An immunologic deficiency state characterized by selective deficiencies of one or more, but not all, classes of immunoglobulins.
An acquired disease of unknown etiology, chronic course, and tendency to recur. It is characterized by inflammation and degeneration of cartilage and can result in deformities such as floppy ear and saddle nose. Loss of cartilage in the respiratory tract can lead to respiratory obstruction.
Cartilage of the EAR AURICLE and the EXTERNAL EAR CANAL.
Distortion or disfigurement of the ear caused by disease or injury after birth.
A congenital or acquired condition of underdeveloped or degeneration of CARTILAGE in the TRACHEA and the BRONCHI. This results in a floppy non-rigid airway making patency difficult to maintain.
The essential part of the hearing organ consists of two labyrinthine compartments: the bony labyrinthine and the membranous labyrinth. The bony labyrinth is a complex of three interconnecting cavities or spaces (COCHLEA; VESTIBULAR LABYRINTH; and SEMICIRCULAR CANALS) in the TEMPORAL BONE. Within the bony labyrinth lies the membranous labyrinth which is a complex of sacs and tubules (COCHLEAR DUCT; SACCULE AND UTRICLE; and SEMICIRCULAR DUCTS) forming a continuous space enclosed by EPITHELIUM and connective tissue. These spaces are filled with LABYRINTHINE FLUIDS of various compositions.
Condition characterized by large, rapidly extending, erythematous, tender plaques on the upper body usually accompanied by fever and dermal infiltration of neutrophilic leukocytes. It occurs mostly in middle-aged women, is often preceded by an upper respiratory infection, and clinically resembles ERYTHEMA MULTIFORME. Sweet syndrome is associated with LEUKEMIA.

Epstein-Barr virus-negative boys with non-Hodgkin lymphoma are mutated in the SH2D1A gene, as are patients with X-linked lymphoproliferative disease (XLP). (1/136)

X-linked lymphoproliferative disease (XLP) is a primary immunodeficiency, which most often manifests itself after Epstein-Barr virus (EBV) infection. The main clinical phenotypes include fulminant or fatal infectious mononucleosis, dysgammaglobulinaemia and malignant lymphoma. We have recently cloned the SH2D1A gene, which has been shown to be mutated in approximately 70% of XLP patients. Now we report five novel SH2D1A mutations in patients from five unrelated XLP families. No mutations were found in another three XLP families. In three boys with early onset non-Hodgkin lymphoma (NHL) from two unrelated families a deletion of SH2D1A exon 1 and a splice site mutation were found, respectively. These patients did not show any laboratory or clinical signs of a previous EBV infection. A fourth EBV-uninfected and unrelated boy with a stop mutation in the SH2D1A gene shows only signs of dysgammaglobulinaemia. Development of dysgamma-globulinaemia and lymphoma without evidence of prior EBV infection in four of our patients suggests that EBV is unrelated to these phenotypes, in contrast to fulminant or fatal infectious mononucleosis. The role of SH2D1A as a putative tumour suppressor gene remains to be investigated.  (+info)

Rosette formation with mouse erythrocytes. III. Studies in patients with primary immunodeficiency and lymphoproliferative disorders. (2/136)

Rosette formation with mouse erythrocytes and other cell-surface markers were examined on lymphocytes from patients with a variety of primary immunodeficiency and lymphoproliferative disorders. Mouse erythrocyte rosette-forming cells and lymphocytes with surface immunoglobulins were regularly absent in patients with Bruton type agammaglobulinaemia, immunodeficiency and thymoma syndrome and severe combined immunodeficiency disease. However, they were present in normal or low numbers in patients with common variable immunodeficiency, selective IgA deficiency and ataxis telangiectasia. Lymphocytes from patients with acute lymphoblastic leukaemia Sezary syndrome and mycosis fungoides made no or few rosettes with mouse erythrocytes. Increased numbers of mouse erythrocyte rosette-forming cells were present in patients with chronic lymphocytic leukaemia and Waldenstrom's macroglobulinaemia. The significance of the mouse erythrocyte rosette as a B-cell marker in the analysis of primary immunodeficiency and lymphoproliferative disorders is discussed.  (+info)

Immunogenetics: changing the face of immunodeficiency. (3/136)

