CHILD Syndrome: Case Report of a Chinese Patient and Literature Review of the NAD[P]H Steroid Dehydrogenase-Like Protein Gene Mutation.

Congenital hemidysplasia with ichthyosiform nevus and limb defects (CHILD) syndrome is an X-linked autosomal dominant disorder characterized by unilateral congenital hemidysplasia with ichthyosiform erythroderma and ipsilateral limb defects caused by a mutation in the gene encoding NAD[P]H steroid dehydrogenase-like protein (NSDHL) at Xq28. The histopathologic hallmark of skin lesions in CHILD syndrome is psoriasiform epidermis with hyperkeratosis and parakeratosis, and its most striking feature affecting the upper dermis is filling of the papillary dermis with foam cells. Here we present the case of a 9-year-old Chinese girl born with the typical clinical features of CHILD syndrome.

Propranolol in the Treatment of Infantile Hemangiomas: A Meta-Analysis in Chinese Patients.

A meta-analysis was conducted to evaluate the efficacy of propranolol in the treatment of infantile hemangiomas (IHs) in Chinese infants. A statistically significant difference was found between infants treated using propranolol and those treated using corticosteroids (p < 0.001).

Association of anti-acidic ribosomal protein P0 and anti-galectin 3 antibodies with the development of skin lesions in systemic lupus erythematosus.

Objective: The specific autoantibodies and antigens that mediate systemic lupus erythematosus (SLE)-related organ injuries remain largely unknown. This study was undertaken to investigate the antibody-mediated immune response that leads to SLE skin lesions.

Methods: The study included 85 SLE patients with lupus-specific skin lesions and 31 without skin lesions.

Hypomethylation of interleukin-4 and -6 promoters in T cells from systemic lupus erythematosus patients.

Aim: DNA methylation regulates gene expression, and hypomethylation is associated with abnormal T-cell function in systemic lupus erythematosus (SLE). However, little is known about the methylation levels of the interleukin (IL)-4 and -6 promoters in SLE patients.

Methods: T cells were isolated from 20 SLE patients and 10 healthy controls, activated in vitro in the presence or absence of 5- azacytidine (5-azaC), and their IL-4 and -6 transcripts were characterized using semiquantitative RT-PCR.