Medical hypotheses
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Lethal cancer and chronic untreatable viral disease with life threatening consequences are among the major burden for morbidity and mortality in the western world. A large number of resources are employed every year in identification of new drugs to treat this condition. A remarkable percentage of resources are wasted for safety concerns about possible acute cardiac or pulmonary toxicity of the new identified compounds, that are rejected without further development even when promising. ⋯ ECMO has been used with success to treat acute life-threatening cardiac and pulmonary toxicity. Our hypothesis is that the new ECMO technological improvement could make this technique available to other setting, such as lethal cancer and infectious diseases, where it can provide a safe base to overwhelm acute cardiac and pulmonary toxicity of chemotoxic drugs and techniques. New drugs and old promising compounds rejected for toxicity could thus be re-introduced and employed, opening a new scenario in the treatment of life-threatening diseases.
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Despite the abundance of information on cerebral malaria (CM), the pathogenesis of this disease is not completely understood. At present, two nonexclusive dominant hypotheses exist to explain how the neurological syndrome manifests: the sequestration (or mechanical) hypothesis and the inflammatory hypothesis. The sequestration hypothesis states that sequestration of Plasmodium falciparum-parasitized red blood cells (pRBCs) to brain capillary endothelia causes obstruction of capillary blood flow followed by brain tissue anoxia and coma. ⋯ BBB dysfunction would thus occur in CM by a mechanism similar to the one occurring in sepsis and is in agreement with the inflammatory hypothesis. Nevertheless, differently from in the inflammatory hypothesis, BBB leakage would facilitate the penetration of ammonia and other toxins into the brain parenchyma, but would not be sufficient to cause CM when occurring alone. We believe our hypothesis better explains the pathogenesis of CM, does not have problems to deal with the exception data not explained by the previous hypotheses, and reveals new targets for adjunctive therapy.
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Postherpetic neuralgia is the most common complication of herpes zoster which is caused by a reactivation of latent varicella zoster virus. The pathogenesis of postherpetic neuralgia may involve peripheral and central mechanisms. Reported risk factors for postherpetic neuralgia include female gender, old age, diminished cell-mediated immunity and nutritional deficiencies. ⋯ We further propose that a follow-up study that contains two groups of herpes zoster patients, i.e., with or without gastroendoscopy-proven PUD, be conducted to determine their incidence of postherpetic neuralgia. In addition, despite of the high proportion of zoster patients having been treated with antiviral therapies, prevention and treatment of postherpetic neuralgia remain challenging in clinical practice. The potential risk of postherpetic neuralgia in zoster patients with PUD could mean that physicians need to pay more attention to the comorbidity--PUD in patients with herpes zoster and treat PUD earlier in order to prevent the development of postherpetic neuralgia.