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Ed Dewke's Rebound Diary
Part 1 — January-February, 2004

(go to Part 2)

Monday, January 26, 2004 - Why I Know I’m Rebounding (My Immune System has Left the Building)

Tuesday, February 3, 2004 - Retrospection: My First P; How Hate Grows

Thursday, February 12, 2004 - Foot P, How Charming ... Hand P, Too ... Remembering Cyclosporine with Affection

Saturday, February 14, 2004 - Meeting a Young Old Wife

Wednesday, February 18, 2004 - Topography: From Dots to Continents

Tuesday, February 24, 2004 - On Ears, on Changing Topicals, and a Weird Arthritic Reprieve


Monday, January 26, 2004

 Why I Know I’m Rebounding (My Immune System has Left the Building)

It’s been four weeks since I’ve taken any systemic medication for my P.  The week between Christmas and New Years I stopped taking cyclosporine, an oral immunosuppressive drug that does well clearing my skin and keeping my psoriatic arthritis (PA) at bay.  But six weeks before that I’d started dropping my dosage on a weekly basis.  My normal dose was 350 mgs a day and by Christmas I was taking 100 mgs a day and after that I just stopped.

About the second week in December all my P symptoms were returning.  Big lesion on my right knee and arthritic swelling obvious in that knee.  (Not so bad, though, as it would have been were I not taking glucosamine/chondroitin as a daily dietary supplement.)  Big lesion on my right buttock.  Nine of ten fingernails showing corruption at the cuticle, and inflammation in the mantles of all fingers and thumbs.  Itchy scalp.  Lesion starting small above my navel.

I should be into my third week of a 12 week course of Amevive right now, but that didn’t happen because my CD4 helper T-cell count was way too low (111 and Amevive isn’t supposed to be used by anyone with a count below 250).  This caught everybody by surprise.  Ms A. (my derm-physician's' assistant) called my radiation oncologist, Dr. M., to find out if my 25 days of radiation last year might have anything to do with it he said it could.  But more derms put their two cents in on the subject and they suggested the fact that I’ve been on immunosuppressive drugs without cessation for over two years might have something to do with it.

What bothers me is that there were no tests during those two-plus years to determine what effect all my immunosuppressive drugs were having on me.  If CD4s — for example — are important, and these drugs I’ve been on can wipe them out, why wasn’t there some concern to find out a long time ago?  (This is not to suggest I didn’t have tests while undergoing methotrexate, Enbrel, and cyclosporine therapies.  Indeed, I had blood work done almost every month.  But as far as I know, the performance of my immune system was not the subject of inquiry.  Rather, they were looking for indications that there might be liver or kidney damage.)

I went on line and tried to figure out just how important my CD4s are.  After a couple of hours of largely over-my-head reading, I was prepared to conclude CD4s protect us against “opportunistic infection.”  The HIV virus either stops or wipes out CD4s, and a couple of readings pointed out that counts as low as mine (111 at the lowest so far) are what they expect to see when someone who has tested positive to HIV has finally decayed into full-blown AIDS.  That, I thought, was pretty enlightening.

So it’s been three weeks now since this Revelation about my CD4s.  I’m off all systemic P-medication and depending on topicals to keep the skin lesions at bay.  I spend about an hour a day working clobetasol propionate ointment into my finger tips, knee, butt, navel and growing collection of dime-sized lesions here and there.  I found my medical forceps hidden in a rarely-used drawer the other day and right away set to work peeling my largest lesion, the one on my right knee.  It’s been four or more years since I did this last, but I didn’t have to think about it.  I hadn’t forgotten a thing.  I remembered perfectly how to look for the loose edges of the largest scales, work the a pointy end of the forceps deep under the scale and jiggle very gently to break it away without much blood.  But I didn’t remove any record-breaking scales.  I think the largest one I got off intact was about the size of a dime.  I remember times, ten years ago, when I could peel skin scales the size of silver dollars off my calves and I would tack these with push pins onto my bulletin board.

