NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2014.

Cover of GeneReviews®

GeneReviews® [Internet].

Show details

Majeed Syndrome

, MD and , MD.

Author Information
, MD
Director, Shafallah Medical Genetics Center
Doha, Qatar
, MD
Associate Professor of Pediatrics
University of Iowa
Iowa City, Iowa

Initial Posting: ; Last Update: March 14, 2013.

Summary

Disease characteristics. Majeed syndrome is characterized by:

  • Chronic recurrent multifocal osteomyelitis (CRMO) that is of early onset with a lifelong course; and
  • Congenital dyserythropoietic anemia (CDA) that presents as hypochromic, microcytic anemia during the first year of life and ranges from mild to transfusion dependent.

Some individuals also develop a transient inflammatory dermatosis, often manifesting as Sweet syndrome (neutrophilic skin infiltration).

Diagnosis/testing. The diagnosis is based on clinical findings and molecular genetic testing of LPIN2, the only gene in which mutations are known to cause Majeed syndrome.

Management. Treatment of manifestations: CRMO is treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy to avoid disuse atrophy of muscles and contractures. If CRMO does not respond to NSAIDs, corticosteroids can be used short term to control CRMO and skin manifestations; however, the complications of long-term use of corticosteroids limit their use in children. Two affected children had resolution of their bone inflammation when treated with an IL-1 inhibitor. Physical therapy should be employed to avoid disuse atrophy of muscles or contractures. CDA is treated with red blood cell transfusion if indicated.

Surveillance: Routine complete blood count (CBC) to determine if red blood cell transfusion is necessary.

Agents/circumstances to avoid: Prolonged bed rest.

Genetic counseling. Majeed syndrome is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Carrier testing for at-risk relatives is possible if the disease-causing mutations in the family are known. If the disease-causing mutations in the family have been identified, prenatal testing for pregnancies at increased risk is possible through laboratories offering either testing for the gene of interest or custom testing.

Diagnosis

Clinical Diagnosis

The diagnosis of Majeed syndrome is based on the following findings [El-Shanti & Ferguson 2007, Ferguson & El-Shanti 2007]:

  • Chronic recurrent multifocal osteomyelitis (CRMO) that is of early onset with a lifelong course
    • Skeletal radiographs show irregular osteolytic (radiolucent) lesions with surrounding sclerosis, usually in the metaphyses of long bones. Hyperostosis may be present in clavicular lesions.
    • Tc-99 or Ga-67 skeletal scan shows increased uptake at the inflammatory lesions; silent (asymptomatic) lesions may be identified.
    • MRI may be required to confirm the diagnosis, follow up lesions, or guide biopsy of an active bone lesion. Active bone lesions show increased signal intensity on T2-weighted and STIR images and decreased signal intensity on T1-weighted images. MRI is the imaging modality of choice for vertebral body lesions.
    • Biopsy of a bone lesion shows nonspecific inflammatory changes with granulocytic infiltration.
  • Congenital dyserythropoietic anemia (CDA)
    • Hypochromic, microcytic anemia manifests during the first year of life and ranges from mild to transfusion dependent.
    • Bone marrow examination shows increased erythropoiesis associated with evidence of dyserythropoiesis including up to 25% of normoblasts that are binucleated and trinucleated. The Ham test is negative.
  • Inflammatory dermatosis [Majeed et al 2000, Majeed et al 2001, Al-Mosawi et al 2007] that may be transient and is often Sweet syndrome (neutrophilic skin infiltration)
    • Biopsy of pustular skin lesions usually shows intraepidermal collection of neutrophils.

Testing

Laboratory testing is nonspecific:

Cultures from blood, bone biopsies, and pustular lesions are always negative.

Molecular Genetic Testing

Gene. LPIN2 is the only gene in which mutations are known to cause Majeed syndrome.

Clinical testing

Table 1. Summary of Molecular Genetic Testing Used in Majeed Syndrome

Gene SymbolTest MethodMutations DetectedMutation Detection Frequency by Test Method 1
LPIN2Sequence analysis / mutation scanning 2Sequence variants 3See footnote 4

1. The ability of the test method used to detect a mutation that is present in the indicated gene

2. Sequence analysis and mutation scanning of the entire gene can have similar mutation detection frequencies; however, mutation detection rates for mutation scanning may vary considerably between laboratories depending on the specific protocol used.

