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Zebras, Not Horses
“When you hear hoof beats, look for horses, not zebras”. This is a principle most doctors learn in medical school. What it means, basically, is that a doctor should look to the most obvious for an answer, not the exotic. This may be a sound diagnostic principle, but for a subset of people who have rare diseases, it is perhaps not the most effective approach to medical care.
I speak, of course, from personal experience. Not only did it take four years for a doctor to decide that I had lupus, but there also was a span of about twenty years when I suffered, without treatment, mysterious episodes of acute abdominal pain. A whole herd of horses was pulled out to explain these episodes. But not until an emergency room physician insisted on taking a CT scan during one episode was a clue to my gut disturbances obtained. And not until a very astute and careful gastroenterologist studied these CT images was the puzzle further unraveled. It finally took my rheumatologist, a creative and talented physician, to spot the zebra in the herd of horses: he determined that I was experiencing lupus-induced inflammation of the gut.
As idiosyncratic as lupus can be, there is still the conviction among many in the medical community that horses and not zebras predominate. In a Lupus Foundation article, for example, the transcript of a dialogue is presented. The dialogue is between Dr. David Isenberg , a noted gastroenterologist, and lupus patients. Dr. Isenberg explains to the patients the low probability that certain GI conditions will occur as a direct result of lupus. The doctor is asked about ascites (fluid in the abdomen), for example. He asserts that ascites are most likely to be caused by kidney or liver problems.
Of course, my experience refutes Dr. Isenberg’s perspective. Ascites was detected during several of my GI episodes. I did not have liver or kidney disease, although once I did have pancreatitis.
I came across another article which suggests my experience is not unique, though it certainly may not be common. In the medical journal RadioGraphics, which is dedicated to the field of radiology, I found the description of a young woman who had an acute episode of small bowel inflammation, with ascites. The woman also had systemic lupus. Her inflammation was successfully treated with high-dose steroids.
While Dr. Isenberg is an esteemed and accomplished researcher, in his interview he entertains as very remote the scenario suggested in the RadioGraphics article. Dr. Isenberg apparently not only expects to see horses, but he also recommends that everyone else does, too. This is not his “fault”; it is standard medical practice.
I have read that sometimes ten years can pass between the time lupus is first suspected to the time when it is ultimately diagnosed. Perhaps the reason for this diagnostic lag has something to do with the horse/zebra dynamic. When dealing with an idiosyncratic disease like lupus, which can confuse and confound, maybe doctors should think more often about zebras. Because something is amiss in a protocol which leaves patients, for so long, without appropriate treatment.
I know that in the ordinary course of events, hoof beats will be produced by horses. But sometimes, when the possibility, or strong suspicion, of lupus exists, a doctor might consider the extraordinary. I think a lot of unnecessary suffering and true harm could be avoided if doctors would just allow themselves to look a little bit harder at what seems to be obvious.
A Gene for Autoimmunity?
Some years ago I bought stock in a company that investigated the genetic origins of disease. The company went bankrupt and I lost all my money, but there was nothing wrong with the research–just the business plan. Hope of finding a cure–for lupus and other diseases–may rest precisely in understanding the genetic basis of illness.
It was with this idea in mind that a study–A Comprehensive Analysis of Shared Loci between Systemic Lupus Erythematosus (SLE) and Sixteen Autoimmune Diseases Reveals Limited Genetic Overlap—was undertaken. As the title suggests, the study failed to produce evidence that there is a strong genetic link between people SLE and other autoimmune diseases. The authors of the study hypothesize that the correlation may be weak between SLE and many other autoimmune diseases because SLE is so “heterogenous”. That is, there are many ways in which SLE can manifest. Perhaps each manifestation of lupus has a different genetic association.
Interestingly (according to the authors), the strongest genetic association found was between SLE and rheumatoid arthritis. The authors hypothesize that maybe this strong link has something to do with the fact that the two diseases share a major symptom: arthritis. There was another, though weaker, genetic association found between SLE and scleroderma.
The authors also noted that several established genetic links to SLE were not found in other autoimmune diseases. The authors admit that the failure to find these links may be due to a problem with the study’s methodology and that future efforts may be able to detect these associations.
So where do I think this leaves us? Well, there doesn’t seem to be an autoimmune gene, one common cause for a multiplicity of autoimmune diseases. And what the study shows, what it reinforces, is the fact that SLE, even on the genetic level, is a very complicated disease. Systemic lupus is more like several diseases than one and its cure may ultimately involve solving many genetic riddles, not just a single puzzle.
