Δρ. Αἴας-Θεόδωρος Παπασταύρου
Χειρουργικὴ Κεφαλῆς & Τραχήλου
Τὸ 35% περίπου τοῦ γενικοῦ πληθυσμοῦ παρουσιάζει φταρνίσματα ἀπὸ καιρὸ σὲ καιρό, καὶ μερικὲς φορὲς αὐτὰ συνοδεύονται ἀπὸ δάκρυα καὶ φαγούρα στὰ μάτια, καὶ ἄλλα περισσότερο ἢ λιγότερο ἐνοχλητικὰ μικροσυμπτώματα. Ἰδίως μέσα στὴν ἄνοιξι, σχεδὸν ὅλοι μας ἔχουμε μπουκώματα στὴ μύτη. Αὐτὰ θεωροῦνται ἀπ΄ τὸν κόσμο ὡς φυσιολογικὴ ἀντίδρασι στὴν παρουσία ηὐξημένης σκόνης στὸ περιβάλλον, καθὼς καὶ στὴν παρουσία "κίτρινης σκόνης" ἀπὸ τὰ πεῦκα, κάμπιες κλπ. Ὅλοι προφέρουν μὲ ἐλαφρότητα τὴ λέξι "ἀλλεργία", ὅ,τι κι ἂν σημαίνῃ αὐτὸ στὴν ἀντίληψι τοῦ καθενός. Καὶ βέβαια οἱ περισσότεροι καταφεύγουν στη χρῆσι σπρέϋ ἢ ἀντι-ισταμινικῶν γιὰ νὰ ἐλέγξουν κατὰ τὸ δυνατὸν τὰ συμπτώματα.
If that’s all there was to it, Doc Gumshoe would not be composing this epistle. But, as it happens, seasonal allergic rhinitis is more than a normal vexation, to be weathered with a packet of OTC pills and a big wad of Kleenex. Here are some tidbits of data:
Beyond concluding that hay fever, or allergic rhinitis (whether perennial or seasonal) is definitely more than a trivial bother, I don’t want to make too much of those numbers. Experts like to put numbers to things, but what I want to stress is that allergic rhinitis is common, consequential, and costly.
Seasonal versus perennial allergic rhinitis
The difference between these is the particular allergic trigger. People with seasonal allergic rhinitis (SAR) are allergic to tree pollens, which are prevalent in early to late spring, or also possibly to grass pollens, prevalent in late spring through summer, or also possibly to various weeds (ragweed et al), prevalent in late summer to early fall, or also possibly to outdoor mold spores (late summer until winter).
People with perennial allergic rhinitis (PAR) can be allergic to indoor molds, house dust mites, cockroaches, and some animals, especially cats. As it happens, as more of our population lives in urban environments, PAR is gaining on SAR in prevalence.
Another factor in allergic rhinitis, whether seasonal or perennial, is a vexing phenomenon called “priming.” The way it works is this: a person is initially exposed to a high enough dose of a particular allergic trigger to set off an allergic reaction. It usually takes a fairly high initial concentration of the allergen to trigger the allergic reaction, but once that has taken place, the person is primed, and subsequent exposures to very small concentrations of that allergen may be enough to trigger another allergic reaction. Thus, when ragweed season sets in, the person may go for several days before feeling any of the usual symptoms, but once the first bout of “hay fever” takes place, the symptoms will persist, triggered daily by much smaller amounts of the ragweed pollen, because the person has become primed, or hypersensitive to that particular allergen. The amounts of allergen that can trigger subsequent symptoms may be as small as one one-hundredth as the original trigger.
Also, and perhaps of even greater consequence, once primed, the person can develop sensitivity to other triggers in the environment – not necessarily allergens of any kind – and those triggers can also result in the same symptoms as the allergens to which the person is sensitive. Those non-allergic triggers include such stimuli as tobacco smoke, perfume, air pollution (e.g. car exhaust), hot or cold drinks, exercise, or even strong emotions.
Allergic response and immune response – what’s the difference?
An allergic response is a kind of immune response. In general, any physiologic response to any invader is an immune response. Our bodies learn to recognize harmful invaders, such as pathogenic microbes, and attempt to mount defenses. Part of the immune response consists in identifying the dangerous invaders and calling out a defending army, which can be cells or complex molecules that attack and destroy the enemy.
An autoimmune response is when this process is turned against our own cells, and is the underlying cause of a great many serious diseases.
