As most of you know there are 2 kinds of herpes infections:

Herpes 1 (HSV-1), which when activated causes sores on the lips, gums and even the eyes. (It used to be called the herpes above the waist.)
Herpes 2 (HSV-2) or genital herpes, which can appear on the labia, vagina cervix (obviously in men in different genital areas…) and all sorts of places on the lower body (inner thighs, buttocks, back)….this is the one we are most concerned about.
A recent postgraduate Obstetrics and Gynecology publication gives an excellent synopsis on herpes and I thought it would be appropriate to go over some of the facts that were presented in this review.

HSV is a DNA virus and is classified as either 1 or 2 by its glycoproteins (i.e. not by where it infects but what is in its molecular structure). It’s transmitted though direct contact with mucosa or abraded skin. That’s the official wording…. when it comes to HSV-1 in “lay” expression you get it from kissing, or oral contact including oral sex. When it comes to HSV-2, transmission is through genital contact…. pretty easy to imagine how it can occur with intercourse, but those lesions women often get on their buttocks, back or thigh can occur via post coital contact (spooning, or getting close to a member that is shedding the virus…. member here usually refers to a penis).

Once transmitted, the virus incubates for 2 to 12 days and then replicates in the layers of the skin causing inflammation and ulceration. But that’s not all…. the virus then enters the sensory neurons and then travels to their root (or ganglia) where it then becomes dormant.  Weeks, months or years later it can become reactivated, spread back down along the nerve root to the skin and cause a recurrent ulcer-like lesion or simply shed from the skin without a visible sore or irritation. Antibodies to the virus develop within several weeks of the infection. The initial infections tend to be more severe than recurrent ones; there may be swelling of adjacent lymph nodes and the lesions may last 3 to 6 weeks. Recurrent infections are usually mild and last 3 to 10 days.  The frequency of recurrences can vary…. they are more likely to occur when your resistance is diminished, i.e. you are sick, have a fever, or are physically or emotionally stressed. After the first infection, about 50% of individuals will have a recurrence in 6 months.

The estimate of how many of us have had HSV-1 or HSV-2 is based on antibody testing which if positive is termed seroprevalence. The seroprevalence of HSV-2 in the US is 16.2% but women are at higher risk with a rate of 20.9%. The amazing fact is that only 19% of adults who are HSV-2 positive (and hence can spread the virus) are aware or their diagnosis! (I have frequently seen patients who come to my office with a complaint of “something down there” but deny any previous history of herpes…they may have had similar symptoms in the past but thought they were due to yeast infections or friction and never had these checked or diagnosed. Now… I am telling them that they have herpes. (And of course, the recriminations begin.) In most cases, especially if they are abstinent or have been with the same partner for years, it’s a recurrent infection. Remember that the virus can also be transmitted from the skin without a viable lesion. This is an STD that is chiefly spread without knowledge that it was there in the first place.

So what is the best way to diagnose HSV? When a “classic” group of vesicles (blisters) or ulcers occur, a culture of the lesions can be done. Especially in primary (first) infections, the culture will be positive in 48 to 72 hours. The sensitivity of the culture decreases the longer the lesion has been present. A positive culture is evidence of herpes, but a negative one doesn’t mean it’s not there, it simply means it was too late to find it or that the culture wasn’t sensitive enough. So ultimately the way to definitively diagnosis herpes and to distinguish between types 1 and 2 is with antibody testing…in a blood test called HerpesSelect 1 and 2. It can usually detect antibodies within 2 to 3 weeks of infection.

