Cartilage-Hair Hypoplasia

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Cartilage-hair hypoplasia (CHH), which is Online Mendelian Inheritance in Man (OMIM) disease number 250250, is an autosomal recessive inherited disorder that results in short-limb dwarfism associated with T-cell and B-cell immunodeficiency. [1] Cartilage-hair hypoplasia and other short-limb dwarfism phenotypes are associated with metaphyseal or spondyloepiphyseal dysplasia. Cartilage-hair hypoplasia is a variant of short-limb dwarfism in which fine sparse hair is also present.

The immunodeficiency in cartilage-hair hypoplasia may be an isolated T-cell immunodeficiency, isolated B-cell immunodeficiency, or combined T-cell and B-cell immunodeficiency.

Although originally described by McKusik et al in 1964 in Amish children and known as metaphyseal chondrodysplasia McKusick type, cartilage-hair hypoplasia has been described in non-Amish persons throughout the United States, Europe, and Mexico. [2] The genetic defect in cartilage-hair hypoplasia has been confirmed to be mutations in the RMRP gene.

The genetic defect in cartilage-hair hypoplasia has been identified as a mutation in the gene for RNAase RMRP, mapped to 9p12. [3, 4, 5, 6, 7, 8, 9, 52, 56] RMRP is a ribonucleoprotein present in the nucleus and mitochondria. RNAase RMRP has multiple functions: cleavage of the upstream 5.8S rRNA junction site necessary for ribosome assembly and associated with bone dysplasia; mRNA cleavage of cyclin B2 mRNA necessary for cell cycle progression, associated with susceptibility to cancer, immune deficiency, anemia, and hair hypoplasia; processing of mitochondrial RNA in the yeast RMRP ortholog; and interaction of RMRP and hTERT leads to an RNA-dependent RNA polymerase activity leading to siRNA altering gene expression. RMRP is required for cell growth, consistent with observations that a generalized defect in cell growth is observed in T cells, B cells, and fibroblasts. [4]

RMRP has 2 types of mutations. The first are insertions or duplications of 6-30 nucleotides that reside in the region between the TATA box and the transcription initiation site. [10] These mutations interfere with the transcription of the RMRP gene and are considered null mutations. Kavadas et al reported that mutations in the promoter region are associated with immune defects. [11] The second consists of single nucleotide substitutions and other changes that involve at most 2 nucleotides in highly conserved regions of the gene.These are considered leaky mutations and result in variable expression of the gene, which may explain the variable phenotype seen in cartilage-hair hypoplasia. These latter mutations result in variable expression of the gene, which may explain the variable phenotype seen in cartilage-hair hypoplasia. The most commonly found mutation in patients with cartilage-hair hypoplasia is 70A>G, which occurs in 30-50% of patients with cartilage-hair hypoplasia and causes an alteration in ribosomal processing. [9] RMRP mutations that reduce ribosomal RNA cleavage are associated with bone dysplasia; whereas, mutations that affect mRNA cleavage are associatedwith hair hypoplasia, immunodeficiency, and dermatologic abnormalities. [7]   Recently, it was observed that RMRP associates with the human telomerase catalytic subunit (hTERT). [54] The 3’ end of RMRP is essential for RNA dependent RNA polymerase acitivity of the RMRP-hTERT complex. 

Although the immune defect primarily affects the T-cell system, mutations of RMRP result in more generalized hematopoietic impairments. [12] In studies from Makitie et al, defective in vitro colony formation in all myeloid lineages was present, including erythroid, granulocyte-macrophage, and megakaryocyte colony formation. This suggests a common cell proliferation defect in cartilage-hair hypoplasia. How the recently identified genetic defects correlate with immunologic defects remains to be determined.

United States

Cartilage-hair hypoplasia is a rare defect. It has been described in both Amish and non-Amish populations. In the Amish, the gene frequency was reported to be 1 per 1340 population with a carrier rate of 1 per 19 population. [5] A recent study examined the temporal trends of primary immunodeficiency diseases. [13]

International

In Finland, the frequency of cartilage-hair hypoplasia was reported to be 1 case per 23,000 live births, with a carrier rate of 1 case per 76 live births. [14]

Persons with cartilage-hair hypoplasia may be subject to infections with opportunistic microorganisms, principally life-threatening varicella infections. In one report, approximately 88% of 108 Finnish patients with cartilage-hair hypoplasia had defective cellular immunity and 56% had increased susceptibility to infections. [15] Individuals with more severe impaired cellular immunity are more susceptible to malignancies, especially leukemia and lymphoma. In their series, the incidence rate of malignancies was 6%. The risk of infections and malignancies correlates with the severity of impaired T-cell immunity.

However, cartilage hair-hypoplasia is a rare cause of severe combined immunodeficiency (SCID). In a large series of 108 patients with SCID, only one patient with cartilage hair-hypoplasia was identified. [16] Individuals with cartilage hair-hypoplasia and SCID have a greater susceptibility to opportunistic infections, such as Pneumocystis carinii pneumonia and graft versus host disease, and may succumb to overwhelming infections in infancy.

