Harvey S. Marchbein, MD

Endometriosis - defined as the presence of endometrial-like glands and stroma in any extrauterine site - is a common disease occurring in 7-10% of all women, and is often associated with chronic pelvic pain and infertility. Apart from these significant individual problems women with endometriosis and their families may face, this disease has a significant impact our society due to its chronic nature 

The symptoms of endometrioses are variable and its course is often unpredictable. While some women may be asymptomatic, the most common manifestations are pelvic pain, particularly with periods, dispaureunia, pain associated with bowel movements, and dysuria or hematuria in cases of bladder involvement.  Despite significant improvements in understanding of this disease, the pathogenesis of endometriosis remains unclear. There are several theories that were suggested; most prominent includes theory of retrograde menstruation associated potentially with genetic susceptibility for the disease. Also theories of hematogeneous and/or lymphogenic spread, genetic link, or defects in immunocompetency have been suggested

The link between endometriosis and ovarian cancer is well recognized and has perplexed physicians for a long time 

. Epidemiological studies have suggested a specific link with endometrioid and clear-cell ovarian cancers, but no firm evidence established endometriosis as an ovarian cancer precursor lesion. Several lines of clinical evidence have supported the observation that non-serous ovarian carcinomas such as endometrioid and clear-cell carcinomas arising from atypical endometriotic foci have a higher likelihood of early diagnosis, as the associated endometriosis can cause pelvic pain or infertility requiring specialized gynecologic care including diagnostic laparoscopy. Deligdisch et al. reported a series of 76 cases of stage I ovarian carcinomas and documented that non-serous carcinomas (54/76) were diagnosed because of the associated symptoms including pelvic pain associated with endometriosis or vaginal bleeding associated with hyperestrogenism and endometrial pathology

. Interestingly they also found that serous carcinomas were frequently found in asymptomatic women with breast cancer diagnoses 

. These and similar observations support the emerging dual model of ovarian carcinogenesis. According to this model, Type I cancers are low grade, slowly developing ovarian carcinomas (including endometrioid, mucinous and low grade serous) associated with KRAS, BRAF, PTEN and B-catenin mutations and often associated with endometriosis. Type 2 is high-grade serous carcinomas associated with TP53 mutations that develop rapidly, are more aggressive and their origin is now thought to be tubal epithelium 

In the recent remarkable study reported in Lancet Oncology, the team of researchers from the Ovarian Cancer Association Consortium (OCAC) performed pooled analysis of 13 case-control studies and confirmed that women with self-reported history of endometriosis have significantly increased of clear cell carcinoma (odds ratio 3.05) and endometrioid ovarian cancer (odds ratio 2.04) 

. In addition the authors show, for the first time, that endometriosis is associated low-grade serous ovarian carcinomas, doubling its risk in women with endometriosis

.  However, there was no association between endometriosis and high-grade serous carcinomas or other subtypes of ovarian cancer in the study.

Taken together these findings will have considerable clinical implications and may affect the ways we think about strategies for ovarian cancer screening and prevention. In particular, the emerging knowledge of the link between ovarian cancer and endometriosis gives us an unprecedented opportunity to develop comprehensive screening plans to aid in the early detection and prevention of specific types of ovarian cancer in women with endometriosis. Such planning should include:

1) Identification of all women with endometriosis – either surgically documented or self-reported by symptoms;

2) Careful  follow up of ovarian presumed endometriomas by imaging studies, perhaps by MRI, for any characteristics changes such as mural formation;

3) Complete surgical resection of all endometriotic foci in women undergoing surgical treatment and tissue evaluation of ovarian endometriomas to rule out malignancy;

4) Hormonal treatment aimed at reducing the risk of cancer in high-risk women.

While it is well known that most women with endometriosis do not develop ovarian cancer, the women and their physicians should always discuss these new findings, carefully document and discuss any new symptoms and formulate plan for regular evaluations and treatment.