I personally think SLE might be approached the way cancer is increasingly treated: though it falls under the rubric of oncology, cancer responds to a variety of very specific therapies that have been designed for different manifestations of the disease. Something like that may evolve (is already evolving to some extent) for lupus. Though there may not be one gene that causes SLE, there may be different places on the genetic map where a susceptibility for distinct forms of lupus exist. And, just as tailored treatments are developed for different cancers, targeted treatments may need to be developed for different kinds of lupus.
There was a time when certain cancers carried with them very high mortality rates. Some of these, like lymphoma, today have dramatically improved cure rates. The day will surely come when people with lupus will experience the same success. They then will be able to look forward to futures that include the prospect of a complete cure.
A Handful of Pills
Image by Ayena
If you have systemic lupus, there’s a pretty good chance you have been prescribed a NSAID (example: aspirin, ibuprofen, Naproxen, etc.) over the course of your illness. Given that likelihood, I have dedicated some time to seeking an understanding of this broad class of drugs. The following essay is one of several I hope to post on the subject.
In writing this post, I have tried to be very careful in my use of language; I draw no conclusions. The available information about NSAIDs indicates that caution should be exercised in their use. Some of the reasons for the caution are explained below. Since research on these drugs continues, the recommendations of the American Heart Association and the FDA for their use reflect only what is currently known. Recommendations of both organizations will likely change over time.
The American Heart Association has issued repeated advisories about the use of NSAIDs; while the Association allows that NSAIDS may still be prescribed under certain circumstances in clinical practice, caution is required. The Association recommends that NSAID use be tempered by an awareness of associated risks. These are risks about which the patient should be informed if NSAID therapy is decided upon. As the Heart Association explains in its report, An Update for clinicians: A Scientific Statement From the American Heart Association (Feb, 2007), the issues surrounding NSAIDS “highlight” the obligation of patients and doctors to balance “the risks and benefits of medications for pain relief”.
So, what are these risks? This is a question that still has not been completely answered. Part of the answer is certainly that there is evidence of increased heart attack, heart failure, stroke and vascular events. The most recent advisory I found from the Heart Association (Sept, 2012) is entitled, “Taking painkillers increases death risk, second heart attack in survivors“. The article explains that the painkillers in question are NSAIDs. Anne-Marie Schjerning Olsen, the physician who led the relevant study, states: “It is important to get the message out to clinicians taking care of patients with cardiovascular disease that NSAIDs are harmful, even several years after a heart attack”.
According to the Heart Association’s 2007 study (cited above), not all painkillers appear to carry an equal risk of potentially lethal side effects. The Association cautions that results are suggestive and more information needs to be collected about the relative risks of each drug. With this cautionary note, they publish a chart that is meant to guide physicians in their use of NSAIDs. The chart describes a “stepped approach” to prescribing painkillers. In this approach, the least dangerous (according to Heart Association information) should be prescribed before moving on to those drugs that are seen to carry greatest risk. The Heart Association chart can be found at Figure 7, http://circ.ahajournals.org/content/115/12/1634.full.
Studies seem to suggest that NSAID risk is dose dependent, though what a safe dose is for an individual has not been established. The risk to individuals from NSAIDs (available over the counter in many cases) is considered so serious that the U. S. FDA has mandated inclusion of black box warnings in their packaging. A description of this black box warning can be found at the NIH website; APPENDIX BLACK BOX WARNINGS OF INCLUDED DRUGS
As I repeat throughout my posts on this website: I am not a doctor or a researcher. I am a patient who reads and who seeks to understand. What I get from the research about NSAIDs is that these readily available drugs are serious medicine. The fact that they are over-the-counter and easily accessed belies the danger they may present to the medical consumer. Before taking any one of these, think for a moment. Be sure that the drug is important to your care. And, consult your doctor. Between the two of you, an informed decision about taking NSAIDs can be made.
By A. G. Moore 2/16/2013
National Cancer Institute
While this essay specifically addresses the connection between sulfasalazine and lupus, the principles involved in the discussion have wider application. As an article in Pharmacological Review explains, “Individual variability in drug efficacy and drug safety is a major challenge in current clinical practice, drug development, and drug regulation” (Pharmacogenetics, Pharmacogenomics, and Individualized Medicine ). In other words, drug effectiveness varies according to the individual. The challenge is to find the most effective drug for each patient.
