Death immunoglobulin

BW) Throughout gestation Reduced growth and altered serum immunoglobulins of progeny some deaths 7... 

IMMUNODEFICIENCY WITH HYPER-IGM (HIGMl), AN IMMUNOGLOBULIN ISOTYPE SWITCH DEFECT CHARACTERIZED BY ELEVATED CONCENTRATIONS OF SERUM IGM AND DECREASED AMOUNTS OF ALL OTHER ISOTYPES. AFFECTED MALES PRESENT AT AN EARLY AGE (USUALLY WITHIN THE FIRST YEAR OF LIFE) RECURRENT BACTERIAL AND OPPORTUNISTIC INFECTIONS, INCLUDING PNEUMOCYSTIS CARINII PNEUMONIA AND INTRACTABLE DIARRHEA DUE TO CRYPTOSPORIDIUM INFECTION. DESPITE SUBSTITUTION TREATMENT WITH INTRAVENOUS IMMUNOGLOBULIN, THE OVERALL PROGNOSIS IS RATHER POOR, WITH A DEATH RATE OF ABOUT 10% BEFORE ADOLESCENCE. 

In twelve of sixty-three patients, both the serum IgM and the serum IgG concentrations were depressed. Two of these Burkitt s lymphoma children also had low IgA, but in the other 10 children the scrum IgA was normal. There were 5 known deaths in children classified with this type II deficiency. Seven of these children had tumor classification of the grade III type III immunoglobulin deficiency. There were 14 children with Burkitt s lymphoma classified with this type III immunoglobulin deficiency with moderately reduced levels of scrum IgG and normal levels of IgM. One child in the grouji had a moderately elevated IgA,... 

Lam, K. P., R. Kuhn, and K. Rajewsky. 1997. In vivo ablation of surface immunoglobulin on mature B cells by inducible gene targeting results in rapid cell death. Ce//90 1073-1083. 

Whereas idiopathic OM often resolves, spontaneously or after administration of intravenous immunoglobuline or corticosteroids [58], the outcome of paraneoplastic OM is more variable and depends on the tumor response to therapy. Children with paraneoplastic OM frequently respond to chemotherapy, adrenocorticotropic hormone, or immunomodulation [223], The response to immune therapy in adults with paraneoplastic OM is very modest, but prompt tumor therapy, immunomodulation, and depletion of IgG may be of some benefit [62, 224], Without antineoplastic therapy, the prognosis is usually poor, and symptoms often progress, ultimately causing death [62],... 

In addition to cancer, too little apoptosis can also result in diseases such as autoimmune lymphoproliferative syndrome (ALPS). This occurs when there is insufficient apoptosis of auto-aggressive T cells, resulting in multiple autoimmune diseases. An overproliferation of B cells occurs as well, resulting in excess immunoglobulin production, leading to autoimmunity. Some of the common diseases of ALPS include hemolytic anemia, immune-mediated thrombocytopenia, and autoimmune neutropenia. The different types of this condition are caused by different mutations. Type 1A results from a mutation in the death domain of the Fas receptor, Type IB results from a mutation in Fas ligand, and Type 2 results from a mutation in caspase 10, reducing its activity. 

Haemorrhagic lesions are characteristic of experimental thiamine deficiency and WE in humans indicative of a breakdown of the blood-brain barrier (BBB). A study using immunoglobulin G (IgG) as an indicator of BBB integrity in thiamine-deficient rats revealed increased IgG immunoreactivity in the inferior colliculus and inferior olive prior to the onset of cell death in these regions (Calingasan et al.,... 

Liver injury is immune mediated with cytolytic T cells maintaining the primary role in cell destruction. Death of hepatocytes results in viral elimination and eventual resolution of the clinical illness. Viremia begins soon after infection and continues throughout the time liver enzymes are elevated. The host antibody response to HAV initially appears as the viral particles begin to disappear from stool. Like most host antibody responses, antibodies of the IgM class appear first and imply recent infection. IgM anti-HAV usually is detectable 5 to 10 days before symptoms appear. After 2 to 6 months, the IgM antibodies are replaced with IgG antibodies, which usually persist throughout life and confer immunity to HAV. Patients who receive immunoglobulin will have low titers of anti-HAV for several weeks after inoculation. Patients who receive hepatitis A vaccine will also have anti-HAV. ... 

Infection is the primary cause of death in patients with chronic GVHD, and antimicrobial prophylaxis is an important component of the care of patients being treated for chronic GVHD. Patients should receive oral trimethoprim-sulfamethoxazole, penicillin, and acyclovir to prevent those infections commonly seen in immunocompromised patients. Some centers will also administer intravenous immunoglobulin to patients with low serum immunoglobulin G levels. 

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