<?xml version="1.0"?>
<Articles JournalTitle="Iranian Journal of Allergy, Asthma and Immunology">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">TGF-&#x3B2; Codon 25 Polymorphism and the Risk of Graft-Versus-Host Disease after Allogenic Hematopoietic Stem Cell Transplantation</title>
    <FirstPage>1</FirstPage>
    <LastPage>6</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Ali</FirstName>
        <LastName>Rashidi&#x2013;Nezhad</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Cyrus</FirstName>
        <LastName>Azimi</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Kamran</FirstName>
        <LastName>Alimoghaddam</LastName>
        <affiliation locale="en_US">Hematology&#x2013;Oncology and BMT Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ardeshir</FirstName>
        <LastName>Ghavamzadeh</LastName>
        <affiliation locale="en_US">Hematology&#x2013;Oncology and BMT Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Arash</FirstName>
        <LastName>Hossein-Nezhad</LastName>
        <affiliation locale="en_US">Endocrinology and Metabolism Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Pantea</FirstName>
        <LastName>Izadi</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Sobhani</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali-Reza</FirstName>
        <LastName>Noori&#x2013;Daloii</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad&#x2013;Reza</FirstName>
        <LastName>Noori&#x2013;Daloii</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Some of the genotypes of cytokines are associated with acute graft versus host disease after bone marrow transplantation. The purpose of the present investigation was to find out the possible association between transforming growth factor beta-1 (TGF-&#x3B2;1) codon 25 polymorphism (rs:1800471) and acute graft versus host disease (aGVHD) after bone marrow transplantation from the sibling with the similar HLA among the Iranian population. 
In this retrospective case-control investigation, 172 subjects including 86 Iranian patients and their siblings with the similar HLA as donor/recipient pairs were recruited. All of the patients were diagnosed with one group of blood disorder consisting of Acute Myeloid Leukemia (AML)=40, Acute Lymphoblastic Leukemia (ALL)=25 and Chronic Myeloid Leukemia (CML)=21. PCR-SSP method was carried out to ascertain TGF- &#x3B2;1 codon 25 G/C polymorphism genotypes. 
The frequency of TGF- &#x3B2;1 codon 25 GG, GC and CC genotypes among all cases were 77.3%, 21.5% and 1.2%, respectively. Recipients with the GG genotype developed severe aGVHD significantly more than those with CC or GC genotypes (Odds Ratio =12.133, P=0.015). 
Genetic background of TGF-&#x3B2;1 may be involved in aGVHD development and/or severity in the patients who received Bone Marrow Transplantation (BMT) from their siblings with the similar HLA among the Iranian population.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/262</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/262/262</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Adenosine Deaminase Activity in COPD Patients and Healthy Subjects</title>
    <FirstPage>7</FirstPage>
    <LastPage>12</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Mohammad Taghi</FirstName>
        <LastName>Goodarzi</LastName>
        <affiliation locale="en_US">Research Center for Molecular Medicine, Hamadan University of Medical Sciences. Hamadan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Abdi</LastName>
        <affiliation locale="en_US">Department of Pathology and Medical Laboratory Sciences, Faculty of Para Medicine, Kurdistan University of Medical Sciences. Sannandaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Heidar</FirstName>
        <LastName>Tavilani</LastName>
        <affiliation locale="en_US">Department of Biochemistry and Nutrition, Faculty of Medicine, Hamadan University of Medical Sciences. Hamadan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ebrahim</FirstName>
        <LastName>Nadi</LastName>
        <affiliation locale="en_US">Research group of pulmonary disease and tuberculosis, Faculty of Medicine, Hamadan University of Medical Science. Hamadan Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojtaba</FirstName>
        <LastName>Rashidi</LastName>
        <affiliation locale="en_US">Department of Biochemistry and Nutrition, Faculty of Medicine, Hamadan University of Medical Sciences. Hamadan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Chronic obstructive pulmonary disease (COPD) has been defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), as a disease state characterized by airflow limitation which is not fully reversible. COPD consists of emphysema which is the destruction and inflammation of the lung alveoli. Adenosine deaminase (ADA, E.C.3.5.4.4) converts adenosine to inosine. There are two isoenzymes of ADA in serum; ADA1 and ADA2. It has been established that in COPD patients the adenosine levels increase, which can contribute to decrease of ADA activity. In this research we studied the ADA and its isoenzyme activity in COPD patients.
This descriptive analytical case-control study was performed on thirty patients who were hospitalized in the pulmonary wards with an acute exacerbation of COPD. ADA activity was determined in 30 COPD patients, 30 nonsmokers and 30 smokers controls. All subjects were male. We used colorimetric (Giusti) method for measuring of ADA activity. The data were analyzed using SPSS 13 software and Kruskall-Wallis and two-way ANOVA tests.