3. Examples of mutations detected by sequence analysis may include small intragenic deletions/insertions and missense, nonsense, and splice site mutations; typically, exonic or whole-gene deletions/duplications are not detected.

4. The mutation detection frequency using sequence analysis in individuals with CRMO and microcytic CDA is 100%; the mutation detection frequency using mutation scanning is unknown.

Interpretation of test results. For issues to consider in interpretation of sequence analysis results, click here.

Information on specific allelic variants may be available in Molecular Genetics (see Table A. Genes and Databases and/or Pathologic allelic variants).

Testing Strategy

To confirm/establish the diagnosis in a proband

  • Clinical evaluation to identify the three components of Majeed syndrome (may require bone biopsy of affected osteolytic lesion, bone marrow biopsy to document dyserythropoiesis, and skin biopsy to document neutrophilic dermatosis)
  • Sequence analysis/mutation scanning of LPIN2 in those who meet clinical diagnostic criteria

Carrier testing for at-risk relatives requires prior identification of the disease-causing mutations in the family.

Note: Carriers are heterozygotes for this autosomal recessive disorder and are not at risk of developing the disorder.

Prenatal diagnosis and preimplantation genetic diagnosis (PGD) for at-risk pregnancies require prior identification of the disease-causing mutations in the family.

Clinical Description

Natural History

Majeed syndrome is characterized by chronic recurrent multifocal osteomyelitis (CRMO), congenital dyserythropoietic anemia (CDA), and inflammatory dermatosis.

Onset of CRMO ranges from age three weeks to no later than age two years. It is characterized by short remissions, one to three exacerbations per month with each remaining for a few days, and a prolonged, probably lifelong, course. Each exacerbation consists of high fever, severe pain, and the appearance of periarticular tender soft tissue swelling, mainly involving large joints and occasionally small joints. The CRMO in Majeed syndrome is often associated with delayed bone age, growth failure, and development of permanent flexion contractures.

CDA usually presents during the first year of life and varies in severity from mild to transfusion dependent.

The inflammatory dermatosis is not a consistent phenotypic component of Majeed syndrome, although this may be a result of its transient nature. Of the affected individuals reported to date, two brothers had Sweet syndrome, their father had psoriasis, and an affected member of another family had cutaneous pustulosis.

Hepatomegaly, neutropenia, and transient cholestatic jaundice may occur during the neonatal period. These findings have no clinical consequences because they are transient. In rare instances, neutropenia may predispose to infections.

Individuals with Majeed syndrome have linear growth retardation with short adult stature.

If left untreated, the quality of life is poor as a result of recurrent pain, chronic anemia, and possible complications of contractures and disuse atrophy of the muscles.

The oldest individual known to have Majeed syndrome has been lost to follow up since he was about 28 years old.

Genotype-Phenotype Correlations

Although the number of individuals reported with Majeed syndrome is too small to study genotype-phenotype correlations, the affected individuals in the family with a frameshift mutation [Majeed et al 2001] appear to have a more severe course and complications than families with other classes of mutations. Conversely, another affected individual with a splice site mutation [Al-Mosawi et al 2007] and two affected Turkish brothers with a frameshift mutation [Herlin et al 2013], who were all diagnosed and treated early, had a less complicated course. It is unclear whether their milder clinical course is attributable to the earlier detection and treatment.

Penetrance

Penetrance is 100%.

Nomenclature

Majeed syndrome has been known by its components (i.e., CRMO, CDA, and neutrophilic dermatosis).

Prevalence

Majeed syndrome is very rare. The four affected families reported to date are from the Middle East:

  • One of Jordanian/Palestinian origin, reported from Kuwait
  • One Jordanian, reported from Jordan
  • One from Bahrain
  • One Turkish family residing in Denmark

Differential Diagnosis

The clinical diagnosis of Majeed syndrome is straightforward once the complete triad is established, and can be confirmed by demonstrating any of the various mutations in LPIN2. However, suspicion should be raised in the presence of any component, especially with an early onset in infancy and early childhood, such as unexplained congenital anemia and multifocal osteomyelitis in infancy.

Because of its recurrent febrile episodic course, Majeed syndrome should also be included in the differential diagnosis of the periodic fever syndromes.

