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Interface Dermatitis, the ID reaction—another face of the Herxheimer-type "die-off" reaction

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The legitimate “Jarisch–Herxheimer reaction” classically follows antibiotic (eg, first with mercury, then with penicillin) treatment of syphilis as a result of microbial debris from dead bacteria triggering a systemic inflammatory response, which can range in severity from mild to life-threatening.

Later and as expected, “Herxheimer reaction” was applied more loosely to reactions following other treatments for other infections, and was appreciated to have several variants, depending on how loosely or strictly one wishes to apply language. Also as expected, the term has been misapplied and is therefore at risk of losing its meaning, especially among overly casual “influencer”-level conversations.

See my previous discussions and linked resources in the following 4 pages for more information.

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Interface Dermatitis, the ID reaction—another face of the Herxheimer-type “die-off” reaction

I personally have experienced at least two events of Interface Dermatitis (ID reaction), first following poison ivy/oak exposure, and second this past week following antibiotic treatment for early sinusitis. Both of these are discussed in the video excerpt above.

Since this topic is unknown to most patients and doctors, I have included several (impressively lackluster) PDF articles below, but again I think my casual coverage of this topic in the video excerpt above is plainly sufficient.

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Interface Dermatitis Sjogren’s Syndrome
2.51MB ∙ PDF file
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Interface Dermatitis Dermatopathology 2021
6.83MB ∙ PDF file
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Interface Dermatitis
1.67MB ∙ PDF file
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Acute And Recurrent Vesicular Hand Dermatitis Veien2009
674KB ∙ PDF file
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In the video excerpt above, I talk about my recent experience with the interface dermatitis (ID) reaction while en route to my detailing of intracellular calcium—stay tuned for the complete video.

Can you ANSWER me 8 questions with 12 answers on INTRACELLULAR CALCIUM?

  1. Describe the physiological roles of intracellular calcium (iCalcium, iCa).

    1. __________________________________________

  2. Describe the pathophysiological roles of intracellular calcium.

    1. __________________________________________

  3. What is the main molecular trigger for the cellular entry of calcium?

    1. __________________________________________

  4. How is the main molecular trigger for the entry of calcium converted to its opposite?

    1. __________________________________________

  5. What is the main biochemical requirement for this conversion?

    1. __________________________________________

  6. Name the two requirements for the requirement (answer) for question no5 above, ie what are the cofactors and coenzymes for no5 above?

    1. __________________________________________

    2. __________________________________________

  7. What single characteristic distinguishes physiologic from pathologic iCalcium?

    1. __________________________________________

  8. Name the 4 main “areas” or “relocations” for iCalcium

    1. __________________________________________

    2. __________________________________________

    3. __________________________________________

    4. __________________________________________

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INTRACELLULAR HYPERCALCINOSIS: 20 years later, this remains a topic of major and emerging importance

INTRACELLULAR HYPERCALCINOSIS: 20 years later, this remains a topic of major and emerging importance

Toward the end of one of my recent videos (LINKED HERE and below) I mentioned an update to my diagram explaining the clinical importance of elevated intracellular calcium. You can also see more discussion of this toward the end of this weekend’s video “

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