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Journal articles on the topic 'Immunodeficiency disease'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Burton, Janet, Elyse Murphy, and Patty Riley. "Primary Immunodeficiency Disease." Professional Case Management 15, no. 1 (January 2010): 5–14. http://dx.doi.org/10.1097/ncm.0b013e3181b5dec4.

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2

&NA;. "Primary Immunodeficiency Disease." Professional Case Management 15, no. 1 (January 2010): 15–16. http://dx.doi.org/10.1097/ncm.0b013e3181d06874.

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3

Dinakar, Chitra. "Alleviating disease burden in primary immunodeficiency diseases." Annals of Allergy, Asthma & Immunology 96, no. 2 (February 2006): 260–62. http://dx.doi.org/10.1016/s1081-1206(10)61234-3.

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4

Iritani, Brian M. "Metabolism meets immunodeficiency disease." Blood 137, no. 4 (January 28, 2021): 436–37. http://dx.doi.org/10.1182/blood.2020008875.

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5

Yamamoto-Furusho, Jesus K. "Crohn’s disease: Innate immunodeficiency?" World Journal of Gastroenterology 12, no. 42 (2006): 6751. http://dx.doi.org/10.3748/wjg.v12.i42.6751.

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6

Jones, Kimmith M. "Human Immunodeficiency Virus Disease." Critical Care Nursing Clinics of North America 11, no. 4 (December 1999): 455–64. http://dx.doi.org/10.1016/s0899-5885(18)30137-0.

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7

Shiraki, Mayuka, Saori Kadowaki, Tomonori Kadowaki, Norio Kawamoto, and Hidenori Ohnishi. "Primary Immunodeficiency Disease Mimicking Pediatric Bechet’s Disease." Children 8, no. 2 (January 22, 2021): 75. http://dx.doi.org/10.3390/children8020075.

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Behcet’s disease (BD) is a chronic inflammatory disease with multisystemic involvement. Its etiology is considered to involve complex environmental and genetic factors. Several susceptibility genes for BD, such as human leukocyte antigen (HLA)-A26, IL23R-IL12RB2, IL10 and ERAP1, in addition to the well-studied HLA-B51, were mainly identified by genome-wide association studies. A heterozygous mutation in TNFAIP3, which leads to A20 haploinsufficiency, was found to cause an early-onset autoinflammatory disease resembling BD in 2016. Several monogenic diseases associated with primary immunodeficiency disease and trisomy 8 have recently been reported to display BD-like phenotypes. Among the genes causing these diseases, TNFAIP3, NEMO, RELA, NFKB1 and TNFRSF1A are involved in the NF-κB (nuclear factor κ light-chain enhancer of activated B cells) signaling pathway, indicating that this pathway plays an important role in the pathogenesis of BD. Because appropriate treatment may vary depending on the disease, analyzing the genetic background of patients with such diseases is expected to help elucidate the etiology of pediatric BD and assist with its treatment. Here, we summarize recently emerging knowledge about genetic predisposition to BD.
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8

Sleasman, J. W. "The Association Between Immunodeficiency and the Development of Autoimmune Disease." Advances in Dental Research 10, no. 1 (April 1996): 57–61. http://dx.doi.org/10.1177/08959374960100011101.