The combination of bone and skin involvement, in particular, is shared by a variety of disorders including the following:

  • Synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is believed to be the CRMO of adults with skin, bone, and synovial membrane inflammation. The contribution of genetics to the etiology of SAPHO syndrome is unclear. The early onset and CDA of Majeed syndrome distinguish it from SAPHO syndrome.
  • Pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome is characterized by oligoarticular, corticosteroid-responsive arthritis beginning in childhood. Pyoderma gangrenosum and severe cystic acne begin in adolescence. Mutations in PSTPIP1 are causative; inheritance is autosomal dominant. In contrast, Majeed syndrome is associated with CDA and not associated with pyoderma gangrenosum or cystic acne, and inheritance is autosomal recessive.
  • Sporadic nonsyndromic CRMO is an autoinflammatory bone disease characterized by bone pain with or without fever with an unpredictable course of exacerbation and spontaneous remissions [El-Shanti & Ferguson 2007, Ferguson & El-Shanti 2007]. It is a sporadic disease. However, some indications suggest that it is a multifactorial disease with both genetic and environmental causes, although most causes have not yet been identified. The CRMO in Majeed syndrome is distinguished from sporadic CRMO as shown in Table 2. Furthermore, CDA is not a feature of sporadic CRMO.

Table 2. Comparison of Sporadic CRMO and CRMO of Majeed Syndrome

FeatureSporadic CRMOCRMO of Majeed Syndrome
Age at onsetLater onset (≤55 yrs)Early onset (1-19 months)
Frequency2-4/year1-4/month
Duration1-20 yearsLifelong
RemissionFrequentRare and brief
Long termBenign course for mostGrowth delay
ContracturesInfrequentCommon

CRMO = chronic recurrent multifocal osteomyelitis

Other disorders to consider:

  • Chronic multifocal non-bacterial osteomyelitis in hypophosphatasia mimicking malignancy [Girschick et al 2007]
  • Cherubism, characterized by painless bilateral, symmetric enlargement of the mandible and/or maxilla resulting from replacement of bone with multilocular cysts composed of fibrotic stromal cells and osteoclast-like cells. Onset is typically between ages two and five years. Other bones are usually not affected and the affected person is otherwise normal. The jaw lesions progress slowly until puberty when they stabilize and then regress such that by age 30 years facial abnormalities are no longer apparent. SH3BP2 is the only gene associated with cherubism. PTPN11 mutations have also been associated with a cherubism-like phenotype in a small number of patients. Inheritance is autosomal dominant.
  • Chronic infantile neurologic, cutaneous, and articular (CINCA) syndrome, a chronic congenital inflammatory disorder characterized by cutaneous rash, neurologic impairment, and arthropathy. CINCA is caused by heterozygous mutations in CIAS1 [Aksentijevich et al 2002] and is distinguished from Majeed syndrome by the presence of neurologic involvement, joint symptoms, and a distinctive appearance (frontal bossing, protruding eyes, and limb shortening) and the absence of CDA.
  • Deficiency of the interleukin-1 receptor antagonist (DIRA), a chronic inflammatory disorder that begins in the neonatal period. It presents with generalized pustulosis and osteitis. If not recognized and treated appropriately, affected individuals can develop systemic inflammatory response syndrome (SIRS) which can be a fatal complication of the disease. DIRA is an autosomal recessive disorder caused by mutations in IL1RN [Aksentijevich et al 2009]. It is distinguished from Majeed syndrome by the absence of CDA and by the distinctive radiographic bone lesions.
  • Congenital dyserythropoietic anemia (CDA). The CDAs are a heterogeneous group of diseases in which the anemia is predominantly caused by dyserythropoiesis and marked ineffective erythropoiesis [Wickramasinghe & Wood 2005]. Three major types (I, II, and III) have been identified, as well as a few minor types. CDA I is an autosomal dominant disorder (caused by mutations in CDAN1) characterized by macrocytic anemia and occasionally associated with acrodysostosis, nail hypoplasia, and scoliosis. In contrast, Majeed syndrome is autosomal recessive and associated with microcytic CDA and no bone dysplasia or deformity.

Note to clinicians: For a patient-specific ‘simultaneous consult’ related to this disorder, go to Image SimulConsult.jpg, an interactive diagnostic decision support software tool that provides differential diagnoses based on patient findings (registration or institutional access required).