Tables 1 and 2 highlight the enormous advances that have been made in the definition of the molecular defects underlying primary immunodeficiencies in the past decade. The identification of SAP as the gene defective in XLP now completes the molecular bases of all the recognised X linked syndromes. Of the autosomally inherited syndromes, only the genes for DiGeorge syndrome, hyper-IgE, and perhaps most importantly, common variable immunodeficiency remain to be elucidated. The major clinical benefits of this information have primarily been in offering more accurate and rapid molecular diagnoses. The ability to make a molecular diagnosis also increases the options for earlier definitive treatments such as bone marrow transplantation and somatic gene therapy. Finally, as illustrated by the studies on the functions of WASP and the gamma c/JAK-3 pathway, identification of the gene defect is the first step to understanding the molecular pathogenesis of the immunological abnormalities.  (+info)

Decreased vaginal disease in J-chain-deficient mice following herpes simplex type 2 genital infection. (4/136)

J-chain-deficient (Jch(-/-)) mice were used to study the role of polymeric IgA (pIgA) in primary disease and protective immunity following genital herpes simplex type 2 (HSV-2) infection. Vaginal IgA in the Jch(-/-) mice was composed primarily of monomeric IgA and was not associated with secretory component (SC). In contrast, vaginal IgA in wild-type (WT) mice was predominantly polymeric and bound to SC. Following HSV-2 genital infection, the Jch(-/-) mice consistently exhibited fewer vaginal symptoms (P = 0.010) and mortality (P = 0.075) than did the WT mice. The variation in disease expression could not be explained by differences in local viral replication, since titers in vaginal wash fluid were comparable. To assess the effect of J chain deficiency on protective immunity, WT and Jch(-/-) mice were immunized intravaginally with attenuated HSV-2, challenged intravaginally with wild-type virus 5 weeks later, and evaluated for vaginal infection and neurological disease. Although the Jch(-/-) mice had reduced vaginal HSV-specific IgA and IgG levels following immunization, both WT and Jch(-/-) mice were protected from symptoms following wild-type virus challenge. We conclude that pIgA is not required for protective immunity against genital HSV-2 disease and that J chain deficiency offers some protection against symptoms following primary HSV-2 genital infection.  (+info)

Cellular aspects of selective IgA deficiency. (5/136)

Five patients with no detectable serum IgA (less than 20 mug/ml) and one patient with low serum IgA were compared to normal subjects. The number of circulating E-RFC was normal as was the lymphocyte DNA synthesis induced by PHA, Con A, and streptokinase-streptodornase. The patients had normal numbers of IgA-bearing lymphocytes and normal or increased numbers of B cells. Purified anti-immunoglobulin antibodies specific for IgG, IgA and IgM induced a normal lymphocyte DNA synthesis as did PWM. The patients' lymphocytes were able in vitro to transform into actively secreting IgA plasmocytes. This transformation was determined by counting the IgA and immunoglobulin-containing cells and then measuring the IgA and IgG secretion in the cultures. In some patients PWM was selectively suppressive in IgA B-cell transformation into IgA secreting cells; in the other patients PWM had no effect on the IgA B-cell differentiation. PWM enhanced the IgG secretion in the patients' cultures as well as IgA and IgG secretion in the normal controls.  (+info)

Severe combined immunodeficiency with B lymphocytes: in vitro correction of defective immunoglobulin production by addition of normal T lymphocytes. (6/136)

A 6 1/2-month-old male with severe combined immunodeficiency (SCID) had a low percentage and number of T cells (11%; 241/mm3) and a high percentage and number of B cells (52%; 1187/mm3) and null cells (37%; 868/mm3). In vitro studies were performed to determine if this child's primary defect involved differentiation of both T and B lymphocytes or if failure of B lymphocytes to differentiate into immunoglobulin producing cells was secondary to T lymphocyte abnormalities. Immunoglobulin production by lymphocytes in response to polyclonal mitogens (pokeweed mitogen and foetal calf serum) was measured by pulse-labelling cells with 3H-leucine and then precipitating cytoplasmic and secreted immunoglobulins with polyvalent anti-human immunoglobulin and S. aureus (Cowan strain I) protein A. The patient's lymphocytes did not synthesize immunoglobulins in vitro in response to mitogens. They did not suppress synthesis of immunoglobulins by normal lymphocytes. However, addition of normal purified T cells, which themselves did not synthesize immunoglobulins, enabled the patient's B lymphocytes to become immunoglobulin synthesizing and secreting cells. Gamma, mu, and light chains were secreted. This suggests that the primary abnormality was in the T-cell axis at the level of lymphoid stem cells or prothymocytes and that failure of B lymphocytes to become immunoglobulin-producing cells was secondary to this defect.  (+info)