Total ADA activity in the COPD and smoker control groups was significantly lower than in non smoker group (18.99 &#xB1; 7, 19.03 &#xB1; 9.1 and 22.95 &#xB1; 6.7 U/L, respectively). There was a significant difference for ADA2 between the three groups. Whereas the ADA1 activity in the three groups had no significant difference. 
Based on the obtained data, decrease of ADA activity may play an important role in the formation of pulmonary injury in COPD patients.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/263</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/263/263</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Role of Nitric Oxide in Airway Responsiveness in Diabetic-Antigen Sensitized Guinea Pigs in Vitro</title>
    <FirstPage>13</FirstPage>
    <LastPage>20</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Saeed</FirstName>
        <LastName>Kolahian</LastName>
        <affiliation locale="en_US">Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Goudarz</FirstName>
        <LastName>Sadeghi-Hashjin</LastName>
        <affiliation locale="en_US">Department of Pharmacology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farzad</FirstName>
        <LastName>Asadi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mostafa</FirstName>
        <LastName>Moin</LastName>
        <affiliation locale="en_US">Department of Clinical Immunology and Allergy, Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Clinical asthma and airway responsiveness appear to be less severe when diabetes is superimposed. The aim of the present study was to determine the possible role of Nitric Oxide (NO) in the airway reactivity under diabetic and diabetic-allergic conditions. 
Twenty-five male guinea-pigs were divided into five groups of five each as follows: diabetic, antigen sensitized, diabetic- antigen sensitized, insulin-treated diabetic- antigen ovalbumin sensitized and control animals. Tracheal rings of all groups were mounted in an organ bath system for isometric contraction measurements. Tissues were pre-incubated with either of the following chemicals: L-NAME, L-arginine or methylene blue. Cumulative concentration response curve was made with histamine. 
Decrease in the airway reactivity in diabetic and diabetic- antigen sensitized animals were shown compared to the antigen sensitized animals. pEC50 values of histamine in the presence of L-Arg showed increase in diabetic and diabetic- antigen sensitized animals compared to the controls. In the presence of methylene blue, these values showed an increase in diabetic and diabetic- antigen sensitized animals compared to the controls. However, incubation with L-NAME did not change the airway responsiveness to histamine in diabetic and diabetic- antigen sensitized animals compared to the controls. 
Experimental diabetes causes were found to decrease the responsiveness of tracheal rings in the presence or absence of allergy. 
Findings of this research work showed that NO had no role in hypo-responsiveness of airway in diabetic and diabetic- antigen sensitized animals.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/264</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/264/264</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Rhinitis is also Common in Infants with Asthma</title>
    <FirstPage>21</FirstPage>
    <LastPage>25</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Herberto</FirstName>
        <LastName>Jos&#xE9; Chong Neto</LastName>
        <affiliation locale="en_US">Pediatric Allergy Division, Federal University of Paran&#xE1; Curitiba, Paran&#xE1;, Brazil</affiliation>
      </Author>
      <Author>
        <FirstName>Nelson</FirstName>
        <LastName>Augusto Ros&#xE1;rio</LastName>
        <affiliation locale="en_US">Pediatric Allergy Division, Federal University of Paran&#xE1; Curitiba, Paran&#xE1;, Brazil</affiliation>
      </Author>
      <Author>
        <FirstName>Gabriele</FirstName>
        <LastName>Cardoso Westphal</LastName>
        <affiliation locale="en_US">Pediatric Allergy Division, Federal University of Paran&#xE1; Curitiba, Paran&#xE1;, Brazil</affiliation>
      </Author>
      <Author>
        <FirstName>Carlos</FirstName>
        <LastName>Ant&#xF4;nio Riedi</LastName>
        <affiliation locale="en_US">Pediatric Allergy Division, Federal University of Paran&#xE1; Curitiba, Paran&#xE1;, Brazil</affiliation>
      </Author>
      <Author>
        <FirstName>Hevertton</FirstName>
        <LastName>Luiz Bozzo Silva dos Santos</LastName>
        <affiliation locale="en_US">Pediatric Allergy Division, Federal University of Paran&#xE1; Curitiba, Paran&#xE1;, Brazil</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The aim of this study was to assess the frequency of rhinitis in asthmatic infants.
A cross-sectional study was conducted using clinical data obtained from a standardized allergy work-up form that includes specific questions on common allergic diseases. Asthmatic patients were seen at the first visit to the Pediatric Allergy Unit, from January 2001 to January 2006, were selected for analysis. Diagnosis of allergic rhinitis was based on the presence of two or more nasal symptoms (sneezing, itching, congestion and rhinorrhea). Allergic sensitization was assessed by skin prick test for Dermatophagoides pteronyssinus, Blomia tropicalis, Blattella germanica, Lolium perenne, dog and cat danders.
