The dermatology staff was called to evaluate abnormal hair on a 22-month-old Hispanic girl whose parents were first cousins. Her medical history was significant for leptomeningitis with subsequent neurologic devastation, gastroesophageal reflux disease, and recurrent respiratory infections. Her hospital course was complicated by sepsis, liver dysfunction, pan-cytopenia, and disseminated intravascular coagulation. She had developed normally for the first year of life. At 13 months she became progressively lethargic and developed floppy muscle tone; a delay in mental and motor milestones was recognized. Results of a metabolic workup were negative. On examination she was noted to have generalized excessively fair skin when compared with her parents. She had silver-gray hair (Figure 1) and white eyebrows and body hair. Her maternal grandfather and granduncles had silver hair since childhood, but were without health problems. A maternal family member was said to have light skin. The presumed diagnosis before pathologic examination was Chediak-Higashi syndrome. Hematoxylin and eosin stain tests revealed prominent melanocytes in the basal layer of the epidermis. The melanocytes were large and distended with a large volume of melanin (Figure 2). The adjacent keratinocytes were completely devoid of melanin. Application of Masson-Fontana ammoniac silver stain highlighted prominent melanocytic melanin and a relative paucity of melanin in the adjacent keratinocytes (Figure 3). Microscopic examination of her hair revealed clumps of melanin of various sizes and shapes irregularly distributed throughout the hair shaft. Ultrastructural examination of the epidermis showed the melanocytes were distended by an accumulation of large stage IV mature melanosomes. Peripheral blood smear failed to show abnormal granules, even after repeated examination. Based on the clinical features and the pathologic findings, a diagnosis of Griscelli syndrome type 2 was made.
[1]
Jo Lambert,et al.
Griscelli syndrome: a model system to study vesicular trafficking
,
2009,
Pigment cell & melanoma research.
[2]
J. Voltarelli,et al.
Griscelli Syndrome: Characterization of a New Mutation and Rescue of T-Cytotoxic Activity by Retroviral Transfer of RAB27A Gene
,
2004,
Journal of Clinical Immunology.
[3]
A. Fischer,et al.
Griscelli syndrome restricted to hypopigmentation results from a melanophilin defect (GS3) or a MYO5A F-exon deletion (GS1).
,
2003,
The Journal of clinical investigation.
[4]
W. Gahl,et al.
Evidence that Griscelli syndrome with neurological involvement is caused by mutations in RAB27A, not MYO5A.
,
2002,
American journal of human genetics.
[5]
A. Fischer,et al.
Mutations in RAB27A cause Griscelli syndrome associated with haemophagocytic syndrome
,
2000,
Nature Genetics.
[6]
A. Fischer,et al.
Griscelli disease maps to chromosome 15q21 and is associated with mutations in the Myosin-Va gene
,
1997,
Nature Genetics.