The Sex Series – Part Nine: Female pelvic floor dysfunction (2 of 2)

Muscular dysfunction in the pelvic floor starts when something happens that causes an injury or large scale inflammation to the pelvic floor.  This causes a large scale release of calcium, which causes the muscle to become too tight (hypertrophic).  As a result of this tightness, metabolism in the tissues increases and substances like histamine, serotonin and prostaglandins are released.  These mediators trigger neurologic pain perception.   The pain causes tightness, which causes more pain, and the cycle continues.

Hypertrophic muscles become musculodystrophic as fibrosis occurs.  The muscle becomes atrophied and is replaced by less extensible connective tissue.  As a result, the muscles aren’t as flexible as they should be. This also means that they cannot relax normally.  This activates trigger points in the pelvic floor and increases tone and spasm in pelvic structures, including the bladder, uterus, and rectum.

Treatment for pelvic floor dysfunction of women is very well described in literature.  It relies largely upon patient education and compliance with various exercises to retrain the muscles to relax completely at will.  Trigger-point pressure, both internal and external, can be applied by the patient or partner to help the muscles relax.  Vaginal or anal dilators, vaginal cones and bladder training can also be effective. Physical therapy including myofascial release and biofeedback are also important to treatment.

While initial treatment of PFD can be complex and time-consuming, the results are very good.  One study followed a cohort for ten years. 71% of women in this cohort reported major reduction or elimination of pain level following physical therapy and exercises done at home. After ten years, 89% of women reported major reduction or elimination of pain.  Many patients continued their home exercises during that time.

 

References:

Bortolami A, et al. Relationship between female pelvic floor dysfunction and sexual function: an observational study. J Sex Med 2015; 12: 1233-1241.

Hartmann D, Sarton J. Chronic pelvic floor dysfunction. Best Practice & Research Clinical Obstetrics and Gynaecology 2014, 28: 977-990.

Espuña-Pons M, et al. Pelvic floor symptoms and severity of pelvic organ prolapse in women seeking care for pelvic floor problems. European Journal of Obstetrics and Gynecology and Reproductive Biology 2014, 177: 141-145.

Ramalindam K, Monga A. Obesity and pelvic floor dysfunction. Best Practice and Research Clinical Obstetrics and Gynaecology 2015, 29: 541-547.

Graziottin A, et al. Mast cells in chronic inflammation, pelvic pain and depression in women. Gynecol Endocrinol 2014; 30 (7): 472-477.

Ahangari A. Prevalence of chronic pelvic pain among women: an updated review. Pain Physician 2014; 17: e141-147.

The Sex Series – Part Eight: Female pelvic floor dysfunction (1 of 2)

Chronic pelvic pain (CPP) in women is staggeringly common, with incidence ranging from 5.7-26.6%, depending on the study. CPP is marked by intermittent or constant pain in the lower abdomen or pelvis, lasts at least six months, and is not associated directly with menstruation, pregnancy or intercourse. Mast cells are known to be involved in the inflammatory processes of these conditions and are therefore linked to CPP.

It can be caused a wide variety of conditions that affect organs or structures in the pelvis, including endometriosis, inflammatory bowel diseases affecting the lower tract, interstitial cystitis, ovarian cysts and hypermobility type Ehlers Danlos Syndrome (HEDS).  Over half of women with CPP report chronic bladder pain, for which interstitial cystitis is a common cause.  Interstitial cystitis is widely accepted to be a mast cell mediated disease.

Despite the frequency of CPP, many exploratory surgeries to identify the cause find nothing (28-55%). Chronic pain from these conditions alters the way the sensory nerves in the pelvic cavity send signals to the spinal cord.  This in turn disrupts interpretation of pain and sensation by the nerves, creating more visceral pelvic pain.

Pelvic floor dysfunction (PFD) affects about 26% of women with CPP.  This dysfunction can cause embarrassing and disabling symptoms, including urinary and fecal incontinence. Pelvic organ prolapse occurs when organs such as the bladder move out of the correct position and impinge on other structures, such as the vagina. Pelvic organ prolapse can be called by pelvic floor dysfunction and it can cause pelvic floor dysfunction.

Sexual dysfunction affects 15-65% of PFD patients. PDF interferes with correct function of a number of muscles, including the levator ani, which hold urogenital structures in place and allow them stretch and contract during penetration and orgasm.  Patients with pelvic organ prolapse often feel a bulge pushing against the vaginal wall that interferes with vaginal penetration.  Vulvodynia, vestibulodynia, vaginismus and painful intercourse are commonly seen in PFD.