A paraprotein in severe combined immunodefeciency disease detected by immunoelectrophoretic analysis of plasma. (7/136)

A qualitative study was made of the plasma immunoglobulins of a child with severe combined immunodeficiency. By immunoelectrophoresis an immunoglobulin with an abnormal electrophoretic mobility was detected. This protein possessed mu heavy chain determinants, gave no detectable reaction with antisera specific for light chains, was of a relatively small molecular size, and was probably not composed of subunits held together by easily reduced disulfide bonds. The light chains that were present in this patient's plasma had a homogeneous electrophoretic mobility. The patient's plasma also contained at least two other immunoglobulins whose antigenic identity could not be established. One of these was abnormal in its electrophoretic mobility. The presence of the abnormal protein with mu determinants in the plasma of the second unrelated child with a similar disease suggests that the detection of this protein may have implications for the diagnosis or classification of immunodeficiency diseases.  (+info)

X-linked hyper IgM syndrome: a report of the first case in Thailand with a confirmed mutation of CD40 ligand gene. (8/136)

X-linked hyper IgM (XHIM) syndrome is a rare congenital immunodeficiency disease caused by failure of B cell to isotype switch from IgM to other classes of immunoglobulins in response to infections. Recently, a molecular cloning of the gene responsible for the syndrome, the CD40L gene has been accomplished and the gene was successfully mapped to the long arm of X chromosome at the position Xq26. We, herein, report the first case of molecular proven XHIM in a Thai boy with a classic presentation and with a confirmed mutation of the CD40L gene. CASE REPORT: A.S. was a 1 year 7 month old boy referred from Buriram Provincial Hospital for a work up and treatment for his recurrent infections consisted of chronic respiratory tract infections with otitis media (since 6 months of age), chronic diarrhea (since 9 months of age) and malnutrition (marasmus) secondary to his longstanding illnesses. He was a product of a consanguineous marriage but without history of similar illness observed in his pedigree. Abnormal laboratory works up included IgG of 300 mg/dl, IgA 10 mg/dl, IgM 1,635 mg/dl, positive stool examinations for Cryptosporidium, chronic colitis on radiographic gastrointestinal follow through study, a positive acid fast bacillus (AFB) stain of gastric aspirate and multiple positive bacterial cultures from various body sources. His anti-HIV serology was negative. His hospital course was significant for several bouts of infections of gastrointestinal, respiratory, and genitourinary systems. His treatment consisted of multiple courses of antibiotics, antituberculous drugs and IVIG administrations. His hospital course was complicated with feeding problem from an esophageal stricture requiring several esophageal dilatations. The analysis of CD40L gene revealed a point mutation of exon 5 (A619T) of the CD40L gene resulting in a stop codon confirming that indeed he had XHIM. He died with Pseudomonas septicemia during the waiting period for a bone marrow transplantation from a cord-blood stem cell.  (+info)

Dysgammaglobulinemia is a medical term that refers to an abnormal gamma globulin or immunoglobulin (antibody) level in the blood. Gamma globulins are proteins that play a crucial role in the immune system and help fight off infections. Immunoglobulins are classified into five types (IgA, IgD, IgE, IgG, and IgM), each with a specific function in the immune response.

In dysgammaglobulinemia, there is an imbalance in the levels of these immunoglobulins, which can be either elevated or decreased. This condition can result from various underlying causes, including genetic disorders, autoimmune diseases, infections, and malignancies that affect the bone marrow or lymphatic system.

Depending on the specific pattern of immunoglobulin levels, dysgammaglobulinemia can be further classified into different types, such as:

1. Hypogammaglobulinemia - a decrease in one or more classes of immunoglobulins
2. Agammaglobulinemia - a severe deficiency or absence of all classes of immunoglobulins
3. Hypergammaglobulinemia - an elevation of one or more classes of immunoglobulins

Dysgammaglobulinemia can lead to increased susceptibility to infections, autoimmune disorders, and other health complications. Therefore, it is essential to identify the underlying cause and provide appropriate treatment to manage the condition and prevent further complications.

Relapsing polychondritis is a rare autoimmune disease characterized by inflammation and damage to the cartilaginous structures in the body. The condition can affect multiple organs and tissues, including the ears, nose, trachea, bronchi, joints, and cardiovascular system. It is called "relapsing" because it tends to involve recurring episodes of inflammation and damage, followed by periods of remission.

