedighipour L, et al (2006). " Effect of regular intravenous immunoglobulin therapy on prevention of pneumonia in patients with common variable immunodeficiency " (abstract). J Microbiol Immunol Infect 39 (2): 114–20. PMID 16604243. ^ Common Variable Immunodeficiency : Article by A Schwartz at eMedicine ^ Janeway CA, Apt L, Gitlin D. Agammaglobulinemia. Trans Assoc Am Physicians 1953;66:200-2. PMID 13136263 [edit] External links Primary Immunodeficiency Association (UK) Immune Deficiency Foundation (US) Michigan Immunodeficiency Foundation (US) Immune Deficiencies Foundation of Australia Immune Deficiencies Foundation of New Zealand IPOPI (International Patient Organisation for Patients with Primary Immunodeficiency) Canadian Immunodeficiencies Patient Organization (Canada) Dutch Patient Organisation for Primary Immunodeficiencies (SAS) Maker of SCIG product [hide] v • d • ePathology: Immune disorders (primarily D80-D89, 273, 279) Immunodeficiency Primary Antibody/humoral ( Hypogammaglobulinemia/agammaglobulinemia (X-linked, Transient of infancy) - Dysgammaglobulinemia (IgA, IgG, IgM) - Hyper IgM syndrome (2, 3, 4, 5) - Common variable immunodeficiency Cell-mediated (T) Di syndrome - Nezelof syndrome - Purine nucleoside phosphorylase deficiency - Ataxia telangiectasia - Hyper IgM syndrome (1) Severe combined (B+T) x-linked: X-SCID autosomal: Adenosine deaminase deficiency - Omenn syndrome - ZAP70 deficiency - Bare lymphocyte syndrome Complement deficiency Angioedema - Complement 2 deficiency PBD chemotaxis/degranulation (Leukocyte adhesion deficiency, Chediak-Higashi syndrome, Hyper-IgE syndrome) respiratory burst (Chronic granulomatous disease, Myeloperoxidase deficiency) Other ICF syndrome - Wiskott-Aldrich syndrome - WHIM syndrome Acquired AIDS Immunoproliferative Hypergammaglobulinemia Paraproteinemia (Cryoglobulinemia, Heavy chain disease, POEMS syndrome, Monoclonal gammopathy of undetermined significance)Lymphoproliferative disorders (Sarcoidosis) Other Hypersensitivity and Autoimmunity/Autoimmune disease See also hematological malignancy and hematology Retrieved from " http://en.wikipedia.org/wiki/Common_variable_immunodeficiency " Categories: Immune system disorders | Immunodeficiency " Children are like butterflies in the wind. Some fly higher than others, BUT each one flies the best they can!!!! " Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 5, 2008 Report Share Posted November 5, 2008 I Found this....Hope it helps My son Blake was first DX'ed with Hypogammaglobulinemia with hypocomplementemia(T-Cell Dysfunction) That was age 3. At age 6 we were sent to DUKE. His DX'ed was Changed to CommonVariabe Immunodeficiency with hypocomplementemia(T-Cell Dysfunction) They then thought Blake had OMEN SYNDROME....Total T-Cell Depletion. Blake still had a lot of break through infections and was STILL spending most of his days in a hospital. He started IVIG at age 6. The increased the doasage on a regular basis. Blake wound up with & losing 7 ports, thousands of PICC Lines and 4 Broviac. We finally removed his last line in July last yr. because of a resistant Pseudomonas infection that would NOT clear. We Started Sub-Q in August last yr. and have not looked back.....he has not been in the hospital (for infections) since then!!!! Getting that DX is very hard. What deterred the Drs. from giving Blake the DX was he was born a Micro Preemie. The Preemie part was a catch all....since he was not gestationaly up to age....he would out grow this problem...Transient(Our Immune Dr, told us that Hyopgammaglobulinemia is often used for Transient....will eventually out grow) But his status was changed when they found he would NOT out grow and definitely NEEDED IgG Therapy. Blake does have a Total T-Cell Dysfunction.....He has no function of what is made by his body. His Titers for all vaccines and Pneumovaxes & anything that tested his T-Cells....everything came back as NON existant!!! at age 9 his DX was changed to Severe Combined Immunodeficiency...he is IgG Threapy dependant!!! Mom to Blake age 16, SCID with Complete T-Cell Dysfuntion http://www3.caringbridge.org/sc/blakester Come & see why I call him: The Greatest Adventure of MY Lifetime " Children are like butterflies in the wind. Some fly higher than others, BUT each one flies the best they can!!!! " Hope this helps with the CVID understanding: Common variable immunodeficiency From Wikipedia, the free encyclopedia Jump to: navigation, search Common variable immunodeficiency Classification and external resources ICD-10 D83. ICD-9 279.06 OMIM 240500 DiseasesDB 3274 eMedicine ped/444 derm/870 MeSH D017074 Common variable immunodeficiency (CVID) is a group of 20-30 primary immunodeficiencies (PIDs) which have a common set of symptoms (including hypogammaglobulinemia)[1] but with different underlying causes. Common variable immunodeficiency is the most commonly encountered primary immunodeficiency.