When the Provider is the Patient: My Accutane Story, Part 3

In the great pharmacological arsenal of Western medicine, a few drugs are so embedded in the collective American consciousness that their names alone conjure up powerful, even emotional, associations. Oxycontin is one. Plan B, another. And Accutane, while not at the root of a nationwide opioid epidemic or vilified by pro-life extremists, is arguably the most controversial medication prescribed today by dermatologists in the U.S. For many patients, Accutane seems like an oral atomic bomb, evoking images of deformed babies and horrific suicides. But for dermatology providers, Accutane occupies an almost sacred status, the gold standard for patients with recalcitrant acne, folliculitis, and a few other skin disorders that fail to respond to first-line treatments like antibiotics and retinoids. I should know: I am one such patient.

 

If you have read parts 1 and 2 of my “Accutane story,” you know by now that I have struggled with a rare form of folliculitis in my beard area for almost a year. In the spring of 2017, I grew a beard for the first time ever and enjoyed a few liberating months of facial hirsutism before my follicles and I met our match: Enterobacter aerogenes. These Gram-negative bacteria, acquired most likely during a hospital rotation in my clinical year of physician assistant school, found a happy home in my beard and overstayed their welcome, to say the least. Despite multiple rounds of topical and oral antibiotics, these unexpected visitors simply refused to die. By mid-November, after three months of painful, inflammatory outbreaks, I was desperate for a different approach. If Accutane was the dermatological nuclear option, I was prepared to hit the “Detonate” button and deal with the aftermath later.

 

In many ways, I was not the typical “Accutane patient” I had encountered in my years at the dermatology clinic. There is a sort of dermatological inner voice, if you will, when seeing an acne patient for the first time that says, “This patient should be on Accutane.” He or she is usually a teen or early twenty-something, has a laundry list of over-the-counter and prescription acne products that have failed, and a face—and sometimes back and chest—bearing the telltales signs of inflammatory acne: papules (small elevated lesions), pustules (small lesions containing pus), and nodules (larger elevated lesions). Often the patient has some degree of acne scarring and, more subtly, a kind of psychological scarring—a sense of dejection and resignation to an unfair but inescapable dermatological fate. It is at this moment, with this archetypal acne patient, that dermatology providers like to have the “Accutane conversation.” It may include some, but hopefully not all, of the following:

 

What is Accutane?

To start, Accutane was the brand name concocted by Roche Pharmaceuticals for isotretinoin (13-cis retinoic acid), an oral medication that was approved by the FDA in 1982 for the treatment of cystic acne. Embraced enthusiastically by dermatologists and acne sufferers alike, Accutane—like Band-Aid, Chapstick, and Kleenex—became a proprietary eponym, in which a brand name is so successful, it is used as frequently or more than the generic object it refers to. It would be twenty years before a generic form of isotretinoin called Amnesteem was approved by the FDA. And while Roche removed Accutane from the market in 2009, amid increasing allegations of gastrointestinal and psychiatric side effects (more on this later), the brand name endures. For eligible patients now, it is usually a question of which generic “Accutane” their insurance providers will approve. I took one called Myorisan. To my knowledge, they are all more or less the same, with some manufacturers claiming better absorbency.

Isotretinoin falls under the umbrella of retinoids, synthetic analogs of vitamin A. Like its sister medication, topical tretinoin—also better known by its original brand name, Retin-A—isotretinoin is a first-generation retinoid. These are the most studied retinoids, with significant research substantiating both their acne fighting and anti-aging properties. I was—and still am—a proponent of topical retinoids, long before I swallowed my first Accutane capsule.

 

What does Accutane do?

This is the part patients may actually want to hear if they are not pharmaceutical history buffs. As with so many medications I studied in PA school, the mechanism of action of Accutane is “not fully understood.” The simplest explanations I have read suggest that Accutane induces apoptosis, or programmed cell death, in various cells in the body. These include cells in sebaceous glands, which are the oil- or sebum-producing glands attached to hair follicles that are typically overactive in patients with acne. Excessive sebum can block the sebaceous gland duct, leading to a closed comedo (whitehead) or open comedo (blackhead). Then the bacteria Proprionibacterium acnes, which live deep within the follicles, feast on the sebum as their primary food source and overpopulate. Finally, the body responds to this bacterial colonization by releasing pro-inflammatory chemicals, leading to the inflamed lesions characteristic of acne.