First reported among Amish children, the disorder has also been reported in other groups throughout the United States, Europe, Asia, and Mexico.

Cartilage-hair hypoplasia is inherited as an autosomal recessive disorder with equal male-to-female frequency.

The predominant clinical feature of cartilage-hair hypoplasia is short-limb dwarfism evident at birth. The onset of dwarfism may be detected in utero, manifesting as shortening and bowing of the femur.

The onset of increased susceptibility to recurrent infections and severity of infections is somewhat more variable in cartilage-hair hypoplasia.

In two studies, increased susceptibility to infections was reported in only 31-56% of individuals with cartilage-hair hypoplasia. [15, 14] In addition, infections may be limited to varicella and may occur in early childhood. Thus, immunodeficiency in individuals with cartilage-hair hypoplasia varies, often with limited susceptibility to infections, and many children with cartilage-hair hypoplasia may live healthy lives.

Children with cartilage-hair hypoplasia that causes SCID present in early infancy with susceptibility to overwhelming and opportunistic infections.

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Thiel CT, Horn D, Zabel B, et al. Severely incapacitating mutations in patients with extreme short stature identify RNA-processing endoribonuclease RMRP as an essential cell growth regulator. Am J Hum Genet. 2005 Nov. 77(5):795-806. [Medline].

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Hirose Y, Nakashima E, Ohashi H, Mochizuki H, Bando Y, Ogata T, et al. Identification of novel RMRP mutations and specific founder haplotypes in Japanese patients with cartilage-hair hypoplasia. J Hum Genet. July 2011. 51:706-710. [Medline].

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Ridanpää M, Sistonen P, Rockas S, Rimoin DL, Mäkitie O, Kaitila I. Worldwide mutation spectrum in cartilage-hair hypoplasia: ancient founder origin of the major70A–>G mutation of the untranslated RMRP. Eur J Hum Genet. July 2002. 10:439-447. [Medline].

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Makitie O, Pukkala E, Teppo L, Kaitila I. Increased incidence of cancer in patients with cartilage-hair hypoplasia. J Pediatr. 1999 Mar. 134(3):315-8. [Medline].

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Ammann RA, Duppenthaler A, Bux J, Aebi C. Granulocyte colony-stimulating factor-responsive chronic neutropenia in cartilage-hair hypoplasia. J Pediatr Hematol Oncol. 2004 Jun. 26(6):379-81. [Medline].

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de la Fuente MA, Recher M, Rider NL, Strauss KA, Morton DH, Adair M, et al. Reduced thymic output, cell cycle abnormalities, and increased apoptosis of T lymphocytes in patients with cartilage-hair hypoplasia. J Allergy Clin Immunol. July 2011. 128:139-146. [Medline].

Lux SE, Johnston RB Jr, August CS, et al. Chronic neutropenia and abnormal cellular immunity in cartilage-hair hypoplasia. N Engl J Med. 1970 Jan 29. 282(5):231-6. [Medline].

Williams MS, Ettinger RS, Hermanns P, et al. The natural history of severe anemia in cartilage-hair hypoplasia. Am J Med Genet A. 2005 Sep 15. 138(1):35-40. [Medline].

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Berthet F, Siegrist CA, Ozsahin H, et al. Bone marrow transplantation in cartilage-hair hypoplasia: correction of the immunodeficiency but not of the chondrodysplasia. Eur J Pediatr. 1996 Apr. 155(4):286-90. [Medline].

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Bordon V, Gennery AR, Slatter MA, Vandecruys E, Laureys G, Veys P, et al. Clinical and immunologic outcome of patients with cartilage hair hypoplasia after hematopoietic stem cell transplantation. Blood. July 2010. 116(1):27-35. [Medline].

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Harada D, Yamanaka Y, Ueda K, et al. An effective case of growth hormone treatment on cartilage-hair hypoplasia. Bone. 2005 Feb. 36(2):317-22. [Medline].

Bocca G, Weemaes CM, van der Burgt I, Otten BJ. Growth hormone treatment in cartilage-hair hypoplasia: effects on growth and the immune system. J Pediatr Endocrinol Metab. 2004 Jan. 17(1):47-54. [Medline].

Obara-Moszynska M, Wielanowska W, Rojek A, Wolnik-Brzozowska D, Niedziela M. Treatment of cartilage-hair hypoplasia with recombinant human growth hormone. Pediatr Int. December 2013. 55(6):e162-164. [Medline].

Riley P Jr, Weiner DS, Leighley B, Jonah D, Morton DH, Strauss KA, et al. Cartilage hair hypoplasia: characteristics and orthopaedic manifestations. J Child Orthop. 2015 Apr. 9 (2):145-52. [Medline].

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Thiel CT, Mortier G, Kaitila I, Reis A, Rauch A. Type and level of RMRP functional impairment predicts phenotype in the cartilage hair hypoplasia-anauxetic dysplasia spectrum. Am J Hum Genet. Sep 2007. 81(3):519-529. [Medline].