In PDF patients, muscles in the pelvic floor can be hypotonic (not tight enough), hypertonic (too tight), or have normal tone. Hypotonic dysfunction is more likely to cause incontinence, bladder symptoms and pelvic organ prolapse.  Hypertonic dysfunction is associated much more with pain and sexual dysfunction. Reduction of the high tone is necessary to reduce pain.

References:

Bortolami A, et al. Relationship between female pelvic floor dysfunction and sexual function: an observational study. J Sex Med 2015; 12: 1233-1241.

Hartmann D, Sarton J. Chronic pelvic floor dysfunction. Best Practice & Research Clinical Obstetrics and Gynaecology 2014, 28: 977-990.

Espuña-Pons M, et al. Pelvic floor symptoms and severity of pelvic organ prolapse in women seeking care for pelvic floor problems. European Journal of Obstetrics and Gynecology and Reproductive Biology 2014, 177: 141-145.

Ramalindam K, Monga A. Obesity and pelvic floor dysfunction. Best Practice and Research Clinical Obstetrics and Gynaecology 2015, 29: 541-547.

Graziottin A, et al. Mast cells in chronic inflammation, pelvic pain and depression in women. Gynecol Endocrinol 2014; 30 (7): 472-477.

Ahangari A. Prevalence of chronic pelvic pain among women: an updated review. Pain Physician 2014; 17: e141-147.

The Sex Series – Part Seven: Mast cell activation and anal penetration

So far in this series, we have talked a lot about vaginally penetrating sex.  But that’s not the only way to have sex so for now, let’s move on.

Anally penetrating sex can be safe, painless and pleasurable for many people.  It is enjoyed by many partners of various sexual orientations.  The anus is an inherently different environment than the vagina and as such, preparation for and participation in anally penetrating sex is a bit different.

An obvious difference is that the anus does not self-lubricate in preparation for sex.  Use of external lubricant is HUGELY important.  Silicone based lubes are often used for anally penetrating sex because it is slicker and is not broken down as quickly by your body as water based lubricants. When selecting a lubricant, be sure to research whether components can irritate the anus and rectum.  In particular, many spermicides are very irritating to rectal tissue. Of course, in the same way that a person can react to lubricant in the vagina, you can react to lubricant in the rectum and anus.  Contact dermatitis or other types of allergic reaction can occur.

Though “vigorous anal penetration” is often considered a risk factor for anal or rectal injury, the actual incidence of these injuries is low and mostly occurs in sexual assault situations.  Injury to the sphincter musculature is unusual.  Large patient groups of gay men who engage in anal sex have been surveyed regarding issues or injuries associated with receiving anal penetration over a long period of time.  Some patients reported infrequent or “slight” incontinence, attributed by medical professionals to the inability of the anal sphincter to close as tightly in the immediate time after penetration.  However, in other studies, no patients have reported this issue.  The most frequent problem, as also seen in vaginal intercourse, is the transmission of sexually transmitted infections.  This can be mitigated by using condoms.

Anal penetration should not hurt.  The person receiving and giving should take steps to relax the anal sphincter, use adequate lubrication, and be sensitive to any pain.  Painful penetration can indicate a problem and should be taken seriously by both partners. Regardless of how an injury was acquired, anal sex can irritate any condition that affects the rectum or anus.

Hemorrhoids are blood vessels that become distended.  They can occur internally or externally, and are often painless.  The first indication of hemorrhoid is often bright red blood on toilet paper.  If a blood clot forms in the hemorrhoid, it can become very painful and swollen.  It is not entirely understood how hemorrhoids form, but straining to stool, increased pressure in the abdominal cavity, obesity and pelvic floor dysfunction are often linked to formation.

Mast cells are increased in hemorrhoid associated tissue and may affect hemorrhoid formation and resolution through release of mediators like tryptase, chymase and platelet activating factor. One study found that the number of mast cells in acute and chronic hemorrhoids is not different, indicating that mast cells can be associated throughout the lifecycle.

