Table 2. Diffrential dianosis of Griscelli syndrome.

MYO5A: Myosin-Va; RAB27A: Ras-related protein Rab-27A

Condition	Clinical Manifestations	Genetics	Epidemiology
Chédiak–Higashi syndrome [8]	Partial albinism. Retina pigmentation, impaired visual acuity, photophobia, increase red reflex, nystagmus. Early-onset immunodeficiency. Mucosal bleeding, easy bruising. Neurologic manifestations appeared in early adulthood. They included: ataxia, tremors, motor, and sensory neuropathies, absent deep tendon reflexes. Accelerated phase: fever, hepatosplenomegaly, lymphadenopathy, neutropenia, anemia, thrombocytopenia, most patients die within the first ten years of life. Patients have an increased risk of developing a stroke.	Autosomal recessive. Lysosomal trafficking regulator is located in chromosome 1 (1q2-q44).	Unknown exact prevalence. Fewer than 500 cases worldwide.
Elejalde ­­syndrome [7]	Partial albinism, not immunocompromised early-onset neurologic dysfunction: marked hypotonia, hyporeflexia or hyperreflexia, spastic or flaccid hemiplegia or quadriplegia, seizures, ataxia, developmental delay. Ophthalmologic manifestations included: nystagmus, diplopia, pupilar areflexia, congenital amaurosis.	Autosomal recessive. MYO5A gene mutations.	20 cases have been reported up to 2019.
Hermansky-Pudlak syndrome type 2 [9]	Partial albinism, neutropenia, low platelet count, microcephaly, horizontal nystagmus, mental retardation.	Autosomal recessive disease. Mutations in AP3B1 gene on chromosome 5. The protein function is lysosomal trafficking.	Unknown
Griscelli Type 1 [4]	Partial albinism, not immunocompromised, neurological deficits, severe developmental delay, and mental retardation.	Mutation in the MYO5A gene on chromosome 15q21.	Only 150 cases have been reported.
Griscelli Type 2 [4]	Partial albinism, immunodeficiency, hemophagocytic syndrome. The hemophagocytic syndrome cause infiltration in the organs, including the brain.	Mutation in the RAB27A gene on chromosome 15q21.
Griscelli Type 3 [4]	Partial albinism. without neurological or immunological compromise. Only minor features are seen in GS3.	Mutation in either melanophilin or MYO5A genes.