The treatment is usually oral with an antiviral medication. The generic and oldest form of medication is acyclovir. The dose for a primary infection is 400mg tablets three times a day for 7 to 10 days. There are 2 other antiviral medications that have somewhat better absorption and longer half-lives than acyclovir but essentially are converted to the same substance in the body. These are valcyclovir (Valtrex) and famcyclovir (Famvir). These are generally more expensive. The dose for Valtrex in a primary infection is 1 g twice daily, again for 7 to 10 days.  For Famvir it’s also 1g twice daily… recurrent infections, less is needed (and works best if started with the very first sign of infection, such as local tingling or pain). Acyclovir is given in a dose of 400mg, 3 times a day for 5 days, Valtrex, 500mg, twice a day for 3 days and Famvir two tabs of 500mg twice a day for just one day. And for suppression (it’s not complete but may decrease viral shedding and transmission to a partner) the prescribed dose is 500 mg of Valtrex daily or 250 mg of Famvir twice daily.  (I know this is getting very specific, but so many women ask for prescriptions, I thought I should include dosing.)

What should be done if herpes occurs during pregnancy?  How great is the risk for neonatal infection? About 1200 to 1500 babies are born in the US each year with neonatal herpes. The most likely cause for their infection is through contact with the active virus in the lower maternal genital tract during vaginal delivery. The majority of the infected babies are born to women who had no history of HSV infection (i.e. they acquired a new infection before delivery) and one third of the cases are caused by HSV-1. Only 3% of the infections are among women with recurrent clinically evident HSV-2 infection. A primary genital herpes outbreak is associated with a higher risk of perinatal transmission than a recurrent outbreak, presumably because the mother has no preformed antibodies that are transferred to the fetus. Neonatal herpes can be serious; 30% of seriously infected babies die and up to 40% of survivors have serious neurological problems. In the past, many women underwent C-section just because they had a history of herpes even though they didn’t have any active lesions at the time of delivery. (This falls into to the “you never know, let’s be safe” category.) But it’s the women who are seronegative (have no antibodies) and who get infected in the last trimester that are the most likely to pass the virus to the baby during delivery. Nor is it completely “safe” for women with active vaginal lesions to deliver vaginally. The current recommendations are:

During pregnancy all symptomatic infections (primary or recurrent) should be treated with a 7-day course of antiviral medication.
All women who have had recurrent herpes or a new infection in pregnancy should be given prophylactic antiviral medication beginning at 36 weeks (And if at risk for a preterm delivery, this should be started earlier.)
C-section is indicated in any women with active perineal (in and around the vagina and labia) lesions or prodromal symptoms (sense that a herpes lesion is starting).
C-section is not indicated in women with a history of HSV without active lesions or symptoms at the time of labor,
C-section is not indicated for nongenital lesions (if there is a lesion on the thigh or buttock in can just be covered with a bandage.)
Bottom line: Many of us have herpes. No, we don’t have a vaccine but short courses of antiviral therapy or daily medication will help diminish recurrence of lesions and spread of the virus.  Recurrences should be treated during pregnancy and at 36 weeks prophylactic antiviral medication may help prevent the need for C-section. If, however, an active lesion is present at time of labor, C-section is advised.

Every year the American College of Obstetricians and Gynecologists (of which I am a “fellow” or FACOG…not very gender appropriate) comes out with new and official committee opinions which I duly read, file and sometimes (if not relevant to my practice) forget. In this March issue of ACOG’s Journal, a new committee opinion on colonoscopy and colorectal cancer screening was published and I felt I should share it with you.

Just to remind you: colorectal cancer is the third leading cause of cancer deaths in women. (The leading cause is lung cancer …remember when we were told we’ve come a long way “baby”… the second cause for cancer death is breast cancer.) Over 70,000 women develop colorectal cancer in the USA every year and more than 24,000 die from this disease. This cancer develops from certain types of initially benign polyps (unlike other cancers) and thus there is a window of opportunity to find and remove them before they become malignant. And obviously if a cancer is found at an early stage with appropriate screening, the surgery is lessened and survival increased.

The risk for colon cancer is increased in women who have strong family histories of colorectal cancer as well as women who have had certain chronic bowel diseases. Waiting for a sign “that something is wrong down there” just doesn’t work…. over 90% of women diagnosed with colorectal cancer had no warning clinical symptoms! Despite these stats, in a recent study it was found that only 63% of women over 50 had been screened by colonoscopy, sigmoidoscopy in the past 10 years or had fecal blood test within the past year. If 90% of the population were screened as recommended, it’s estimated that 310,000 lifetime quality life years would be saved.

