eMedicine Specialties > Dermatology > Internal Medicine

LEOPARD Syndrome

Author: Sergiusz Jozwiak, MD, PhD, Head, Professor, Department of Child Neurology, The Children's Memorial Health Institute of Warsaw, Poland
Coauthor(s): Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Jan 7, 2009

Introduction

Background

LEOPARD syndrome is a complex dysmorphogenetic disorder of variable penetrance and expressivity. Gorlin et al introduced the acronym LEOPARD as the name of the syndrome in 1969 to recall the main features of the disorder.

  • Lentigines (multiple)
  • Electrocardiographic conduction abnormalities
  • Ocular hypertelorism
  • Pulmonary stenosis
  • Abnormalities of genitalia
  • Retardation of growth
  • Deafness

Not all of the findings are present in any given patient. Zeisler and Becker first described the syndrome in 1936 in a 24-year-old woman with progressive generalized lentigines, hypertelorism, pectus carinatum, and prognathism. The first familial cases were reported in twins by Rosen and subsequently in 8 persons from a large 3-generation pedigree reported by Pipkin. Subsequent communications added new findings in isolated patients or families. Moynahan first documented the association of the syndrome with cardiac abnormalities and short stature in 1962.

Pathophysiology

Molecular studies have proven that LEOPARD syndrome and Noonan syndrome are allelic disorders caused by different missense mutations in PTPN11, a gene encoding the protein tyrosine phosphatase SHP-2 located at band 12q24.1.

In 2005, Ogata and Yoshida documented that PTPN11 mutations can be identified in approximately 40% of Noonan syndrome patients and in greater than 80% of LEOPARD syndrome patients.1 Because the vast majority of mutations reside in and around the broad intramolecular interaction surface between the N-SH2 and PTP domains of the PTPN11 protein, they have been suggested to affect the intramolecular N-SH2/PTP binding in the absence of a phosphopeptide, leading to excessive phosphatase activities.

In 2006, Hanna et al found that Noonan syndrome mutations enhance SHP-2 catalytic activity, whereas the activity of representative LS mutants is undetectable when assayed using a standard PTP substrate.2 The results are also supported by studies by Kontaridis et al.3 They revealed that whereas Noonan syndrome is caused by gain-of-function PTPN11 mutations, LEOPARD syndrome mutants are catalytically defective and act as dominant negative mutations that interfere with growth factor/Erk-mitogen-activated protein kinase–mediated signaling.

In 2006, Tartaglia et al reported that germline mutations in the PTPN11 gene cause LEOPARD and Noonan syndromes, whereas somatic mutations in the same gene contribute to leukemogenesis.4 To date, 2 patients with LEOPARD syndrome and myelomonocytic or acute lymphoblastic leukemias have been reported.5,6

Importantly, however, not all patients with LEOPARD syndrome demonstrate linkage to 12q24.1.

Reported in 2005, Kalidas et al performed mutation screening and linkage analysis of PTPN11 in 3 families, each of which had a history of LEOPARD syndrome for 3 generations.7 One family was found to carry a novel mutation (Q510P; 176876.0022). No variations in sequence were observed in the other 2 families, and negative lod scores excluded linkage to the PTPN11 locus, showing that LEOPARD syndrome is genetically heterogeneous.

Writzl et al reported a family with molecularly proven (p.Thr468Met in PTPN11) LEOPARD syndrome in a father and his adult son.8 The father had multiple lentigines equally dispersed over his body, whereas his son was devoid of lentigines on the left part of the thorax, back, and left arm. In addition, the son was found to have a mosaic karyotype in lymphocytes (47, XXY/46XY). On skin biopsy, mainly 47,XXY karyotype was present in the pigmented skin and 46,XY karyotype in the unpigmented areas. The authors considered various pathogenetic mechanisms: revertant mosaicism, silencing of a second PTPN11 mutation, genes located on a sex chromosome influencing the phenotype, and epigenetic influences.

Frequency

International

No epidemiologic data are available. The syndrome seems to be rare both in the United States and internationally.

Mortality/Morbidity

Most patients with LEOPARD syndrome lead a normal life. Cardiac pathologic findings (eg, obstructive cardiomyopathy, cardiac dysrhythmias) may be a cause of death in selected patients. A 19-year-old woman who died as a result of respiratory insufficiency secondary to thoracic deformities and a congenital heart defect has been reported.

Race

LEOPARD syndrome has no clear racial predilection.

Sex

In a large collected series of 77 patients, a slight preponderance of men has been documented (47 men, 30 women).

Age

Lentigines may be present at birth or develop during childhood. They become more numerous and darker with age. Other skin lesions, such as nevocellular nevi and malignant melanomas, reported sporadically in the LEOPARD syndrome, may undergo depigmentation.