In the past, an appropriate patient/drug match was achieved through trial and error. Increasingly, though, science has improved the process of prescribing appropriate drugs for patients; often, a doctor can know in advance physical characteristics of patients which might make them more receptive to a drug or more likely to experience side effects.
Targeting medication to enhance effectiveness and avoid side effects is a gift to everyone: patients don’t lose precious, sometimes irreplaceable time with a therapy that doesn’t work; and dangerous, even lethal, side effects may be avoided.
Sulfasalazine is a drug therapy which can be administered today with greater confidence because of advances in genotyping–that is, identifying genetic elements which influence the way a patient processes medication. The history of this drug and its associated risks has been well-documented. In 1965 a physician from the Mayo Clinic reported that a patient he had been treating for inflammatory bowel disease went on to develop lupus. The doctor, Donato Alarcón-Segovia, attributed this development to the drug the patient had been taking: sulfasalazine. Since the 1965 case, sulfasalazine has been recognized as a drug which can induce lupus; the phenomenon is known as drug-induced lupus, or DIL. Sulfasalazine also may exacerbate disease in established lupus.
While doctors have known for a long time that drugs can induce lupus (first case was reported in 1945 in response to Sulfadiazine), this manifestation of lupus, known as drug-induced lupus or DIL, is usually described as being “mild”. However, “mild” lupus is not always the experience of a DIL patient. For example, an article which appears in Postgraduate Medical Journal (Postgrad Med J. 1982 February; 58(676): 98–99) describes a comatose 19-year old girl with “sulphasalazine-induced cerebral lupus erythematosus”.
Sulfasalazine has its uses: among other applications, some doctors find it a good alternative for controlling inflammatory bowel disease, rheumatoid arthritis, and, ironically, discoid lupus (see: Treatment of discoid lupus erythematosus with sulfasalazine: 11 cases ). According to the Lupus Foundation, sulfasalazine may even be prescribed to someone who has lupus if symptoms of rhuematoid arthritis are evident (see Lupus and Overlap).
So, what is a patient to do with this information? Whether sulfasalazine induces a “mild” or severe case of lupus, the development is obviously one a patient would like to avoid. As it turns out, this may be possible–without completely eliminating sulfasalazine from the physician’s list of viable treatment options. There is a way for doctors to profile individual patients and approximately assess their risk for developing sulfasalazine-induced lupus. Research has shown that almost all people who develop lupus after taking sulfasalazine fall in a group known as “slow acetylators” (see my blog: Medication Alert ). Those at high risk for developing sulfasalazine-induced lupus also tend to have specific genetic markers: HLA A1, HLA B8, and HLA DR3. If a patient does not have these markers and is not a “slow acetylator”, then the risk of developing drug-induced lupus may be greatly reduced.
Of course, it‘s impossible to tell how someone will respond to a drug. A serious discussion with the physician is in order before the decision is made to take sulfasalazine, or any medication. Risk and benefits need to be assessed.
Every drug has associated risks–not taking a drug also has associated risks. The more information a patient and doctor have about a proposed course of treatment, the more confidently can they assess the relative risk. In the case of sulfasalazine, it seems patients and doctors have the opportunity to weigh the medication’s benefits with more confidence than was available in the past.
Some articles helpful in learning about sulfasalazine and sulfasalazine-induced lupus:
Sulfasalazine-induced Lupus and Hypersensitivity, by Qingping Yao, and Bevra Hahn UCLA School of Medicine
Drug-induced lupus erythematosus on DermNet NZ
By A. G. Moore 2/28/2013
by Liz West on Wikimedia Commons
Today’s blog was prompted by a question I read recently on Lupus UK.
Pancreatitis, whether related to lupus or not, is a very serious development and requires immediate medical attention. During an attack, the pancreas starts to digest itself because certain pancreatic enzymes have been released prematurely. These enzymes usually break down food in the small intestine but, since they have been put to work in the wrong place, they instead begin to break down the pancreas. The situation can quickly become life-threatening.
A doctor diagnoses pancreatitis by reviewing blood tests and abdominal scans. The reason the attack occurred, however, may not be easy to discover. Without knowing the cause, it will be difficult to design an appropriate treatment plan.
