Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As procalcitonin concentrations have been shown to be elevated in patients with septicemia and gram-negative infections in particular, we proceeded to investigate the effect of endotoxin, a product of gram-negative bacteria, on procalcitonin concentrations in normal human volunteers. Endotoxin from Escherichia coli 0113:H10:k, was injected i.v. at a dose of 4 mg/kg BW into these healthy volunteers. Blood samples were obtained before and 1, 2, 4, 6, 8, and 24 h after injection of the endotoxin. Each patient's cardiovascular and overall clinical status was monitored over this period. The patients developed chills and rigors, myalgia, and fever between 1-3 h. Tumor necrosis factor-alpha levels increased sharply at 1 h and peaked at 90 min, reaching the baseline concentration thereafter by 6 h. Interleukin-6 levels increased more gradually, peaking at 3 h and reaching the baseline concentration at 8 h. The procalcitonin concentration, which was undetectable (< 10 pg/mL) at 0, 1, and 2 h, was detectable at 4 h and peaked at 6 h, maintaining a plateau through 8 and 24 h (4 ng/mL). There was no elevation of calcitonin concentrations, which remained below 10 pg/mL, the lowest sensitivity of the assay. Procalcitonin was measured by a two-antibody immunoradiometric assay specific for this peptide, with no cross-reactivity with calcitonin, katacalcin, or calcitonin gene-related peptide. We conclude that endotoxin induces the release of procalcitonin systemically, that this increase is not associated with an increase in calcitonin, and that the increase in procalcitonin associated with septicemia in patients may be mediated through the effect of endotoxin described here. Whether procalcitonin participates in the mechanisms underlying inflammation remains to be investigated.
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PMID:Procalcitonin increase after endotoxin injection in normal subjects. 798 63

Hot flashes (HFs), defined as transient sensations of heat, sweating, flushing, anxiety, and chills lasting for 1-5 min, constitute one of the most common symptoms of menopause among women though only a few seek treatment for these. The basis of HFs lies in abnormal hypothalamic thermoregulatory control resulting in abnormal vasodilatory response to minor elevations of core body temperature. Recent data suggest an important role for calcitonin gene-related peptide, hypothalamic kisspeptin, neurokinin B and dynorphin signal system, serotonin, norepinephrine in causation of HFs in addition to estrogen deficiency which plays a cardinal role. The mainstay of treatment includes hormonal replacement therapy, selective serotonin, and norepinephrine reuptake inhibitors in addition to lifestyle modification. In this review, we address common issues related to menopause HFs and suggest a stepwise approach to their management.
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PMID:Menopausal Hot Flashes: A Concise Review. 3100 Oct 50