Saturday, March 29, 2014

Yoga may lower homocysteine (one study found) and perchance, pain?

 Here is a reference to a small study demonstrating that yoga helps menstrual pain by lowering homocysteine levels.  My own personal experience is that yoga has helped me in dealing with my endometriosis/chronic pelvic pain; and both my doctor and pelvic physical therapist recommend that I continue with it. It doesn't always take the pain away, but I think overall it lessens it, lessens the reaction my body has to pain, and helps me feel better mentally and emotionally too.
"More recent research has reported on the potential scientific relationship between yoga and easing of menstrual symptoms. During menstruation, women who have painful periods have been observed to have higher serum levels of nitric oxide (NO), homocysteine, and other factors related to possible endothelial dysfunction. Research by Chien and colleagues assessed such blood serum levels for such markers in 30 women with dysmenorrhea and in 30 controls. Participants were instructed in yoga therapy 2x/week for 8 weeks, and each session was 30 minutes in length. The study concludes that yoga intervention can reduce severity of dysmenorrhea and may be effective in reducing serum homocysteine levels."  

"In the study by Rakhshaee, 92 female students (ages 18-22) were randomly assigned to a treatment group (n=50) and to a control group (n=42). Over a period of 3 menstrual cycles, participants recorded pain using a Visual Analog Scale and reported pain duration in terms of hours. During the first menstrual cycle, symptoms were recorded, and then during the second and third cycles, the treatment group was asked to complete 3 yoga poses during the luteal phase. The control group received no intervention. Yoga poses instructed include the Cat, Fish, and Cobra.

"In the experimental group, both the pain intensity and the pain duration showed significant differences with the participants who completed yoga poses having less pain intensity and pain duration. The authors conclude that yoga is  a safe and simple treatment for primary dysmenorrhea. Oftentimes, patients who complain of dysmenorrhea lack access to care for this other than medications that might include pain medication or birth control pills. Instructing a patient in basic yoga postures presented in this research may be a simple alternative to such medications. There are several websites that offer free access not only to images of poses, but also to free classes. I often hear from patients that they enjoy taking advantage of free fitness classes including yoga on various television stations. This may be another "tool in the toolbox" that we can offer to patients who have pain related to the menstrual cycle."

From Yoga Journal, poses for endometriosis:  (they do mention retrograde menstruation once but in this article they say "One study, however, found that retrograde menstruation naturally occurs in 90 percent of women, most of whom never develop endometriosis. So we do not know for sure if inversions increase retrograde flow or whether the backward flow increases the risk of endometriosis.")

Yoga for Endometriosis and Pelvic Pain:

YinYoga Video for endo:

Older blog post about stretches/yoga to help with pelvic pain:

Yoga for Pelvic Pain DVD:

Peripheral vs Central Sensitization in Pelvic PT

In pelvic pain rehabilitation, they often use what's called myofascial trigger point release. Before we've discussed peripheral and central sensitization. Here we see it being discussed as to the difference in treating chronic pelvic pain: "If a trigger point, by definition, is a hyperirritable spot in a taut band of skeletal muscle that may or not have referred pain, what then, is driving the soft tissue dysfunction? Some authors argue that the peripheral nervous system is at fault, while others point to the central nervous system as the driver. Peripherally, nociceptive input may sensitize dorsal horn neurons. Centrally, patients who have chronic pain will have larger areas of pain, described as being a result of higher central neural plasticity. This is a controversial topic, and the authors are quick to point out that experimental evidence is "sparse." While there is support in the literature for peripheral trigger points creating central sensitization, the article states that "…preliminary evidence suggests that central sensitization can also promote TrP activity." ...the summary points are that trigger points may be both a central and peripheral phenomena, and that chronicity of the condition may drive the focus of rehabilitation efforts. Specifically, the authors state that when a patient presents with peripheral sensitization, treatment should be directed towards inactivation of the trigger point, mobilizing joints and nerves, and functional activity. Patients who present with persistent pain may require more attention directed to the central system utilizing a multidisciplinary approach such as medications, medical and physical therapy management, and psychological therapy. Fear, anxiety, and the neuroscience approach to pain should be addressed."

Tuesday, March 11, 2014

Progesterone resistance

Progesterone resistance in endometriosis: link to failure to metabolize estradiol.

AuthorsBulun SE, et al. Show allJournal

Mol Cell Endocrinol. 2006 Mar 27;248(1-2):94-103. Epub 2006 Jan 10.