[2] Contents[hide] 1 Causes and types 2 Clinical Features 3 Diagnosis 4 Associated conditions 5 Treatment 5.1 Reactions 6 Research 7 Epidemiology 8 History 9 References 10 External links // [edit] Causes and types CVID is believed to be a genetically determined primary immune defect; however, the underlying causes are different. The result of these defects is that the patient doesn't produce sufficient antibodies in response to exposure to pathogens. As a result, the patient's immune system fails to protect them against common bacterial and viral (and occasionally parasitic and protozoan) infections. The net result is that the patient is susceptible to illness. In CVID, the B cells are affected. In combined severe immunodeficiency, a more severe condition than CVID, diagnosed in infancy, both parts of the immune system (the cellular and humoral system) are affected, hence its classified as combined immunodeficiency. CVID appears to include a number of defects, some of which have been identified. For the majority, the genetic causes are still unknown. ICOS, TACI and CD19 have been identified as candidates.[3][4] It is possible that environmental agents provoke the immune defect, due to genetic predisposition, but this has not been clarified. [/] [edit] Clinical Features Signs and Symptoms of CVID include: hypogammaglobulinemia, or low levels of immunoglobulin G (IgG), immunoglobulin A (IgA) and/or immunoglobulin M (IgM). lack of normal levels of antibody in the serum is part of the diagnosis Chronic swelling of the lymph glands Enlarged spleen atrophic gastritis with pernicious anemia nodular lymphoid hyperplasia of the intestine. This finding can be mistaken for intestinal lymphoma bacterial overgrowth of the intestine. increased intestinal permeability (i.e. leaky gut) villous atrophy in the small intestine, which can resemble coeliac disease and cause diarrhoea and malabsorption increased incidence of inflammatory bowel disease bronchiectasis (lung tissue damage as a result of repeated chest infections) leading to shortness of breath poor titer levels in response to vaccination. Responsiveness may be tested after administration of polysaccharide and non-polysaccharide coated pathogens (e.g. streptococci and tetanus respectively) polyarthritis, or joint pain, spread across most joints, but specifically fingers, wrists, elbows, toes, ankles and knees chronic infections. (most common symptom) Specifically: upper respiratory tract infection - e.g. bronchitis, sinusitis which respond to antibiotics but return or recur. Viral infections that usually respond to antivirals, sinusitis, tonsilitis, epiglottitis, dermatological abscesses/boils (often, but not exclusively, facial and axillary), pneumonia, bronchitis, pleurisy, stomach/intestinal infections, colds, influenza, shingles, conjunctivitis Tiredness chronic diarrhoea (often arises as a result of " minor " intestinal infections, including protozoan and parasitic infections) children may show a " failure to thrive " - they may be underweight and underdeveloped compared with " normal " peers patients may lose weight [edit] Diagnosis Diagnosis is often delayed; and diagnosis is often made in the second or third decade of life after referral to an immunologist. It is a diagnosis of exclusion,[5] and sometimes considered a wastebasket diagnosis.[6] It presents similar to X-linked agammaglobulinemia, but the conditions can be distinguished with flow cytometry.[7] [edit] Associated conditions As with several other immune cell disorders, CVID may predispose to lymphoma or possibly stomach cancer.[8] There also appears to be a predilection for autoimmune diseases, with a risk of up to 25%. Autoimmune destruction of platelets or red blood cells are the most common of these. [edit] Treatment Treatment usually consists of immunoglobulin therapy, which is an injection of human antibodies harvested from blood donations: intravenous immunoglobulin (IVIG, most common treatment in the US)[9] subcutaneous immunoglobulin G (SCIG, relatively new treatment in the US) intramuscular immunglobulin (IMIG, less effective, painful) This is not a cure, but it strengthens immunity by ensuring that the patient has " normal " levels of antibodies, which helps to prevent recurrent upper respiratory infections. IG therapy can't be used if the patient has anti-IgA antibodies but in this case, products low in IgA