So here are the screening guidelines put out by The American College of Obstetricians and Gynecologists:

1. Colonoscopy:  This is the preferred test. It provides a full examination of both the colon and the rectum in one session and allows the physician to perform a biopsy or polypectomy if indicated. Colonoscopy is recommended every 10 years beginning at age 50. (Obviously if polyps or pre-cancer is found than this needs to be repeated more often….also if a first degree relative had colorectal cancer at a relatively young age, screening should begin before 50 and be done more frequently.) In one study, it was shown that the incidence of colorectal cancer was reduced by 76-90% among those having colonoscopy and appropriate polypectomy compared with individuals in the general population. But like every diagnostic test, it’s not perfect. The miss rate for adenomas (polyp growths) measuring 1 cm or more is 5-12% and for cancer is 5%. Colonoscopy also requires (as most of you know) clear fluids the day prior to the procedure and a thorough bowel preparation (major laxatives that cause diarrhea in order to clean out the colon). And there can be complications: around 2.8 (including perforations and hemorrhage) per 1,000 procedures. Most occur during biopsy; it is also felt that the experience of the colonoscopist is a factor. The test is usually done with “conscious sedation” or rapid anesthesia in a specialty center and hence you’ll need someone to drive you home. This procedure can also be quite expensive, especially for individuals who have no or inadequate insurance coverage. (I always tell my patients to check to see if the physician who will perform the procedure and surgical center where it is done are covered by their insurance.)

2. Flexible Sigmoidoscopy: This requires insertion of a thin, flexible tube into the rectum. It only visualizes a portion of the colon. It should be done every 5 years. It clearly is not as “all colon encompassing” as colonoscopy but can be done in an office without significant sedation.  Sigmoidoscopy will miss any polyps or cancers in portions of the colon that are not visualized (the proximal colon, i.e. high up) and those are the kind that are most likely to occur in women and African Americans. If a polyp in the distal (or lower) colon is found, there is a two fold or higher risk that a tumor is in the proximal colon (not seen) and a subsequent, full colonoscopy is then advisable. Sigmiodoscopy requires a bowel preparation but enemas may suffice. Studies have shown that sigmoidoscopy reduces 60-80% of colorectal mortality but only if the tumors are in the part of the colon that is viewed.

3. Double Contrast Barium Enema: Actually this test is not recommended due to low pickup, but the ACOG committee states that this procedure (which requires a bowel prep) is an option in cases in which colonoscopy is not available or contradicted.

4. Stool tests for occult (hidden) blood: There are 2 kinds….the first is a high sensitivity guiac fecal occult blood test. It has to be collected at home after abstaining from certain foods and medications. In order to have any reliability, three separate stool samples (smeared on a special card) are necessary. Testing of just one sample after a rectal exam is essentially useless. The second type of test is done with a special kit that allows for fecal immunochemical testing (which also detects blood). In this case, perhaps only two home samples are needed (and no special diet). Both tests are positive only if large polyps or a cancer disrupt the mucosa of the bowel (i.e. push though it and cause very slight  bleeding)…otherwise they will not pick up small or early tumors. If the tests are negative the recommendation is to repeat then yearly. If positive, a colonoscopy should be done.

The College then has a section on developing technologies. This is where the committee addresses virtual colonoscopy. This noninvasive procedure requires the same bowel preparation as regular colonoscopy. Gas is injected through the rectum and a CT (computed tomography) is performed. It is quick and requires no anesthesia. In trials to date, virtual colonoscopy has shown 39% sensitivity and 90.5% specificity in detecting lesions that are at least 6 mm. It also can detect incidental pathology outside the colon. The authors state that the “lifetime cumulative radiation risk must be evaluated”. If a polyp or tumor is found, then a true colonoscopy must be done so a biopsy can be performed. That means another prep unless a same day colonoscopy can be scheduled. The committee members also state that the U.S. Preventive Task Force does not currently recommend the test. (Having given you this information I have to divulge that those of my patients who had this test and had negative findings were delighted that they could “get by” with it.) If the test is negative, it should be repeated every 5 years.

