1

Let us assume we have a patient with this history and let us try to explain his/her normal CRP values on the end of this post given the fact of commorbid high fever and neutrophilia.

The questions to intrigue are here

  • If it is bacterial, how come CRP is not elevated?
  • If it is viral, how come there is neutrophilia?
  • If it is autoimmune, how come it is not autoimmune (ruled out by hematology and clinic)?

The patient wrote this:

Here are some fact about my fever of unknown origin, the diagnosis is apparently unknown, I am waiting now for some more serology, blood tests, urine cultivation and throat culture results.

The illness had 4 onsets, connected by a "feeling well" periods, 3 of them were cured by ATB, the four is being left untreated for diagnostic purposes.

First onset

before seeing a doctor:

duration:

  • one week

symptoms:

  • high fever on first day (39 Celsius)
  • elevated temperature the rest of the week (37.7 Celsius)
  • violent unproductive cough
  • conjunctivitis (bloody eyes)
  • congested nose (not runny, just swelled)
  • sore throat

therapy:

  • rest, hot tea, sore throat and cough off-the-counter medicine
  • w/o medical attention

after seeing a doctor:

diagnostics:

  • CRP elevated to 33
  • stethoscope test found "something" on the lungs

therapy:

  • clarithromycin 500mg 2 times a day
  • some otc mucolytics and antitusics (not codeine like)

duration:

  • four days

symtoms:

  • resolved after 4 days, but on the 7th day on ATB, the sore throat returned

Second onset

duration:

  • three days

therapy:

  • azithromycin 500mg for 3 days once a day

symtoms:

  • resolved after 3 days

Third onset

After another 4 days being ok, I went to sauna to strengthen my immunity. The next day...

symptoms:

  • high fever, used antipyretics when reached 39 Celsius
  • vomitting (due to fever)
  • violent unproductive cough

diagnostics:

  • referred to pneumologist
  • CRP elevated to 48
  • RTG of the lungs and hearth OK
  • stethoscope, lymph nodes, abdomine ok
  • the "pulse oximetry and arterial blood gas test" showed high pulse
  • blood: true left shift
    • leukocytes 18 (<10)
    • neutrophils 0.856 (<0.7)
    • lymphocytes 0.091 (>0.2)
    • neutrophils# 15 (<7)

therapy:

  • cefurixim (cephalosporines 2nd gen) 500mg twice a day for 2 weeks

duration:

  • resolved completely in a day or two

Fourth onset

After three weeks feeling healthy and one alright blood test (cell count+diff, antigens, CRP and biochemistry), I went into a hot shower after a train trip and ended it with a very short cold shower to strengthen immunity. The next day...

symptoms:

  • high fever (39 Celsius)
  • vomiting (due to fever)
  • mild unproductive cough

diagnostics:

  • RTG of the lungs OK
  • lymphnodes OK
  • sthetoscope OK
  • blood: true left shift
    • bilirubin 24 (<21)
    • ALT 1.04 (<0.83)
    • leukocytes 19 (<10)
    • neutrophiles 0.92 (<0.8)
    • lymphocytes 0.038 (>0.2)
    • neutrophiles# 17 (<7)
    • lymphocytes# 0.72 (>0.8)
    • sedimentation 1 (>2)
    • BUT CRP NOT (much) ELEVATED 6.2 (<5)

At this point, the pneumologist was kind of stunned by these results and referred me to the hemmatology the same day. The test there were pretty much the same, except a bit elevated CRP (~20). Hematologist ruled out malignity and referred me to the infections diseases. They ruled out some viruses Eppstein-Barr, HIV, heppatitis and perhaps boreliosis and referred me to USG of abdomen and RTG of sinuses, which were ok.

1

C-reactive protein synthesis is driven primarily by interleukin-6

IL-6 induces CRP production in the liver by activating Janus kinases. Signal transducers and activators of transcription subsequently switch on the CRP gene expression, leading to the production of CRP.

but fever is caused by a range of cytokines including IL-6, IL-1, TNF-a. So, at the time a fever appears, IL-6 levels may not have been high enough and present long enough to stimulate hepatic synthesis of CRP.

Whereas proinflammatory cytokines (e.g., IL-1, IL-6, and tumor necrosis factor) appear within one hour after the start of bacterial infection, and procalcitonin (PCT) after 5 hours, the hepatic synthesis of CRP starts 6 to 8 hours after onset and peak concentrations are reached between 36 to 50 hours after infection has started. [1]

  1. http://www.hindawi.com/journals/bmri/2013/124021/

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