I remember some controversy about the value of exfoliating this way.  One school of thought says never to “peel.”  When a lesion is moist, rub gently with terrycloth and be happy with whatever comes off.  Stop if anything starts bleeding.  But I’ll tell you why I take the forceps and make a project of it.  The goop — in this case, the clobetasol propionate ointment — is largely useless if it’s just smeared on top of scale.  It must hit the layers of skin that are still alive and growing too fast and these, depending on the lesion, may be quite deep beneath the outermost layer of scale.  When I have peeled down to bright red skin — beneath the white and yellow scale — I know I have reached an area where the ointment can do some good.  And since I found the forceps and peeled my knee, once more I have proven this to myself.  The lesion is still active, and I peel scale off it every day, but it is far less inflamed than it was — the skin is salmon pink rather than scarlet — which means the clobetasol is doing its job.

Tuesday, February 3, 2004

Retrospection: My First P ... How Hate Grows

My P first appeared in 1990, when I was 39 years old.  For many months it was only on my scalp.  The first person to use the word “psoriasis” was a barber and I didn’t think much about it.  He pointed me towards a few brands of shampoo that were supposed to help “psoriasis” and I naively thought following his advice and using these shampoos would take care of the problem.  Months passed. I developed a lesion on the tip of my nose.  This one finally drove me to a dermatologist.  As is so frequently the case for flakers, P wasn’t her first choice diagnosis.  First she treated me for pre-cancerous skin cells on my nose.  This involved killing the lesion with super-cool gas and hoping the nose would heal lesion-free.  It worked for awhile, then the lesion came back and I switched dermatologists.  This derm looked at my nose, my scalp, and said “psoriasis.”  I’d heard the word twice, now.  I went off in search of information.  And became depressed.

It seems identifying the demon enraged it.  The moment we started targeting treatment to P, it erupted with an unimaginable magnificence.  The speed with which my skin turned from normal to grotesque was breathtaking.  It occurs to me, now, that it came then with all the strength and speed of the rebound I’m currently experiencing.

First, all the earliest lesions become hardened against whatever topical palliative I use.  This means they might stop growing under the influence of the goop, but they don’t subside.  They remain inflamed and they flake — while new lesions crop up everywhere.  At first the new lesions are red spots about the size of BBs.  Sometimes they are isolated, but more often than not they appear in clusters, three to six of them within an inch or so of each other.  It happens on the calves and forearms first, then on the thighs and upper arms, then on the back, chest and abdomen. The unknowing will say, “It looks like measles.” 

All these tiny, colonial lesions grow rapidly.  Those that are clustered closely conjoin and form the big lesions that will ultimately be the most difficult to clear — the lesions that cover elbows and knees like yarmulkes.  The more isolated spots will achieve some indeterminate size — dime, quarter, half-dollar — and then settle there.

Watching all this occur now is a unwanted trip down Memory Lane, like returning to an alley where, in childhood, you were beaten up by bullies.  The only thing different I bring to the party this time is knowledge about how bad it’s going to get and the fruitlessness of all the attempts I’m going to make to thwart it.

There is an order to how we object to flaking, a hierarchy to our hatred of lesions, and I imagine, though we all possess this, the details differ as significantly as our gender and our personalities.  So in defining mine I’m attempting to build no case for anyone else.  My most hated lesions are the ones that hurt or itch.  The next most hated are those that are most visible.  My attitude about all the other lesions borderlines indifference. 

Thursday, February 12, 2004

Foot P, How Charming ... Hand P, Too ... 
Remembering Cyclosporine with Affection

P on the soles of my feet is much different than P anywhere else on my body.  I believe the P is active for quite a while before it is noticeable, because it doesn’t turn into scale.  At first the skin just thickens.  I’ve thought about this and the only logical explanation I can come up with (with no more real knowledge than I possess) is that the pressure on the skin on the bottoms of my feet compacts the dead layers of skin into leather-like calluses.  Eventually, where the dead skin is thickest, the outer-most layer turns whitish, and though it still doesn’t scale, the color is the same as the fine scale common to plaque lesions on knees and elbows.  It’s at this point that what’s going on becomes noticeably psoriasis.