Allergies are responses to invading substances that are not necessarily harmful. I am fiercely allergic to crabmeat, but not, thank Heaven to any other seafood – and my wife loves crabmeat. What would be harmful to me is not the crabmeat itself, but the reaction that I mount if I should happen, by mistake, to eat crabmeat.
People with allergies appear to be somewhat different from our luckier non-allergic fellow humans. We tend to produce a different variety of immunoglobulins – IgE – when challenged with certain substances, whereas the rest of the population produces IgG.
When an allergic person (sometimes also called an atopic person) is exposed to certain substances, he or she will express IgE molecules, which will coat cells in the throat, nasal passages, eyes, and even the entrance to the GI tract. These cells, called mast cells, then degranulate (break up) and set in motion a great number of different responses. The one most prominent in many allergic reactions is the release of histamine, which cases edema (swelling) of the mucous tissues in the nasal passages and the eyes and itching in various parts of the body. The histamine reaction typically occurs very quickly, usually within 15 minutes.
The allergic response also includes the summoning of other cells – eosinophils, neutrophils, basophils – to the site of the allergic reaction. These cells bring about an inflammatory response, usually about 8 to 12 hours after the initial histamine response. The histamine response is sometimes called the early-phase response, and the inflammatory response is called the late-phase response.
In plain language, that’s why, when hay fever strikes, people first respond with sneezing and itching and watery eyes, and later on they get stuffed-up noses.
But that’s also why, in trying to deal with hay fever (or SAR) the antihistamine pill often doesn’t do the job.
Symptoms of SAR and/or PAR
“What!” you say. “Doc Gumshoe is going to tell me about my symptoms? I know darn well what they are and what they feel like.” Well, maybe so and maybe not.
Starting with the eyes, there’s itching, tearing, puffiness around the eyes, redness in the eyes themselves caused by too much blood in the blood vessels on the surface, and also actual pain. Of course, nasal symptoms are foremost – the nose runs (rhinorrhea) or is stuffed up, and the annoying post-nasal drip is common. And then there are those paroxysmal sneezing fits.
Typically, the parade of symptoms in the course of a day during the time when a person is affected by seasonal allergies is sneezing in the morning, runny nose and more sneezing as the day goes on, and then – perhaps the most bothersome symptom of all – the stuffy nose at bedtime.
One of the little tricks that folks with hay fever try to stave off a sneezing fit is to put a finger to the tip of the nose and push upward. (Sometimes it does work; I’ve done it during a concert where the sound of a sneeze would be unwelcome.) People sometimes also try to open their nasal passages that way. This is called the “allergic salute.” It may result in a little wrinkle across the bridge of the nose, which some doctors can spot the minute you walk into the consulting room.
And then there are other symptoms. People in the grip of a bout of allergic rhinitis can develop painful sinus headaches or earaches, as well as sore throats (usually mild). And sometimes the whole oral cavity and throat develop persistent itching sensations, which, of course, are almost impossible to alleviate by scratching, although people try to deal with the itch by means of stratagems like clearing the throat or forcing air through a constricted pharynx.
The sense of taste and smell may also be diminished. Or, to be more precise, when for any reason our sense of smell is dialed down, we find that we can’t taste much of anything – that’s because a major part of what we think of as the taste of food is conveyed by the sense of smell.
Finally, some people find that hay fever season leaves them tired and unable to get a good night’s sleep, which is doubtless why those who are most susceptible find that they are less effective at work.
There is also non-allergic rhinitis. Some people can develop similar symptoms from exposure to non-allergens, such as perfumes, some spicy foods, tobacco smoke, and even some bright lights and sudden changes in temperature. Mostly these people don’t itch, but then can certainly have the usual hay fever nasal symptoms. It’s important for those people to understand their condition, because trying to treat the non-allergic variant with anti-allergic remedies like antihistamines has a scant chance of success.
By now surely everybody knows that you have to go easy on nasal decongestant sprays. The temptation, in hay fever season, to deal with the stuffed-up nose with decongestant sprays is hard to resist. A few squirts in each nostril opens the nasal passages just fine. The only problem is that after as few as 4 or 5 doses, the treatment backfires – the nasal passages block up worse than ever. There’s obstruction, inflammation, hyperemia (meaning that the nose is suffused with blood), sometimes breakthrough nosebleeds, and the nose may take on an unattractive purple hue. Some people (certainly not any readers of these sermons) may think that when they get this result from the nasal decongestant it’s because they haven’t used enough, so they redouble the dose, which may work, but just a little bit. Then the congestion comes back with a vengeance. There are unfortunate souls out there who are addicted to nasal decongestants. Most of the time their nasal passages are as though packed with concrete, with only brief periods of respite during which they can breathe through their noses. It can take weeks for addicted persons to get weaned off nasal decongestants.
