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At least 343 records · Page 19Linked to original sources
PubMed1986

[Association of a pediatric bullous eruption, cutaneous and muscular atrophy, hyperpigmentation and dysmorphism. A new entity?].

We report the case of a young patient who presented with dysmorphism, bullous eruption of childhood, cutaneous and muscular atrophy and hyperpigmentation. Attempts were made to find out where this case fits in the nosological framework. This young boy without any particular family history was born with facial dysmorphism consisting of micrognathia, right microphtalmos, gothic palate and left facial palsy of the peripheral type. At the age of 2 years and 9 months, generalized fragility of the skin appeared in the form of a recurrent bullous eruption. The bullae left numerous atrophic and depigmented scars; they spared the mucosae, and there was no photosensitivity. At the same time, generalized skin atrophy developed: the subcutaneous venous network was abnormally visible and there was diffuse hyperpigmentation. The hair was fine, curly and thin. The teeth dystrophic and abnormally positioned. The cornea of the right eye was invaded by conjunctiva. The bullous eruption subsided when the child was about 6 years' old, but the skin atrophy became worse and was accompanied with amyotrophy of the limbs and retraction in flexion of the joints at the extremities. Chronic ulcerations were present on the lower limbs. Statural and ponderal growth, as well as mental development were normal. The biochemical examinations performed revealed no abnormality. Light and electron microscopy of the skin showed a normal dermis-epidermis junction, but the anchorage fibres were rarefied. The dermal connective tissue was abnormal, with thin collagen fibres and disorganized fibrillae. Fibroblasts were hypoplastic and numerous. The elastic network was meagre and elastic fibres had a slashed appearance. Biopsy of a palmar nodule showed cheloid-like lesions. The nosological discussion involved some congenital bullous diseases and certain forms of connective tissue dystrophia. Among the bullous diseases, congenital poikiloderma, as described by Weary and Kindler, is unaccompanied with amyotrophy, articular retraction or dysmorphism. According to Verret et al., the bulla is located at the dermis-epidermis junction. Recessive dystrophic epidermolysis bullosa seems to differ from our case in that skin atrophy is localized and amyotrophy, dysmorphism and disorders of pigmentation are absent. In addition, we found no histological evidence of collagenolysis. Mendes Da Costa's bullous dystrophy can be excluded, as there was no nanism, microcephaly or diffuse alopecia in our patient. Among connective tissue dystrophias, acrogeria Ehlers-Danlos type IV syndrome does not include bullous eruption, amyotrophy or articular retraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Abnormalities, Multiple↗
PubMed1985

Biochemical and clinical study of calcium pantetheine-S-sulfonate.

Calcium pantetheine-S-sulfonate (PaSSO3Ca) is one of the pantothenic acid derivatives. We examined PaSSO3Ca inhibition capacity of tyrosinase activity in vitro. For the safety evaluation when it will be applied to the human skin, we tested PaSSO3Ca creams to the fifty one patients with skin diseases by 48 hours closed patch test method. And clinical evaluation of PaSSO3Ca creams were performed in fifty patients with chloasma by half side method. Results were as follow: 1, PaSSO3Ca was proved to inhibit the tyrosinase activity in vitro. 2, PaSSO3Ca cream was shown to be safe to human skin. 3, 10% PaSSO3Ca cream lightened the skin hyperpigmentation.

Administration, Topical↗
PubMed1985

Paralysis and lipofuscin-like pigmentation of farm stock caused by the plant, Trachyandra laxa var. laxa.

A paralytic condition of farm stock in South West Africa, characterized by prominent neuronal and some mild extraneuronal pigmentation, is described. The distribution of the pigment, which was mainly located in the larger neurones of the brain and spinal cord, is given. Experimental evidence, obtained by feeding the plant, is presented that the condition is caused by Trachyandra laxa var. laxa. The histochemical features of the pigment proved to be compatible with a lipofuscin.

Animals↗