First, the thick white stuff showed up between my little toe and the next one on my right foot.  I could not see it from the top and it was difficult to see from the bottom because the P arthritis in my knee doesn’t permit me to hold my foot in my lap and turn it over for many seconds at a time.  I discovered it while scratching my foot and peeling off about an inch of this white dead skin between the toes.  Between the toes, these thickened plaques will slough off by themselves because of the natural moisture and the abrasion that occurs from walking.  Once I saw what had come off in my fingers, I took a closer look.  The whole outside edge of the bottom of my foot is one big lesion and at the pressure points — ball of my big toe, narrow tendon just outside the arch, and the heal — had developed the white patches.  I started to peal more from the patch I’d torn off between the toes and it was, literally, like skinning my foot.  Two or three square inches of thick skin came off easily.  I knew I could peel the whole sole if I wanted to.  I recalled something else that I’d forgotten about foot P.  If you peel too much, the thinner, formerly unexposed skin beneath will dry out fast and crack.  And cracks on the bottom of a psoriatic foot can be very painful.  So I stopped peeling where I could (without leaving dangling flaps of skin).  I used nail clippers to cut away some rough edges around the peeled area. 

But I stopped peeling too late.  By the next evening the skin under where I peeled had cracked in two places.  Ah, now I remember.  The Joy of Foot P!

I had an appointment Monday of this week with Ms. A. (my derm-physician's assistant).  I showed her my foot and most of the new blossoms on my limbs and remembered, while we were talking, that the last time I had foot P this bad (which was several years ago) I had occluded them overnight by taping 8 gal plastic trash bags over a liberal application of topical corticosteroid ointment.  I asked her if she’d still recommended it.  She said sure, but also recommended something new.  It’s a cream called Vanamide (Dermik Laboratories, a Division of Aventis Pharmaceuticals Inc.) and its active ingredient is urea (40%).  Yeap, this is stuff from our urine, a toxic product of protein metabolism.  (Years ago someone emailed me and asked if I’d heard slathering pee on lesions helped.  I laughed in response.  This is why I swear never to dismiss anything as foolish!) 

Here’s how the Vanamide package insert describes Urea:  “Urea dissolves the intercellular matrix and thereby softens hyperkeratotic [abnormally thick horny layer of skin] areas by enhancing the shedding of scales.... For enzymatic debridement [surgical removal] and promotion of normal healing of surface lesions, particularly where healing is retarded by local infection, necrotic [dead] tissue, fibrinous [diseased connective tissue] or purulent [containing pus] debris, or eschar [hard crust or scab]. [Bracketed defining words looked up by Ed.  Sorry their inclusion here busts up the otherwise poetic rhythm of this package insert prose.]  The insert for Vanamide goes on to actually recommend using it under occlusion.  They say it is strong enough to soften ingrown toenails.  Had I not peeled away the necrotic, fibrinous eschar accounting for most of the P lesion on my right foot, I would have been tempted to occlude Vanamide on there last night or the night before.  As it is, with the lesion now tender and cracked, I’m afraid a dose of Urea might penetrate further than intended giving me dissolved intercellular matrices in all the wrong places.

(Excuse me while I take a minute to go wash the Latin out of my mouth....)

Last Spring, when I was in the final three months of my uneventful Enbrel regimen, my hands looked about as bad as they do now.  (It is amazing, on reflection, that six months of cyclosporine in the Summer and Fall was able to completely clear them! Including the nails!) One day last Spring I took my two oldest granddaughters to Dairy Queen.  We stood in line, ordered our treats, picked them up and sat in a booth to eat.  A group of young people walked by us laughing.  Alexandria (age 10) said, “I hate those people,” and scrunched her face up like only 10 year-olds can.  “Why do you say that?” I asked.  “Do you know them?”  “They were behind us in line,” she said, “and they were staring at your hands and talking about how gross they looked.”  It seems like it took me way too long to come up with a response to this.  Finally, I said, “Well, if those folks knew me, if they were familiar with my lightening wit and charismatic personality, they wouldn’t pay any attention to my hands.”  To this, Stephanie (also 10 years old) said, “What’s carey-spastic, Papaw?”  Alexandria added, “If they knew you, do you think they would understand you?”

