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I've long been interested in the so-called "smoker's corn", which I attach as an example.
Having seen some work by Craig Camasta DPM, I am interested in wether there is any other literature on the subject. These intractable yellow, macerated lesions are quite peculiar.
I think what may be confusing the issue is the basic terminology. Describing the presenting skin symptoms there appears to be an indentation in the epidermis which has localised hyperkeratotic hypertrophy. The whiter underling skin which surrounds the yellow mass would be consistent with increased hydration (water trapped in the side salt linkages of the keratin molecules). These kinds of lesion are often long standing and thought to be the result of secondary changes within the dermis where the yellow elastic tissue is replaced by white fibrous bands binding the Stratum Germinitum to the fibrous capsule beneath. These are often referred to in chiropody text as fibrous corns. All too frequently the white maceration is confused with the microscopic white fibrous tissue within the dermis. This would be impossible to see with the naked eye and as the lesion is not a second intension wound, there would be no visible keloids. Daily enucleating the hyperkeratosis followed by paints with an alcoholic base will quickly change the colour from white to yellow. Effectively the whiteness disappears, this would be impossible if the cells were fibrous tissue.
Discoluration similar to the macerated appearance can be found on the skin surfaces after applications of salicylic acids. This is thought to represent a microscopic hydration of the keratin cells and when the cells are physically remove the colour of skin reverts to normal.
The association with smokers
I worked with a chap in NZ and he was convinced smoking could influence chemical deposits in skin cells. He thought smoker's hard skin was darker brown than no smokers. There was some preliminary studies done with a skin light/ colour instrument but the results were inconclusive. It has been shown that chemical deposits have been found in the skin and nails from systemic ingestion e.g. gold and arsenic, so it is not beyond belief nicotine or other tar derivatives may stain skin under certain circumstances. The circumstances have never been proven.
Another plausible explanation is the fibrous lesions are chronic and painful feet in the client group are borne stoically. Often those most severely affected have co moribund complications which might involve compulsive behaviours such smoking and dependency on alcohol and drugs. In the thirties when most of the text concerning this skin lesion classification was made many of the clients described were institutionalised individuals who smoked incessantly.
I think the colour of the hyperkeratosis may become more pigmented in smokers but the association between smoking and localised hyperkeratosis on weighbearing areas is zero.
I think this condition is something that is steeped in anecdote - but I really believe it exists as a distinct pathology separate to typical discreet hyperkertotic lesions and IPK.
Certainly since being made aware of these lesions by podiatric surgeons, who refuse to operate on them in the presence of a continued smoking habit, I can almost predict a person has a heavy smoking habit based soley on the clinical appearance of the 'corn'.
Craig Camasta I think had some ?unpublished work on changes in incidence pre/post smoking which was quite interesting.
Although this condition seems universally known about by all podiatric surgeons I speak with, general podiatrist are usually quite astounded at the proposition. :p
Dr. Camasta has made a few presentations on this topic at the Podiatry Institute Seminars - why not check with him directly. I have been a patient of his over the years and he has never failed to answer any questions I had - from the complex to the mundane. He is very approachable and would be pleased to help in any way that he can. His e-mail address is posted on the faculty page of the Podiatry Institute's website ( www.podiatryinstitute.com ).
Becca
Last edited by Becca : 28th October 2005 at 04:34 AM.
I posed a similar question a while ago (maybe May/June)on Podiatry Arena, IPK and smokers. Some interesting info came from that and even though I have made the suggestion to a few people that there may be an association between their smoking and the pain in/on their foot they would still rather ask "isn't there anything else you can do" (besides debriding/ deflective padding than stop lighting their nicotine sticks.
Would be interested to see what comes back from Craig Camasta.
OMG. I thought I was imagining it! But the only times I've seen these corns presenting have been with smokers! Would love to read more on this and maybe even do some research!
Have seen a number of patients over the years with large intractible fibrous plantar HDs which didn't respond to orthotic/footwear management and/or keratolytics and local debridment - sometimes as regularly as 4 week intervals. On several of these patients, within two months of quitting smoking, their lesions resolved. At least two patients resumed smoking after a year or two - and within weeks, their lesions returned. One man in particular had an on/off relationship with the weed - and his fibrous HDs treated his feet to the same regime! Not all smokers present with fibrous HDs or other keratosis and not all patients with these lesions are smokers. Perhaps some are more susceptible to one or more of the chemicals contained in ciggarette smoke, which may then act as a potentiate to trigger the localised keratosis.
Most recent success case was after 20 yrs of suggesting to patient she had a 50/50 chance of resolving the corn within 12 months. 9 Months into smoking cessation the corns we had been debriding for 20 yrs had resolved.
I think one of the theories is that smoking affects the collagen synthesis and flexibility of dermis and epidermis. More so in women than men ...
I have too many of these cases over the years to mention but my treatment is enuculation followed by application of trichloroacetic acid with return visits within 2-4 days then progressively lengthening intervals between return visits.
Have fun ...I have been having these anecdotal conversations for over 25 yrs now and funny no one has come up with the money to study it...maybe should ask the tobacco industry
I believe there is a link with these type of corns and smoking. I havea Pt whoi gave up smoking and these lesions changes dramtically in there composition ? Perhaps Localised Ischaemia due to vascular effects of smoking?
Smoker's corns - aetiology
Re: Smoker's corns - aetiology
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Hybrid Mode