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There is a paradoxical relationship between immunodeficiency diseases and autoimmunity. While not all individuals with immunodeficiency develop autoimmunity, nor are all individuals with autoimmunity immunodeficient, defects within certain components of the immune system carry a high risk for the development of autoimmune disease. Inherited deficiencies of the complement system have a high incidence of systemic lupus erythematosus (SLE), glomerulonephritis, and vasculitis. Carrier mothers of children with chronic granulomatous disease, an X-linked defect of phagocytosis, often develop discoid lupus. Several antibody deficiencies are associated with autoimmune disease. Autoimmune cytopenias are commonly observed in individuals with selective IgA deficiency and common variable immune deficiency. Polyarticular arthritis can be seen in children with X-linked agammaglobulinemia. Combined cellular and antibody deficiencies, such as Wiskott-Aldrich syndrome, carry an increased risk for juvenile rheumatoid arthritis and autoimmune hemolytic anemia. Several hypothetical mechanisms have been proposed to explain the associations between autoimmunity and immunodeficiency. Immunologic defects may result in a failure to exclude microbial antigens, resulting in chronic immunologic activation and autoimmune symptoms. There may be shared genetic factors, such as common HLA alleles, which predispose an individual to both autoimmunity and immunodeficiency. Defects within one component of the immune system may alter the way a pathogen induces an immune response and lead to an inflammatory response directed at self-antigens. An understanding of the immunologic defects that contribute to the development of autoimmunity will provide an insight into the pathogenesis of the autoimmune process.
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9

McShane, Pamela J. "Common Variable Immunodeficiency and Other Immunodeficiency Syndromes in Bronchiectasis." Seminars in Respiratory and Critical Care Medicine 42, no. 04 (July 14, 2021): 525–36. http://dx.doi.org/10.1055/s-0041-1730893.

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AbstractImmunodeficiency represents a vast number of diseases and syndromes. Both primary and secondary forms of immunodeficiency are important contributors to the development of bronchiectasis. Primary immune deficiencies, in particular, are increasingly identified and defined as contributors. Specific immune deficiencies that are closely associated with bronchiectasis and as discussed in this article are common variable immunodeficiency, specific antibody deficiency, immunodeficiencies involving immunoglobulin E, DOCK8 immunodeficiency, phosphoglucomutase 3 deficiency, activated phosphoinositide 3-kinase delta syndrome, and X-linked agammaglobulinemia. Each of these primary immune deficiencies has unique nuances. Vigilance for these unique signs and symptoms is likely to improve recognition of specific immunodeficiency in the idiopathic bronchiectasis patient. Secondary forms of immunodeficiency occur as a result of a separate disease process. Graft versus host disease, malignancy, and human immunodeficiency virus are three classic examples discussed in this article. An awareness of the potential for these disease settings to lead to bronchiectasis is necessary to optimize patient care. With understanding and mindfulness toward the intricate relationship between bronchiectasis and immunodeficiency, there is an opportunity to elucidate pathophysiologic underpinnings between these two syndromes.
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10

Bodemer, W. "Immunodeficiency viruses and prion disease." Primate Biology 2, no. 1 (August 24, 2015): 65–69. http://dx.doi.org/10.5194/pb-2-65-2015.

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Abstract. Two threatening human diseases have emerged during the past 35 years. Human immunodeficiency virus (HIV) was transmitted from non-human primates – e.g., the chimpanzee to humans – and then spread into populations all over the world. To date, around 35 million people are infected and no vaccine is available because the virus undergoes rapid mutation, resulting in a swarm of virus strains. At best, therapeutical intervention is possible with antiviral drugs; however because of its capacity to rapidly mutate, resistant virus strains develop. Since non-human primates (NHPs) carry simian immunodeficiency virus (SIV), we could assess infection and immunity by SIV/HIV in rhesus monkeys (M. mulatta) as a model for acquired immunodeficiency syndrome (AIDS). Transmissible spongiform encephalopathy (TSE) emerged in ruminants in the 1980s and shortly thereafter appeared in humans, leading to variant Creutzfeldt–Jakob disease (vCJD). The vCJD is a terminal neurological disorder since it heavily and irreversibly damages the brain. No cure is at hand. The causative agents for TSE are prions. They are unusual pathogens and enigmatic since they lack nucleic acid as inheritable information. On the other hand, prions were suspected as infectious agents for years and suspected to be the etiological agent of scrapie in sheep. Molecular biology and medicine have clearly identified prions in recent years as the responsible agent for bovine spongiform encephalopathy in ruminants (BSE). BSE has been transmitted to humans, resulting in around 225 vCJD cases. Similar to the SIV/HIV model for Acquired Immunodeficiency Syndrome (AIDS), we could establish a prion infection model in rhesus monkeys. HIV/AIDS and vCJD are zoonoses since their original pathogens can be transmitted from animals to humans. Our experimental efforts to understand these intriguing pathogens and their corresponding diseases in rhesus monkeys as a valid model for both human diseases are summarized in this review.
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11