This incident added a new layer of stigma to the reality of having serious hand P.  I’m usually super-conscious of my  hands when they’re flaming and I’m out in public, but my family is used to it and when in the company of my kids and grandkids my P is ignored.  (Even I can forget about it in this company.)  Well, on this occasion, public and family were mixed.  I was caught up in the family (on a outing with my two granddaughters) and oblivious to the public.  What I hadn’t realized would occur was their stigma on my account.  My granddaughter was upset by the reaction of strangers to my hand P — even though I hadn’t noticed that reaction.  And it occurred to me right away that this was worse — by a considerable margin — than being stigmatized myself.

I suppose that lesions on one’s face are worse, even, than hand P.  Ironically, my nose was the second place P showed up [see January 26 entry].  It had been in my scalp for some time and then, before any of it had been properly diagnosed, it showed up on my nose: a red lesion right on the end — very Rudolphian. As I wrote earlier, the first derm I went to didn’t diagnose P and my nose lesion was “burned off” with super-cool gas.  Not surprisingly, it returned quickly.  Once I started treating the face lesions as P, they proved to be very responsive to topicals and, as a result, I haven’t had to live for long periods wearing my disease on my nose, or my cheeks or my chin.

However, three or four years into my tryst with P, symmetric lesions showed up on the right and left of my chin, just above the jaw bone.  Both would grow fast to about the size of a nickel.  Sometimes it seemed this would happen over night!  I couldn’t be fast enough with my topicals to guarantee being rid of these unsightly blemishes when I had to make appearances, so I grew a beard.  I wore that beard — with only a couple of brief respites — for a decade.  I’ve no idea how often those two lesions were active beneath the beard (they rarely itched), and it wasn’t until I’d been clear or nearly clear for several years on the systemics that, in 2003, I finally shaved it off. 

As you might expect, I’ve been paying close attention to my face during this rebound.  The nose has already flared and I’ve responded, as always, with a mild topical corticosteroid that works very well.  The trick is not to over use it.  I must catch the lesion early in its eruption if only one or two daily applications of the steroid are to do the trick.  Any later and it will take up to a week to subdue the lesion.  Any earlier and too much healthy skin absorbs the steroid and, eventually, will become immune to its palliative effect. 

Every day when I check for activity on my nose, I also check those places on the right and left of my chin that once gave me so much grief.  I’m typing with one hand, now, while I pound on wood with the other:  So far, no chin lesions.

Saturday, February 14, 2004

Meeting a Young Old Wife

An interesting experience at my county public library today.  I’d taken grandchildren Stephanie (10) and Brandon (7) to the library to get set up with library cards.  We’d stopped at the front check-out station where I picked up the forms to fill out, then we headed up to the second floor so they could browse in the young reader’s section while I filled out the forms.  (First challenge, the staircase.  Before my P arthritis I would have called such a staircase “impressive.”  Now the better word choice seemed to be “brutal.”  One cannot appreciate a good banister until joint problems open your mind.)

I sat at a table while the kids browsed.  I did not notice the young lady sit down across from me.  I didn’t look up from my forms until she asked, “Is your sugar low or high?”  I’d guess she was in her early twenties.  Judging from her clothes, she was a Pentecostal woman: long hair pulled tightly back, ankle-length skirt. Long sleeves. Her inquiry shocked me because my blood sugar had been higher than usual that morning.  But since when was this something noticeable by a stranger?  As a conversation opener, she picked a sure bet for me.  “Well, as a matter of fact, today it’s high,” I said, “but how did you know?”

“Your fingernails,” she said.  “My grandfather had high sugar and his toenails looked like your fingernails.  But I’ve known other people with low sugar and their toenails get like that, too.”

“Actually,” I said, “my nail problem is psoriasis, and I’ve had it for quite a bit longer than my diabetes.”  She accepted my explanation most graciously and thereafter we spent several minutes discussing other symptoms of hypoglycemia and diabetes.