Endometriosis is the most common cause of pelvic pain and affects an estimated 5 million women in the US. The biologically active estrogen estradiol (E2) is the best-defined mitogen for the growth and inflammation processes in the ectopic endometriotic tissue that commonly resides on the pelvic organs. Progesterone and progestins may relieve pain by limiting growth and inflammation in endometriosis but a portion of patients with endometriosis and pelvic pain do not respond to treatment with progestins. Moreover, progesterone-induced molecular changes in the eutopic (intrauterine) endometrial tissue of women with endometriosis are either blunted or undetectable. These in vivo observations are indicative of resistance to progesterone action in endometriosis. The molecular basis of progesterone resistance in endometriosis may be related to an overall reduction in the levels of progesterone receptors (PRs) and the lack of the PR isoform named progesterone receptor B (PR-B). In normal endometrium, progesterone acts on stromal cells to induce secretion of paracrine factor(s). These unknown factor(s) act on neighboring epithelial cells to induce the expression of the enzyme 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD-2), which metabolizes the biologically active estrogen E2 to estrone (E1). In endometriotic tissue, progesterone does not induce epithelial 17beta-HSD-2 expression due to a defect in stromal cells. The inability of endometriotic stromal cells to produce progesterone-induced paracrine factors that stimulate 17beta-HSD-2 may be due to the lack of PR-B and very low levels of progesterone receptor A (PR-A) observed in vivo in endometriotic tissue. The end result is deficient metabolism of E2 in endometriosis giving rise to high local concentrations of this local mitogen. The cellular and molecular mechanisms underlying progesterone resistance and failure to metabolize E2 in endometriosis are reviewed.

Sunday, March 9, 2014

EndoMarch is almost here!

The time for the EndoMarch is drawing close and yellow is the theme color! I'm looking forward to meeting my endosisters, to all the activities for the event, and most of all to help promoting awareness. Awareness, not just that endometriosis exists, but awareness for the toll it can take on the lives it affects and why research and education is so important.
Please join us in any way you can-
by being there physically, virtually, or in spirit.

Webcast for the day:

Worldwide EndoMarch

Preliminary Program – Washington, DC

Thursday, March 13, 2014

REGISTRATION CHECK-IN: National Mall (Outdoors)
11:00 AM 12:00 PM Registration Check-in outside on the National Mall,
located near 7th Street & Jefferson Street

CALL TO ACTION CEREMONY: National Mall (Outdoors)
12:00 PM 2:00 PM Opening Ceremony & Various Guest Speakers
National Mall | 7th Street & Jefferson Street, Washington, D.C.

THE MARCH BEGINS: National Mall (Outdoors)
2:00 PM The march begins- Beginning Point: National Mall at 7th Street & Jefferson Street

Want to learn more about endometriosis? Then please also join us for the educational symposium that takes place in the Andrew W. Mellon Auditorium, from 9:30 am – 11:30 am.

Cost $$ of Endo

"...Estimates of endometriosis costs for the USA in 2002. Total costs are substantial and ranged $2–110 billion depending on prevalence rates. Direct healthcare costs make up 78% of total costs arising from endometriosis. Annual indirect costs of time lost from work due to endometriosis amounted to $0.5–24 billion....Endometriosis imposes a substantial economic burden on society. The high burden originates from the time delay between onset of symptoms and diagnosis, costly medical and surgical treatments, the chronic nature of endometriosis and the indirect costs associated with reduced quality of life and ability to work. Increasing awareness of the disease, cutting the time to diagnosis and providing centralized evidence-based specialized care are crucial steps in reducing the morbidity, health care expenditure and lost productivity associated with endometriosis. The substantial economic burden underlines the need for further research into cost-effective approaches to diagnosing and treating endometriosis...."
"The ability to diagnose endometriosis by means of laparoscopy depends on the surgeon's skills and experience. As a result, 3–12 years may pass between symptom onset and definitive diagnosis (Arruda et al., 2003; Husby et al., 2003). During this time period, unnecessary investigations and treatments are likely to be initiated, thus representing a cost of obtaining a diagnosis for women presenting with symptoms that may have several different causes. Better diagnostic methods would alleviate some of the distress felt between symptom onset and diagnosis and treatment, although the net effect on costs is unclear....In addition to difficulties involved in diagnosing endometriosis, costs appear to be influenced by the patient profile, specific diagnosis of endometriosis and principal procedure performed. An analysis of inpatient endometriosis treatment showed that costs were higher in older women and in African-American women as compared with Caucasian women. The specific diagnosis appears to play a role: endometriosis of the intestine and of the skin was associated with higher and lower inpatient costs, respectively, than endometriosis at other sites (Zhao et al., 1998a). Of the surgical interventions of endometriosis, total abdominal hysterectomy generated higher inpatient costs than other procedures (Zhao et al., 1998a; Gao et al., 2006).... Employed women incur indirect costs of time lost from work due to endometriosis....Little is known about the productivity loss associated with endometriosis, although available estimates from cost-of-illness analyses suggest that endometriosis may impose considerable indirect costs. Estimates of the number of hours missed from work due to endometriosis ranged 19.2–86.4 h per patient per year (Kunz et al., 1995; Mathias et al., 1996)....First of all, there is currently no reliable non-surgical diagnostic test for endometriosis. Thus diagnosis requires laparoscopy, preferably with histological confirmation. If endometriosis is present at laparoscopy, it is recommended that it is surgically removed at the same time as diagnosis, as an effective treatment for endometriosis-associated subfertility and pain (Kennedy et al., 2005). Secondly, the lower costs of medical treatment need to be balanced by additional costs due to higher recurrence rates of endometriosis with medical when compared with surgical treatment (Wellbery, 1999; D'Hooghe et al., 2003b; Winkel, 2003)...."