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pH

Additives (IVIG products containing sucrose are more often associated with renal dysfunction, acute renal failure, and osmotic nephrosis, particularly with preexisting risk factors [eg, history of renal insufficiency, diabetes mellitus, age >65 y, dehydration, sepsis, paraproteinemia, nephrotoxic drugs])

Parenteral Form and Final Concentrations

IgA Content (mcg/mL)

Carimune NF

(CSL Behring)

Kistler-Nitschmann fractionation; pH 4, nanofiltration

6.4-6.8

6% solution: 10% sucrose, < 20 mg NaCl/g protein

Lyophilized powder 3%, 6%, 9%, 12%

Trace

Flebogamma

(Grifols USA)

Cohn-Oncley fractionation, PEG precipitation, ion-exchange chromatography, pasteurization

5.1-6

Sucrose free, contains 5% D-sorbitol

Liquid 5%

< 50

Gammagard Liquid 10%

(Baxter Bioscience)

Cohn-Oncley cold ethanol fractionation, cation and anion exchange chromatography, solvent detergent treated, nanofiltration, low pH incubation

4.6-5.1

0.25M glycine

Ready-for-use liquid 10%

37

Gamunex

(Talecris Biotherapeutics)

Cohn-Oncley fractionation, caprylate-chromatography purification, cloth and depth filtration, low pH incubation

4-4.5

Does not contain carbohydrate stabilizers (eg, sucrose, maltose), contains glycine

Liquid 10%

46

Gammaplex

(Bio Products)

Solvent/detergent treatment targeted to enveloped viruses; virus filtration using Pall Ultipor to remove small viruses including nonenveloped viruses; low pH incubation

4.8-5.1

Contains sorbitol (40 mg/mL); do not administer if fructose intolerant

Ready-for-use solution 5%

< 10

Iveegam EN

(Baxter Bioscience)

Cohn-Oncley fraction II/III; ultrafiltration; pasteurization

6.4-7.2

5% solution: 5% glucose, 0.3% NaCl

Lyophilized powder 5%

< 10

Polygam S/D

Gammagard S/D

(Baxter Bioscience for the American Red Cross)

Cohn-Oncley cold ethanol fractionation, followed by ultracentrafiltration and ion exchange chromatography; solvent detergent treated

6.4-7.2

5% solution: 0.3% albumin, 2.25% glycine, 2% glucose

Lyophilized powder 5%, 10%

< 1.6 (5% solution)

Octagam

(Octapharma USA)

Cohn-Oncley fraction II/III; ultrafiltration; low pH incubation; S/D treatment pasteurization

5.1-6

10% maltose

Liquid 5%

200

Panglobulin

(Swiss Red Cross for the American Red Cross)

Kistler-Nitschmann fractionation; pH 4 incubation, trace pepsin, nanofiltration

6.6

Per gram of IgG: 1.67 g sucrose, < 20 mg NaCl

Lyophilized powder 3%, 6%, 9%, 12%

720

Privigen Liquid 10%

(CSL Behring)

Cold ethanol fractionation, octanoic acid fractionation, and anion exchange chromatography; pH 4 incubation and depth filtration

4.6-5

L-proline (~250 mmol/L) as stabilizer; trace sodium; does not contain carbohydrate stabilizers (eg, sucrose, maltose)

Ready-for-use liquid 10%

< 25

Alan P Knutsen, MD Professor of Pediatrics, Director of Pediatric Allergy and Immunology, Director Jeffrey Modell Diagnostic & Research Center for Primary Immuodeficiences (CGCMC), Director of Pediatric Clinical Immunology Laboratory, Department of Pathology, St Louis University Health Sciences Center

Alan P Knutsen, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, Clinical Immunology Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Harumi Jyonouchi, MD Faculty, Division of Allergy/Immunology and Infectious Diseases, Department of Pediatrics, Saint Peter’s University Hospital

Harumi Jyonouchi, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association of Immunologists, American Medical Association, Clinical Immunology Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, Society for Pediatric Research, Society for Mucosal Immunology

Disclosure: Nothing to disclose.

James M Oleske, MD, MPH François-Xavier Bagnoud Professor of Pediatrics, Director, Division of Pulmonary, Allergy, Immunology and Infectious Diseases, Department of Pediatrics, Rutgers New Jersey Medical School; Professor, Department of Quantitative Methods, Rutgers New Jersey Medical School

James M Oleske, MD, MPH is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Allergy Asthma and Immunology, American Academy of Hospice and Palliative Medicine, American Association of Public Health Physicians, American College of Preventive Medicine, American Pain Society, Infectious Diseases Society of America, Infectious Diseases Society of New Jersey, Medical Society of New Jersey, Pediatric Infectious Diseases Society, Arab Board of Family Medicine, American Academy of Pain Management, National Association of Pediatric Nurse Practitioners, Association of Clinical Researchers and Educators, American Academy of HIV Medicine, American Thoracic Society, American Academy of Pediatrics, American Public Health Association, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

John Wilson Georgitis, MD Consulting Staff, Lafayette Allergy Services

John Wilson Georgitis, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association for the Advancement of Science, American College of Chest Physicians, American Lung Association, American Medical Writers Association, and American Thoracic Society

Disclosure: Nothing to disclose.

Cartilage-Hair Hypoplasia

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