If pancreatitis is related to lupus, a specific protocol is recommended. In the medical journal Clinical and Developmental Immunology, outcomes for groups of patients with lupus pancreatitis are compared. Those patients who are treated promptly and aggressively fare far better than patients who do not receive this level of care. (See: Clinical and Developmental Immunology, Systemic Lupus Erythemtaosus-Related Acute Pancreatitis: A Cohort from South China.)
Pancreatitis occurs for a variety of reasons. In some people, the condition may be a result of lifestyle–excess consumption of alcohol is generally included in this category. For other people, medication may precipitate an attack. Azathioprine and steroids are often suspected antagonists in this scenario. Evidence about the link between pancreatitis and these two drugs is not uniformly persuasive; while azathioprine clearly may cause pancreatitis in some people, steroids are another matter. There is disagreement about whether steroid-induced pancreatitis actually exists.
Estimates vary about the risk of developing pancreatitis while on azathioprine. According to a 2003 study published in the American Journal of Gastroenterology, patients on azathioprine ran a 0.4% increased risk of developing pancreatitis. Another medical journal, Annals of Gastroenterology, reported that patients on azathioprine (or mercaptopurine, into which azathioprine is converted by the liver) who had inflammatory bowel disease stood a 3.1% increased risk of developing pancreatitis. So, if someone is on azathioprine therapy and pancreatitis develops, suspicion will first fall on the medicine as culprit. The drug will be discontinued and an alternate medication prescribed.
As for steroids and pancreatitis: there is growing disagreement about this relationship. The Lupus Foundation describes steroid-induced pancreatitis, and indicates that the cessation of steroid therapy is the remedy for this condition. However, a recent article in Clinical and Developmental Immunology states: “Increasingly accumulated evidence showed that steroids do not trigger acute pancreatitis or cause increased mortality” in lupus patients. The lack of unanimity about the steroid/pancreatitis link increases the element of speculation in the diagnosis and treatment of pancreatitis.
When a situation exists where lupus has evidently caused pancreatitis, the way forward is clear for the doctor. High-dose steroids are the cure. This type of pancreatitis is called idiopathic lupus pancreatitis and is a very serious condition; it needs to be treated by experts in lupus care.
Since idiopathic lupus pancreatitis is thought to be rare, it can easily be overlooked by a physician who is not experienced in treating lupus. The complexity of treatment decisions facing a clinician increases if the lupus patient with pancreatitis is already on steroid therapy. Now the doctor has to figure out whether steroid therapy is appropriate or will make matters worse. The critical question has to be answered: Did steroids cause pancreatitis or will steroids cure pancreatitis?
An incident that occurred in a Slovenian hospital llustrates this point. A 33-year-old man evidently had pancreatitis. He also had lupus. Idiopathic lupus pancreatitis was suspected but high-dose steroid therapy did not elicit an improvement. Since the patient had been on steroid therapy, steroid-induced pancreatitis was suspected, but historically the use of steroids had not been a problem for this patient, so this theory fell out of favor. Finally, close examination of the many tests to which the patient had been subjected revealed that he had cytomegalovirus. It was this virus, the doctors concluded, which caused the pancreas to become inflamed. Treatment with Ganciclovir (an antiviral) was begun. The patient improved and eventually recovered.
The 33-year-old Slovenian patient obviously benefited from excellent medical care. The team of doctors who treated him were skilled and creative. They did not think in a box but used the latest research to problem-solve for their patient. Anyone with lupus who becomes ill wants just such a medical team in charge of their care.
Pancreatitis is a serious condition, for anyone. If you have lupus, the situation is even more perilous. If you do have lupus, know in advance who the best lupus doctors are and where the best lupus treatment facilities are located. When illness strikes, whether it’s pancreatitis or another ailment, be sure you are in a place that offers the best chance of a successful outcome.
Lupus: Signs and Tells
By A. G. Moore 4/28/2013
Public Domain Wikimedia Commons
Sometimes I don’t take my own advice. Acknowledging this helps to keep me modest. Yesterday I received a strong dose of modesty as my husband’s predictions of impending trouble were realized. The truth of his insight became obvious during the night: my body confirmed what my husband had observed for several days, what he had insisted on before we turned in the night before. A flare was upon me. The thing about catching a flare early is that it’s usually easier to chase lupus away if the disease is caught on the upswing, before it’s taken hold.