Fissures are tears in the anal or rectal tissue.  Fissures can be very painful, especially during and after defecation.  Fissures also cause bright red blood on the toilet paper or stool.  Patients who have fissures often have increased resting pressure when tested with anorectal manometry, meaning their muscles are more tense than usual.  Fissures can also be mast cell activating, as mast cells are active in wound healing.  Tears in the rectum and anus do not heal as quickly as those in the vagina.

Rectal itching is not unusual in allergy/mast cell patients.  Mast cells are natively present in the rectum and can degranulate in response to stimuli just like mast cells anywhere else.  Mediators released can also cause pain.  Care should be taken to reduce friction as much as possible to try to prevent degranulation from pressure.  Itching and pain can also be signs of reacting to condoms or lubricants used.

Pelvic floor dysfunction can also make anal sex painful, as the rectum and anus may not be properly supported by connective tissue.  Patients with pelvic floor dysfunction or connective tissue defects should be cautious to observe any pain or discomfort when receiving anal penetration. Pelvic floor dysfunction, and the other conditions mentioned above, can be irritated by anal penetration.

As described earlier in the series, it is possible to have an allergic reaction to semen, either due to the presence of allergens or to the composition of the semen itself. If semen enters the body during anally penetrating sex, it is possible to have an allergic reaction.  Condoms can prevent these reactions, and are also recommended to decrease risk of infection due to contact with GI flora.

 

References:

Chond PS, Bartolo DCC. Hemorrhoids and fissure in ano. Gastroenterol Clin N Am 2008, 37: 627-644.

Cawich SO, et al. Complete anal sphincter complex disruption from intercourse: A case report and literature review. International Journal of Surgery Case Reports 2012: 3, 565-568.

Zamvar V, et al. Severe anal pain caused by food allergy?: A case report. European e-Journal of Clinical Nutrition and Metabolism 2010, 5: e144-e145.

Taweevisit M, et al. Increased mast cell density in haemorrhoid venous blood vessels suggests a role in pathogenesis. Singapore Med J 2008; 49 (12): 977-979.

The Sex Series – Part Six: Male pelvic dysfunction and mast cells

Chronic pelvic pain syndrome (CPPS) affects about 15% of male patients and 90% of patients with chronic prostatitis. Patients with these conditions experience pain in the pelvis, abdomen and genitalia, as well as urinary tract symptoms without evidence of infection. Pain can be intermittent or constant, and can interfere with daily activities including sitting, standing, urination and defecation.

CPPS also causes sexual symptoms. Painful ejaculation, erectile dysfunction, and other types of ejaculation dysfunction are all common in this patient group.  In one study, 40% of patients with CPPS were found to have erectile dysfunction.  In another, 72% of patients reported either erectile dysfunction or difficulty with ejaculation.

Pelvic floor dysfunction is a component of CPPS. Many of these patients have abnormally tense pelvic floor muscles, which can cause muscle spasm and obstruct bloodflow. CPPS patients are more likely than healthy controls to have vascular dysfunction associated with nitric oxide level. In a group of 146 patients with CPPS and verified pelvic floor spasm, 56% experienced painful ejaculation.  Visceral and myofascial pain and spasm of the muscles in the pelvic floor contribute to CPPS.  While pelvic floor dysfunction has been well researched for female patients, there are far fewer studies on pelvic floor dysfunction in men.  Biofeedback and pelvic floor physical therapy can resolve issues with erectile dysfunction and other sexual issues.

IL-17, expressed by special T cells called Th17 cells, is required to develop CPPS-like conditions in animal models. IL-17 triggers mast cell degranulation and secretion of many inflammatory molecules.  A number of mast cell mediators are elevated in patients with CPPS. IL-1b, TNF, IL-6 and IL-8 are higher in seminal fluid of these patients.  CCL2 and CCL3 expression is also increased. In the prostate of animals with a CPPS model, TNF, IL-17a, IFN-γ and IL-1b are all increased.

Tryptase has been found to induce pelvic pain. Levels of tryptase and carboxypeptidase A3 are higher in CPPS patients than in healthy controls.  Tryptase binds to a receptor called PAR2.  When tryptase binds to this PAR2 receptor, it is thought that it makes nerves oversensitive. If the PAR2 receptor is blocked, pelvic pain is mitigated.  In animal models where they cannot make tryptase-like products, pelvic pain does not develop in CPPS.