Hayee, Bu’Hussain, Farooq Z. Rahman, Gavin Sewell, Andrew M. Smith, and Anthony W. Segal. "Crohn’s disease as an immunodeficiency." Expert Review of Clinical Immunology 6, no. 4 (July 2010): 585–96. http://dx.doi.org/10.1586/eci.10.32.

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12

STRAYPEDERSEN, A. "Primary immunodeficiency disease in Norway." Molecular Immunology 35, no. 11-12 (August 1998): 792. http://dx.doi.org/10.1016/s0161-5890(98)90508-9.

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13

Itescu, Silviu. "ADULT IMMUNODEFICIENCY AND RHEUMATIC DISEASE." Rheumatic Disease Clinics of North America 22, no. 1 (February 1996): 53–73. http://dx.doi.org/10.1016/s0889-857x(05)70262-3.

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14

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245. http://dx.doi.org/10.1016/0197-0070(88)90082-4.

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15

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245. http://dx.doi.org/10.1016/0197-0070(88)90083-6.

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16

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245. http://dx.doi.org/10.1016/0197-0070(88)90084-8.

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17

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245. http://dx.doi.org/10.1016/0197-0070(88)90085-x.

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18

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245. http://dx.doi.org/10.1016/0197-0070(88)90086-1.

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19

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 245–46. http://dx.doi.org/10.1016/0197-0070(88)90087-3.

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20

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90088-5.

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21

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90089-7.

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22

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90090-3.

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23

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90091-5.

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24

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90092-7.

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25

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90093-9.

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26

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246. http://dx.doi.org/10.1016/0197-0070(88)90094-0.

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27

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 246–47. http://dx.doi.org/10.1016/0197-0070(88)90095-2.

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28

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90096-4.

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29

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90097-6.

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30

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90098-8.

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31

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90099-x.

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32

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90100-3.

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33

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90101-5.

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34

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247. http://dx.doi.org/10.1016/0197-0070(88)90102-7.

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35

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 247–48. http://dx.doi.org/10.1016/0197-0070(88)90103-9.

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36

Brookman, Richard R. "Infectious disease: Acquired immunodeficiency syndrome." Journal of Adolescent Health Care 9, no. 3 (May 1988): 248. http://dx.doi.org/10.1016/0197-0070(88)90107-6.

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37

Dvorak, Christopher C., and Morton J. Cowan. "Radiosensitive Severe Combined Immunodeficiency Disease." Immunology and Allergy Clinics of North America 30, no. 1 (February 2010): 125–42. http://dx.doi.org/10.1016/j.iac.2009.10.004.

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38

Zent, Clive S. "CLL: an acquired immunodeficiency disease." Blood 128, no. 15 (October 13, 2016): 1908–9. http://dx.doi.org/10.1182/blood-2016-08-734475.

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39

Saifi, Maryam, and Christian A. Wysocki. "Autoimmune Disease in Primary Immunodeficiency." Immunology and Allergy Clinics of North America 35, no. 4 (November 2015): 731–52. http://dx.doi.org/10.1016/j.iac.2015.07.007.

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40

Hassan, S. N., and F. C. Schmalstieg. "Sarcoid, infectious disease, or immunodeficiency?" Journal of Allergy and Clinical Immunology 115, no. 2 (February 2005): S85. http://dx.doi.org/10.1016/j.jaci.2004.12.352.