Saturday, March 8, 2014

How far we have to go for care

OHIP turns blind eye to suffering | The London Free Press  The long waiting times and denial of coverage to a patient with endometriosis in Ontario- and her trip to the USA to finally get the help she needed.

Wednesday, March 5, 2014

Women With Endo Have Higher Rates of Some Diseases

Women with Endometriosis Have Higher Rates of Some Diseases
 "Women who have endometriosis are more likely than other women to have disorders in which the immune system attacks the body's own tissues, according to researchers at the National Institute of Child Health and Human Development (NICHD), the George Washington University, and the Endometriosis Association.  The researchers also found that women with endometriosis are more likely to have chronic fatigue syndrome and to suffer from fibromyalgia syndrome — a disease involving pain in the muscles, tendons, and ligaments. Women with endometriosis are more likely to have asthma, allergies, and the skin condition eczema. The researchers surveyed 3,680 women who said they had been surgically diagnosed with endometriosis. “This study indicates that women with endometriosis may be more likely to have a variety of diseases involving the immune system,” said Duane Alexander, M.D., Director of the NICHD. “Further study of the immune system in endometriosis may yield important clues to identifying the causes and treatment of the disease.”  In women who have endometriosis, tissue like the lining of the uterus — the endometrium — grows in other parts of the abdominal cavity. The endometrial tissue may attach itself to the ovaries, the outside of the uterus, the intestines, or other abdominal organs. Endometriosis affects an estimated eight to ten percent of reproductive age women. It may cause infertility or pelvic pain, although researchers believe that some women with the disease may not experience symptoms. In addition, the researchers found that family members of women with endometriosis more commonly had the disease, as reported by others.  The researchers published their findings in the October 2002 issue of Human Reproduction. Roughly 99 percent of the women in the study said they had experienced pelvic pain for about 10 years before they were diagnosed with endometriosis. The women in the study reported that their pain began shortly after their first periods. The researchers do not know whether endometriosis actually occurs at the first period or if it develops over time. It is also unclear whether treating pain early could prevent chronic pelvic pain from developing in these women. For this reason, the study authors suggested that physicians treating patients with pelvic pain — particularly adolescents — consider whether endometriosis might be causing the problem.   Ninet Sinaii, MPH, of NICHD’s Pediatric and Reproductive Endocrinology Branch, and her colleagues analyzed information from a 1998 survey of members of the Endometriosis Association. The researchers focused on the 3,680 women who said they had been surgically diagnosed with the disease. The study authors compared the likelihood of women with endometriosis having a variety of disorders to the likelihood of women in the general population having these same conditions. These included:
  • Autoimmune diseases — disorders in which the immune system attacks the body's own tissues.
  • Chronic fatigue syndrome — a strong feeling of fatigue that lasts for at least six months without letting up.
  • Fibromyalgia — a recurrent pain in the muscles, tendons, and ligaments.
  • Endocrine diseases — disorders of the glandular tissue
  • Atopic diseases — such as allergies or asthma 