Management

Evaluations Following Initial Diagnosis

To establish the extent of disease and needs in an individual diagnosed with Majeed syndrome, the following evaluations are recommended:

  • Skeletal radiographs, if not already performed
  • CBC, if not already performed
  • Bone marrow biopsy if significant anemia is present
  • Examination of the skin
  • Medical genetics consultation

Treatment of Manifestations

Because of the rarity of Majeed syndrome, treatment is empiric.

CRMO is treated as follows:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs), which provide moderate improvement. If there is an inadequate response to NSAIDs, corticosteroids are useful in controlling CRMO and skin manifestations; however, their long-term use in children is limited by side effects such as growth delay and cataracts.
  • Tumor necrosis factor inhibitors and bisphosphonates have been reported to improve sporadic CRMO; however, the two individuals with Majeed syndrome treated with TNF-alpha inhibitors did not improve [Herlin et al 2013]. To date, bisphosphonates have not been used to treat individuals with Majeed syndrome; thus, their efficacy in this disorder is unknown.
  • The same two affected individuals reported by Herlin et al who failed to improve with TNF blockade did respond to IL-1 blockade (IL-1 receptor antagonist [anakinra] and IL-1β antibody [canakinumab]) with clinical, radiographic, and laboratory evidence of improvement [Herlin et al 2013].
  • Physical therapy to avoid disuse atrophy of muscles or contractures

CDA is treated with periodic monitoring with complete blood count (CBC) and blood transfusion if indicated. One patient had a splenectomy, after which the anemia markedly improved. In the two affected individuals reported by Herlin et al [2013] it is unclear if the CDA completely resolved, as a repeat bone marrow biopsy was not performed.

Prevention of Secondary Complications

Physical therapy can help to prevent contractures.

Surveillance

The following are appropriate:

  • Routine CBC to determine if red blood cell transfusion is necessary
  • Regular pediatric care

Agents/Circumstances to Avoid

Prolonged bed rest should be avoided because it can result in joint contractures and disuse atrophy.

Evaluation of Relatives at Risk

See Genetic Counseling for issues related to testing of at-risk relatives for genetic counseling purposes.

Therapies Under Investigation

Search ClinicalTrials.gov for access to information on clinical studies for a wide range of diseases and conditions. Note: There may not be clinical trials for this disorder.

Other

Three patients were treated with colchicine for four months with no improvement.

Genetic Counseling

Genetic counseling is the process of providing individuals and families with information on the nature, inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. The following section deals with genetic risk assessment and the use of family history and genetic testing to clarify genetic status for family members. This section is not meant to address all personal, cultural, or ethical issues that individuals may face or to substitute for consultation with a genetics professional. —ED.

Mode of Inheritance

Majeed syndrome is inherited in an autosomal recessive manner.

Risk to Family Members

Parents of a proband

  • The parents of an affected child are obligate heterozygotes (i.e., carriers of one mutant allele).
  • Heterozygotes (carriers) do not have Majeed syndrome, but may have psoriasis.

Sibs of a proband

  • At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.
  • Once an at-risk sib is known to be unaffected, the risk of his/her being a carrier is 2/3.
  • Heterozygotes (carriers) do not develop Majeed syndrome, but may have psoriasis.

Offspring of a proband. The offspring of an individual with Majeed syndrome are obligate heterozygotes (carriers) for a disease-causing mutation.

Other family members of a proband. Each sib of the proband’s parents is at a 50% risk of being a carrier.

Carrier Detection

Carrier testing for at-risk family members is possible once the mutations have been identified in the family.

In populations with a high carrier rate and/or a high rate of consanguinity, it is possible that the reproductive partner of the proband may be affected or heterozygous. Thus, the risk to offspring is most accurately determined after molecular genetic testing of the proband's reproductive partner.

Related Genetic Counseling Issues

Family planning

  • The optimal time for determination of genetic risk, clarification of carrier status, and discussion of the availability of prenatal testing is before pregnancy.
  • It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected, are carriers, or are at risk of being carriers.

DNA banking is the storage of DNA (typically extracted from white blood cells) for possible future use. Because it is likely that testing methodology and our understanding of genes, mutations, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

Prenatal Testing

If the disease-causing mutations have been identified in an affected family member, prenatal testing for at-risk pregnancies is possible through laboratories offering either prenatal testing for the gene of interest or custom testing.

Preimplantation genetic diagnosis (PGD) may be an option for some families in which the disease-causing mutations have been identified.

