ABSTRACT
Relapsing polychondritis is a rare systemic disorder characterized by recurrent inflammation of cartilaginous structures, the eye, the audiovestibular and cardiovascular systems. Skin lesions, found in 17% to 38% of cases, include leukocytoclastic vasculitis, livedo reticularis, erythema nodosum, erythema multiforme, keratoderma blenorrhagicum, psoriasis, polyarteritis nodosa, thrombophlebitis and other various conditions. We report a 65-year old man with relapsing polychondritis and associated thrombophlebitis. The patient was treated with oral dapsone and systemic steroid with complete resolution of symptoms. However, the patient died of severe intractable pneumonia.
Subject(s)
Aged , Humans , Cardiovascular System , Dapsone , Erythema Multiforme , Erythema Nodosum , Inflammation , Livedo Reticularis , Pneumonia , Polyarteritis Nodosa , Polychondritis, Relapsing , Psoriasis , Skin , Thrombophlebitis , VasculitisABSTRACT
Damage produced by radiation elicits a complex response in mammalian cells. Including growth rate changes and the induction of a variety of genes associated with growth control and apoptosis.At doses of 10,000 cGy or greater, the exposed indivisual was killed in a matter of minutes to a couple of days. With symptoms consistent with pathology of the central nervous system(CNS) including degenerative changes. The nature of the damege in irradiated cells underlies the unique hazads of ionizing radiation. Radiation injury CNS is a rare event in clinical medicine, but it is catastrophic for the patient in whom it occurs. The incidience of cerebral necrosis has been reportes as high as 16% for doses greater than 6,000 cGy.In this study, the effect of radiation on brain tissues was studied in vivo. Jun and p53 genes in the rat brain were induced by whole body irradiation of rat with 60Co in doses between 1 Gy and analyzed for expression analyses were done using 1.8 Kb & 0.8 Kb-pGEM-2-JUN/Eco RI/Pst I fragments, 2.0 Kb-php53B/Bam HI fragment and 1.1 Kb-pBluescript SK-ACTIN/Eco RI fragment as the digoxigenin or [alpha32P]dCTPlabeled probes for Jun, p53 and beta-actin genes, respectively.Jun gene seemed to be expressed near the threshold levels in 1 hour after irradiation of 60Co in dose less than 1 Gy and was expressed in maximum at 1 hour after irradiation of 60Co in dose of 30 Gy. Jun was expressed increasingly with time until 5 or 6 hours after irradiation of 60Co in dose of 1 Gy and 10 Gy . After irradition of 60Co in dose between 20 Gy and 100Gy, the expression of Jun was however increased to peak in 2 hours and decreased thereafter.P53 gene in this study also seemed to be expressed near the threshold levels in 1 hours after irradiation of 60Co in less than 1 Gy and was expressed in maximum and 6 hours after irradiation of 60Co in dose of 1 Gy. P53 was expressed increasingly with time until 5 or 6 hours after irradition of 60Co in dose between 1 Gy and 40 Gy. After irradition of 60Co in dose of 50 Gy and 100Gy. The expression of p53 was however increased in peak in 2 hours and decreased thereafter. The expression of Jun and p53 genes was not correlative in the brain tissue from rats.It seemed to be very important for the establishment of the optimum conditions for the animal studies relevant to the response of genes inducible on DNA damage to ionizing radiation in mammalian cells. But there are many limitations to the animal studies such as the ununiform patterns of gene expression from the tissue because of its complex compositions. It is necessary to overcome the limitations for development of in situ Northern analysis.