 The researchers found that women with endometriosis were at greater risk than were other women for such autoimmune diseases as systemic lupus erythematosus, Sjögren’s Syndrome, rheumatoid arthritis, and multiple sclerosis.  The women in the study were over a hundred times more likely to experience chronic fatigue syndrome than the general population of U.S. women. The women with endometriosis were more than twice as likely as other women to experience fibromyalgia. In addition, 20 percent had more than one other disease, and up to 31 percent of those with more than one disease had also been diagnosed with either fibromyalgia or chronic fatigue syndrome. Hypothyroidism — an underactive thyroid gland — was seven times more common in the endometriosis patients. In many cases, hypothyroidism may also be an autoimmune disorder, resulting from an immune system attack on the thyroid gland. The researchers also found that the rates of allergies and asthma were higher among women with endometriosis than among women in the U.S. population, and higher still if they had other diseases. The researchers found that 61 percent of the women with endometriosis reported allergies (as compared to 18 percent of the general female population) and 12 percent had asthma (as compared to 5 percent). If a woman had endometriosis and an endocrine disease, the percent with allergies rose to 72 percent, and if a woman had endometriosis plus fibromyalgia or chronic fatigue syndrome, the rate for allergies rose to 88 percent. Two-thirds of the women reported that relatives also had diagnosed or suspected endometriosis, suggesting a familial basis for the condition.  
The study authors cautioned, however, that the study may not be representative of all patients with endometriosis. First, the women may have joined the Endometriosis Association because they were experiencing pain from their condition and so may not be typical of all patients with endometriosis. Also, such self-reported surveys may be more open to error than are surveys taken by a trained interviewer. For example, some of the women who answered the survey may have misinterpreted questions, may not have recognized the names of specific diseases, or may not have accurately reported conditions experienced by their family members. The women who responded to the Endometriosis Association survey were predominantly white (nearly 95 percent) and educated (90 percent had at least some college education), and ninety-one percent were of reproductive age (15-45 years old). To compensate for such possible sources of bias, the researchers conducted a type of statistical test known as a sensitivity analysis. This analysis helps to confirm that even if a disease is underestimated in the general population and overestimated in the study sample, the rates of the various conditions reported in women with endometriosis are probably still significantly higher than in the general population. “These findings suggest a strong association between endometriosis and autoimmune disorders, chronic fatigue syndrome and fibromyalgia" said Ms. Sinaii. “Health care professionals may need to consider endometriosis when evaluating their patients for these disorders.” More information about endometriosis is available from the NICHD publication, Endometriosis, at Information about endometriosis is also available from the Endometriosis Association, 8585 North 76th Place, Milwaukee, WI 53223; phone, 414-355-2200; The NICHD is part of the National Institutes of Health, the biomedical research arm of the federal government. The Institute sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. NICHD publications, as well as information about the Institute, are available from the NICHD Web site,, or from the NICHD Clearinghouse, 1-800-370-2943; e-mail "

Gluten free and endo

Some report feeling better by going gluten free? Is there a reason behind this? Read on:

"Gluten-free diet: a new strategy for management of painful endometriosis related symptoms?

Marziali M. 1, Venza M. 2, Lazzaro S. 2, Lazzaro A. 2, Micossi C. 2, Stolfi V. M. 2
1 Department of Gynecology and Obsterics, Tor Vergata University, Rome, Italy;
2 Department of General Surgery, Villa Tiberia Hospital, Rome, Italy
AIM: Pelvic pain affects 4% to 39% of women and accounts for 10-40% of all outpatient gynecologic visits. The etiology of painful endometriosis-related has not been fully delineated. No studies have been published concerning gluten-free diet administered to achieved relief of painful symptoms endometriosis-related. The aim of this retrospective study was to evaluate the effectiveness for the outcomes of endometriosis-related pain and quality of life of gluten-free diet in a follow-up of 12 months in patients with chronic pelvic pain endometriosis-related.

METHODS: Two hundred seven patients with severe painful endometriosis-related symptoms entered the study. At enrolment time, the baseline values of painful symptoms were assessed by Visual Analogue Scale (VAS) for dysmenorrhoea, non-menstrual pelvic pain, and dyspareunia. According to VAS, pain severity was scored from 0-10; 0 indicating the absence of pain, and 1-4, 5-7 and 8-10 mild, moderate and severe respectively. A gluten-free diet was submitted to all patients and a new evaluation was performed after 12 months of diet. Student t test was used for statistical analysis.

