Adv Exp Med Biol
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The diagnosis, treatment and prevention of high altitude cerebral edema (HACE) are fairly well established. The major unresolved issues are 1) the pathophysiology, 2) the individual susceptibility, and 3) the relationship of HACE to acute mountain sickness (AMS) and to high altitude pulmonary edema (HAPE). In the context of the two types of cerebral edema, cytotoxic (intracellular) and vasogenic, a leaking of proteins and water through the blood-brain barrier (BBB), a recent MRI study in persons ill with HACE (16) suggested a predominantly vasogenic mechanism. ⋯ New work suggests that the brain swells on ascent to altitude, but that this is unrelated to AMS. Preliminary data showing that those with less cerebrospinal fluid volume (a tighter fit of the brain in the cranium) were more likely to develop AMS supports the hypothesis of Ross that those with less ability to accommodate the increased brain volume are the ones that suffer AMS. The blood-brain barrier and intracranial hemodynamics are the two key elements in the pathophysiology of HACE and AMS.
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Case Reports
Accelerated nodulosis during methotrexate therapy for refractory rheumatoid arthritis. A case report.
Accelerated nodulosis (AN) is a potential complication of methotrexate (MTX) therapy for rheumatoid arthritis (RA). We report on a 62-year old man affected by seropositive RA who developed AN after five months of MTX treatment. MTX-dose reduction was followed by rapid regression of the skin nodules. The Authors describe the typical features of AN and discuss on the pathogenetic mechanisms.
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Comparative Study
Plasma and urinary serotonin and 5-hydroxyindol-3-acetic acid in adults with migraine and tension-type headache.
Each headache can be a complex diagnostic, therapeutic, prognostic and social problem. The pain in the head can be connected with many organic and non-organic causes. ⋯ Based on the data obtained and their correlation with clinical features and in comparison with a control group, the following can be stated: (1) there is involvement of serotonin in migraine and tension-type headache during the attacks, although the positive 5-HT values from plasma were small; (2) urinary 5-HT values in migraine and tension-type headache were normal in comparison to the control group; (3) significantly decreased values of 5-HIAA in urine were found both in migraine and tension-type headache groups. These findings show that catabolism of 5-HT is probably decreased during headache periods; (4) visual aura was found in five out of ten subjects with tension-type headache.
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Traditionally, many advances in medicine have been serendipitous. Are serendipitous and anecdotal synonymous? Many of our materia medica today relate to initial probes and anecdotal reports that matured to full investigation and therapeutic indications. The recent situation regarding Skin Cap is one that highlights the downside of this scenario. ⋯ This product, over the period of twelve months, got rave reviews in the lay press in the non-peer reviewed dermatologic periodicals, and amassed impressive sales figures in this period of time. It was extremely effective, and most dermatologists who used it have patients who consider it the most effective therapy in the last year. The formulation of a low concentration of zinc pyrithione seemed unusual, and this truly was an anecdotal approach, using a homeopathic dosage of a commonly used p
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Oxygen tension (pO2) in rat renal cortex and outer medulla was studied after an intravenous injection of mannitol or furosemide, followed 10 minutes later by an intravenous injection of the non-ionic X-ray contrast medium (CM) iopromide (370 mg iodine/ml). Ten minutes after mannitol injection, before injection of CM, pO2 in the medulla had decreased from a control level of 32 +/- 3 to 28 +/- 4 mm Hg. The addition of CM caused a further decrease, to 24 +/- 5 mm Hg, which was a significant reduction. ⋯ Injection of CM caused a significant decrease in pO2 to 37 +/- 3 mm. Ringer's solution (n = 6) caused no changes. We conclude that pretreatment with mannitol or furosemide does not prevent the CM-induced decrease in pO2 in the outer medulla.