Nerve growth factor (NGF) is a mast cell mediator that has been implicated in CPPS. It is elevated in seminal plasma of CPPS patients and directly correlates with pain level. It is thought that NGF makes the peripheral nerves oversensitive and causes more nerve cells than usual to be present. NGF and tryptase were elevated in prostate secretions of most CPPS patients in a small patient group. Of note, NGF release occurs and increases weeks after initial symptoms.

In animal models, injecting cetirizine (H1 antihistamine) into the peritoneal cavity decreased pain by about 13.8%; ranitidine (H2 antihistamine), 6.1%; cromolyn, 31.4%. A combination of all three decreased pain by 69.3%. When cromolyn and cetirizine were used together, larger pain relief was achieved than when used individually, but this was not seen when using ranitidine and cromolyn together.  These data suggest that H2 signaling is not a major contributor in chronic pelvic pain in male patients.

Pelvic floor dysfunction is also common in heritable connective tissue diseases and is often present in hypermobile patients.

References:

Done JD, et al. Role of mast cells in male chronic pelvic pain. Journal of Urology 2012: 187, 1473-1482.

Roman K, et al. Tryptase-PAR2 axis in experimental autoimmune prostatitis, a model for chronic pelvic pain syndrome. Pain 2014: 155 (7), 1328-1338.

Cohen D, et al. The role of pelvic floor muscles in male sexual dysfunction and pelvic pain. Sex Med Rev 2016; 4, 53-62.

Murphy SF, et al. IL17 mediates pelvic pain in experimental autoimmune prostatitis (EAP). PLoS ONE 2015, 10(5) : e0125623.

 

The Sex Series – Part Five: Seminal allergy, post-orgasmic illness syndrome and burning semen syndrome

Allergy to semen has only been well documented and studied in cisgender (non-transgender) women. Some papers go so far as to state that this problem is exclusive to (cisgender) women.  Despite this, there is evidence that (cisgender) males can have allergy to semen, including their own.  Furthermore, semen allergy is not restricted to vaginal intercourse and can be seen in anal and oral sex, as well as local reactions when semen contacts skin outside of the vaginal area.

Semen contains a number of inflammatory molecules, including TGFb1, MCP-1, IL-13 and IL-17.  MCP-1 has a well described role in mast cell activation in which it draws mast cells toward an inflammatory site and directly induces histamine release.  The physical effects of orgasm use opioids made in the body.  Some patients experience a days-long reaction to orgasm.

Termed “postorgasmic illness syndrome”, allergic symptoms affecting the genitals and general flu-like symptoms present 2-8 hours after ejaculation. These symptoms can persist for up to a week, with the day after ejaculation often being the worst.  Postorgasmic illness syndrome causes excessive sweating, rhinitis, anxiety, depression and difficulty concentrating.  This condition is recognized as a rare disorder by the NIH.  It has been hypothesized that these patients are in fact suffering from opioid withdrawal caused by the rapid depletion of opioids by orgasm.

Semen allergy has been associated with serum IgE to prostate-specific antigen (PSA), a molecule involved in the kallikrein-kinin system.  Autologous semen allergy, or allergy to one’s own semen, can be confirmed by reaction to semen in skin prick allergy testing or by specific IgE in the blood. One study found that 88% of patients who experienced burning and pain after ejaculation were positive for allergy to their own semen.

The phenomenon of burning after ejaculation is called “Burning semen syndrome”. In these patients, burning, pain and swelling of the UG tract occurs following ejaculation.  This study also evaluated partners of these patients receiving vaginal sex.  In many instances, both members of the couples evaluated were positive for allergy to semen. 89% of these couples had at least one member who exhibited allergic reaction to semen.

 

References:

Van Dijk F, et al. Non-oncological and non-infectious diseases of the penis (penile lesions). EAU-EBU Update series 4 2006; 13-19.

Ghosh D, Bernstein J. Systemic and localized seminal plasma hypersensitivity patients exhibit divergent immunologic characteristics. J Allergy Clin Immunol 2014: 134 (4): 969-972.

Jiang N, et al. Postorgasmic illness syndrome (POIS) in a Chinese man: No proof for IgE-mediated allergy to semen. J Sex Med 2015; 12: 840-845.

Bernstein JA, et al. Is burning semen syndrome a variant form of seminal plasma hypersensitivity? Obstetrics & Gynecology 2003; 101 (1): 93-102.

Chen WW, Baskin M. A 33-year-old woman with burning and blistering of perivaginal tissue following sexual intercourse. Annals of Allergy, Asthma & Immunology 2004; 93: 126-130.