Unfortunately, for my husband and others I love, signs of the flare included a compromise of my ordinarily good nature. Today, I must apologize to people–not for the first time–because I was irritable and rude.
Then I’ll take my prednisone.
As everyone who has lupus knows, reluctance to begin an immune-suppressive regimen can seem reasonable. When lupus consists mostly of pain and lack of vigor, then taking medicine can seem self-indulgent. In my case, lupus has run a relatively mild course, so the temptation to ride out a storm without medicine is quite strong.
There are risks, though, to this laissez-faire approach. Lupus has, on occasion, turned on me and become vicious. Doctors have scratched their heads and alarm bells have gone off as I lay on a stretcher with symptoms that didn’t fit into any recognized pattern.
So I’m careful now, about guarding against vicious lupus episodes. I look for signs that tell me when a serious storm is brewing and I need to take action.
Signs of trouble for me do not always occur in a cluster. Some by themselves are compelling. For example, if I start to twitch–not just an eye or a jerk or two in my leg, but unremitting, sleep depriving, multi-site twitching–then I take action. ‘Cause there’s trouble coming.
If my gut acts up and no amount of coddling will sooth it, I take action. ‘Cause there’s surely trouble coming and I never play chicken with when my gut is involved.
I don’t have lupus nephritis, which can be active without any signs such as those I just described. Though some 40% of lupus patients present with nephritis early in the disease (first 5 years), about 5% of patients will develop kidney problems later. The material I cite below suggests that the best outcome for nephritis patients is realized with early diagnosis and treatment. Since lupus nephritis can be silent, invisible, without early signs, it’s important that all lupus patients be monitored from time to time to see if this condition is developing.
What the literature says about treating early
There is little disagreement in the research community about the wisdom of getting early treatment when lupus attacks organs. To illustrate this cautious approach, I did some reading on two common manifestations of lupus. In both these cases, lupus nephrttis and GI lupus, early diagnosis and treatment are uniformly recommended. I am assuming we can extrapolate this cautious attitude to other forms of lupus where there is organ involvement.
While not everyone with lupus has nephritis, this symptom is one of the first a doctor will look for when diagnosing the disease. The consensus about management of lupus nephritis is clear: early intervention saves lives and helps to prevent kidney failure. In 2008, the American Association of Kidney Patients issued a report about pediatric lupus nephritis. The report concluded: “Early recognition of the pediatric patient…with prompt intervention…may prevent kidney failure…”.
In 2006, an article in the The Journal of Rheumatology concluded:”…early initiation of immune-suppressive treatment might be critical for the outcome of patients with lupus nephritis”.
And, finally, a 1999 article in the American Journal of Nephrology stated: “In most patients today, there is a gratifying response to early treatment…”
The consensus about early treatment of lupus nephritis is mirrored in recommendations for treatment of gastrointestinal lupus. Most sources suggest that GI lupus is often caused by lupus vasculitis, which is a very serious, life-threatening condition. However, there are aspects of lupus expressed in the GI tract which may not be caused by vasculitis. Two of these are pancreatitis and intestinal pseudo–obstruction. Early treatment in any of these instances is essential.
A 2010 article in The World Journal of Gastroenterology described lupus mesenteric vasculitis, as “…a main cause of acute abdominal pain in SLE patients”. The authors of this posited that prompt diagnosis and “….appropriate intervention can avoid potentially fatal complications of…lupus mesenteric vasculitis”.
With regard to lupus pancreatitis, the same authors concluded: “As many as 57% of SLE-related acute pancreatitis cases may develop complications if not treated promptly.” And, finally, the authors discussed psuedo-obstruction. The recommendation for early treatment was unequivocal: “Early diagnosis and prompt treatment is critical to improve the overall outcome of SLE-related IPO (intestinal pseudo-obstruction) patients.”
As for my current lupus flare, this is small potatoes. I’m paying attention and treating early. I am confident that this flare, like so many others, will subside quickly. Then my bottle of prednisone will be retired to a dark corner in the cabinet where it will wait until the next time one of my “signs” appears.
This article is about sulfa drugs, which can be separated into two categories: antibiotic and non-antibiotic. What I hope to do in writing this post is offer some insight into the issues surrounding sulfonamide hypersensitivity.
Recently I wrote about sulfasalazine, which is a sulfonamide (sulfa drug). In that blog I report that sulfasalazine can cause drug-induced lupus. Though there always exists the possibility of adverse reaction to medication, sulfa drugs as a class seem to pose a particular threat to lupus patients.