Later, at home, I spent an hour surfing the net for links between nail problems and diabetes.  I could find nothing specific. Was it an old wife’s tale?  I decided to ask an in-law, my wife’s aunt who lives in the mountains of Eastern Kentucky and has been a social worker in the hospice field for many years. “Have you ever heard of anybody associating corrupted fingernails or toenails with diabetes or hyperglycemia?”  “Oh yes,” she said.  “It can be a sign.  I had a client for nearly a decade who was bad diabetic, one of those whose blood sugar would bottom out and then get super high all of a sudden, and his toenails looked awful.  He lived a long time, though.” 

I haven’t been able to get this subject out of my mind.  In the fourteen years I’ve lived in Kentucky I’ve had probably half-a-dozen occasions like this, where old grassroots erudition and modern knowledge seem continents apart.  I was raised in a much younger State than Kentucky, and though I’ve lived in many communities just as “old” as the Blue Grass, I’d not “married into” any of those others.  Here I’ve married into a community with a long, rich and colorful past.  I’ve begun to think that people of European ancestry, like me, born and raised in the western United States, grow up with a palpable lack of history.  I’d never seen a gravestone with a date earlier than 1860 until I moved East.  I can think of only a handful of things I was taught as a child that didn’t come out of Reader’s Digests of the 1950s.  (The two most significant of those exceptions being to draw poison out of a bee sting with a mud pack, and knowledge that it was possible to make a chocolate cake without chocolate or sugar.)  Here and now is different.  It is not uncommon to find in a “family section” of a cemetery, graves going back to the 1700s.  People possess diaries and paintings and letters that document their heritage that far back.  People still hold onto clothes and furniture “of museum age.” I’ve seen in the poorest homes furniture that, with a little restoration, would sell for thousands in finer antique stores. I think it is from this rich and palpable history that connections like bad nails and poor blood sugar control emerge. 

And so what, way back when, did people do when they finally decided that corrupted nails probably meant poor blood sugar (“high” OR “low”)?  About the only thing they could do was modify their diet.  That means they probably ate more or less sweets, and they probably consumed greater amounts of natural things — plant parts and extracts — that were believed to have curative powers.  They probably bought and tried all sorts of snake oil, too.  And for some of them, some of it worked, some of the time.  It must also be noted that living to be 60 was considered a feat.  Death in one’s late forties or fifties meant a long life had been lived.  And if, having been married as a teenager, that long life produced many children and many more grandchildren, well, that person ought not complain.

Wednesday, February 18, 2004

Topography: From Dots to Continents

There are several one-liners in the FlakeHQ “Don’t Say This” collection that refer to playing connect the dots with one’s P lesions.  It’s also been mentioned in several emails through the years.  I think, for some people, when they are flaming there are dozens of coin-sized (or smaller) lesions on their limbs and torso.  For me, though, that particular topography is an intermediate stage.  I’m in it now.

Do you recall seeing in magazines or on TV some of the high-resolution, high-altitude photographs of islands in the Earth’s oceans?  Remember how, from that perspective — looking straight down from on high — it is so obvious that the above-sea-level islands are only the peaks of submarine mountains that spread out beneath them until their color blends into the dark blue of the ocean depths?  Those photographs remind me of what I look like now, when I’m at the connect-the-dots stage in my P rebound. The submarine mountains come in shades of blue and green; my P lesion landmasses come in shades of red.

Consider my calves.  When I try to remember the worst my P has ever been, I recall a large lesion on each of my calves.  These cover the back part of the calves from just above the ankle to just beneath the backside of the knee, and each wraps around its leg about 160 degrees.  They itch fiercely, and since the itch cannot be completely ignored, I irritate these lesions and that’s part of what makes them so hard to treat.  Their location makes them easy to pick at, so I peel the scale off of them when I’m wasting time.  While this may enable my topical medicine to work a little better, you wouldn’t know it because the peeling irritates the lesion, inflaming it more, giving it strength to resist the palliative effect of the topical drug.  So it’s a vicious circle, and I play it with all the instinctive regularity of the lowest mammal on the food chain.  Me and my lesions:  Keeping mutually destructive company in perpetuity. 

In fact, these humongous, calf-covering lesions are the eroded plateaus of a rugged subsurface landscape that first emerges as dozens of smaller scaly “islands” in the oceans of skin on my calves.  Watching this happen — a process that takes between two and three months (unless something is done to quell it) — is to observe a simulation of the emergence of land masses from the primordial Earth’s ocean.