The Sex Series – Part Four: Seminal allergy

Author’s note: This series is long and covers a number of topics other than vaginally penetrating sex, including male and female orgasms, reactions of the penis, testicles and prostate, anal sex, and pelvic floor dysfunction and pelvic pain.  The first several posts are about vaginally penetrating sex because this is what I get asked the most questions about.  It is not meant to be exclusive to anyone on the basis of gender or sexual orientation.

**
It is possible to be truly allergic to semen, although this is rare.  One of the hallmarks of this condition is that it is completely preventable with condom use.

Most patients react during or after their first experience with vaginal penetration by a penis resulting in ejaculation.  Each subsequent exposure generally causes a worsening reaction. However, it is possible to develop an allergy after a number of intercourse encounters. In studies, patients with seminal allergy are allergic to semen from multiple partners, although there are anecdotes about patients reacting to semen from a single partner and not only.

This type of allergy has been linked to IgE.  The testing for this sensitivity involves skin prick tests with seminal protein that produce wheal and flare response.  Semen specific IgE is often appreciable in the blood following exposure.  Some patients have type III and type IV hypersensitivity reactions to semen and symptoms can occur days after the exposure.

Like all other forms of allergy, the range of reactions is massive.  It can range from a low level itching to anaphylaxis requiring epinephrine.  Itching, burning, redness, swelling, pain, and blistering in the vagina have all been reported. Trouble breathing, cough, wheezing, GI symptoms, generalized hives, disseminated angioedema and full anaphylaxis can occur.  Anaphylaxis has been reported in 16 cases, with one case causing loss of consciousness.

Across studies, most patients have either a personal or family history of allergic conditions.  80% of patients in one study had a family history of atopic disease.  One study found that the onset of seminal allergy often coincides with genital system conditions or procedures like hysterectomy, IUD placement or removal, pregnancy and tubal ligation.  It is hypothesized that the disruption of the normal state of immune activity in the vagina by these activities can trigger seminal allergy, but this has not been proven.

References:

Schlosser BJ. Contact dermatitis of the vulva. Dermatol Clin 2010: 28; 697-706.

Moraes PSA, Taketomi EA. Allergic vulvovaginitis. Ann Allergy Asthma Immunol 2000; 85: 253-267.

Chen WW, Baskin M. A 33-year-old woman with burning and blistering of perivaginal tissue following sexual intercourse. Annals of Allergy, Asthma & Immunology 2004; 93: 126-130.

Harlow BL, He W, Nguyen RHN. Allergic reactions and risk of vulvodynia. Ann Epidemiol 2009; 19: 771-777.

Liccardi G, et al. Intimate behavior and allergy: a narrative review. Annals of Allergy, Asthma & Immunology 2007; 99: 394-400.

Sonnex C. Genital allergy. Sex Transm Infect 2004; 80: 4-7.

The Sex Series – Part Three: Allergic reactions of the vagina and vulva

Most of what I said about kissing applies to genitally penetrating intercourse, too.  It is not uncommon for people to develop hives as a result of the vibration, pressure, heat and friction of intercourse. Swelling after sex, called postcoital edema, is also not unusual.  Sex is also a known trigger for asthma and rhinitis.  Several aspects of sex, including the heat and emotion, can activate the autonomic nervous system and cause release of mast cell mediators.  Importantly, studies have revealed that the allergic effects of sex are not due to the physical exertion (ie. exercise anaphylaxis).

While local reactions are more common, there is precedent for sex causing multisystem allergic response or anaphylaxis.  The person receiving the vaginal penetration is more likely to have anaphylaxis following sex, especially if they are strongly sensitized to food or medications.  Seminal fluid can contain food or drug allergens.  Aspirin and penicillin derivatives have been reported to cause allergic reactions from sex, called postcoital hypersensitivity. Transfer of pollens from the clothes or skin of the partner can also cause allergic reactions.

One product we have not yet discussed that can cause contact dermatitis and anaphylaxis is condoms. 25% of reactions to latex condoms cause hives over large portions of the body, angioedema and respiratory symptoms. There are latex alternative condoms, but many patients react to those as well.

Vaginally penetrating intercourse often causes microscopic tearing, mostly due to inadequate lubrication.  As a former sex educator, if you think you are using enough lubrication, you are not.  It is my personal experience that water based lubricants are better tolerated by most allergy patients for vaginal intercourse.  Silicone lubricant is popular because it’s not absorbed by the body and is therefore slicker, whereas water based lubricant often requires reapplication.  But that’s okay.  That’s why you get a whole bottle.