1. Simoens S, Hummelshoj L, D’Hooghe T. Endometriosis-cost estimates and methotologic perspective. 

 2007;13:395-404.
2. Burney RO, Giudice LC: The Pathogenesis of Endometriosis. In Nezhat C, Nezhat F, Nezhat C, (eds): Nezhat’s Operative Gynecologic Laparoscopy and Hysteroscopy. 

New York, New York: Cambridge University Press

, 2008:251-7.
3. Munksgaard PS, Blaakaer J. The association between endometriosis and ovarian cancer: a review of histological, genetic and molecular alterations. 

 2012;124:164-69.
4. Nezhat F, Datta MS, Hanson V, et al. The relationship of endometriosis and ovarian malignancy: a review. 

 2008;90:1559-70.
5. Deligdisch L, PÃ©nault-Llorca F, Schlosshauer P, et al. Stage I ovarian carcinoma: different clinical pathologic patterns. 

 2007;88:906-10. 6. Levanon K, Crum C, Drapkin R. New insights into the pathogenesis of serous ovarian cancer and its clinical impact. 

 2008;26:5284-93.
7. Pearce CL, Templeman C, Rossing MA, et al. on behalf of the Ovarian Cancer Association Consortium. Association between endometriosis and risk of histological subtypes of ovarian cancer: a pooled analysis of case-control studies. 

Articles

Emerging information on the link between ovarian cancer and endometriosis gives us an unprecedented opportunity to develop comprehensive screening plans for early detection and prevention of specific types of ovarian cancer.

Endometriosis and Risk of Ovarian Cancer: An update

 A Novel Device for Peritoneal Access in Laparoscopic Surgery

"Safe abdominal entry and prevention of retroperitoneal vascular  injuries during laparoscopic surgery are the ultimate goals of any  laparoscopic surgeon.  Dr. Linda Nicoll and colleagues very capably have  been able to describe a new technique and technology that prevent  almost all retroperitoneal vascular injuries during laparoscopic entry."

 -    Linda M. Nicoll MD, Madelein Lemyre MD, Dorian Bosev MD, Jian Qun Huang MD, Lisa Bhagan MD and Camran Nezhat MD

 email us with their comments and questions

 by using the comment links at the end of each article.


           Editor-in-Chief
 "New Frontiers in Reproductive Medicine"
           OBGYN.net

afe abdominal entry and prevention of retroperitoneal vascular injuries during laparoscopic surgery are the ultimate goals of any laparoscopic surgeon.  Dr. Linda Nicoll and colleagues very capably have been able to describe a new technique and technology that prevent almost all retroperitoneal vascular injuries during laparoscopic entry.

Frontiers in Reproductive Medicine

 I developed Osteoporosis from taking Lupron for seven months. (To treat Endometriosis. I took 3.75mg monthly). My doctor put me on Fosamax, 5mg daily for the first month, and then 10mg daily for another 5 months. Is this treatment adequate, or should I have taken Fosamax for a longer period? If so, what is recommended? Also, at what point should the bone density test be repeated?

 My first thought is as to whether or not add back therapy was used to prevent the osteoporosis that can accompany prolonged GnRH therapy. The reason for therapy with Lupron was not mentioned so the point is one of academic interest but not practical at this time.

Fosamax 10mg daily is an adequate dose but the duration of therapy has to be customized to the level of osteoporosis and the speed of return to normal density levels. This is variable. During therapy, a urinary NTX could have been done to insure reduced bone turnover and it can still be done now, after therapy, to confirm premenopausal NTX levels if you, indeed, are premenopausal (not mentioned above).

Osteoporosis is frequently reversible in premenopausal women with adequate Calcium supplementation and weight bearing exercise because endogenous circulating estrogen should be helpful in and of itself. An important point is that we don't know your pre-treatment bone density or physical exam or family history which may also impact on your recent bone density.