Resources

GeneReviews staff has selected the following disease-specific and/or umbrella support organizations and/or registries for the benefit of individuals with this disorder and their families. GeneReviews is not responsible for the information provided by other organizations. For information on selection criteria, click here.

  • Eurofever Registry
    Largo Gaslini, 5
    Genova 16147
    Italy
    Phone: +39 010 382854; +39 010 393425
    Fax: +39 010 393324; +39 010 4211018
    Email: marcogattorno@ospedale-gaslini.ge.it; printo@ospedale-gaslini.ge.it

Molecular Genetics

Information in the Molecular Genetics and OMIM tables may differ from that elsewhere in the GeneReview: tables may contain more recent information. —ED.

Table A. Majeed Syndrome: Genes and Databases

Data are compiled from the following standard references: gene symbol from HGNC; chromosomal locus, locus name, critical region, complementation group from OMIM; protein name from UniProt. For a description of databases (Locus Specific, HGMD) to which links are provided, click here.

Table B. OMIM Entries for Majeed Syndrome (View All in OMIM)

605519LIPIN 2; LPIN2
609628MAJEED SYNDROME

Normal allelic variants. The genomic sequence of LPIN2 is approximately 95 kb and comprises 20 exons. Exon 1 and the majority of exon 20 are non-coding (5’ and 3’ untranslated regions). The mRNA is approximately 6245 bp and encodes a protein of 896 amino acids. It is expressed in almost all tissues.

Pathologic allelic variants. Three pathologic mutations have been identified: two frameshifts and one splice site change. Four pathologic mutations have been identified: two frameshift mutations resulting from a 2-bp deletion, one splice site mutation, and one missense mutation.

The fourth nucleotide variant is a missense mutation that changes an evolutionarily conserved amino acid (see Table 3).

Table 3. Selected LPIN2 Allelic Variants

Class of Variant AlleleDNA Nucleotide Change (Alias 1)Protein Amino Acid Change (Alias 1)Reference Sequences
Normalc.991G>Tp.Ala331SerNM_014646​.2
NP_055461​.1
c.1043C>Tp.Pro348Leu
Pathologicc.540_541delp.Cys181X
c.2201C>Tp.Ser734Leu
c.2327+1G>Cp.Arg776Serfs*66 2
c.1316_1317del
(1312_1313del)
p.Ser439Trpfs*15
(Leu438fs+16X) 3

Note on variant classification: Variants listed in the table have been provided by the author(s). GeneReviews staff have not independently verified the classification of variants.

Note on nomenclature: GeneReviews follows the standard naming conventions of the Human Genome Variation Society (www​.hgvs.org). See Quick Reference for an explanation of nomenclature.

1. Variant designation that does not conform to current naming conventions

2. Al-Mosawi et al [2007]

3. Herlin et al [2013]

Normal gene product. The protein product comprises 896 amino acids and has a lipin domain and a SMP2 domain. The protein plays a role in lipid metabolism and may play a role in lipodystrophy in mice. In humans it is apparent that it plays a role in inflammation, probably in the innate immune response.

Abnormal gene product. Three out of the four identified mutations produce a truncated protein. The fourth mutation is a missense mutation that changes an evolutionarily conserved amino acid.