Clinical

History

Highly variable expressivity of the syndrome makes the diagnosis difficult, especially in sporadic patients. Seventy percent of reported cases are familial. Based on clinical analysis of a large series of patients collected from the literature, in 1976 Voron et al proposed minimum criteria for the diagnosis.9

  • Multiple lentigines must be present.
  • Features of at least 2 other categories must be present.
    • Other cutaneous abnormalities
    • Cardiac structural or electrocardiographic abnormalities
    • Genitourinary abnormalities
    • Endocrine abnormalities
    • Neurologic defects
    • Cephalofacial dysmorphism
    • Shortness of stature
    • Skeletal abnormalities
  • If lentigines are absent, a diagnosis of LEOPARD syndrome may be established if the patient has features in at least 3 above-mentioned categories and has an immediate relative with the defined diagnosis.
  • Diagnosis of LEOPARD syndrome is very difficult in small children. According to Digilio et al, the diagnosis can be clinically suspected in the first months of life in patients who have 3 main features: characteristic facial features (100%), hypertrophic cardiomyopathy (87%), and café au lait spots (75%).10

Physical

  • Lentigines are small, dark brown, polygonal, irregularly shaped macules, usually 2-5 mm in diameter, but sometimes larger, even up to 1-1.5 cm. These large and darkly pigmented lesions are called by some authors café noir spots, by analogy to café au lait spots observed in neurofibromatosis type 1.11
  • They are often present on the face, neck, and upper part of the trunk but also on the palms, soles, and the sclerae.
  • Lentigines are the most prominent manifestation of the LEOPARD syndrome and are present in more than 90% of the patients; however, an absence of the feature does not exclude the diagnosis of the syndrome. Speculation about generalized lentiginosis always being a part of the spectrum of LEOPARD syndrome have been recently weakened by a study from Xing et al,12 who mapped familial generalized lentiginosis without systemic involvement to band 4q21.1-q22.3.
  • On careful skin examination, other cutaneous abnormalities may be detected.
    • Axillary freckling
    • Café au lait spots
    • Localized hypopigmentation
    • Onychodystrophy
    • Interdigital webs
    • Hyperelastic skin
  • Mental retardation, usually of mild degree, is observed in about 30% of the affected persons.
  • About 25% of patients have sensorineural hearing loss.
  • Seizures, nystagmus, or hyposmia have been documented in a few patients.
  • One third of the patients demonstrate short stature (in 20% of the cases below third percentile), which seems to become evident soon after birth (most newborns are of normal birth weight).
  • Despite frequent cardiac involvement, most patients are asymptomatic, and findings upon routine physical examinations may be negative. Interestingly, a higher frequency of family history of sudden death and atrial fibrillation has been reported in patients with left ventricular hypertrophy without PTPN11 mutations.13 A comprehensive review of 26 patients with LEOPARD syndrome documented left ventricular hypertrophy in 19 patients (73%) and right ventricular hypertrophy in 8 patients (30%). Long-term prognosis was overall benign, but the occurrence of 4 fatal events in patients with left ventricular hypertrophy indicates that such patients require careful risk assessment.14
  • In 2004, Yagubyan et al reported a patient with recurrent upper extremity aneurysms that required multiple operations.15 This patient also had multiple other peripheral aneurysms, thus far asymptomatic. Abnormal, extremely elongated vertebral and basilar arteries have also been reported.16
  • About 35% of the patients demonstrate various cephalofacial findings. Ocular hypertelorism was the most frequently reported (25%). Other findings include the following:
    • Mandibular prognathism
    • Broad nasal root
    • Dysmorphic skull
    • Low-set ears
    • Dental abnormalities
    • High palate arch
    • Epicanthal folds
    • Ptosis
    • Corneal tumors
  • Developmental anomalies of the genitourinary system are described in 26% of patients, predominantly in men. Abnormalities of the external genitals, such as cryptorchidism or hypospadias, may be observed on physical examination.
  • Different types of skeletal anomalies have been documented in affected patients, including chest deformity (pectus excavatum, pectus carinatum), kyphoscoliosis, winging of the scapulae, rib anomalies, syndactyly, delayed development or agenesis of permanent teeth, or supernumerary teeth.
  • In 2004, Rudolph et al reported colobomas of the iris, the retina, and the choroid in 3 members of one family.17

Causes

Familial cases suggest an autosomal dominant mode of inheritance with variable expressivity. Speculation exists on the more severe course of the disease in males, which may partially explain the slight preponderance of men in the large collected series of Voron et al in 1976.9

More on LEOPARD Syndrome

Overview: LEOPARD Syndrome
Differential Diagnoses & Workup: LEOPARD Syndrome
Treatment & Medication: LEOPARD Syndrome
Follow-up: LEOPARD Syndrome
Multimedia: LEOPARD Syndrome
References
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References

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  2. Hanna N, Montagner A, Lee WH, Miteva M, Vidal M, Vidaud M, et al. Reduced phosphatase activity of SHP-2 in LEOPARD syndrome: consequences for PI3K binding on Gab1. FEBS Lett. May 1 2006;580(10):2477-82. [Medline].

  3. Kontaridis MI, Swanson KD, David FS, Barford D, Neel BG. PTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effects. J Biol Chem. Mar 10 2006;281(10):6785-92. [Medline].

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Further Reading

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Keywords

LEOPARD syndrome, cardiocutaneous lentiginosis syndrome, multiple lentigines syndrome, generalized lentiginosis, centrofacial lentiginosis, lentiginosis profusa syndrome, lentiginosis-deafness-cardiopathy syndrome, cardiocutaneous syndrome, progressive cardiomyopathic lentiginosis, Moynahan syndrome, OMIM 151100

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Contributor Information and Disclosures

Author

Sergiusz Jozwiak, MD, PhD, Head, Professor, Department of Child Neurology, The Children's Memorial Health Institute of Warsaw, Poland
Sergiusz Jozwiak, MD, PhD is a member of the following medical societies: Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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