Congenital giant hydronephrosis in adults

Giant hydronephrosis is the term designating the presence of more than 1,000 ml. of fluid in the collecting system. Of 4 cases of congenital hydronephrosis found over a three-year period at the Ochsner Medical Institutions, 2 were associated with unsuspected carcinomas. Hydronephrosis may first be detected as a mass palpable in the abdomen and displacing the intestines on gastrointestinal films. Excretory urography, retrograde pyelography, and angiography confirm the diagnosis. The treatment of choice is nephrectomy.     

Cotton-wool spots and the early diagnosis of giant cell arteritis

BACKGROUND: Giant cell arteritis is a common cause of severe visual loss in older individuals. Patients often present to the ophthalmologist having already lost vision in one eye. Detection of early ophthalmoscopic signs that precede irreversible visual loss in giant cell arteritis would allow preventative treatment in an otherwise frequently blinding disease. METHODS: Case presentations. RESULTS: Seven patients with mild visual symptoms and results of an ophthalmologic examination significant for cotton-wool spots were found to have giant cell arteritis. On specific questioning, six of seven patients described constitutional symptoms consistent with giant cell arteritis. Six patients had an abnormally elevated Westergren erythrocyte sedimentation rate. Temporal artery biopsy confirmed giant cell arteritis in six patients. The seventh patient received a diagnosis of polymyalgia rheumatica. Prompt treatment with corticosteroids led to preservation of vision and uneventful resolution of the cotton-wool spots in all seven patients. CONCLUSION: Cotton-wool spots are an early ophthalmoscopic finding in giant cell arteritis and can precede severe visual loss. Recognition of the significance of cotton-wool spots, use of laboratory studies, and prompt treatment may preserve vision in an otherwise frequently blinding disease.     

Expression of cyclo-oxygenase-2 in human airway smooth muscle is associated with profound reductions in cell growth

1. It is now accepted that uncontrolled proliferation of human airway smooth muscle (HASM) cells contributes, in many cases, to the chronic stages of asthma. However, the physiological and pathophysiological processes regulating cell growth and division in the airway are not clear. We have recently shown that the immediate early gene, cyclo-oxygenase-2, is induced by cytokines in HASM cells. Since cyclo-oxygenase metabolites, such as prostaglandin (PG) E2 have been shown to modulate HASM cell growth, we have investigated any autocrine action of endogenously released cyclo-oxygenase-1/2 products on the proliferative responses in these cells. 2. HASM cells were cultured from healthy tissue obtained at lung or heart/lung transplantation. HASM cell proliferation was measured by [3H]-methyl thymidine uptake by cells and by cell counts. Cyclo-oxygenase-2 expression was measured by Western blot analysis and activity measured by the release of PGE2, by radioimmunoasay. 3. HASM cells proliferated in response to foetal calf serum, a response that was greatly inhibited when cyclo-oxygenase-2 was induced with either interleukin-1beta plus tumour necrosis factor-alpha or interleukin-1beta, tumour necrosis factor alpha plus interferon gamma (each at 10 ng ml(-1)). The inhibitory effect of cytokines on HASM cell proliferation was reversed in a concentration dependent manner by either the mixed cyclo-oxygenase-1/-2 inhibitor, indomethacin or the selective cyclo-oxygenase-2 inhibitor, L-745,337 (each at 10 microM). 4. PGE2 or the stable analogue of prostacyclin, cicaprost concentration-dependently (0.1 pmol to 1 microM) inhibited serum induced proliferation of HASM cells. By contrast, the TP receptor agonist, U46619 stimulated proliferation of HASM cells when cells were cultured without but not with serum. Other cyclo-oxygenase products, PGD2, PGF2alpha had no effect on cellular proliferation at concentrations up to 1 microM. 5. These observations illustrate a profound inhibitory effect of cyclo-oxygenase-2 induction on HASM cell proliferation, possibly via IP or EP receptor activation. Cyclo-oxygenase-2 induction has, thus far, been associated with the pro-inflammatory responses of plasma exudation and oedema formation and is assumed to be an enzyme worthy of selective inhibition in many disease states. However, our observations suggest that cyclo-oxygenase-2 can have an anti-inflammatory, anti-proliferative function in the airways. These observations may have importance in the use and development of therapies for airway disease such as asthma.     

Is oral levamisole immunostimulation in rats mediated by reduced levels of free plasma corticosterone?

A brief review of the immunostimulative and anti-inflammatory properties of levamisole is followed by a research report which indicates that in rats under antigenic challenge by ovalbumin, oral levamisole (18 mg/kg) decreases corticosterone levels. This previously unreported finding may belie the immunostimulative effect of levamisole.