References

Literature Cited

  1. Aksentijevich I, Masters SL, Ferguson PJ, Dancey P, Frenkel J, van Royen-Kerkhoff A, Laxer R, Tedgård U, Cowen E, Pham T-H, Booty M, Estes JD, Sandler NG, Plass N, Stone DL, Turner ML, Hill S, Butman JA, Schneider R, Babyn P, El-Shanti HI, Pope E, Barron K, Bing X, Laurence A, Lee C-CR, Chapelle D, Clarke GI, Ohson K, Nicholson M, Gadina M, Yang B, Korman BD, Gregersen PK, van Hagen PM, Hak AE, Huizing M, Rahman P, Douek DC, Remmers EF, Kastner DL, Goldbach-Mansky R. An autoinflammatory disease with deficiency of the interleukin-1 receptor antagonist. N Engl J Med. 2009;360:2426–37. [PMC free article: PMC2876877] [PubMed: 19494218]
  2. Aksentijevich I, Nowak M, Mallah M, Chae JJ, Watford WT, Hofmann SR, Stein L, Russo R, Goldsmith D, Dent P, Rosenberg HF, Austin F, Remmers EF, Balow JE, Rosenzweig S, Komarow H, Shoham NG, Wood G, Jones J, Mangra N, Carrero H, Adams BS, Moore TL, Schikler K, Hoffman H, Lovell DJ, Lipnick R, Barron K, O'Shea JJ, Kastner DL, Goldbach-Mansky R. De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID): a new member of the expanding family of pyrin-associated autoinflammatory diseases. Arthritis Rheum. 2002;46:3340–8. [PubMed: 12483741]
  3. Al-Mosawi ZS, Al-Saad KK, Ijadi-Maghsoodi R, El-Shanti HI, Ferguson PJ. A splice site mutation confirms the role of LPIN2 in Majeed syndrome. Arthritis Rheum. 2007;56:960–4. [PubMed: 17330256]
  4. El-Shanti HI, Ferguson PJ. Chronic recurrent multifocal osteomyelitis: a concise review and genetic update. Clin Orthop Relat Res. 2007;462:11–9. [PubMed: 17496555]
  5. Ferguson PJ, El-Shanti HI. Autoinflammatory bone disorders. Curr Opin Rheumatol. 2007;19:492–8. [PubMed: 17762617]
  6. Girschick HJ, Mornet E, Beer M, Warmuth-Metz M, Schneider P. Chronic multifocal non-bacterial osteomyelitis in hypophosphatasia mimicking malignancy. BMC Pediatr. 2007;7:3. [PMC free article: PMC1784091] [PubMed: 17241478]
  7. Herlin T, Fiirgaard B, Bjerre M, Kerndrup G, Hasle H, Bing X, Ferguson PJ. Efficacy of anti-IL-1 treatment in Majeed syndrome. Ann Rheum Dis. 2013;72:410–3. [PMC free article: PMC3660147] [PubMed: 23087183]
  8. Majeed HA, Al-Tarawna M, El-Shanti H, Kamel B, Al-Khalaileh F. The syndrome of chronic recurrent multifocal osteomyelitis and congenital dyserythropoietic anaemia. Report of a new family and a review. Eur J Pediatr. 2001;160:705–10. [PubMed: 11795677]
  9. Majeed HA, El-Shanti H, Al-Rimawi H, Al-Masri N. On mice and men: An autosomal recessive syndrome of chronic recurrent multifocal osteomyelitis and congenital dyserythropoietic anemia. J Pediatr. 2000;137:441–2. [PubMed: 10969284]
  10. Wickramasinghe SN, Wood WG. Advances in the understanding of the congenital dyserythropoietic anaemias. Br J Haematol. 2005;131:431–46. [PubMed: 16281933]

Chapter Notes

Author Notes

Shafallah Medical Genetics Center: www.smgc.org.qa

Author History

Hatem El-Shanti, MD, Shafallah Medical Genetics Center, Doha, Qatar (2008-present)
Polly Ferguson, MD (2013-present)
Hasan A Majeed, FRCPI, DCH, Jordan University, Amman (2008-2009)

Professor Hasan A. Majeed was a distinguished pediatrician and astute scientist. He was a world-renowned expert on autoinflammatory disorders contributing tens of manuscripts on the topic in the form of published journal articles, chapters in books and proceedings in international conferences. Professor Majeed died in November, 2009 at the age of 75 years. He was a great teacher who took pride in educating and training hundreds of physicians. He is greatly missed by his family, friends, colleagues, students, and patients.

Revision History

  • 14 March 2013 (me) Comprehensive update posted live
  • 23 September 2008 (cg) Review posted live
  • 26 June 2008 (ham) Original submission
Copyright © 1993-2014, University of Washington, Seattle. All rights reserved.

For more information, see the GeneReviews Copyright Notice and Usage Disclaimer.

For questions regarding permissions: ude.wu@tssamda.

Bookshelf ID: NBK1974PMID: 20301735
PubReader format: click here to try

Views

Tests in GTR by Gene

Tests in GTR by Condition

Related information

  • MedGen
    Related information in MedGen
  • OMIM
    Related OMIM records
  • PMC
    PubMed Central citations
  • PubMed
    Links to pubmed
  • Gene
    Gene records cited in chapters on the NCBI bookshelf. Links are provided by the authors or the NCBI Bookshelf staff.

Related citations in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...