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41

Broides, Arnon, Ronit Gavrieli, Jacov Levy, Rachel Levy, Nurit Hadad, Dirk Roos, Baruch Wolach, and Amit Nahum. "Chronic granulomatous disease due to different mutations in patients from the same consanguineous extended family." LymphoSign Journal 5, no. 2 (June 1, 2018): 57–60. http://dx.doi.org/10.14785/lymphosign-2018-0004.

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Chronic granulomatous disease is a primary immunodeficiency disease caused by a genetic mutation in any of the 5 genes encoding the different components of the Nicotinamide Adenine Dinucleotide Phosphate reduced (NADPH)-Oxidase enzyme complex. Since primary immunodeficiency diseases are considered to be rare diseases, the genetic diagnosis of a certain primary immunodeficiency leads to the reasonable assumption that all patients with the same disease within the same family will have the same genetic mutation. We report 2 patients with chronic granulomatous disease from the same extended consanguineous family who had different genetic causes of their disease. Therefore, it is crucial to obtain a definitive genetic diagnosis of primary immunodeficiency disease even in patients from the same family, where the same genetic diagnosis is presumed to be the cause of the disease. Statement of novelty: Genetic causes of chronic granulomatous disease may be different in patients from the same family.
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42

Geffner, Mitchell E. "Probable Autoimmune Thyroid Disease and Combined Immunodeficiency Disease." Archives of Pediatrics & Adolescent Medicine 140, no. 11 (November 1, 1986): 1194. http://dx.doi.org/10.1001/archpedi.1986.02140250120047.

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43

Drljevic-Todic, Vanja, Andrej Preveden, Daniela Maric, Vanja Andric, Bozidar Dejanovic, and Aleksandra Vulin. "Prediction of cardiovascular risk among male patients infected with human immunodeficiency virus in Vojvodina, Serbia: A single centre study." Medical review 72, no. 9-10 (2019): 286–90. http://dx.doi.org/10.2298/mpns1910286d.

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Introduction. Human immunodeficiency virus infection is a disease of the modern era and it is estimated that there are more than 30 million infected individuals worldwide. Although the major cause is still unclear, patients infected with human immunodeficiency virus are at higher risk of ardiovascular diseases by 61% compared to general population. Material and Methods. This study included 111 male patients infected with human immunodeficiency virus treated at the Clinic of Infectious Diseases, Novi Sad, Serbia from January 2008 to December 2018. Five cardiovascular risk scores were used: Data Collection on Adverse Events of Antihuman immunodeficiency virus Drugs, Framingham 10-year Heart Score, Framingham 5-year Heart Score, prediction algorithm for cardiovascular disease and atherosclerotic cardiovascular disease risk estimator, at the beginning of the treatment, whereas cardiovascular events were recorded during the following 10 years. Results. Data Collection on Adverse Events of Anti-human immunodeficiency virus Drugs, Framingham 10-year Heart Score, Framingham 5-year Heart Score, and prediction algorithm for cardiovascular disease are tools that can identify individuals infected with human immunodeficiency virus at cardiovascular risk with statistical significance. The prediction algorithm for cardiovascular disease provides superior risk estimation compared to other scores. The atherosclerotic cardiovascular disease risk estimator did not show to be a marker of cardiovascular risk prediction among this population of patients. Conlusion. The above mentioned cardiovascular risk prediction algorithms, developed for general population, and Data Collection on Adverse Events of Anti-human immunodeficiency virus Drugs score, specific for population infected with human immunodeficiency virus, allow accurate cardiovascular risk estimation. Until the development of more specific algorithms, these scores are adequate tools for identification of patients at risk, providing prevention measures and treatment of cardiovascular disease.
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44

Hunter, Paul R., and Gordon Nichols. "Epidemiology and Clinical Features of Cryptosporidium Infection in Immunocompromised Patients." Clinical Microbiology Reviews 15, no. 1 (January 2002): 145–54. http://dx.doi.org/10.1128/cmr.15.1.145-154.2002.