Sulfa drugs were the first antibiotics ever discovered; in 1936 a researcher at Bayer Laboratories in Germany formulated a drug called Prontosil. One of the first patients treated with this drug was the researcher’s own daughter.
Prontosil was considered a “wonder drug” and revolutionized medical care; in time, other sulfa drugs were formulated. However, resistance to sulfa drugs soon developed as some microorganisms became immune to them. Eventually, alternative antibiotics, such as penicillin, were discovered.
Sulfonamides still have a place in the doctor’s bag of tricks. These drugs are especially effective in treating urinary tract infections. Though a doctor might be tempted to resort to a sulfa drug when susceptible organisms are detected, caution is advised, especially caution in patients who have certain conditions. These conditions include lupus and HIV. Individuals who have an established sensitivity to penicillin are also at increased risk.
There is little question today about the risk of using sulfonamide antibiotics in lupus patients—that question has been asked and answered. There is an elevated risk. The question still open is whether the sensitivity to sulfonamide antibiotics carries over to non-antibiotic sulfonamides.
Non-antibiotic sulfonamides have a different chemical structure from their antimocrobial cousins; this different structure seems to limit the number of adverse reactions. I have read a number of research articles and a few case reports about the possibility of a cross-over hypersensitivity between the antibiotic sulfonamide and the non-antibiotic. Not all researchers agree about the level of risk.
It seems that most researchers feel non-antibiotic sulfonamides are safer for lupus patients (or anyone with a sulfonamide hypersensitivity) than antimicrobial sulfonamides. However, case reports do exist which show that there can be a crossover–people can be allergic to both antibiotic and non-antibiotic sulfonamides. This is especially true in people who are allergic to penicillin.
One case illustrates the dilemma a doctor may face when sorting through the conflicting research: A Canadian physician reports that a 70-year old patient has symptoms of mild heart failure. She also has a history of antibiotic sulfonamide hypersensitivity. The doctor prescribes furosemide (Lasix), an non-antibiotic sulfonamide diuretic, despite the patient’s history of allergy. He’s not concerned about a cross-over hypersensitivity between the two types of sulfonamides.
A few hours after the patient leaves his office, the doctor receives a call from the pharmacist. He points out that the patient also has a history of hypersensitivity to hydrochlorothiazide, a non-antibiotic sulfonamide. The doctor reconsiders his prescription; he agrees that a non-sulfonamide diuretic might be wiser in this case. In a follow-up consult with his patient, the doctor recommends she wear a Medic Alert bracelet.
In the mind of at least this one doctor, there is now a heightened concern about cross-over sensitivity between anti-biotic and non-anti-biotic sulfonamides. He concludes his report by suggesting that in the future he will proceed more cautiously in prescribing sulfonamides of any kind to someone with a demonstrated sulfonamide hypersensitivity.
Some researchers have concluded that a cross-over sensitivity between sulfonamides is not due so much to a sulfonamide allergy as it is to a general sensitivity to all medication. This would explain why people with penicillin allergy are more likely to have a allergy to both kinds of sulfonamides.
Non-antibiotic sulfonamides are present in many prescription drugs. The names of some of these are (this is not a comprehensive list–always check with your doctor and pharmacist if sulfonamide allergy is a concern): furosemide (one brand name of this drug is Lasix), Celecoxib (one brand name is Celebrex) and hydrochlorothiazide (which is sold under a variety to names and which is also used in the preparation of a number of hypertensive drugs, including Atacand, Benicar and Zestoretic).
The names of a few antibiotic sulfonamides are (once again, this is not a comprehensive list; check with your doctor and pharmacist if sulfonamide sensistivity is a concern): Septra and Bactrim; Silvadene; Azulfadine; Gantrisin; and Erythromycin-sulfisoxazole (combination drug sold under a number of brand names).
I emphasize here, as I always do: have a conversation with your doctor if you think sulfonamide sensitivity may be an issue. Report to your doctor any history of adverse reaction to medication of any kind. Patients cannot always know the class of drugs to which a medication belongs (I didn’t know, for example, that Celebrex was a sulfonamide). Pharmacists are also good sources of information. As the example from Canada (described above) illustrates, sometimes pharmacists catch things doctors miss.
A few articles that were helpful to me in putting together this blog were: