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Results for “Immunologic Deficiency Syndromes”

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PubMedDate not supplied

Immune deficiency: office evaluation and treatment.

Congenital deficiencies of the immune system occur in children or adults and can cause severe or recurrent infections. The overall incidence of these immunodeficiency diseases is estimated at approximately 1 in 10,000, excluding selective immunoglobulin A deficiency, but this estimation is based on population studies, not hospital or clinic populations. The majority of immune defects involve antibody production; these immune deficiencies are found more often in adults than infants and children. In an allergy practice, recurrent infections are common, and determining if an immune defect is likely to be present can be problematic. Some guidelines concerning the clinical presentation and laboratory evaluation and treatment options can aid the practicing clinician.

Anti-Bacterial Agents↗
PubMed1978

[Immunostaging (author's transl)].

This survey covers the problems of immunologic monitoring of patients and the spectrum of methods of diagnosing various types of immunopathological reactions.

Allergens↗
PubMedDate not supplied

[Immunology laboratory].

Explore the source record for details and available documents.

Academies and Institutes↗
PubMed1991

[Diagnosis of cytomegalovirus infections in hospitalized patients].

Rapid detection of cytomegalovirus (CMV) infections, especially in immunocompromised patients, is important and sometimes lifesaving. We describe one year's experience of using a combination of several methods: detection of "immediate early" CMV antigen in blood, detection of "early" virus antigen after brief incubation in cell culture, detection of viral DNA by polymerase chain reaction, regular culture in human embryo fibroblasts, and serological detection of IgM and IgG antibodies. A quick and early diagnosis was achieved by all three rapid methods. However, none of the methods is sufficiently sensitive or specific to allow it to be used alone. A combination of several methods is recommended in order to achieve maximum efficiency and safety.

Cytomegalovirus Infections↗
PubMed1991

Laboratory screening for the diagnosis of children with primary immunodeficiencies.

To select simple and low-cost laboratory tests that contribute to the diagnosis of primary immunodeficiencies (PID) in children, the medical records of 98 patients with PID were analyzed. White blood cell counts, serum IgG, IgM and IgA determinations, Shick test, isohemagglutinin titers, delayed cutaneous hypersensitivity tests, nitro blue tetrazolium test and hemolytic complement (CH50) determination associated with clinical data led to the diagnosis in 95% of cases. Applying this laboratory screening to patient series studies in other countries, the diagnosis was suggested in at least 92% of the cases. This screening proposal may be used as a guideline in the standardization of complementary tests for the diagnosis of immunodeficiencies in pediatric centers of developing countries and also at the primary medical care level in developed countries.

Clinical Laboratory Techniques↗
PubMed2006

Immunity status in children with Bacille Calmette-Guerin adenitis. A prospective study in Tehran, Iran.

OBJECTIVE: To determine the immunity status of children with Bacille Calmette-Guerin (BCG) lymphadenitis (patient group) and unaffected children (control group) in Iran. METHODS: We performed this longitudinal case-control study on 75 children between 2 months to 14 years old in Rasool Akram and Markaz Tebbi Hospital, Tehran, Iran during the period of 2 years (2000-2002). RESULTS: Ninety percent of patients had normal immunoglobulin, 10% had low level, 96.1% had normal nitro blue tetrazolium test and 3.9% had lower activity. There was a significant difference in the total lymphocyte CD3, CD8, CD19, CD16/CD56 and natural killers (NK) cell but no significant difference in the CD4/CD8 ratio and CD4 between case (n=75) and control (n=100) groups. Thirty-eight cases with mild lymphopenia, isolated CD4, CD3, CD19, NK cells (CD16/CD56) deficiency in 3 (22%); idiopathic disseminated BCG infection (unknown immunodeficiency type) in 3 (22%) patients were observed. Thirty-eight cases were diagnosed as mild immune deficient without any previous recurrent infections (mild lymphopenia; Isolated CD4; CD3 or CD19 deficiency. Natural killers (CD16/CD56) deficiency in 3 (22%); idiopathic disseminated BCG infection (unknown immunodeficiency type) in 3 (22%) patients. The natural killers (CD16/CD56) deficient cases responded well to 3 antimycobacterial drugs without immunomodulator. Natural killers cell deficiency not yet reported as a risk factor for progression and complication of BCG infection. All cases of idiopathic disseminated BCG infection (unknown immunodeficiency type) with nonlethal and indulgent BCG infections responded well to needle aspiration and antimycobacterial drugs with immunomodulator (gamma interferon). CONCLUSION: In cases with multiple and recurrent BCG lymphadenitis without any previous recurrent infection complete immunological studies should be carried out. Most cases with mild immune deficiency usually response well to needle aspiration alone or combine with antimycobacterial drugs. The combination of IFN-gamma and chemotherapy in cases of idiopathic disseminated infections caused by BCG and without previous recurrent other infection except mycobacterium species, can limit the disease.

Adolescent↗
PubMed1991

[Angioedema due to acquired complement-C1-inhibitor deficiency in a female patient with non-Hodgkin lymphoma and autoimmune hemolytic anemia].

A case of angioedema due to acquired deficiency of the regulatory protein C1-esterase-inhibitor (C1-INH) is reported. The edematous attack occurred 3 1/2 weeks after initiation of successful therapy for autoimmune-hemolytic anemia in the course of long-standing non-Hodgkin's lymphoma. At the time of acute edema the complement profile was typical: virtual absence of C1-INH function was associated with diminished concentrations of the components of the classical pathway of complement (C1q, C1r, C1s, C2, C4) and reduced complement hemolytic activity (CH50). Anti-C1-INH-autoantibodies were not detected. The angioedema lasted for about one week, and no further attacks occurred during the five-months follow-up period. Although there was only a minor adjustment to the therapy, the C1q, C2, C4 and CH50 values gradually increased to levels close to the lower limit of the normal range, while C1r and C1s showed normal values. In contrast to most other reports, this case was characterized by angioedema which was precipitated only after initiation of appropriate treatment for the underlying disease rather than before therapy or even diagnosis of the underlying disease.

Aged↗