First there is the coming of the islands.  One ... another ... then several usually rather close together.  This is the connect-the-dots stage.  This morning I count sixty-three islands on my left calf, at least thirty of them in two large clusters. 

Then the sea of normal skin between and around the tightest clusters of islands begins to change, to redden.  This is when the calf resembles a satellite photograph of an island cluster in any of Earth’s oceans.  You see the “islands” you have been counting in that cluster are merely high knolls on a larger land mass that is just now emerging from your skin’s depths.

The emergence of the larger land mass happens quickly, in a week or two.  The reddish outline continues to darken and then thicken (as though it were rising up out of the skin) and soon the earlier dot-sized lesions can no longer be distinguished.  A cluster of islands has become a continent.

The continent quickly takes on its own characteristics.  Different continents will slough the dead skin (cells being replaced 14 times faster than normal) in different ways.  In some places the dead skin won’t scale, but stays compacted and builds up into a hard, whitish, scabrous substance that can be chipped away and bleeds easily.  In other places, the continents form yellowish scales with defined edges (where natural exfoliation is separating the dead tissue from the rest).  You can plunge fingernails or tweezers under the edges of this scale and peel it away.  Sometimes, pin-point bleeding will occur.  Another kind of continent won’t scab or scale, instead it stays supple and becomes covered with raised pimples that make one suspect pustular P, but it isn’t pustular when the pimples aren’t filled with fluid.  This kind of continent reminds me of the skin on horny toads.  In my own case, these continents are often the oldest — meaning they were among the first to form — and the most treated with topical corticosteroids.  In fact, I’m inclined to think this peculiar topography might be a consequence of the steroids.  Such lesions can neither be chipped nor peeled.  Scratching the pimples merely tears them away and they are sure to bleed.  But there is one benefit, this kind of continent-lesion, in my case at least, doesn’t itch.

Today the massive continent which will be a single calf-encompassing lesion on my right leg is visible but still largely submerged.  Many of the clusters of islands have already merged, but I see from the larger salmon colored area beneath all the scaling islands that the massive continent is merely weeks away. 

The same is true for the right calf, but it is perhaps a week behind the left in its formation.  There are still clusters of islands on the right — only a couple are conjoined — and the outline of the massive continent is still very dim. 

I think if I were to start on cyclosporine today (which I can’t, this is purely a musing) the continent on my left leg would never fully emerge, but the continent on my right would see dry air for a brief time.  Cyclosporine is, for me, a P continent preventative and killer.  Taking the proper dosage of cyclo will reverse the creation of these huge lesions in a matter of weeks.  They will disappear faster than they emerged.  Methotrexate works nearly as well but, sometimes, it cannot ever completely tame the most recalcitrant continents.  They may dwindle but never entirely disappear.

Contemplating improvement is depressing me.  Enough for now.

Tuesday, February 24, 2004

On Ears, on Changing Topicals, and a Weird Arthritic Twist

A few days ago, when I removed my finger from my ear a comet’s tail of flakes came with it, dusting my collar and shoulder with the old familiar detritus of ear P.

Hm.  My ear must have itched.  Why else would my finger have been in there?  Truth is, ear P has never been one of my serious complaints though, come to think of it, whenever I’m flaming widely I’m bound to have it.

I think the truth is I’m somehow consciously “turned off” to the sensation of itching in my ears, but I respond to it subconsciously.  I do it and don’t know it.  I didn’t know why my finger had been in my ear — would no doubt have never remembered it being there — until that comet’s tail of flakes brought my attention to it.

So now I know. I’d have just as soon not been reminded. 

A derm was the first person to bring my ear P to my attention.  He was trying to get a handle on how widespread the problem was and, at some point, he said, “Let’s take a look in your ears.”  A millisecond after he stuck the probe in the first ear he went, “Yeap.  In there, too.” 

It means another medicine.  For me this has always been fluocinonide solution, a corticosteroid in an alcohol base.  (Dermacin and Lidex are two of the well-known brands, but I buy it as a generic.)  I apply it to the inner ear by soaking a Q-Tip with it and swabbing thoroughly.  (Once a day, though twice is recommended.)