These are the classic four factors at the root of acne: 1) increased sebum production, 2) clogged sebaceous glands, 3) P. acnes overgrowth, and 4) the body’s inflammatory response. And while first-line acne medications like benzoyl peroxide, topical retinoids (like Retin-A), and oral and topical antibiotics affect one or more of these factors, Accutane affects all of them. It is the proverbial “big gun” of acne, and most patients who have been through the ringer with severe acne are ready to step up to the line of fire and accept the side effects. There are several major side effects every Accutane patient should know about, more than a few of which I experienced first-hand.

 

What to expect on Accutane

First things first: it is well established that Accutane causes birth defects if taken by a female patient during pregnancy. Not long after the market release of Accutane in 1982, cases of birth defects—including cardiovascular and neurological deformities—began emerging. The New York Times reported in 1988 that over 1,000 babies had been born in the U.S. with birth defects attributed to Accutane in the six years since its release. The FDA responded by imposing stricter labels, including a black box warning, and by developing physician training materials.

In 2006 the FDA launched iPLEDGE, a mandatory distribution program for isotretinoin intended to prevent use of the medication during pregnancy. All prescribers of isotretinoin in the U.S. must be registered and activated on the iPLEDGE web site. And every single Accutane patient in the U.S., male or female, must be registered and activated, as well. Women must have two negative pregnancy tests, taken 30 days apart, before even being able to start Accutane. They must declare two forms of birth control—or abstinence—and take monthly pregnancy tests, included in their routine blood work monitoring, throughout their Accutane course. Men must also get monthly blood work but are spared the requisite “Hey, Doc, I’m still not pregnant” song and dance. Ask most dermatology providers, and they will tell you that iPLEDGE is a frustrating, inflexible system that often delays patients in getting the medication they most need. Suffice it to say that birth defects are the most serious side effect for female patients of childbearing age, should they get pregnant on Accutane, but there is no evidence that Accutane affects fertility or causes birth defects once a course is completed.

But what of the other side effects that perpetuate Accutane’s status as the so-called nuclear option? Without question, the most common side effect is dryness—affecting the lips, nose, eyes, and skin over all. If you are on Accutane, you will be dry, as the medication targets the very glands in the skin that secrete oil. For most patients, the dryness can be tolerable with frequent applications of lip balm, Aquaphor or Vaseline to the nostrils, lubricating drops for the eyes, and moisturizer (oil-free!) to the face and body. Patients may experience dryness severe enough to evolve into a rash (often on the tops of the hands), for which mild topical steroids are effective.

While dryness on Accutane is inevitable, other side effects are highly variable. Among the more common side effects include elevated triglycerides and cholesterol, so a lipid panel is included in every Accutane patient’s monthly blood work. Providers often recommend taking fish oil supplements containing omega-3 fatty acids, which may help to lower cholesterol levels. Other common side effects include headache, nausea, vomiting, and muscle and joint pain.

But the “big ones,” the side effects that patients most worry about—and which, unfortunately, scare away many ideal Accutane candidates—are also the most rare and highly debated. Accutane has been associated with both gastrointestinal disorders (namely inflammatory bowel disease and ulcerative colitis) and psychiatric disorders (including anxiety, depression, psychosis, and suicidal ideation). In both cases, however, causation has never been demonstrated, after numerous case studies and lawsuits. The possibility of rare idiosyncratic adverse effects does exist, but patients should be reassured that Accutane is not a straight ticket to IBD and suicidality. The most important guidance patients should receive is to notify their provider immediately if any unusual or worrying side effects occur during an Accutane course. The dosage can always be decreased, or the medication discontinued altogether.