The hallmark symptom of relapsing polychondritis is pain and swelling in the ears, nose, or airways. Other symptoms may include:

* Redness, tenderness, and warmth in affected areas
* Hearing loss or tinnitus (ringing in the ears)
* Nasal congestion, runny nose, or nosebleeds
* Hoarseness or difficulty speaking
* Wheezing, shortness of breath, or coughing
* Joint pain, stiffness, or swelling
* Skin rashes or sores
* Eye inflammation or dryness
* Heart murmurs or other cardiovascular symptoms

The exact cause of relapsing polychondritis is not known, but it is thought to involve an abnormal immune response in which the body's own antibodies attack and damage cartilage and other tissues. The diagnosis of relapsing polychondritis is typically based on a combination of clinical symptoms, laboratory tests, and imaging studies.

There is no cure for relapsing polychondritis, but treatment can help manage the symptoms and prevent complications. Treatment may include corticosteroids, immunosuppressive drugs, and other medications to reduce inflammation and suppress the immune system. In severe cases, surgery may be necessary to repair or replace damaged tissues.

Ear cartilage, also known as auricular cartilage, refers to the flexible connective tissue that makes up the structural framework of the external ear or pinna. The ear cartilage provides support and shape to the ear, helping to direct sound waves into the ear canal and towards the eardrum.

The ear cartilage is composed of type II collagen fibers and proteoglycans, which give it its flexibility and resiliency. It is covered by a thin layer of skin on both sides and contains no bones. Instead, the ear cartilage is shaped and maintained by the surrounding muscles and connective tissue.

There are three main parts of the ear cartilage: the helix, the antihelix, and the tragus. The helix is the outer rim of the ear, while the antihelix is the curved ridge that runs parallel to the helix. The tragus is the small piece of cartilage that projects from the front of the ear canal.

Ear cartilage can be affected by various conditions, including trauma, infection, and degenerative changes associated with aging. In some cases, surgical procedures may be required to reshape or reconstruct damaged ear cartilage.

Acquired ear deformities refer to abnormal shapes or structures of the ear that result from injury, infection, inflammation, or other external factors after birth. These deformities can affect the appearance and function of the ear, causing symptoms such as hearing loss or discomfort. Examples of acquired ear deformities include:

1. Cauliflower ear: a condition characterized by swelling, thickening, and distortion of the ear caused by repeated trauma or injury to the ear cartilage.
2. Microtia: a congenital ear abnormality that can become worse over time due to infection, inflammation, or trauma, resulting in an underdeveloped or absent ear.
3. Macrotia: an abnormally large ear that may result from injury or other external factors.
4. Stenosis: a narrowing of the ear canal that can result from chronic inflammation, infection, or scarring.
5. Hematoma: a collection of blood in the ear tissue caused by trauma or injury, which can lead to deformity if not treated promptly.
6. Keloids: overgrowths of scar tissue that can form after injury or surgery and distort the shape of the ear.

Treatment for acquired ear deformities may include surgical reconstruction, splinting, or other interventions depending on the severity and underlying cause of the condition.

Tracheobronchomalacia is a medical condition that refers to the abnormal softening and weakness of the tracheal and bronchial walls, leading to their collapse or narrowing during breathing, particularly during expiration. This collapse can cause symptoms such as wheezing, shortness of breath, coughing, and recurrent respiratory infections. The condition can be congenital or acquired, with common causes including aging, chronic obstructive pulmonary disease (COPD), and long-term intubation. In severe cases, tracheobronchomalacia may require surgical intervention to stabilize the airway and improve breathing.

The inner ear is the innermost part of the ear that contains the sensory organs for hearing and balance. It consists of a complex system of fluid-filled tubes and sacs called the vestibular system, which is responsible for maintaining balance and spatial orientation, and the cochlea, a spiral-shaped organ that converts sound vibrations into electrical signals that are sent to the brain.

The inner ear is located deep within the temporal bone of the skull and is protected by a bony labyrinth. The vestibular system includes the semicircular canals, which detect rotational movements of the head, and the otolith organs (the saccule and utricle), which detect linear acceleration and gravity.

Damage to the inner ear can result in hearing loss, tinnitus (ringing in the ears), vertigo (a spinning sensation), and balance problems.

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, is a skin condition characterized by the rapid onset of painful, red, and swollen skin lesions. The lesions are often accompanied by fever and elevated white blood cell count, particularly an increase in neutrophils.