can be used; subcutaneous delivery also is a means of permitting such patients to have adequate antibody replacement. IVIG treatment can be received by patients with a complete IgA deficiency if the IgA is completely removed from the treatment. [edit] Reactions Some CVID patients may experience reactions to IG therapies; reactions may include: anaphylactic shock (very rare) hives (rare) difficulty breathing headache (relatively common, may be relieved by an antihistamine, paracetamol/acetaminophen, or an anti-inflammatory (naproxen, advil, aspirin) nausea (common in IVIG) fever (common in IVIG and rare in SCIG) aseptic meningitis (rare) severe fatigue (common in IVIG) muscle aches and pain, or joint pain thrombotic events (rare) swelling at the insertion site (common in SCIG) Patients should not receive therapy if they are fighting an active infection as this increases the risk of reaction. Also, patients changing from one brand of product to another may be at higher risk of reaction for the first couple of treatments on the new brand. Reactions can be minimised by taking an antihistamine and/or hydrocortisone and some paracetamol/acetaminophen/anti-inflammatory (naproxen, advil, aspirin) prior to treatment; patients should also be thoroughly hydrated and continue to drink water before, after and during treatment (if possible). [edit] Research Research is currently focussing on genetic analysis, and in differentiating between the various different disorders in order to allow a cure to be developed. Cures are likely to be genetic in nature, repairing faulty genes and allowing the individual to start producing antibodies. Funding for research in the US is provided by the National Institutes of Health. Key research in the UK is funded by the Primary Immunodeficiency Association (PiA), and funding is raised through the annual Jeans for Genes campaign. [edit] Epidemiology CVID has an estimated prevalence is about 1:50,000.[10] The typical patient is between 20 and 40, and males and females are equally affected. About 20% of patients are diagnosed in childhood. [edit] History Janeway et al (1953) is generally credited with the description of the first case of CVID.[11] [edit] References ^ common variable immunodeficiency at Dorland's Medical Dictionary ^ Park MA, Li JT, Hagan JB, Maddox DE, Abraham RS (August 2008). " Common variable immunodeficiency: a new look at an old disease " . Lancet 372 (9637): 489–502. doi:10.1016/S0140-6736(08)61199-X. PMID 18692715. ^ Salzer U, Neumann C, Thiel J, et al (2008). " Screening of functional and positional candidate genes in families with common variable immunodeficiency " . BMC Immunol. 9 (1): 3. doi:10.1186/1471-2172-9-3. PMID 18254984. ^ Blanco-Quirós A, Solís-Sánchez P, Garrote-Adrados JA, Arranz-Sanz E (2006). " Common variable immunodeficiency. Old questions are getting clearer " . Allergol Immunopathol (Madr) 34 (6): 263–75. PMID 17173844. ^ Common Variable Immunodeficiency : Article by C Lucy Park at eMedicine ^ Online 'Mendelian Inheritance in Man' (OMIM) COMMON VARIABLE IMMUNODEFICIENCY; CVID -240500 ^ Common Variable Immunodeficiency at Merck Manual of Diagnosis and Therapy Professional Edition ^ Mellemkjaer L, Hammarstrom L, Andersen V, et al (2002). " Cancer risk among patients with IgA deficiency or common variable immunodeficiency and their relatives: a combined Danish and Swedish study " . Clin. Exp. Immunol. 130 (3): 495–500. doi:10.1046/j.1365-2249.2002.02004.x. PMID 12452841. ^ Pourpak Z, Aghamohammadi A, Sedighipour L, et al (2006). " Effect of regular intravenous immunoglobulin therapy on prevention of pneumonia in patients with common variable immunodeficiency " (abstract). J Microbiol Immunol Infect 39 (2): 114–20. PMID 16604243. ^ Common Variable Immunodeficiency : Article by A Schwartz at eMedicine ^ Janeway CA, Apt L, Gitlin D. Agammaglobulinemia. Trans Assoc Am Physicians 1953;66:200-2. PMID 13136263 [edit] External links Primary Immunodeficiency Association (UK) Immune Deficiency Foundation (US) Michigan Immunodeficiency Foundation (US) Immune Deficiencies Foundation of Australia Immune Deficiencies Foundation of New Zealand IPOPI (International Patient Organisation for Patients with Primary Immunodeficiency) Canadian Immunodeficiencies Patient Organization (Canada) Dutch Patient Organisation for Primary Immunodeficiencies (SAS) Maker of SCIG product [hide] v • d • ePathology: Immune disorders (primarily D80-D89, 273, 279) Immunodeficiency Primary Antibody/humoral ( Hypogammaglobulinemia/agammaglobulinemia (X-linked, Transient of infancy) - Dysgammaglobulinemia (IgA, IgG, IgM) - Hyper IgM syndrome (2, 3, 4, 5) - Common