About one in five persons with allergic rhinitis, whether seasonal or perennial, will also have bronchial symptoms – wheezing, coughing, shortness of breath, chest tightness. These tend not to be part of the early-phase allergic response, but to develop hours or even days after the onset of the usual allergic rhinitis symptoms. Bronchial symptoms are due to an inflammatory response, due not so much to histamine release from mast cells, but to the release of inflammatory cells in the pharynx which travel to the bronchi and cause trouble.
The late-phase allergic response and the possibility of bronchial symptoms are important factors in managing SAR or PAR; in severely-affected individuals, trying to deal with the early-phase response with antihistamines may not be sufficient.
I’m steering clear of asthma in this installment, because it’s a large and very important subject and I don’t want to give it short shrift. Enough to say for now that asthma attacks can certainly be triggered by an allergic response, and are subject to the same priming phenomenon as SAR, meaning that once having manifested an allergic response with an asthma attack, the patient can (and likely will) have repeated asthma attacks in response to a large range of other non-allergenic stimuli. But the management of asthma differs greatly from the management of allergic rhinitis and deserves another epistle.
Now we come to the management of hay fever, or whatever …
People who aren’t susceptible to allergic rhinitis are apt to say, “What’s the big deal?” It’s true that people with mild cases can mostly just ride it out. They sneeze and itch for a few days, then the worst of it passes, and life returns to normal. But there are some people who are made genuinely miserable, for more than just a few days, and it’s not just a small minority (as those pesky statistics I put up at the beginning of this piece attest). A factor in the management of SAR, however, is that there are lots of people who are too embarrassed to seek medical help for a supposedly trivial ailment. Beyond looking for some over-the-counter antihistamines, they grit their teeth and apply tissues to their noses.
The question is, what should they do instead?
A first move is to figure out what it is that they are allergic to, and avoid it if at all possible. This is more crucial in the case of perennial AR, since the culprit is apt to be in the afflicted person’s normal environment – the cat, the carpet, the upholstered furniture, the attic, the cellar, the air conditioner, the humidifier.
It’s a bit easier with seasonal allergies, because we can figure out what’s producing pollens when we’re most affected. For example, if you live in a part of the country where there’s a lot of Russian thistle (aka tumbleweed), and you’re allergic to tumbleweed pollen, of which there are huge quantities, you might keep the windows in your house shut and run the air conditioner when these nasty (although picturesque) weeds are putting out the pollen. Same thing with the car. And, of course, the same thing goes for other common allergens: if you know what your allergens are, try to avoid them.
So how can you be sure what your allergens are?
Well, there are tests. The simplest is the skin prick test. Little sample dabs of the suspected allergens are put on the skin, and the skin is lightly pricked to permit the allergens to penetrate. In about 15 or 20 minutes, the skin will redden and swell in response to the samples to which the person being tested is allergic. Typically, several samples at a time are tested, and the allergist identifies the patches of skin on the patient by writing numbers next to the test patches, so that if number 6 reacts, by golly, the patient is indeed allergic to maple pollen, or ragweed, or whatever.
A variant of skin testing is intradermal testing, in which the suspected allergic trigger is injected more deeply beneath the skin. This is normally reserved to test whether the patient is allergic to a drug.
A potential problem with the skin test is that if the patient is already in the throes of an allergic episode, he or she is likely to respond positively to just about every challenge, so the test doesn’t single out the culprit. Patients are best advised to do their allergy testing not in the season when they are most susceptible to SAR. For PAR patients, that may not be possible, so the allergist may have to resort to other tactics to get the patient to a state where the test will produce useful results.
Some patients cannot take a skin test because the test will not produce reliable results if the patient it taking certain drugs, such as some older antihistamines, OTC drugs for reflux, or some antidepressants. In that case, the allergist may resort to the enzyme-linked immunosorbent assay (ELISA) blood test.
Specific SAR/PAR treatment strategies
By now, most people have moved beyond the old first-generation antihistamines such as Benadryl (diphenhydramine), Tavist (clemastine) or Chlor-Trimeton (chlorpheniramine). They had their virtues, one of which was that in addition to quelling the immediate allergic reaction, they had a sedative effect. Thus, if a person developed a fierce allergic itch just before bedtime, a Benadryl might be just the ticket. But they had other effects as well, such as making people very thirsty. And the sedating antihistamines as a class are off limits to airplane pilots, according to Air Traffic Control regulations. They are also strongly not recommended for persons who are going to drive a motor vehicle; in fact, some people involved in accidents while “under the influence” of a non-sedating antihistamine have been charged with DUI.