The medical definition of Sweet syndrome includes the following criteria:

1. Abrupt onset of painful, erythematous (red), and edematous (swollen) papules, plaques, or nodules.
2. Fever greater than 38°C (100.4°F).
3. Leukocytosis with a predominance of neutrophils in the peripheral blood.
4. Histopathological evidence of a dense dermal infiltrate of neutrophils without evidence of vasculitis.
5. Rapid response to systemic corticosteroids.

Sweet syndrome can be associated with various medical conditions, such as infections, malignancies, and inflammatory diseases, or it can occur without an identifiable underlying cause (idiopathic).

Immunodeficiency "Dysgammaglobulinemia" at Dorland's Medical Dictionary Dysgammaglobulinemia at eMedicine Dictionary " ... Dysgammaglobulinemia is a type of immune disorder characterized by a reduction in some types of gamma globulins, resulting in ... Andre Cruchaud et al.: "The site of synthesis of the 19S T-globulins in dysgammaglobulinemia" (1962). Accessed 2009-07-17. v t ... Hyper IgM syndrome can be considered a form of dysgammaglobulinemia, because it results from a failure of transformation from ...
"Hypogammaglobulinemia" is distinguished from dysgammaglobulinemia, which is a reduction in some types of gamma globulins, but ... "agammaglobulinemia" at Dorland's Medical Dictionary "Dysgammaglobulinemia" at Dorland's Medical Dictionary Rose, Mark E.; Lang ...
Patients may also develop dysgammaglobulinemia and malignant non-Hodgkin lymphoma, even without exposure to EBV. Other observed ...
MeSH considers hyper IgM syndrome to be a form of dysgammaglobulinemia, not a form of hypergammaglobulinemia. X-linked ...
Laboratory studies showed increased levels of IgM, low levels of IgA, equally low levels of IgG, and dysgammaglobulinemia. ...
... is a form of dysgammaglobulinemia where the proportional levels of the IgG isotype are reduced relative to other ...
The ratios of immunoglobulins vary rapidly in all infants, and the term dysgammaglobulinemia, although theoretically applicable ...
... is a poorly defined dysgammaglobulinemia characterized by decreased levels of IgM ...
Faria syndrome Lopez-Hernandez syndrome Lou Gehrig's disease Louis-Bar syndrome Low birth weight dwarfism dysgammaglobulinemia ...
... dysgammaglobulinemia MeSH C15.378.147.333.500 - iga deficiency MeSH C15.378.147.333.750 - igg deficiency MeSH C15.378.147.542 ...
Immunodeficiency "Dysgammaglobulinemia" at Dorlands Medical Dictionary Dysgammaglobulinemia at eMedicine Dictionary " ... Dysgammaglobulinemia is a type of immune disorder characterized by a reduction in some types of gamma globulins, resulting in ... Andre Cruchaud et al.: "The site of synthesis of the 19S T-globulins in dysgammaglobulinemia" (1962). Accessed 2009-07-17. v t ... Hyper IgM syndrome can be considered a form of dysgammaglobulinemia, because it results from a failure of transformation from ...
Children with Tourettes Syndrome May Suffer Immunoglobulin A Dysgammaglobulinemia: Preliminary Report. Postinfectious ...
Dysgammaglobulinemias. Many people with hypogammaglobulinemia or dysgammaglobulinemia receive periodic doses of IVIG, which can ...
Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.
Dysgammaglobulinemia complicated by disseminated measles. Br Med J 1971;2(758):380-1. ...
Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.
Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.
IgA deficiency is one of the most common of all immune defects. While it is often not associated with clinical illness, presumably due to compensation from other sectors of the immune system, IgA-deficient individuals are distinctly more likely to become ill and have one or more of specific groups o …
Dysgammaglobulinemia complicated by disseminated measles. Br Med J 1971;2(758):380-1.. *Committee on Infectious Diseases, ...
Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.
However, persons with impaired humoral immunity (e.g., hypogammaglobulinemia or dysgammaglobulinemia) can receive zoster ... and dysgammaglobulinemia. Combination MMRV vaccine should not be administered as a substitute for the component vaccines when ...
... autosomal recessive X-linked 279.06 Common variable immunodeficiency Dysgammaglobulinemia (acquired) (congenital) (primary) ...
Selective immunoglobulin M immunodeficiency (SIgMD) is a rare form of dysgammaglobulinemia, which is characterized by a ...
... dysgammaglobulinemia; germline mutation; Ikaros; IKZF1; nuclear localization;. ...