Contributing to the insufficient lubrication is the fact that most people don’t engage in long enough foreplay.  Foreplay provides a number of benefits: it increases naturally secreted vaginal lubrication, increases blood flow to the vagina and tells the cervix to get out of the way. 20 minutes of foreplay is often recommended as a rule of thumb in order to get the vagina in order before penetrating intercourse.

Moisture, friction and heat can cause the vulvar skin to break down. Estrogen plays a large role in keeping this tissue strong and undamaged.  Urine on the skin can cause contact dermatitis.  Malnutrition and history of genital infections can also contribute towards the reactivity of the tissue. It is also possible to be IgE positive for Candida albicans, a yeast that lives normally in the vagina.  Inflammation can upset the balance of the normal flora, resulting not only in vaginal infections but a literal allergy to Candida.

References:

Schlosser BJ. Contact dermatitis of the vulva. Dermatol Clin 2010: 28; 697-706.

Moraes PSA, Taketomi EA. Allergic vulvovaginitis. Ann Allergy Asthma Immunol 2000; 85: 253-267.

Chen WW, Baskin M. A 33-year-old woman with burning and blistering of perivaginal tissue following sexual intercourse. Annals of Allergy, Asthma & Immunology 2004; 93: 126-130.

Harlow BL, He W, Nguyen RHN. Allergic reactions and risk of vulvodynia. Ann Epidemiol 2009; 19: 771-777.

Liccardi G, et al. Intimate behavior and allergy: a narrative review. Annals of Allergy, Asthma & Immunology 2007; 99: 394-400.

Sonnex C. Genital allergy. Sex Transm Infect 2004; 80: 4-7.

The Sex Series – Part Two: Contact dermatitis

Symptoms affecting the genitalia as a result of vaginally penetrating intercourse are not uncommon.  Today we are going to talk about allergic and irritant reactions to products. There are other kinds of symptoms to vaginally penetrating intercourse that we will get to later on in this series.

It is not unusual for people to use specific products only in advance of having sex.  This includes things like lubrication, pleasure creams, and products for shaving and removal of hair.  Contact dermatitis can arise as a result of these products.

Contact dermatitis is inflammation of the skin following contact with a substance that irritates or generates an allergic reaction.  In case it’s not obvious, genital tissue is much more sensitive than other parts of the body.  Irritant contact dermatitis of the vulva is more common than true allergic dermatitis there.

Common irritant triggers include hygiene products like soap, shower gel, and sanitary napkins, spermicides, diaphragms, and sexual lubricants.  In some people, these triggers can also generate a true allergic dermatitis.  Additional triggers commonly associated with allergic contact dermatitis regularly include neomycin, -caine anesthetics and nickel.

Contact dermatitis of the genital (and other) areas can cause a wide range of reactions from mildly irritating to very severe.  Symptoms can include redness, swelling, itching, burning and pain, and can cause chronic thickening of the skin, fissuring of the skin, weeping of the skin and blistering.  In most patients, the substance responsible for the reaction is identified via skin patch testing.  I would not expect this to be reliable in mast cell patients given the inherently reactive nature of our skin.

Irritant contact dermatitis often shows symptoms shortly after product use. True allergic contact dermatitis is a delayed type IV hypersensitivity reaction and can take 2-3 days to appear. Many patients are able to identify the trigger by removing products and symptom resolution upon doing so. Some genital hygiene products include alcohol.  Many more include propylene glycol, a well defined trigger for vulvar dermatitis.  Products that contain sugar and/or change the pH of the internal vaginal environment disturb the natural microbial flora, causing inflammation and increased risk of infection later.

It is also possible for products used by the partner to transfer during vaginal penetration.  If the penetration is made by part of the body and not a toy, transfer can happen in either direction. For persons using toys for external or internal stimulation, it is also possible to react to the material of the product. Something to consider is that many companies sell products to clean up after sex, either to clean genitalia, toys or both.  Please look carefully at the ingredients included in those products.  Additionally, please ensure that any toys used are cleaned before and after use.

 

References:

Schlosser BJ. Contact dermatitis of the vulva. Dermatol Clin 2010: 28; 697-706.