RESULTS: At 12 month follow-up, 156 patients (75%) reported statistically significant change in painful symptoms (P<0.005), 51 patients (25%) reported not improvement of symptoms. No patients reported worsening of pain. A considerable increase of scores for all domains of physical functioning, general health perception, vitality, social functioning, and mental health was observed in all patients (P<0.005).

CONCLUSION: In our experience, painful symptoms of endometriosis decrease after 12 months of gluten free diet.
"Endometriosis is associated with having the HLA-DQ2 and DQ8 genes (which are also present in approximately 96% of patients with Celiac Disease), as well as the DQ7 gene, which has been associated with Celiac Disease in some southern Italians, Sicilians, and Sardinians.

Two studies published within the last few years have shown associations between Celiac Disease and endometriosis. Researchers in Sweden (Stephansson, et al.) reviewed the medical records of over 11,000 women with Celiac Disease in 2011. Compared with controls, women with Celiac Disease were found to be at a much higher risk of having endometriosis, especially in the first year after diagnosis with celiac disease (overall hazard ratio of 1.39). The authors postulate that there must be a shared inflammatory process in both disorders. Likewise, researchers in Brazil found that 2.5% of women diagnosed with endometriosis also had Celiac Disease (Aguiar, et al, 2009). Please see the references section for links to these two studies.

The gluten free diet has recently been recommended as a strategy to manage the pain of endometriosis. In a pilot study in Italy, 75% of women with endometriosis had a decrease in pain symptoms after 12 months on the gluten free diet (see link in reference section). This strongly suggests that gluten sensitivity and/or Celiac Disease plays a role in endometriosis."
"Gluten is a protein found in glutinous grains (including wheat, rye, barley, spelt, kamut, triticale, graham, bulgur and controversially oats) that many people with endometriosis have difficulty with. In fact, a recent study found that 75% of the endometriosis patients studied had reduced pain while following a gluten-free diet.1 It can be very difficult to digest, leading to increased bowel symptoms, bloating and increased pain.  Some people find the problem is specifically wheat and tolerate other glutinous grains just fine.  The key to going gluten-free is to choose foods that are naturally gluten-free, like brown and wild rice, quinoa, millet, amaranth, legumes, sweet potatoes and squash instead of processed gluten-free bread, pasta, baked goods, breakfast cereals, bars and crackers which are typically highly refined and fall into the inflammatory category.  Also be aware that many condiments contain hidden gluten, so read labels or better still make your own salad dressings, sauces, salsas and marinades to avoid gluten and other inflammatory ingredients."


More on gluten and endo, specifically the association between endo and Celiac's:

During the follow-up, 118 individuals with CD and 399 matched controls developed endometriosis. Hence, patients with CD were at increased risk of subsequent endometriosis [HR = 1.39; 95% confidence interval (CI) = 1.14-1.70]. The absolute risk of endometriosis in patients with CD was 112/100,000 person-years with an excess risk of 31/100,000. Risk estimates were highest in the first year after diagnosis (HR = 1.49; 95% CI = 0.83-2.67) and gradually decreased (>5 years after CD diagnosis, HR = 1.33; 95% CI = 1.00-1.79).


Endometriosis seems to be associated with prior CD. Potential explanations include shared etiological factors and CD-mediated inflammation."

Nine of the 120 women in the study group were anti-tTGA positive and five of them were also anti-EMA positive. Four of these five patients were submitted to intestinal biopsy which revealed CD in three cases (2.5% prevalence). The overall CD prevalence among the population control group was 1:136 women (0.66%).


This is the first study reporting the prevalence of CD among women with endometriosis, showing that CD is common in this population group (2.5%) and may be clinically relevant."

Not convinced as this speaks of retrograde menstruation which has been largely refuted as the initial causation of endo but the lab results are interesting to read as is the connections to inflammatory and autoimmune disorders:

"Our study reports a potential association between endometriosis and CD in Italian women, showing a trend for increased prevalence of CD in women affected by endometriosis, even if not statistically significant.
In the last few years, some recent studies about this topic have been performed, showing similar results [17, 18]. The interest arises from shared features of both CD and endometriosis, specifically concerning etiology and ongoing inflammation.
It is well known that CD is an autoimmune disorder in which an abnormal T cell response to gluten occurs. Dieterich et al. recently showed that the tissue enzyme transglutaminase is a target of immunological reaction, generating a complex of the prolamine of gluten with HLA molecule that is recognized by T helper cells [22]. It is noteworthy that CD is strongly associated with some HLA class II genes, in particular with homozygosis for HLA DQ2.5 haplotype; also a condition of heterozygosis for this haplotype associated with the presence of DQ2.2, DQ7, or DQ8 produces a higher risk of CD [2325].
The presence of gut inflammation, resulting from the above-mentioned immunological response, together with abnormal intestinal permeability and consequent increased antigenic exposure and autoantibody production, could be also responsible for the association of CD with other autoimmune diseases: dermatitis herpetiformis, diabetes mellitus type 1, Sjögren’s syndrome, rheumatoid arthritis, primary biliary cirrhosis, and sclerosing cholangitis. This theory is supported by the evidence that a number of autoantigens, normally cryptics, are processed and presented by APC to T cells, because of prolonged intestinal inflammation [26].
Another factor that could explain the association of CD with other autoimmune diseases is a common genetic background, represented by HLA haplotype; in fact, some genes in the region of major histocompatibility complex are involved in multiple autoimmune disorders, such as HLA DQA1 and DQB1 genes that can confer risk to both CD and type 1 diabetes [27].
Despite decades of extensive research, the pathogenesis of endometriosis remains not completely clarified. Actually, endometriosis is considered a multifactorial disorder, in which the primum movens seems to be represented by retrograde endometrial debris reflux into the peritoneal cavity that promotes increase of oxidative stress and consequent low-grade inflammation [3, 28, 29]. Peritoneal macrophages have been identified as key processes, by producing growth and angiogenic factors, as well as various proinflammatory cytokines that could be responsible for maintenance of disorder and impairment of reproductive function, as well as the systemic involvement that characterized endometriosis [30, 31]. In the last years, chronic inflammation with increased oxidative stress has been reported to be involved also in the association of endometriosis with other chronic inflammatory diseases, as atherosclerosis [32]. According to these evidences, endometriosis is now considered a chronic inflammatory disease, with inflammation not limited to peritoneal cavity but spread to systemic level, as signaled by elevated serum levels of markers as Ca-125 and C-reactive protein (CRP) [33, 34].
Also a genetic predisposition has been suggested for development and progression of endometriosis, with HLA DQ7 haplotype being reported as the first allele significantly associated with endometriosis [35, 36].
A potential role of autoimmunity for endometriosis has been suggested, as it fulfills many of the classification criteria of autoimmune diseases: polyclonal B cell activation, immunological abnormalities in T and B cell functions, defective apoptosis, tissue damage, and multiorgan involvement [37, 38]. This topic is supported also by familial occurrence, genetic predisposition, female preponderance, and increased likelihood of other autoimmune diseases, like systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s syndrome, multiple sclerosis, and endocrine disorders [8, 39].
Among these associations, recently some studies have evaluated the relationship with CD. The first study has determined the presence of CD in a Brazilian subpopulation of women with endometriosis suffering from infertility [17]. The authors have found that prevalence rates of positive CD serology for anti-tTG and antiendomysium IgA in a group of 120 patients with endometriosis versus 1500 controls were statistically significant (4.1% in patients versus 0.8% in controls), even if the prevalence rates of the biopsy-confirmed CD did not reach the statistical significance (2.5% cases versus 0.66% controls), showing only a positive trend, maybe also because one patient refused the endoscopic examination. They have concluded that, even if not statistically significant due to small number of cases, CD is more common in women with endometriosis with respect to controls, suggesting a potential clinical relevance. In the interpretation of their results, however, we cannot ignore that control group was constituted by blood donors; these subjects, as underlined by authors themselves, cannot be considered to be representative of the general population. In fact, some conditions, first of all the presence of anemia (one of the possible manifestations of CD), have to be excluded in subjects candidate as donors. Moreover, in this report total serum IgA assessment was not performed, making it not possible to exclude serum IgA deficiency, a condition that compromises the diagnostic power of serological assays for CD. Finally, since patients with endometriosis were enrolled among subjects referring for infertility disorders, women at higher risk of CD could have been screened, infertility being a complaint also of CD. As regards, in our study the enrollment was conducted among women with endometriosis, not necessarily involving the presence of infertility; however, an increased prevalence of infertility among patients with endometriosis with respect to controls was finally found.
Recently, a Swedish nationwide population-based study has evaluated the risk of developing endometriosis in about 11.000 women with known CD [18]. During the follow-up period of study, the authors have found an increased risk of developing endometriosis, hypothesizing that chronic inflammation characterizing CD could act as trigger in endometriosis development. It is not by chance that they reported that this risk was higher in the first year after the diagnosis of CD, when mucosal healing could not be yet achieved, despite gluten-free diet start. The greater awareness to CD presence, together with improved diagnosis and some socioeconomic factors, has led to increased prevalence of CD, especially identifying mild degrees of CD; pursuant to authors’ view, pointing severity of inflammation due to CD to be crucial for endometriosis development, the presence of mild CD could modify the association with endometriosis. As regards, in our study all subjects diagnosed as affected by CD (both patients and controls), although clinically not suspected for CD, presented villous atrophy with high grades of inflammation at intestinal biopsy.
In conclusion, our results confirm the potential association between CD and endometriosis, although this trend does not reach the statistical significance. Further studies with higher number of subjects are desirable to definitively support this relationship. Actually, we can suggest screening a woman with endometriosis for CD if a valid clinical suspect is present."