Four hundred and ninety-three infants (under 2 years of age) were selected from a total of 1543 asthmatics aged 0-14 years, 58% males. Physician diagnosis of rhinitis in infants was registered in 367 (74%) and 131 (36%) had positive skin prick test to at least one allergen. Infants were more frequently sensitized to Dermatophagoides pteronyssinus (43%) and Blomia tropicalis (27%). Among asthmatic children &#x2265;2 years old, 890 (84%) also had rhinitis, 773 (87%) were atopic. Among those children with rhinitis, one hundred and eighty six were fully skin prick tested with a standard panel of common aeroallergens. There was no difference between sensitization in asthmatic infants and older asthmatic children with allergic rhinitis.
Thus the frequency of rhinitis in asthmatic infants as well as atopic sensitization were similar to older children.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/265</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/265/265</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Quercetin Effectively Quells Peanut-Induced Anaphylactic Reactions in the Peanut Sensitized Rats</title>
    <FirstPage>27</FirstPage>
    <LastPage>34</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Farideh</FirstName>
        <LastName>Shishehbor</LastName>
        <affiliation locale="en_US">Department of Nutrition, Faculty of Paramedicine, JondiShapour University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Lotfollah</FirstName>
        <LastName>Behroo</LastName>
        <affiliation locale="en_US">Department of Nutrition, Superintendent of Nutrition and Diet-therapy Unit, Aras Hospital, Ardebil, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehri</FirstName>
        <LastName>Ghafouriyan Broujerdnia</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, JondiShapour University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Forough</FirstName>
        <LastName>Namjoyan</LastName>
        <affiliation locale="en_US">Department of Pharmacology, Faculty of Pharmacy, JondiShapour University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seiyed-Mahmoud</FirstName>
        <LastName>Latifi</LastName>
        <affiliation locale="en_US">Department of Biostatistics, Faculty of Health, Ahvaz JondiShapour University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Peanut allergy is the major leading cause of fatal or life-threatening anaphylactic reactions to foods. At present, there is no remedy for this condition. The applied pharmaceutical cares are merely palliative, while their deleterious side effects have already been established. Hence, many sufferers search for complementary and alternative medicines. A versatile-, "flavonol" subgroup-member of the flavonoid family, quercetin, is of paramount interest to investigators. In this study the effects of quercetin on peanut-induced anaphylactic reactions were investigated in a rat model of peanut allergy. Wistar rats were sensitized with crude peanut extract in the presence of Cholera toxin and Aluminium hydroxide. Sensitized rats were then allotted into three groups; Positive control, Quercetin-treatment and Sham, (n=7, each). Naive rats (n=7) served as negative controls.
One week post-sensitization period, the rats in treatment group were treated with quercetin at a dose of 50 mg/kg(Body Weight)/mL Di-methyl-sulfoxide 5%/rat, over a period of four weeks. Subsequently, rats were challenged, and anaphylactic reaction parameters including variations in plasma histamine levels, vascular permeability, systemic anaphylaxis scores, and total serum Immunoglobulin E levels were measured.
After daily-gavaging for four weeks, quercetin completely abrogated peanut-induced anaphylactic reactions following challenges, so that the mean of plasma histamine levels in the quercetin-treated rats, were lower significantly (p=0.004) as compared with positive control group. Our findings suggest that the flavonoid quercetin is potent enough to suppress the on-going Immunoglobulin E responses against peanut proteins, and can be propounded as an alternative medicine to protect against Immunoglobulin E-mediated food allergies.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/266</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/266/266</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Prevalence, Management and Burden of Asthma-A Nigerian Study</title>
    <FirstPage>35</FirstPage>
    <LastPage>41</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Alexander</FirstName>
        <LastName>O. Oni</LastName>
        <affiliation locale="en_US">Department of Medicine, Niger Delta University/Teaching Hospital, Wilberforce Island, Amassoma, Bayelsa State, Nigeria</affiliation>
      </Author>
      <Author>
        <FirstName>G.E.</FirstName>
        <LastName>Erhabor</LastName>
        <affiliation locale="en_US">Department of Medicine, Obafemi AwolowoUniversity/Teaching Hospital, Ile-Ife, Nigeria</affiliation>
      </Author>
      <Author>
        <FirstName>E.E.</FirstName>
        <LastName>Egbagbe</LastName>
        <affiliation locale="en_US">Department of Medicine, University of Benin/Teaching Hospital, Benin City, Nigeria</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Inadequate attention given to the management of asthma and ways of improving treatment could be a significant factor for the increase morbidity and mortality from asthma despite major advances in our understanding of the pathophysiology of the disease. There seems to be paucity of data concerning the management pattern and burden of asthma in Africa. This study was undertaken to determine the prevalence, management pattern and the burden of asthma.
