Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute thallium poisoning in a 67-year-old Chinese woman is described. She presented with acute pain in the chest, abdomen, and lower limbs. The diagnosis was not made, however, until alopecia developed. Detoxification treatment, which included Prussian blue (potassium ferric hexacyanoferrate) was then given, but further neurological damage occurred. The patient's motor function recovered after 1 year, but residual sensory neuropathy remained. This case illustrates that tissue-bound thallium may cause prolonged neurological damage if detoxification therapy is not commenced within 72 hours of the onset of acute poisoning. Acute abdominal pain and painful neuropathy in the lower extremities are important early diagnostic clues for timely therapy. However, by the time alopecia develops-typically around 2 weeks after the onset of symptoms-detoxification therapy may not be able to prevent the development of prolonged neurological damage.
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PMID:Management of thallium poisoning. 1102 53

Taxane-induced peripheral neurotoxicity (TIPN) is the most common non-hematological side effect of taxane-based chemotherapy, and may result in dose reductions and discontinuations, having as such a detrimental effect on patients' overall survival. Epothilones share similar mechanism of action with taxanes. The typical TIPN clinical presentation is mainly comprised of numbness and paresthesia, in a stocking-and-glove distribution and may progress more proximally over time, with paclitaxel being more neurotoxic than docetaxel. Motor and autonomic involvement is less common, whereas an acute taxane-induced acute pain syndrome is frequent. Patient reported outcomes questionnaires, clinical evaluation, and instrumental tools offer complementary information in TIPN. Its electrodiagnostic features include reduced/abolished sensory action potentials, and less prominent motor involvement, in keeping with a length-dependent, axonal dying back predominately sensory neuropathy. TIPN is dose-dependent and may be reversible within months after the end of chemotherapy. The single and cumulative delivered dose of taxanes is considered the main risk factor of TIPN development. Apart from the cumulative dose, other risk factors for TIPN include demographic, clinical, and pharmacogenetic features with several single-nucleotide polymorphisms potentially linked with increased susceptibility of TIPN. There are currently no neuroprotective strategies to reduce the risk of TIPN, and symptomatic treatments are very limited. This review critically examines the pathogenesis, incidence, risk factors (both clinical and pharmacogenetic), clinical phenotype and management of TIPN.
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PMID:Taxane and epothilone-induced peripheral neurotoxicity: From pathogenesis to treatment. 3164 57