O Dysgammaglobulinemia,O Dysgenesis of the basal ganglia,O Dysgenesis of the cerebellar vermis,O Dysgenesis of the hippocampus, ...
Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.
Dysgammaglobulinemia is typically hypogammaglobulinemia of one or more immunoglobulin subclasses. The malignant lymphomas are ... Dysgammaglobulinemia. Lymphoproliferative disease (malignant lymphoma). XLP2 is most often characterized by HLH (often ... associated with EBV), dysgammaglobulinemia, and inflammatory bowel disease. HLH resulting from EBV infection is associated with ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
... dysgammaglobulinemia // ID F87S(2a); standard; MUTATION; SH2 Accession A0106 Systematic name g.62912T>C, c.260T>C, r.260u>c, p. ... dysgammaglobulinemia Comment -!-Coded as T53I in the ref [1] by mistake // ID Y54C(1); standard; MUTATION; SH2 Accession A0059 ... dysgammaglobulinemia // ID L31P(1); standard; MUTATION; SH2 Accession A0051 Description Missense mutation in the exon 1 Date 09 ... dysgammaglobulinemia // ID R55X(9); standard; MUTATION; SH2 Accession A0062 Description Nonsense mutation in the exon 2 Date 09 ...
Immunodeficiency with Hyper-lgM (Dysgammaglobulinemia Type I) Accompanied by Aortic Calcification. Jin, Dong Kyu; Lee, Hoan ...
People with hypogammaglobulinemia or dysgammaglobulinemia may require vaccination with MMR or varicella vaccine. However, many ...
... with congenital rubella syndrome who survive into adulthood may be plagued by autoimmune disorders and dysgammaglobulinemia. ...
Differential diagnosis of endocrine or metabolic disorders causing depression are ...
The ratios of immunoglobulins vary rapidly in all infants, and the term dysgammaglobulinemia, although theoretically applicable ...
Children with Tourettes syndrome may suffer immunoglobulin A dysgammaglobulinemia: preliminary report. Biological psychiatry, ...
", "dysgammaglobulinemia", "agammaglobulinemia", "hypogammaglobulinemia" (the written text phrases allowed for both American ...
Neutropenia can occur in dysgammaglobulinemia and paroxysmal nocturnal hemoglobinuria Paroxysmal Nocturnal Hemoglobinuria (PNH ...
Diseases involving immunoglobulin production, including X-linked agammaglobulinemia, hyper-IgM syndrome, dysgammaglobulinemia ...
  • Immunodeficiency "Dysgammaglobulinemia" at Dorland's Medical Dictionary Dysgammaglobulinemia at eMedicine Dictionary "hypogammaglobulinemia" at Dorland's Medical Dictionary Raif S. Geha et al. (wikipedia.org)
  • Selective immunoglobulin M immunodeficiency (SIgMD) is a rare form of dysgammaglobulinemia, which is characterized by a selective low level of IgM in conjunction with normal T cell numbers and function and no other identifiable immunodeficiency. (psychiatrist.com)
  • Synonyms for immune system insufficiency included "immunologic insufficiency syndromes", "common adjustable immunodeficiency", "dysgammaglobulinemia", "agammaglobulinemia", "hypogammaglobulinemia" (the written text phrases allowed for both American and English spellings). (edrc2013.org)
  • Hyper IgM syndrome can be considered a form of dysgammaglobulinemia, because it results from a failure of transformation from IgM production to production of other antibodies, and so the condition can be interpreted as a reduction of the other types. (wikipedia.org)
  • Dysgammaglobulinemia is typically hypogammaglobulinemia of one or more immunoglobulin subclasses. (nih.gov)
  • Clinical manifestations include hemophagocytic lymphohistiocytosis , lymphoma , and dysgammaglobulinemia . (bvsalud.org)
  • Individuals with dysgammaglobulinemia are prone to recurrent infections. (medlineplus.gov)
  • Rationale: Lymphoid interstitial pneumonia is a rare benign pulmonary lymphoproliferative disorder usually presenting with a subacute or chronic condition and frequently associated with autoimmune disorders, dysgammaglobulinemia, or infections. (univ-reims.fr)
  • Hyper IgM syndrome can be considered a form of dysgammaglobulinemia, because it results from a failure of transformation from IgM production to production of other antibodies, and so the condition can be interpreted as a reduction of the other types. (wikipedia.org)
  • Dysgammaglobulinemia is a type of immune disorder characterized by a reduction in some types of gamma globulins, resulting in heightened susceptibility to some infectious diseases where primary immunity is antibody based. (wikipedia.org)