Tuesday, March 4, 2014

Laparoscopy in the Diagnosis of CPP

Laparoscopy in the Diagnosis of Chronic Pelvic Pain

Deborah A. Metzger, PhD, MD

(From Chronic Pelvic Pain: An Integrated Approach, eds Steege, Metzger, Levy)

"Clear documentation of the laparoscopic findings will allow the operator to plan the surgical procedures to be performed.   Photographic and written documentation in the operative record allows the surgeon to refer back to the procedure, when planning additional treatment or if another  laparoscopic procedure is performed subsequently.

             It is important that the exam be conducted in a standardized and thorough manner.  Soon after the laparoscope and accessory trocar are inserted, the omentum and bowel directly beneath the trocar should be inspected for Veress needle and trocar injury.  First, a general survey of the pelvis is undertaken so that all of the pelvic structures are in view of the laparoscope.  The blunt probe is used to gently manipulate the organs of interest, in particular areas with scarring or areas which correlate with pelvic tenderness.    The laparoscope is then moved closer to the left adnexa and the ovary is lifted, if possible, and the pelvic sidewall is carefully inspected.  The ovary is then released and the laparoscope then directed over the anterior cul de sac and swept over to the right adnexa.  Again the right ovary is elevated and the pelvic sidewall is carefully inspected.  The posterior borad ligaments and cul de sac are then carefully evaluated.  The surface of the bowel should be examined next, followed by an inspection of the appendix, liver, and diaphragm. 

            The examiner’s efforts should be concentrated primarily in the region of the patient’s pain.  For example, when a pelvic examination suggests that there is tenderness in the right adnexa, most of the laparoscopic effort should be concentrated there.  However, the examiner should also be receptive to other possible abnormalities that could contribute to the pain or
which may be one of several pain sources of the patient.

            Visual records via still photographs or video will aid your post-operative discussion with the family. Patients often benefit immensely when they can “see” what was responsible for their pain or, alternatively,  may be reassured if their pelvis is normal.  Many surgeons give the patient a copy of the photographic and written record.

Specific conditions commonly found in women with chronic pelvic pain will now be reviewed.

While typical endometriosis implants appear as blue-black “powder-burn” implants often surrounded by stellate scarring, the atypical lesions are less apparent visually but more active physiologically as determined by their production of prostaglandins (15).  Atypical implants may  appear as reddish vesicles, clear vesicles, slight irregularities on the surface of the peritoneum or white patches.  Detection of subtle non- pigmented lesions requires laparoscopic inspection at close range (1-2 cm) or inspection of the surface at moderately close range utilizing different lighting angles.

Teenagers are more likely to have atypical implants, particularly the nonpigmented type (16).  Sometimes an extraordinary effort may be required to make a diagnosis including re-cuts of peritoneal biopsies that are negative for endometriosis at first glance.  Early detection of endometriosis has an important impact on treatment selection.

            Sometimes endometriosis implants are buried under scar tissue that develops as a result of the natural progress of the disease or from previous superficial attempts at ablation.  Palpation of these areas with the manipulating probe will allow detection of occult nodules.  Resection of the overlying scar tissue may be necessary in order to discover and remove underlying implants and fibrosis.

            Bowel endometriosis may be difficult to diagnose preoperatively even in the presence of rectal bleeding, dyschezia or deep dysparunia.  Only 20% of women with bowel endometriosis can be identified by either colonoscopy and/or barium enema (Redwine and Sharpe, unpublished). However, if a patient has suspected bowel involvement, there are several techniques which may be helpful in improving the diagnostic yield.  Since most of bowel endometriosis is found associated with the rectosigmoid, a careful examination may yield evidence of scarring and distortion of the serosa of the bowel.  Palpation of any abnormalities with the manipulating probe allows assessment of the extent of the lesion.  Inserting ring forceps or a rectal probe into the rectum and gradually withdrawing it, may disclose retroperitoneal nodules that would otherwise go undetected.  Similarly, the pelvic floor tissues can be palpated in detail using a recto-vaginal examination a blunt laparoscopic probe.   Finally, the diagnosis of significant bowel endometriosis may require a laparotomy in order to run the bowel.         