variable immunodeficiency Cell-mediated (T) Di syndrome - Nezelof syndrome - Purine nucleoside phosphorylase deficiency - Ataxia telangiectasia - Hyper IgM syndrome (1) Severe combined (B+T) x-linked: X-SCID autosomal: Adenosine deaminase deficiency - Omenn syndrome - ZAP70 deficiency - Bare lymphocyte syndrome Complement deficiency Angioedema - Complement 2 deficiency PBD chemotaxis/degranulation (Leukocyte adhesion deficiency, Chediak-Higashi syndrome, Hyper-IgE syndrome) respiratory burst (Chronic granulomatous disease, Myeloperoxidase deficiency) Other ICF syndrome - Wiskott-Aldrich syndrome - WHIM syndrome Acquired AIDS Immunoproliferative Hypergammaglobulinemia Paraproteinemia (Cryoglobulinemia, Heavy chain disease, POEMS syndrome, Monoclonal gammopathy of undetermined significance)Lymphoproliferative disorders (Sarcoidosis) Other Hypersensitivity and Autoimmunity/Autoimmune disease See also hematological malignancy and hematology Retrieved from " http://en.wikipedia.org/wiki/Common_variable_immunodeficiency " Categories: Immune system disorders | Immunodeficiency " Children are like butterflies in the wind. Some fly higher than others, BUT each one flies the best they can!!!! " Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 8, 2008 Report Share Posted November 8, 2008 OK, can someone please give me the low down on titers? I know several parents who are waiting until their child is 2 and then giving them a titers test to see what vax they actually need. My issue is that I was tested with my first babe and was found to NOT be " immune " to rubella. BUT with both my 2nd and 3rd babes I WAS. I've heard that these tests can differ by the day...so, whats the deal? Any and all advice is greatly appreciated! www.BOBYSboutique.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 9, 2008 Report Share Posted November 9, 2008 1. Vaccination is a hoax http://whale.to/vaccines/note.html 2. Titre tests measure antibody levels, I think, which is another hoax re immunity http://whale.to/vaccines/antibody.html Titers? OK, can someone please give me the low down on titers? I know several parents who are waiting until their child is 2 and then giving them a titers test to see what vax they actually need. My issue is that I was tested with my first babe and was found to NOT be " immune " to rubella. BUT with both my 2nd and 3rd babes I WAS. I've heard that these tests can differ by the day...so, whats the deal? Any and all advice is greatly appreciated! www.BOBYSboutique.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 9, 2008 Report Share Posted November 9, 2008 Hi , I’m not an expert on titers, but I do know that they prove nothing and essentially mean nothing. Doing a titer test will only show a snap-shot in time of what your child has recently been exposed to. If you child has not been exposed to rubella recently, then there will be no presence of antibodies in the system. Titer tests in NO WAY shape or form are an indication of immunity to anything. For example, I’ve had chicken pox, and once you’ve had chicken pox, you are immune for life (of course there are exceptions), but a titer test on my blood will not show any antibodies for this disease, unless there has been recent exposure to the disease. Your body is building defense for viruses and disease all the time, everyday, and every time you are exposed to something. Most healthy people with robust immune function will remain healthy and ward off the offending “bugs”; so a titer test will only show what your body is currently being assaulted by, but it doesn’t mean that you have that virus or disease, just that your body has been exposed to it. Once the “threat” is no longer there, there is no more reason for your body to waste it’s time building a defense system, meaning antibodies, to fight the threat, so it focuses it’s efforts elsewhere. Does that make sense? Maybe someone else can explain a bit better than I. ~Chris _____ From: Vaccinations [mailto:Vaccinations ] On Behalf Of jbobys Sent: Saturday, November 08, 2008 11:19 PM Vaccinations Subject: Titers? OK, can someone please give me the low down on titers? I know several parents who are waiting until their child is 2 and then giving them a titers test to see what vax they actually need. My issue is that I was tested with my first babe and was found to NOT be " immune " to rubella. BUT with both my 2nd and 3rd babes I WAS. I've heard that these tests can differ by the day...so, whats the deal? Any and all advice is greatly appreciated! www.BOBYSboutique.com Quote Link to comment Share on other sites More sharing options...
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