Even during a vicious rebound, I don’t think my ear P ever gets too bad.  For example, some people have a collateral problem stemming from their ear P:  The flakes mix with earwax and form a hard compound that plugs their ear canals.  Hearing efficiency diminishes – like listening to the world through a piece of sheet rock.

Other people have bad P in the folds of the outer ear.  I’ve gotten it there occasionally — and do feel the itching when it’s there — but so far, this rebound, it hasn’t crept out.

Here’s an advance notice for younger FlakeHQ readers (those under 40):  As you get older, what comes out of your head’s orifices matters more to you and is usually more consequential. 

Quasi-appendages like your nose and your ears are likely to continue to grow slightly after the rest of you has stopped growing.  Someone with normal (meaning usually unremarkable) ears may find at sixty they look like Dumbo. The cartilage part of your nose can grow like your ears, and it’s shape may change slightly.  Again, a particularly normal nose on a 30 year old might bloom nostrils big enough to be airplane hangers by fifty-five.  A person can be self-conscious about these little (big) things.  That self-consciousness can become full-blown stigma when things like hair and flakes start to flourish with untoward lushness in these places.

(No one likes nose hair.  People spend money on every new device advertised to make short work of nose hair.  Few people remain blind to their own nose hair problem for long because our society does shun it and you can’t help but wonder what people are staring at that resides two to three inches below your eyes.  The exception is men with bushy mustaches.  Nose hair tends to get lost in bushy mustaches.  I know.  When I shaved my mustache I discovered a crop of nose hair that was horrifying.  For years I’d occasionally watch barbers take a few swipes at my mustache with their electric clippers then frown, set down the clippers, pick up the pointy scissors, return to the general area, snip snip, then move on.  Now, shorn of mustache, I cannot go back to those barbers. And I am collecting all sorts of devices for trimming nose hair.)


Last week it was time for me to make a switch between my clobetasol propionate (a.k.a. Temovate) and betamethasone dipropionate (a.k.a. Diprolene).  These are both considered strong topical corticosteroids. 

Back before I used any of the systemic drugs for psoriasis I was totally dependent on topicals to manage the disease.  My derm told me at that time, “We need to establish you on a revolving regimen of different topicals, from potent to not-so-potent, to keep your skin guessing.  If you just stick with one thing it will wear out.  It will stop working.”  So I’d use one kind of topical for as long as it took to exhaust a large (60 gram) tube, and then I’d switch to another.  Temovate and Diprolene were the two most potent corticosteroids in my revolving regimen at that time.

Within three days of using the betamethasone dipropionate I could see an impressive difference in some of my lesions.  It’s true — at least it is for me — that the lesions just become resistant to anything I put on them.  Given time, they will learn to ignore anything.  And it takes long enough for this to happen that I am unwilling to blame it on the medicine.  Quite the contrary, my natural instinct is to slather on more of the medicine and this, of course, just speeds up the lesions’ resistance to it.  But I had forgotten about most of this, at least consciously, until three days into the betamethasone.  The lesion that shocked me the most was the bumpy one covering my right knee (under which lives the psoriatic arthritis).  Wow!  It had diminished from red to salmon color, except for the bumps, which were still red, and I’d swear it was smaller, that the edges were closing in.  This was the most obviously improved lesion, but on inspection I found several others that looked better.

For me this is a bittersweet news.  Now that I’ve experienced it, again, I remember what it really does and doesn’t mean. It doesn’t mean I’m “on the mend.”  Indeed, it would be quite surprising if any lesion subsided completely under the betamethasone.  No, what I’ve done is temporarily shocked them into submission — a little.  I’m still looking at a large portion of my 60 grams of betamethasone dipropionate that is going to get slathered on these lesions over the next couple of weeks and, if experience proves true, my lesions will become familiar with it quickly, then set about working on the strength of their resistance to it.  Probably as early as next week I’ll see this momentary improvement start to backslide.  I won’t know exactly when I return to as bad as I’ve been, and I don’t know if I’ll get worse. 