 

But back to me…

By the time I popped my first Accutane pill on November 13, 2017, I was in pretty rough shape, to say the least. My folliculitis had come back with a vengeance and was redder, crustier, and “angrier” than ever. To make matters worse, I was scheduled for the Physician Assistant National Certification Exam (or “PANCE,” as it is known to all us PAs) on November 20, and my stress level was through the roof. My PA program had none too subtly emphasized the importance of students passing the PANCE on the first attempt, and one classmate had already failed. The fear of disappointing my school, my family, and myself haunted me. I took two weeks off from work—and, effectively, my relationship—to hunker down in my room and become something of a reclusive robot. Subsisting largely off coffee and Chipotle burritos, I answered hundreds of practice exam questions every day as if my life depended on it—and it did. Having taken a leap of faith six years earlier to pursue a career in medicine, I felt like the PANCE was more than a certification exam: it was symbolic, a validation of all that I had worked so hard for.

The good news is, I passed. On November 28, I became a certified physician assistant, or “PA-C.” I was exhilarated—and relieved. The bad new is, my skin had suffered from the enormous stress of this time. If a photo can say a thousand words, my face in photos from this period is silently crying out for help.

November 18, 2017: Six days (and six pills) in

The first change I observed with my skin on Accutane was the same as every other Accutane patient since 1982: dryness. It seemed like within hours of taking my first 40 mg capsule, I was reaching for a sample-sized tube of Aquaphor ointment I had snagged from the office. And while some patients don’t experience dry facial skin, my face became dry almost immediately. If I even lightly rubbed my face, I could expect a mini snow shower of dead skin flakes. For facial dryness, I relied heavily on a light, oil-free moisturizer called Cerave PM Moisturizing Lotion. Throughout my six-month course of Accutane, I kept sample sizes of Aquaphor and Cerave PM in my pockets at all times. Thanks, Spring Street Dermatology sample closet!

 

November 23, 2017

The second major change I observed was a redness I had never experienced before, extending from my lower face all the way up to my cheeks and forehead. This is a phenomenon known as the “Accutane glow,” and I looked particularly glow-y. Since Accutane causes the stratum corneum, the top layer of the epidermis, to turn over at an accelerated rate, patients are “exquisitely sensitive” to the sun. Confession: I was not diligent about sunscreen. Most of my Accutane course took place over the winter, when I rarely saw the sun for more than 10 minutes. And with a beard still in place—because shaving was out of the question—every sunscreen I tried would not absorb and seemed only to add a patchy, sticky layer of white to my beard hairs. And so, red face it was. A few patients asked me if I had rosacea. One asked if I “just blushed all the time.”

 

December 29, 2017

November and December were slow going in terms of progress. This should have been expected, having talked with hundreds of Accutane patients at the practice. Most patients don’t see an appreciable difference until the third month of treatment. But first comes the “purge,” when all the old skin cells start rising—at an accelerated rate, with a potent retinoid—from the bottom layer of the epidermis up to the surface. “It gets worse before it gets better” is the adage. (There should be a framed cross-stitch of this in every dermatology exam room in America. I might market that.) In my case, things simply could not get any worse than they were in mid-November. It could only get better, and I relaxed into that certainty, despite some rather gnarly eruptions.

 

January 13, 2018

February 2, 2018

By February 2018, things were better. The purge was over, and my skin looked decidedly less cystic, inflamed, and “angry.” There were still breakouts, but fewer and less severe. My dose had been increased to 40 mg twice a day, where I would stay for the remainder of my course. But with higher doses of Accutane comes the risk of more pronounced side effects. In my case, I started developing back pain. I was slow to make the association with Accutane. For at least a month, I was convinced that alternating sleep on two different mattresses—mine and my boyfriend’s—was the culprit. I even suggested that he purchase a new mattress. “IKEA mattresses are horrible!” I pleaded. (They are, actually.) Alejandro politely dismissed my request. But as the pain evolved, migrating down my cervical spine into my thoracic and lumbar spine and hips, I had my “Aha! moment” and shifted the blame from IKEA to Accutane.