Moraes PSA, Taketomi EA. Allergic vulvovaginitis. Ann Allergy Asthma Immunol 2000; 85: 253-267.

Chen WW, Baskin M. A 33-year-old woman with burning and blistering of perivaginal tissue following sexual intercourse. Annals of Allergy, Asthma & Immunology 2004; 93: 126-130.

Harlow BL, He W, Nguyen RHN. Allergic reactions and risk of vulvodynia. Ann Epidemiol 2009; 19: 771-777.

Liccardi G, et al. Intimate behavior and allergy: a narrative review. Annals of Allergy, Asthma & Immunology 2007; 99: 394-400.

Sonnex C. Genital allergy. Sex Transm Infect 2004; 80: 4-7.

The Sex Series – Part One: Kissing and allergic reactions

The avenues by which a person can suffer symptoms as a result of sex are almost endless.  I am asked often about the mechanism by which mast cell patients can react to foreplay or intercourse. The reason it has taken so long to put this series together is not because of a dearth of information, but because there is so much.  The research on this topic is deep, if not always to the point: Why do some people react badly to having sex?

There are a number of reasons why sex can cause allergic symptoms, which explains why intimacy is often fraught with anxiety for mast cell patients.  So let’s start with the entry level: kissing.

It is widely accepted that kissing can transfer allergens via saliva, or contact between skin or oral mucosa.  Allergic reaction after kissing is not even especially unusual.  5-12% of IgE food allergic patients have had at least one reaction after kissing.  Peanuts, walnuts, and tree nuts are the most common offenders.  Rash around the mouth, hives around the mouth, flushing, angioedema of lips, mouth, tongue and throat, wheezing and hives all over the body have all been reported in this situation.  Usually symptoms present within minutes, but there are literature references to reactions developing up to three hours later.

In a group of 26 volunteers that ate peanut butter, the protein reached its highest concentration in saliva five minutes after consumption.  After an hour, the protein was undetectable.  Several methods for clearing the protein were tested.  Brushing teeth, rinsing mouth, or both, waiting an hour after consumption, and waiting an hour and then chewing gum, all reduced protein concentration by over 80%.  However, waiting one hour after eating was still the most effective way to clear the protein from the mouth.

Though much less common than transfer of food allergens, it is possible to transmit medications via saliva. In literature, all reports of this phenomenon involve ingestion of β-lactam antibiotics, including penicillin derivatives.  In these cases, the patients had symptoms of oral allergy syndrome with hives over large parts of the body.

The quality of the kissing is certainly a factor.  How deep is it?  How much hard? How much friction?  How wet?  Mast cell patients often react to physical stimuli like this.  It’s not hard to imagine a situation where the pressure and heat of kissing cause local mast cell degranulation.   I found a (non-scientific) article describing a woman with aquagenic urticaria who reacts to kissing because it’s wet.  For patients allergic to sweat, that could also cause a kissing reaction.

I feel like I should throw out there that you can react to allergens returned to the mouth by vomit.  Mostly because there isn’t really anywhere else to put it.  So it’s here.  The warning about vomit is in the kissing post.  How did this get to be my life?

BUT GUESS WHAT GUYS?!?!?!? Kissing can also be good for allergy patients.  One study reported that that kissing decreased wheal response (the formation of red swollen areas) was decreased 28-34% in patient allergic to dust mite and Japanese cedar pollen.  This patient group had allergic rhinitis and atopic dermatitis.  It didn’t decrease the response to injection of histamine, which means the benefit from kissing in this study is not directly blocking histamine.  Plasma levels of neurotrophins were decreased in these patients.  Neurotrophins have a complex relationship to mast cells, so it’s possible that neurotrophins block something that tells mast cells to release histamine.

I know everyone wants to know – how can I kiss safely? So hang in there, because it’s coming.  Along with the answers to all of the “embarrassing” sex questions I have ever been asked.

References:

Liccardi G, et al. Intimate behavior and allergy: a narrative review. Annals of Allergy, Asthma & Immunology 2007; 99: 394-400.

Maloney JM, et al. Peanut allergen exposure through saliva: assessment and interventions to reduce exposure. J Allergy Clin Immunol 2006; 118: 719-724.

Liccardi G, et al. Drug allergy transmitted by passionate kissing. Lancet 2002; 359: 1700.

Sonnex C. Genital allergy. Sex Transm Infect 2004; 80: 4-7.