Finally, Fecal DNA Testing is mentioned in the committee report. This is a stool test for genetic mutations associated with colorectal cancer. They state that the test is evolving and has the potential to be highly specific (better than tests for occult blood) but so far the U.S. Preventive Services Task Force too does not recommend it.

Bottom Line:  Currently, the best way to screen for colorectal cancer is with colonoscopy. Start at age 50….that first test will determine whether you are a polyp “former”. If you are not a former polyp former (I had to play on these words!) and you are considered low risk, repeat it every 10 years. (So I have 2 years to go…) This is a small price to pay in order not to be a victim of this third leading cause of cancer deaths in women.

Ever since cell phones became our most common distant audible communication device, there has been concern as to whether the radio frequency that is emitted will cause harm. (Note: I am using the term audible, not visual or visual plus audible… so I am ruling out anything with text or that requires looking at a screen as we communicate.) Does holding that cell phone to your ear (rather than using a Bluetooth or the speaker) increase the risk of brain cancer, or change brain function?

As you can imagine, there are quite a few studies that have addressed this concern and so far any clinical association between cell phone use and prevalence of brain tumors has been inconsistent, i.e. there is no definitive answer. But there is no question that cell phones emit radio frequency energy (actually it’s called radio frequency-modulated electromagnetic fields or RF-EMF’s) that is absorbed by nearby brain cells. I don’t know about you, but I carry my cell phone everywhere and if it rings, or if I simply have to make a call and am not sitting by a hard line, I don’t hesitate to put it to my ear. One of my daughters doesn’t use her hard line; the other doesn’t even have one but relies entirely on her cell phone!  So it was with great interest that I read the latest JAMA article titled “Effects of Cell Phone Radio frequency Signal Exposure on Brain Glucose Metabolism”. ( I have to admit that the title sounds like something out of a physics journal, and indeed some of the authors came from the medical department of the Brookhaven National Laboratory.)

The investigators placed cell phones on the left and right ears of 47 healthy participants. They then injected them with a minimally radioactive glucose substance and measured its activity with a PET scan of the brain twice, once with the right phone activated (“on” but sound muted) for 50 minutes and once with both phones deactivated ( “off”… this was the control). They found that the radio frequency of the “on” phone increased the rate of glucose metabolism in areas of the brain that were closest to the phone’s antenna. (If you want to know the exact locations, they were the orbitofrontal cortex and temporal pole). Whole brain metabolism did not differ between the “on” and “off” conditions.

So what does this mean? Well, there was a subsequent editorial in the same issue of JAMA (for those of us who need expanded explanations). The editors noted that in the experiment the cell phones were receiving a text (from a recorded text) for 50 minutes. Apparently, cell phones in receiving mode emit less energy, than when a user is speaking into a phone. Therefore, whatever effect was observed on those areas of the brain may have been less than that which occurs in normal-use situations. They then go on to say that “the biologic significance, if any, of increased glucose metabolism from acute cell phone exposure is unknown, (but) the results warrant further investigation”.

Bottom line: The area in your brain close to a hand-held phone can (at least with regard to glucose metabolism) be effected, perhaps more so when you make long phone calls. The clinical significance is still not known, but perhaps we should make a habit of keeping that phone away from our ears (and brain), especially if we initiate long or multiple calls.

Our risk of breast cancer is high…one in eight over our lifetime. (I now consider a lifetime to be 90, my Dad’s birthday was this week; he turned 91… happy birthday, Dad!). The good news is that improved treatments and early detection have significantly improved survival and long-life expectancy in women with a personal history of breast cancer. There are many risk factors for breast cancer, some of which we have little or no control over such as family history of premenopausal breast cancer, genetic mutations in the BRCA genes, not having children at a young age, early onset of menarche (periods), late menopause or radiation for cancer before the age of 30. Whereas there are other risk factors for which we may have control. These include smoking, “excessive” alcohol consumption, obesity, sedentary lifestyle and long-term use of hormones. And if we have a personal history of early breast cancer, our risk of another cancer in the same breast or the other breast is elevated. The overall estimated risk of a second breast cancer after early stage breast cancer is 5.4 to 6.6 per 1000 women years. (Remember, 1000 women years equals one year for 1000 women, or 10 years for 100 women.) 