But I do know that it is not in the nature of my P to submit to the palliating influences of topical corticosteroids.  I don’t know how bad things would get if I did not use them.  It knows that I don’t know this.  So we play this expensive game.  I spend and work to hold it back, to think that I am being proactive; it goes about its life perturbed but far from mortally wounded.  It gives me my noticeable moments of progress, but then it takes them away and shows me how in command it still really is.


Granddaughter Stephanie has enlisted me to help with a project for her fourth grade social studies.  She (and each of her classmates) has been tasked to create a “Kentucky Scrapbook.”  The assignment is detailed enough that they were given a typed list of things needing to be represented in this scrapbook.  Of course, (and I’m sure this is in deference to the parents and grandparents who’d be helping their offspring with this project) considerable latitude of interpretation is permitted.  “Creativity” in filling the pages will earn huge rewards (according to the syllabus).

I approached the assignment like a project (always trying to enhance a child’s educational experience in all ways possible, but primarily in demonstrating an adult approach to the problem), and our first exercise was to “plan” how we would go about finding stuff for the pages.  One thing led to another and it was decided that, over the next six weekends, we will take a series of road trips to acquire experiences and photographs to put in the scrapbook.  This past Saturday was our first.

Papa Ed and his psoriatic knee, took Stephanie and cousin Alexandria to the Woodford Reserve Distillery, to Ashland, home of Henry Clay, and then to Henry Clay’s monument in Lexington Cemetery. That morning was the first time I thought about how much walking all this might entail.  I really had no idea.  What it proved to be was bad planning.

The Woodford Reserve Distillery required walking through three buildings, climbing up 20 and down 93 steps (rather than climb up some I took a van with the other oldsters) and I was on my feet about an hour.  Ashland was another hour on my feet and several flights of stairs up and down inside the home and out.  Plus walking the grounds to visit outbuildings, getting to and from the car in the parking lot.  And, at the cemetery, the closest we could park meant hiking up (and then back down) a steep but stepless hill to the Clay Crypt and Monument. 

By the time we got home I was limping severely and hurting mightily.  Rest that night was tough.  Getting up to go to the bathroom was tougher.  Sunday I made only one trip up to my attic office and came down quickly, using the butt on steps routine that my two year old grandchildren have been taught by their mothers.  The majority of the day I spent on the living room couch, legs up, watching TV.  I dreaded Monday (yesterday) for knowing I’d have to go up to the office and come down several times.

But then nature called about 2:00 a.m. Monday morning and I was halfway to the bathroom when I realized nothing hurt too significantly and my limp was barely occurring.  Back in bed I did a couple of knee lifts and couldn’t believe it.  Twelve hours before I had to use a hand behind my right knee to get it to go anywhere.  I slept fitfully for a few more hours — but not because of pain.

Why did my PA so suddenly diminish?  Monday was a miracle day, I moved with complete freedom anywhere I wanted, in and out of the house, up and down stairs, around town....  No, the knee was not “cured” but the PA hadn’t been this insignificant for months.  It was like time had shifted back to the weeks when I was being weaned off cyclosporine, weeks when I was just beginning to feel the PA again.  What had I done to bring this reprieve about?

Of course, the first thing to think about is Saturday.  My psoriatic knee got a tougher workout that Saturday than it had ever gotten during a flame time.  While I, like everybody, have experienced the truth in the old adage no pain no gain, I’ve never known it to apply to arthritis.  Quite the contrary, typically for me a stressed arthritic joint only gets worse until time dilutes the stress.  (On the other hand, I do know the value of keeping an arthritic joint limber by exercising it when it is not hurting.)

Another possibility:  Upon coming home Saturday and explaining my predicament to Clara, she suggested I forgo the Tylenol/Ultram combination I had been taking for pain and switch to a prescription-strength dose of ibuprofen.  Might this have acted on my arthritis pain the way switching to betamethasone dipropionate has acted on some of my skin lesions? 

Well, I’m only working on my second day after my Sunday Disablement, and though I’m appreciative of the fact that so far, today, the pain is staying low, it’s probably too soon to jump to conclusions.

(Go to Part 2)

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