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SUMMARY Cryptosporidium spp. are a major cause of diarrheal disease in both immunocompetent and immunodeficient individuals. They also cause waterborne disease in both the United States and United Kingdom. Studies on the mechanisms of immunity to cryptosporidiosis indicate the importance of the T-cell response. The spectrum and severity of disease in immunocompromised individuals with cryptosporidiosis reflect this importance since the most severe disease is seen in individuals with defects in the T-cell response. The most commonly studied group is that of patients with AIDS. These patients suffer from more severe and prolonged gastrointestinal disease that can be fatal; in addition, body systems other than the gastrointestinal tract may be affected. The widespread use of antiretroviral therapy does appear to be having a beneficial effect on recovery from cryptosporidiosis and on the frequency of infection in human immunodeficiency virus-positive patients. Other diseases that are associated with increased risk of severe cryptosporidiosis, such as primary immunodeficiencies, most notably severe combined immunodeficiency syndrome, are also predominantly associated with T-cell defects. Of the remaining groups, children with acute leukemia seem to be most at risk from cryptosporidiosis. There is less evidence of severe complications in patients with other malignant diseases or in those receiving immunosuppressive chemotherapy.
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45

Hampson, F. A., A. Chandra, N. J. Screaton, A. Condliffe, D. S. Kumararatne, A. R. Exley, and J. L. Babar. "Respiratory disease in common variable immunodeficiency and other primary immunodeficiency disorders." Clinical Radiology 67, no. 6 (June 2012): 587–95. http://dx.doi.org/10.1016/j.crad.2011.10.028.

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46

Illoh, Orieji C. "Current Applications of Flow Cytometry in the Diagnosis of Primary Immunodeficiency Diseases." Archives of Pathology & Laboratory Medicine 128, no. 1 (January 1, 2004): 23–31. http://dx.doi.org/10.5858/2004-128-23-caofci.

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Abstract Context.—To review the applications of flow cytometry in the diagnosis and management of primary immunodeficiency disease. Data Sources.—Articles describing the use of flow cytometry in the diagnosis of several primary immunodeficiency diseases were obtained through the National Library of Medicine database. Study Selection.—Publications that described novel and known applications of flow cytometry in primary immunodeficiency disease were selected. Review articles were included. Articles describing the different immunodeficiency diseases and methods of diagnosis were also selected. Data Extraction.—Approximately 100 data sources were analyzed, and those with the most relevant information were selected. Data Synthesis.—The diagnosis of many primary immunodeficiency diseases requires the use of several laboratory tests. Flow cytometry has become an important part of the workup of individuals suspected to have such a disorder. Knowledge of the pathogenesis of many of these diseases continues to increase, hence we acquire a better understanding of the laboratory tests that may be helpful in diagnosis. Conclusions.—Flow cytometry is applicable in the initial workup and subsequent management of several primary immunodeficiency diseases. As our understanding of the pathogenesis and management of these diseases increases, the use of many of these assays may become routine in hospitals.
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47

Silk, Howard J. "Immunodeficiency Syndromes and Reactive Airway Disease." Journal of Asthma 31, no. 4 (January 1994): 231–41. http://dx.doi.org/10.3109/02770909409089471.

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48

Mechanic, Laura J. "Granulomatous Disease in Common Variable Immunodeficiency." Annals of Internal Medicine 127, no. 8_Part_1 (October 15, 1997): 613. http://dx.doi.org/10.7326/0003-4819-127-8_part_1-199710150-00005.

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49

Viallard, Jean-Francois. "Granulomatous Disease in Common Variable Immunodeficiency." Annals of Internal Medicine 128, no. 9 (May 1, 1998): 781. http://dx.doi.org/10.7326/0003-4819-128-9-199805010-00026.

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50

Zauber, N. Peter. "Granulomatous Disease in Common Variable Immunodeficiency." Annals of Internal Medicine 128, no. 9 (May 1, 1998): 782. http://dx.doi.org/10.7326/0003-4819-128-9-199805010-00027.

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