Deterioro neurológico y crisis convulsiva / Neurologic impaiment and seizures

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[Eosinophilic fasciitis and related diseases]. / Fascitis eosinofílica y enfermedades relacionadas.

The eosinophilic fasciitis (EF) is characterized clinically by cutaneous swelling (in the initial phases) and fibrosis (in advanced phases) that affects predominantly to the extremities. Differences with scleroderma are, among other, that it affects from a primary way to the fascia and the subcutaneous fat tissue instead to the dermis, and its response to the corticoids. In most instances its causes are ignored (then we could denominate it Shulman's disease), but in a non negligible percentage of cases it can have a toxic origin, and, more rarely, to be a paraneoplastic syndrome. Other disorders with diverse etiologies can cause cutaneous lesions clinical and histologically indistinguishable from EF; the group of all these diseases would constitute the fasciitis-panniculitis syndrome, from Shulman's disease would be an idiopathic form.

Fascitis eosinofílica y enfermedades relacionadas / Eosinophilis fascitiis and related diseases

La fascitis eosinofílica (FE) se caracteriza clínicamente por tumefacción (en las fases iniciales) y fibrosis (en fases avanzadas) cutáneas de predominio en las extremidades. Las diferencias con la esclerodermia son, entre otras, que afecta de forma primaria a la fascia e hipodermis en lugar de la dermis; y su respuesta a los corticoides. En la mayoría de las ocasiones la etiología es desconocida (entonces podríamos denominarla enfermedad de Shulman), pero en un porcentaje no despreciable de casos puede tener un origen tóxico, y, mas raramente, ser un síndrome paraneoplásico. Otras enfermedades con etiologías diversas pueden provocar lesiones cutáneas clínica e histológicamente indistinguibles de la FE; el conjunto de todas estas enfermedades constituirían el síndrome de fascitis-paniculitis, del que la enfermedad de Shulman sería una forma idiopática (AU)

[Glucocorticoid treatment improves glucose tolerance in patients with temporal arteritis or polymyalgia rheumatica]. / El tratamiento con glucocorticoides mejora la tolerancia a la glucosa en pacientes con arteritis de la temporal o polimialgia reumática.

BACKGROUND: Corticosteroid therapy has been shown to improve glucose tolerance in some connective tissue diseases. This fact has been inadequately investigated in vasculitis. OBJECTIVE: To evaluate the effect of glucocorticoid therapy on glucose tolerance in patients with temporal arteritis (TA) or polymyalgia rheumatica (PR). MATERIALS AND METHODS: An oral test with glucose overload (OGO) was performed before and after one month of initiating therapy with corticosteroids in 14 patients with TA or PR (TA/PR group) and in nine patients with other chronic inflammatory diseases (control group). RESULTS: After treatment, patients with TA/PR experienced a decrease in the area under the glucose curve and in serum glucose values at minutes 0, 90, and 120 of the OGTT. Also, a decrease was observed for the area under the insulin curve and for plasma insulin levels at minutes 90 and 120 after OGO. CONCLUSIONS: Therapy with corticosteroids improves glucose tolerance in TA/PR with no increase in insulin secretion.

An open comparison of the diabetogenic effect of deflazacort and prednisone at a dosage ratio of 1.5 mg:1 mg.

OBJECTIVE: To compare the diabetogenic effects of deflazacort (D) versus prednisone (PN) using a dosage ratio of 1.5 mg deflazacort:1 mg prednisone. METHODS: Thirty-three patients suffering from various active connective tissue or chronic inflammatory diseases were randomized to be treated with D or PN, assuming a therapeutic equipotency ratio of 1.5 mg D:1 mg PN. Neither dosage nor glucocorticoid employed were modified during the study. Patients had not received steroid treatment during the month prior to their inclusion date. Fasting glucose, glycosylated haemoglobin and fructosamine were determined before and after 1 month of treatment. Non-diabetic patients were also submitted to an oral glucose tolerance test (OGTT) at entry and after 1 month. Results were compared by univariate, and multivariate tests to correct the effects of age, body mass index and diagnosis. RESULTS: After 1 month of treatment there were no differences between D and PN in fasting glucose, glycosylated haemoglobin, or fructosamine. OGTT performed after treatment showed similar glucose values for both treatment groups. Patients treated with D had insulin levels at min 60 of the post-treatment OGTT which were higher than those treated with PN [114.1 (62.8) mcUI x ml(-1) versus 73.5 (32.7) mcUI x ml(-1), P = 0.049], but the difference lost its statistical significance in the multivariate analysis. CONCLUSION: D and PN have similar effects on glucose tolerance when an equipotency ratio of 1.5 mg D:1 mg PN is employed. Previous studies employing a ratio of 1.2:1 mg may have underestimated the adverse effects of D on glucose metabolism.