This study was a cross sectional design involving clinical and lung function assessment. The diagnosis of asthma was made using the clinical features of asthma and lung function parameters (Forced expiratory volume in one second, Peak expiratory flow rate, Reversibility tests). Totally, 120 asthma patients participated in this study. All subjects completed the clinical asthma control questionnaires. All items were rated with the calculation of their mean and percentages. Student t-test was used to calculate the difference between the mean of the lung function tests for subjects and control. 
The prevalence of asthma among respiratory unit patients was 6.6% and higher in the first three decades of life with female preponderance (F:M=1.5-1).There is a strong family history of asthma(81.7%). Associated allergies include rhinitis (75%), pharyngitis (54%), conjunctivitis (54%) and dermatitis (30%). Percentage of asthma patients treated with bronchodilators alone (70%), combined inhaled bronchodilators and steroid (28.3%). Impaired daily activities include sports (84%), Job career (60%), Physical activity (55%), Social activity (54%), Household chores (61%), Disturbed sleep (53%), Daytime symptoms (51%), Hospitalized(50%). Subjects had significant low lung function values when compared with control (P &lt; 0.05). The burden of asthma is very high despite the advanced knowledge of the pathophysiology and management of asthma.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/267</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/267/267</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>9</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2010</Year>
        <Merized by severe neutropenia and is associated with severe systemic bacterial infections from&#xA0; early&#xA0; infancy.&#xA0; Granulocyte&#xA0; Colony&#xA0; Stimulating&#xA0; Factor&#xA0; (GCSF)&#xA0; is&#xA0; clinically&#xA0; used&#xA0; as&#xA0; a treatment for congenital and acquired neutropenia. The aim of this study was evaluation of GCSF (PD- Grastim) in treatment of these patients.
Patients with severe congenital neutropenia referred to Immunology, Asthma and Allergy Research Institute between Jan 2007 and Dec 2010 enrolled the study. Other causes of neutropenia were excluded by serial CBC and bone marrow studies, medical and drug histories and immunological tests. Patients were visited and examined monthly to evaluate their CBC and ANC&#xA0; (Absolute&#xA0; Neutrophil&#xA0; Count),&#xA0; GCSF&#xA0; side&#xA0; effects&#xA0; and&#xA0; dosage&#xA0; adjustment.&#xA0; Cytogenetic studies were being done for all the patients for early detection of progression to AML/MDS.
From twenty two patients who enrolled this study, 16 patients regularly evaluated. They were ten males and six females, range in age from 2 to 18 years old. Two patients failed to continue our follow up unfortunately and four patients died due to disease complications. Patients were followed for 24 to 48 months. In a period of 12-24 months before treatment, the mean of hospitalization frequency was 3.1 times and duration was 10 days; while during receiving treatment, they decreased to 0.2 times and 3 days, respectively (p&lt;0.01). Also significant increase in mean ANC was observed during follow up (315/&#xB5;l before treatment versus 1749/&#xB5;l after 12 month regular treatment). Bone pain was the most common side effect.
There have been no evidences of developing AML/MDS up to present time. Treatment with GCSF&#xA0; significantly&#xA0; reduced&#xA0; the&#xA0; duration&#xA0; and&#xA0; the&#xA0; frequency&#xA0; of&#xA0; hospitalization.&#xA0; Because&#xA0; of plausible progression to AML/MDS, regular follow-up of patients should be continued.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/330</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/330/330</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>11</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2012</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Physicians Awareness on Primary Immunodeficiency Disorders in Iran</title>
    <FirstPage>57</FirstPage>
    <LastPage>64</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Keramat</FirstName>
        <LastName>Nourijelyani</LastName>
        <affiliation locale="en_US">Department of Epidemiology and Biostatistics, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Asghar</FirstName>
        <LastName>Aghamohammadi</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Salehi Sadaghiani</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nasrin</FirstName>
        <LastName>Behniafard</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hassan</FirstName>
        <LastName>Abolhassani</LastName>
        <affiliation locale="en_US">Department of Epidemiology and Biostatistics, Tehran University of Medical Sciences, Tehran, Iran AND Community Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sarvenaz</FirstName>
        <LastName>Pourjabar</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Rezvanizadeh</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Joobin</FirstName>
        <LastName>Khadamy</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Amir</FirstName>
        <LastName>Imanzaeh</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojtaba</FirstName>
        <LastName>Sedaghat</LastName>
        <affiliation locale="en_US">Community Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nima</FirstName>
        <LastName>Rezaei</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran AND Department of Immunology, Molecular Immunology Research Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
     