The new class of non-sedating antihistamines (now about 20 years old) is said by some to have somewhat less potent allergy-quelling effects than the previous, sedating antihistamines. Among the more widely-used are cetirizine (Zyrtec), desloratadine (Clarinex), fexofenadine (Allegra), and loratadine (Claritin). Loratadine was among the first of the non-sedating antihistamines to come on the market and is the only one of that group of three agents to have survived. The other two, astemizole (Hismanal) and terfenadine (Seldane) have been taken off the US market because of a potentially fatal cardiac arrhythmia that can result from their use in combination with certain other quite common drugs, such as antibiotics and antifungals.
A benefit of these non-sedating antihistamines is that they have a longer half-life than the older agents, and therefore can be taken once daily. Physicians who make a specialty of treating allergies recommend that patients who anticipate developing allergies at a certain point in the season start taking their antihistamines a few days in advance of the appearance of the offending pollens.
With all respect to these physicians, Doc Gumshoe’s eyebrows lift at this recommendation. Yes, depending on where you live, the tree pollens begin to blow around in great abundance starting sometime in April or thereabouts, but this year nothing much happened until May, and then they burst out with a vengeance. I suspect that recommendation hasn’t had much takeup. But if people take their antihistamines daily once whichever allergen they’re susceptible to starts to be abundant, chances are the worst of the allergic rhinitis symptoms can be avoided.
However, this does not solve the whole problem. The inflammatory symptoms still need to be dealt with, and the antihistamines do very little to affect those. If people develop inflammatory symptoms of the nasal passages and upper airways, a good option is an intranasal steroid.
A key difference between the intranasal steroids and the antihistamines is that, while antihistamines work fairly quickly, intranasal steroids need to be taken for several days or as long as a week before their effectiveness is felt. Because these drugs are administered very much like the nasal decongestants we discussed earlier, some people get confused and think that they are decongestants, so when they don’t have an immediate effect they conclude that the drug is not working and quit using it. Or they may think that they may experience a rebound effect, as to the decongestants, and refrain from using the steroid.
From whatever data I have seen, intranasal corticosteroids are exceedingly safe. Yes, I know, the word “steroid” sends up red flags in the view of many people. Without going into excess scientific detail, let me say that the category “steroid” covers an immense range of quite distinct substances. There are two reasons why these intranasal steroids are definitely safe drugs: one, only tiny amounts of the drug are absorbed systemically – most of their activity is limited to the nasal passages, where they combat the immune reaction that brings on inflammation. And two, the tiny amounts that are absorbed are very rapidly metabolized in the liver and excreted.
Some of the more widely-used intranasal corticosteroids are beclomethasone dipropionate (Beconase), budesonide (Rhinocort), flunisolide (AeroBid or Nasalide), fluticasone (Flonase), and triamcinolone acetonide (Nasacort). All of these agents are also used in other formulations, under other names, to control other immune responses, including those associated with asthma.
Finally, for some persons with severe allergic responses who don’t respond adequately to medication, and who can’t get away from the allergens that trigger their symptoms, immunotherapy may be appropriate. This consists of inoculating the patient with tiny but increasing amounts of the allergen to which they are sensitive. Experts debate about the exact mechanism that makes immunotherapy work, when it does work. It might be analogous to the gradual decrease over time in the intensity of the allergic reactions that an individual experiences. In other words, a person who is violently allergic to certain tree pollens and has miserable hay fever seasons might find that as time goes on the allergies aren’t as fierce and the symptoms aren’t as potent.
But by and large, allergies as a problem are on the increase
There are theories as to the reason for this, but the most persuasive theory, from where I sit, is that our lives are becoming increasingly sanitized and isolated from the natural world, so that the natural immunotherapy that comes from exposure, in relatively small quantities, to a great variety of potential allergens, simply doesn’t happen as it used to. Evidence supporting this is that children raised in urban environments have a higher incidence of allergies – SAR, PAR, asthma, you name it – than kids raised in rural environments. Of course, the urban environment has its own panoply of potential allergens, but there apparently is such a thing as excessively sanitized child-rearing.
We shouldn’t exaggerate the problem, though. Allergic rhinitis is rarely fatal. I was going to say “never fatal,” but then I remembered that my mother sneezed while driving her car and crashed (not too hard!) into the car ahead. She escaped injury except for a broken finger. But you should never underestimate the consequences of a sneeze.
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