Most Accutane patients I have seen at Spring Street do not report muscle or joint pain during their course. If they do, it is usually mild and tolerable. But again, at 35—by now, 36—I was not a typical Accutane patient. Some side effects are more severe in “older” patients, and I was 10 to 20 years older than most Accutane patients. With my newfound arthritis, I felt a good 50 years older. Though I tried to keep my “aches and pains” complaints to a select few, a lot of basic movements simply hurt. Every warm-up stretch on the gym mats was a glimpse into what arthritis actually feels like when you get to “that age.” Toward the end of my course, as the pain seemed to settle in my hips, even walking was becoming unbearable. (I am happy to report that all of the pain began to subside in the first weeks after Accutane.)

 

March 18-28, 2018: The “Accutane Glow”

March was a “good month,” when I could say without any hesitation that Accutane was working. When my mom came up to New York for a springtime visit, I looked—and felt, on an emotional level—better. My Accutane glow was borderline radioactive, but I was visibly happier and relatively clear. But there was never a day when I was totally clear. I continued to wake up every morning with the hope that “today is the day,” the tipping point, when my breakouts were behind me. Despite marked over all improvement, there were always two or three infected follicles in my beard—painful, inflamed, angry. Accutane was shutting down the oils on which my nemesis bacteria lived, but they were still holding on, surviving through the famine.

The real kicker came in in late April, when I had one of the worst breakouts since starting Accutane. I frantically texted a barrage of selfies to Dr. Mikhail—on a weekend, no less—and wrote, “This is what I look like after five months of Accutane.” I felt like I had gone backwards when, all along, I had believed in the inevitability of upward progress on Accutane. She was reassuring, as always, urging me to stay the course. And this is exactly what I did for the months of May and June, as I edged toward my maximum cumulative dose. I took my pills and “let go and let God.” There were some emotional lows during this time, particularly when I went to my friend Rachel’s wedding in early June. In every photo of myself from that weekend, I look as red and inflamed as ever. How could my skin revolt on my like this, after months of improvement?

April 28, 2018: Breaking out again

 

May 3, 2018: Approaching the end

 

June 1, 2018: Red for the wedding

By mid-June, Accutane and I were done. It was time to break up. I had surpassed my maximum dose of 11,250 mg and taken 13,200 mg cumulatively since November. I had also paid nearly $400 out of pocket for the last month of treatment, as my crappy insurance denied coverage. My overtaxed liver, aching hips, and empty wallet needed some time to recover. Frustrated with continued breakouts, on June 22 I decided to take matters into my own hands and do a repeat bacterial culture, swabbing what was a fairly characteristic pustule. Five days later, the report came back: “Enterobacter aerogenes, moderate growth.” My Gram-negative bacterial friend had made it, after all.

Rather than feeling disappointed, however, I was surprisingly relieved. I knew definitively what the problem was and what it had always been. I scrutinized the antibiotic sensitivity report like I was studying for the PANCE all over again. I also consulted every single dermatologist in the office to construct a game plan. One of the doctors suggested a topical form of the antibiotic gentamicin. In PA school, I had only learned of its IV form. So it was another “Aha! moment” to learn not only that a topical form existed, but that it was active against Gram-negative species like Enterobacter. For safe measure, I decided to go back on the oral antibiotic that had cleared me in the first place: ciprofloxacin.

Only this time, my boyfriend Alejandro—who had broken out consistently right along with me all along, if to a lesser degree—would be joining me in a combined mission of all-out antibiotic warfare. For two weeks, we slathered on our creams and took our pills, routines that became as familiar as brushing our teeth. It seems obvious in retrospect, but for months we had unwittingly engaged in a kind of bacterial ping-pong: if one of us was flaring, it was only a matter of time before the other would flare, too. Despite the major improvements with Accutane, I was never going to clear—and neither was Alejandro—if we didn’t both combat the causative organism at the same time. For any readers suffering from a stubborn or seemingly resistant folliculitis, consider if you might be passing the bacteria back and forth with your partner.

 

July 12, 2018: One month post-Accutane…with some antibiotic assistance

Within days, we both began to clear. We would cautiously check in with each other, “Are you breaking out?” After about a week, the answer for both of us was, simply, “No.” That was an historic moment, for neither of us to be experiencing a breakout. I am still hesitant to exclaim, “I’m cured!” I was clear briefly before, and it all came back again, likely due to the decidedly not fun game of Gram-negative ping-pong. For now, I am appreciating each day that I wake up, greet my face in the mirror, and am not dejected and defeated.

It is now July 29, almost a year to the day that I first realized that something was terribly, terribly wrong with my face. Call it my year of dermatological hell. It was a complicated diagnosis, one that stumped and stymied numerous dermatology providers—me, most of all—and required a multi-pronged approach to eradicate. And while Accutane didn’t wipe it out by itself, it forever changed my oil production, decreased the bacterial load, and set the stage for antibiotics to work more effectively this time. (Not to mention, I don’t even remember what a blackhead on my nose even looks like.) Am I glad I did it? No regrets here.

I am left with significant scarring along my lower face, where continuous inflammation wreaked havoc for so long. Of course, I hate that. Fortunately, I work in an office with access to lasers and other cosmetic treatments that are effective for scarring. I won’t be able to do any of these for a while, as skin continues to be sensitive for six months to a year after Accutane. I will get there—and more on these in future blogs. For now, I am happy to be clear, to feel a weight slowly lifting off my shoulders, and to share my story with patients and readers. Severe acne and folliculitis are debilitating conditions and should not be marginalized. I know this all too well now—I have been there. But with determination, persistence, and the right medical treatment plan, it can—and will—get better.

 

July 20, 2018: Back to the “old me”

Got Moles? Map Skin Changes with FotoFinder

Spring Street Dermatology

image courtesy of www.fotofinder-systems.com

 

May is the American Academy of Dermatology’s Skin Cancer Awareness Month, and with sunnier weather already upon us in New York, it is the perfect time to think about the health of your skin. Like other cancers, skin cancer is an abnormal growth of cells. It usually develops on areas of the skin exposed over time to damaging rays from the sun. Individuals with light skin who sunburn easily have a higher risk, but skin cancer can affect people of all skin types.

 

There are three cancers dermatologists look for during full-body exams:

  1. basal cell carcinoma, the most common type of skin cancer,
  2. squamous cell carcinoma, the second most common skin cancer, and
  3. melanoma, the deadliest form of skin cancer.

In addition, dermatologists look for premalignant growths known as actinic keratoses (AKs).

If left untreated, AKs have the potential to develop into squamous cell carcinomas.

 

If detected early, all skin cancers are highly treatable. However, the American Academy of Dermatology has some alarming statistics:

  • An estimated one in five Americans will develop skin cancer in their lifetime.
  • Nearly 9,500 Americans are diagnosed with skin cancer every day.
  • On average, one American dies from melanoma every hour.

 

For patients with a lot of moles and sun damage (like me), monitoring skin changes over time is virtually impossible. And for “high risk” patients with family or personal histories of skin cancer, close monitoring is critical. Fortunately, there is an exciting new technology that we are launching at Spring Street Dermatology to supplement full-body skin exams: FotoFinder.

FotoFinder is a whole-body photography program that takes high-resolution images of the body, head to toe, in 20 different positions. In addition, suspicious moles are marked and documented using a dermatoscope that creates highly magnified images. Baseline images are then compared with follow-up images, taken six months to a year later. The software is able to detect microscopic changes that can be analyzed by our dermatologists and reviewed in subsequent full-body skin exams.

A diagnosis of skin cancer is never news anyone wants to hear. FotoFinder uses cutting edge technology to detect subtle changes at their very earliest stages, minimizing the risk of developing into more dangerous skin cancers down the road.

For more information about FotoFinder, please contact Spring Street Dermatology at (212) 431- 4749.

For more information on Skin Cancer Awareness Month, visit:

https://www.aad.org/public/spot-skin-cancer/programs/skin-cancer-awareness-month

When the Provider is the Patient: My Accutane Story, Part 2

The summer of 2017 was a bittersweet season for me. In late July, I celebrated my graduation from the York College/CUNY Physician Assistant Studies program after two grueling years of coursework and clinical rotations. And after months of confinement in New York, I was free to enjoy three weeks off with my friends in Maine and family back home in North Carolina. The only problem was, as I discussed in my previous blog post, my face. A mysterious bacterial infection had developed in my beard area—as if to punish me for growing an actual beard for the first time in my life—and seemingly set up shop. Despite a course of doxycycline and topical clindamycin lotion, the first-line treatments for impetigo and other superficial skin infections, my face went from bad to worse to full-on freak-out.

 

It should come as no surprise, in retrospect, that the bacteria that had colonized my face had a mind of their own.  Bacteria were among the first life forms on Earth, so it stands to reason they know a thing or two about survival. I didn’t know the specific bacterial culprit at this point and, after no improvement with both oral and topical antibiotics, I wasn’t even sure the problem was bacterial in origin. I could only watch in dread as my face morphed from day to day in a feeble attempt to mount a response to this new invader.

 

It was at this point, in mid-August, that the follicular nature of my skin condition became more evident. Whereas before, in late July, it seemed to be a broad, generalized infection of the superficial skin (classically seen in impetigo), it now appeared to be originating in the hair follicles themselves. I still had significant swelling in both cheeks, but I was now developing painful cystic lesions, usually a pustule (by definition, a pus-filled vesicle) with a centrally placed hair. Though I didn’t know it at the time, this presentation is classic for folliculitis, which is broadly any inflammatory reaction of the hair follicle. All I knew was that these beard hairs hurt like tiny, excruciating needles. The only relief I could get was from pulling the offending hair out with a pair of tweezers. Usually the bulb of the hair would be covered with a greasy coating, and from the now empty pore a substantial amount of oily, yellow fluid would inevitably ooze. Unlike traditional “pimples,” there usually was only a minimal amount of pus and very little blood.

 

Of course, self-manipulation and “picking” (which I hope to address in future blogs) only served to prolong and worsen my condition. I also attempted to shave a few times in these early months, reasoning that topical antibiotics would be ineffective if I continued to grow a beard. This also was a mistake, most likely redistributing the bacteria to previously unaffected follicles—like a bee pollinating flowers. While I don’t believe my skin condition was self-inflicted in origin, I now acknowledge that I fell into a vicious “pull-and-pop” cycle. In seeking temporary relief from the painful cystic lesions, I unwittingly delayed long-term control. Without fully realizing it, I was now in the grips of both a dermatological and psychological condition.

August 13, 2017: Crustiness.

 

 

August 21, 2017: Gazing at the eclipse. Looking like a chipmunk.

 

Any time away from New York City, as I’ve come to realize in my fourteen years here, is a welcome opportunity for renewal, especially when that time is with family and friends. But coming back to New York in late August 2017, I was more than a little uneasy about my face. Plan A clearly hadn’t worked, so it was time to move on to Plan B. I was placed on a different antibiotic, Bactrim (trimethoprim-sulfamethoxazole) and prescribed an ointment containing benzoic acid. Bacterial and fungal cultures were also obtained. The working theory was that this was indeed a bacterial infection, and that both oral and topical antibiotics would provide broad Gram-positive and Gram-negative coverage.

 

It was during this time that things really went downhill rapidly for me. Cystic lesions got larger and inflammation swept across the full expanse of my beard. As with the previous course of doxycycline, I had no appreciable response to Bactrim. And the benzoic acid ointment did little more than coat my face in a greasy film. At one point I developed a cyst the size of a golf ball on my right cheek. Within a matter of days, individual beard hairs began falling out on their own, creating a patchy network of hairlessness and inflammation. Though committed to finishing the second course of antibiotics, I resigned myself to the grim reality that, whatever this infection was, it had gone too far. In my PA program at York College, one of my favorite professors, Dr. Edward Rampersaud, had frequently reminded us that in all bodily processes, “Inflammation leads to scarring.” No matter what, I was going to be left with permanent scars, front and center on my face.  

 

August 27, 2017: Redness.

 

 

August 31, 2017: Greasiness.

 

 

September 1, 2017: Patchiness.

 

In future posts, I will come back to the psychological effects of acne and other scarring conditions. Suffice it to say for now, in the late summer of 2017, my face became a preoccupying concern. It became a topic of conversation with almost everyone I knew, particularly my mother, who would text me every morning, “How’s your face?” Usually the response was something along the spectrum of “Not great” to “God awful,” depending on the day.

 

To make matters worse, my boyfriend, Alejandro, was starting to break out in his beard area in the same telltale pattern: painful cysts, needle-like hairs, golden serous fluid. This initiated a new psychological phase in my skin saga: guilt, shame, and worry. Not only was I going through my own dermatological hell, I was responsible for dragging my partner right down with me. I felt like some sort of diseased carrier with the potential to transmit my infection to anyone who got too close. My intimacy with Alejandro—up to this moment so free and uninhibited—became cautious, guarded, wary. But Alejandro was, and is, eternally optimistic. “We’re going to get through this,” he would say. “We’re a team.”

 

In early September, my bacterial culture finally came back, and the microscopic organism at the literal root of my problem was isolated: Enterobacter aerogenes, a Gram-negative bacterium associated with nosocomial—or hospital-acquired—infections. Around the time that everything had started back in July, I had been grinding out one of my last clinical rotations, in Internal Medicine. To put it mildly, there were a lot of very sick patients with very serious problems: C-dif colitis, decubitus ulcers, pneumonia, and sepsis, to name a few. Though I will never know the exact origin of my skin infection, the most plausible theory I have developed is that I: 1) touched a ventilator or other common hospital apparatus, then 2) touched my beard, where my bacterial friend Enterobacter set up a happy home, feeding off the oils in my follicles. The final diagnosis was now established: Gram-negative folliculitis.

 

After two months of suffering and after failing two previous antibiotics, I was placed on a different antibiotic, ciprofloxacin (“cipro”), which has greater efficacy against Gram-negative bacteria. Within days of a two-week course, a miracle happened: I begin to clear. Swelling improved dramatically, and the follicular cysts that had been so painful and pronounced began to dissipate. Looking back on photos from this time, I was so clearly happy. I was moving to a new apartment in Park Slope and preparing for the “PANCE,” or Physician Assistant National Certification Exam. The bacteria had been isolated, the appropriate antibiotic had been selected, and this nightmare folliculitis was behind me.

 

September 18, 2017: Central Park / September 30, 2017: Park Slope

 

But the nightmare was not over, as it would turn out. The course of cipro had afforded me a month-long reprieve, but the Enterobacter was simply too tenacious. In late October, I repeated a course of cipro—my fourth course of oral antibiotics over all—and again had about a week or so of relatively clear skin. By early November, the folliculitis was coming back at an alarming pace. My cheeks looked unhealthily inflamed, and the all-too-familiar cysts reappeared. My smile was gone and replaced with a look of disappointment and anxiety.

 

November 6, 2017 / November 8, 2017

 

This Enterobacter was a multi-drug-resistant survivor and, I had to concede, it had won the antibiotic battle. I simply could not go on another round of oral antibiotics. What good would it do? More than once I fantasized about getting admitted to the hospital. I would calmly study for the boards, catch up on The View, and slurp down Jell-O while more potent IV antibiotics coursed through my veins, drowning these demonic bacteria in liquid poison. Given my luck, however, I would probably pick up a different nosocomial infection and kill off whatever natural gut flora I had left. No Whoopi and Joy marathon for me.

 

But this was war, and I was anything but resigned. Plans A, B, and now C had failed. It was time to unveil Plan D: Accutane. I realize it has taken two full blog posts about “my Accutane story” to get to the part where I actually started this medication. But for anyone who is reading this blog and dealing with severe acne or folliculitis, I wanted to share my own “pre-Accutane” story and images to chronicle my journey from beginning to end. On November 13, I popped my first 40 mg capsule of Accutane and hoped that this medication—what felt like my last resort—would clear me, once and for all.

 

In Part 3, I will get to the heart of the matter: what is Accutane, and what does it do? How does it work in the treatment of acne and, in my case, folliculitis? What are the common side effects—some of which I have experienced myself—and what side effects are rare or unlikely? And, of course, I will discuss my own progress as I now enter my fifth month of treatment.

 

To be continued!

When the Provider is the Patient: My Accutane Story, Part 1

For most of my adulthood, I had maintained what you might call a “clean cut” appearance. I was probably 16 years old when I received a free Gillette Mach 3 in the mail. Since then, every two days during my morning shower, I had dutifully shaved my thick red beard, never letting it grow beyond a respectable stubble. Last spring, however, approaching the end of my clinical year of PA school, I had had enough. Beards were in! I was 35 and late to the trend. Time to relax and give the early morning hacking a rest. I set aside my trusty Mach 3 and let my long repressed beard hairs come in.

 

(Caption: “May 2017. Newly bearded.”)

 

The response was immediately favorable. “Nice scruff!” and “Love the beard!” wrote friends on my Facebook and Instagram pages. Some friends were enthusiastic enough to write “Handsome!” or “Sexy!” In what felt like a human sexuality experiment, I felt an upswing of attention from both men and women. Did I look more rugged? More “manly”? More “masculine”? (Whatever that means?) Perhaps imbued with confidence in my new bearded self, I met my boyfriend Alejandro in early May. We have been happily partnered for almost nine months now.

 

(Caption: “June 2017. New beard + new man!”)

 

Lest you think this just another grow-a-beard-and-find-a-boyfriend tale, however, think again. As is so often the case in life, what goes up must come down—and my face as I knew it was about to go way down. By early July, powering through an Internal Medicine rotation at NewYork-Presbyterian Queens, I began to feel large, tender lumps underneath my beard. The hair was so thick, I couldn’t see the lumps, but trimming had become unusually painful. I also realized that my cheeks had become swollen, as if I had gained a significant amount of weight. (I hadn’t.) I kept the beard in place for my graduation on July 27, thinking I would shave a few days later and address what I thought would be some mild cystic acne that had formed under my beard.

 

(Caption: “July 27, 2017: The calm before the storm.”)

 

When I did shave for the first time in months, it was nothing short of a blood bath. Despite going slowly and carefully, I nicked a few of the cystic nodules with my razor. (This is where the faint of heart may want to skip ahead.) There was no purulent discharge or “pus” to speak of, but I was surprised by how much the lesions bled and oozed an oily yellow serous fluid. One in particular on my right cheek would not stop, but I had a dinner to run to. I grabbed some tissue and daubed at my face as discreetly as I could on my walk to the train. I managed to get through dinner, meeting some friends of Alejandro’s from Mexico and apologizing for the state of my face. It was the just the beginning of a new self-consciousness I had never experienced before.

 

(Caption: “August 2, 2017: Beardless and breaking out.”)

 

Two days later, I was diagnosed with impetigo, a highly contagious bacterial skin infection affecting the superficial skin. Impetigo most frequently affects children, ages two to five, but in adults it is often associated with poverty, crowding, poor hygiene, and underlying scabies.1 I was a poor PA student, and my beard had gotten pretty long—but was I that poor, and was my hygiene that bad? In any case, most cases of impetigo clear within one to two weeks, if treated. As I packed up for a long-awaited summer vacation with friends in northern Maine, I grabbed my prescription of doxycycline and clindamycin lotion with no doubt that I would respond.

 

As luck would have it, my impetigo and I were not “most cases.” Despite faithful adherence to the oral and topical antibiotic regimen, I got worse. The clindamycin lotion created a thick, dry, white cast over my cheeks, under which my cystic nodules poked through, bled, and oozed. The doxycycline, as far as I could tell, did nothing except make me more sensitive to the sun. My cheeks were still swollen, like a baseball player with a dipping problem. But I was enjoying myself, my friends, and the calm of Moosehead Lake. I decided there was nothing to be done until I got back to New York.

 

(Caption: “August 11, 2017: This isn’t working.”)

 

 

To be continued…