It makes sense that women who have had breast cancer would benefit from early detection if a second breast cancer should occur. Are follow-up mammograms enough?


Good question; an article in this week’s edition of The Journal of the American Medical Association titled “Accuracy and Outcomes of Screening in Women with a Personal History of Early-Stage Breast Cancer” tried to address this very prescient query. The authors (of which there were many) identified screening mammograms from 1996 to 2007 in women with an initial early-stage breast cancer including diagnoses of ductal carcinoma in situ (DCIS), stage I or stage II invasive cancer. The women received mammograms at facilities in 5 mammography registries of the National Cancer Institute affiliated with the Breast Cancer Surveillance Consortium (This should mean that the quality of the mammograms was good). They excluded women who had bilateral mastectomy for their first cancer (Presumably, they had no residual breast tissue and were not candidates for mammogram screening). A mammogram performed at least 6 months after the first breast cancer diagnosis was defined as “screening” if it was part of a routine follow-up (i.e. not done solely in the breast that had a lumpectomy or in a woman who reported a new breast lump or discharge from the nipple).  


There were 58,870 screening mammograms in women who had a personal history of breast cancer (PHBC) and the same number matched screening mammograms in women who had no personal history of breast cancer. Moreover, they matched the two groups of women with regards to breast density, age group, mammography year and registry. As expected, the women with previous breast cancer had an increased family history of breast cancer (23.2% vs. 17.6%), history of breast plastic surgery (6.9% vs. 0.8%) and actual mammogram follow-up from 9 to 14 months since their previous screening (82.7% vs. 43.1%… both numbers seem pretty low!). There were more cancers in the PHBC women (499 invasive and 156 ductal carcinoma in situ) than women without PHBC (285 invasive, 57 DCIS) within 1 year of screening mammography. Mammography screening in PHBC women did detect cancers at an early stage but had a lower accuracy. There was a higher interval cancer rate (the difference between screening mammogram date and the date of a breast cancer diagnosis) in the PHBC women than in women who had no previous breast cancer history. 


So does all this mean that screening mammogram is insufficient screening for women who have had breast cancer? And if not, what should the follow-up be? 


As many of you know, I often recommend MRI for my patients who have had a personal history of breast cancer. But I also try to point out that MRI scans can result in false positive findings with subsequent negative biopsies, worry and expense. Moreover, MRI does not improve the diagnosis of DCIS. Micro-calcifications that are the hallmark of DCIS are more likely to be found in mammograms and even if MRI is done mammogram screening should continued to be used. The authors address this stating that, “although there is interest in adjunct (additional) screening for PHBC women; there is no evidence that this improves clinical end points and no consensus regarding which of these women (other than those with proven cancer gene mutations) should have adjunct imaging.” They also felt that although there was a relatively higher rate of interval cancers (those not detected by mammogram) most of the cancers were eventually found at an early stage. They then concluded that: “The data neither support nor negate a role of adjuvant screening in PHBC women.”


Just so you understand how complicated this issue is, neither this study nor others have definitively come out and said NOT to do additional screening. The summary in the article adds that PHBC women may have different factors predisposing them not only to a risk of a second breast cancer, but also to breast cancers that are less likely to be detected with screening and “a more tailored screening strategy than is currently recommended might be warranted.” 


Bottom line: If you have had previous breast cancer, make sure you get a yearly mammogram. But also talk to your doctor about ordering additional tests such as MRI especially if you had breast cancer before the age of 50, your breasts are dense (and hard to “see through” on mammogram) or you have received chemotherapy for your first breast cancer (These were the women in the study whose mammograms had the lowest sensitivity). If your insurance won’t cover an MRI for these indications, you might ask about lower “cash-only” fees.