            Not all adhesions which are found at the time of a laparoscopy for CPP are responsible for the patient’s pain.  In general, filmy adhesions are not associated with chronic pelvic pain, although it is tempting to use their presence as an
explanation.   In contrast, dense adhesions which distort anatomy and/or function may be a significant source of pain.  Careful pelvic mapping prior to the laparoscopy as well as a correlation of laparoscopic findings with a description of the patient’s pain characteristics may allow a certain degree of discrimination.  When the patient has localized pain and the only findings are adhesions limited to the anatomic location of the pain, it is highly probable that the adhesions contribute significantly to the pain.  In other patients, the judicious use of laparoscopy under conscious sedation will allow a more definitive diagnosis.


            Direct inguinal, indirect inguinal and femoral hernias are seldom visible in women at the time of laparoscopy as indentations or defects of the peritoneum.  Moreover, hernias may be difficult to palpate externally, making diagnosis in women problematic (17).  The presence of hernias is suspected on the basis of a vaginal exam associated with inguinal tenderness which reproduces the patient’s pain.  A retroperitoneal laparoscopic examination by an experienced general surgeon confirms the diagnosis and allows treatment at the same time.  

Pelvic congestion

            Dilated ovarian and pelvic veins, when present in the patient with ovarian tenderness and postcoital ache, are diagnostic of pelvic congestion.  However, laparoscopy is not a definitive method of diagnosing pelvic varicosities since Trendelenberg positioning enhances venous drainage and minimizes the size of the veins.  Transvaginal ultrasound and transcervical venography are less invasive and a more definitive means of diagnosing this condition.  Testing should be preferably performed prior to the laparoscopy so that appropriate treatment can be instituted.

Pathology which is rarely associated with CPP

            Some pathology is often encountered during laparoscopic examinations for CPP but is only rarely responsible for chronic pelvic pain.  Findings such as functional ovarian cysts, cysts of Morgagni, filmy adhesions and peritoneal windows (Master-Allen syndrome) should be viewed as “red herrings” which may distract attention from the real reason for pain.  More widespread use of laparoscopy under conscious sedation (Chapter 34) will provide additional information regarding the
spectrum of sources of pelvic pain."          

***Please note that ovarian cysts can rupture and cause pain and endometriosis is often found behind peritoneal windows. "Peritoneal pockets are an unclear pathology Pockets in the peritoneum. They can be large and deep. Peritoneal pockets are believed to be associated with endometriosis
Excision is believed to be the right therapy."

Saturday, March 1, 2014

More on Immune

From (please it for the full length post!):

"...the number of leukocytes was much, much higher in women with endometriosis regardless of whether they were receiving treatment or not. Leukocytes (pronounced loo-co-sites) aka white blood cells, they’re an important part of the immune system, usually the good guys, helping to fight off infection and remove harmful material from the body....The fact that there seems to be an excess of these cells in the peritoneal fluid of women with endometriosis makes it look like they were trying to help fight the endometriosis...Like the other leukocytes macrophages were normally the good guys, it was their job to destroy diseased or infected cells, by engulfing and digesting them and to signal other immune cells to come join the party. Looking over the notes from another case it turns out they hate endometriosis too, they react to the disease as if it were a wound, trying to do their job and ‘fix’ the injury but end up secreting factors that actually encourage the survival of endometriosis instead. Kinda like trying to put out a bonfire with petrol. Is that the end of the case though? Should we just lock up the macrophages and throw away the key? Maybe there’s more going on here, macrophages are trying to be the good guys, but something is telling macrophages to produces these inflammatory factors that help endometriosis...Within the cells of your body there are all sorts of different signals that tell a cell what to do and how to do it. Amongst these signals are ones that switch on genes and one such signalling mechanism, called the JNK signalling pathway, was found to be responsible for the inflammatory activity of macrophages. So the true culprit has been found, case closed? Not quite, endometriosis has many different accomplices and although one of the major ones has been identified there is still much work to do."

Pretty Bad A** !!!
Macrophages be like: