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PubMed · 7331917

[Enteropathic acrodermatitis. Hematologic study with X-ray microanalysis].

J Calap·J Chandler
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AcrodermatitisAdolescentElectron Probe MicroanalysisHumansMalabsorption SyndromesMaleZincCase ReportsJournal Article

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J Calap, J Chandler. [Enteropathic acrodermatitis. Hematologic study with X-ray microanalysis].. https://pubmed.ncbi.nlm.nih.gov/7331917/

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PubMed1998

[Suppurative acrodermatitis continua of Hallopeau. A differential diagnosis of paronychia].

HISTORY AND CLINICAL FINDINGS: A 39-year-old man was admitted for treatment of bilateral inflammatory-pustular skin changes in the area of the large toes and soles of the feet. Antibiotic treatment and an Emmert wedge resection had already been unsuccessfully performed at another hospital for what was diagnosed as paronychia. On admission there were inflammatory, in part erosive, red areas with yellow and partly confluent pustules on the distal phalanges of both great toes. The entire right nail-bed and left medial nail-bed were missing. In the area of the capillitium, both lower arms and the sulcus coronarius there were erythematous squamous plaques. INVESTIGATIONS: Radiography of the great toes demonstrated dystrophic demineralisation, in part with subchondral cystic changes of the spongiosa. Histological examination of the nail-bed showed hyperplasia and papillomatosis, definite hyperkeratosis with a prominent granular layer, as well as ortho- and parahyperkeratosis. Laboratory tests for inflammatory disease were unremarkable and there was no association with HLA B27. DIAGNOSIS, TREATMENT AND COURSE: Suppurative acrodermatitis continua of Hallopeau was diagnosed and immunosuppressive treatment with cyclosporin A given (initially 4.4 mg/kg. stepwise reduction to 2.5 mg/kg within 6 weeks, this dosage then continued for a further 10 weeks). Nearly complete healing was achieved, but the condition recurred in a mild form 2 weeks after the end of treatment. CONCLUSION: Suppurative acrodermatitis continua of Hallopeau should be included in the differential diagnosis of inflammatory changes of the distal phalanges.

Acrodermatitis↗
PubMed1998

Zinc uptake into fibroblasts is inhibited by probenecid.

Cellular zinc transport has not been fully characterized. The role of an anion carrier was investigated by treating normal human fibroblasts, and those carrying a mutation which affects zinc transport, acrodermatitis enteropathica (AE), with the anion carrier inhibitor, probenecid. Zinc uptake (2, 10, or 20 micromol 1(-1) 65zinc) was determined during initial rates of uptake (15 min) following treatment with 0, 10 or 20 mmol 1(-1) probenecid. Probenecid stimulated extracellular zinc binding in normal and AE fibroblasts. Probenecid inhibited the internalization of zinc in normal, but not AE, fibroblasts. Normal fibroblasts exhibited an apparent Km which was reduced by 53% and 44% in the 10 and 20 mmol 1(-1) probenecid treated cells. The Vmax was also reduced in the normal fibroblasts by 51% and 50% in the 10 and 20 mmol 1(-1) probenecid treated cells. The results suggest that a probenecid-sensitive anion carrier is involved in the internalization of zinc in human fibroblasts. The lack of an effect of probenecid on the internalization of zinc in the AE fibroblasts suggests that the mutation involves a probenecid-sensitive anion transport system, and that there may be a secondary mechanism for zinc transport in these cells.

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