The duration of therapy can not be determined in advance so that question is unanswerable. The repeat bone density should not be done earlier than 12 months and many experts recommend 24 months at a minimum due to variability of measurements even in the same person on the same machine on the same day (2-3% variation noted).

I have been diagnosed with Osteoporosis. I am a 60-year-old Caucasian female. I have not had a hysterectomy. I have been talking Ogen and Provera for the past five years. Can/should Fosamax be used in conjunction with HRT to help rebuild bone density?

If this is your first bone density, we have no way of knowing if there has been a decrease in bone density despite HRT (18% of women are genetically incapable of building bone from being on HRT) or if your bone density was always low and the HRT is keeping it stable.

Fosamax can be used in combination with HRT although there are very few papers in the literature at this point, indicating this. Anecdotally, this has been a very effective combination.

Another option is to get a urinary NTX prior to adding medication to determine the bone turnover and see if additional therapy is warranted at this time. Therapeutic modalities will also depend upon the severity of osteoporosis shown on the bone density.

Some small amount of literature speaks about HRT with the addition of small amounts of androgen to increase bone production. Pros and cons of adding this therapy should be discussed with your physician.

 I have an 81 year old female patient who is taking Calcium, ERT (Premarin, .625mg), (s/p hysterectomy), and has taken Fosamax for 3 years for a history of lumbar compression fractures. I ordered her first bone density study, DEXA, which showed Z-scores (compared to young adult) of lumbar: -0.83, hip: -1.87, and radius -3.54. Should her therapy be changed?

 T scores are compared to young adults. Z scores are compared to patients of the same age. I wonder if there is degenerative joint disease along with compression falsely increasing the lumbar reading because that is not consistent with osteoporosis causing vertebral fractures.

Due to history of vertebral fractures, treatment should be maintained. A urinary NTX can be obtained to determine bone turnover to insure adequacy of therapy.

 Should Fosamax be used longer than 3 years?

 No reason why it can't. May depend upon the bone density and what it changes to in that 3 year period.

Regarding the reporting form for DEXA Densitometry , specifically the LUNAR brand

 What is the significance of >2.5 S.D. over young adult values at the distal radius, if the 33% value is normal, and why is this reported?

 For the spine, is the L1-L4 the best marker? Is this an average? Are all values given, in case 1 or 2 are markedly different from osteoarthritis or other disorder, and we should thus not use them in our interpretation?

 Both the separate values and the average are important. With osteoarthritis, the value will be abnormally elevated, making an osteoporotic vertebra appear better than it is and a normal vertebra may have a positive T score indicative of degenerative joint disease.

 For the hip, I have been told that the Wards triangle value is useless, and the only one to pay attention to is the neck value. If so, why are 3 values reported?

 Wartd's traingle is of limited value because there is no agreement on *exactly* where on the bone densitometry Ward's triangle is. The neck has been shown to be the most reliable value. The 3 values are reported as a matter of custom and hopefully, in the future this will be changed by the NOF (National Oseoporosis Foundation or another governing body.

 What do I tell a patient who has very discrepant values from radius to hip to spine, for example, +.09, -2.5, and -0.85, and what is the significance of which bone is the lowest in density?

 You tell the patient she has osteoporosis evident in the hip and considering the mortality associated with hip fracture, treatment is recommended.

 If I have a bone density value in g/cm2 from a SPA study can I compare that value to a subsequent DEXA value?

 My understanding is that only DEXAs can be compared to DEXAs and even that is not completely true due to variations from one machine to another.

Questions by Kathleen Griffin, M.D. Maui, Hawaii
 Answers by Harvey Marchbein, M.D. Great Neck, New York

 I have an 81 year old female patient who is taking Calcium, ERT (Premarin, .625mg), (s/p hysterectomy), and has taken Fosamax for 3 years for a history of lumbar compression fractures. I ordered her first bone density study, DEXA, which showed Z-scores (compared to young adult) of lumbar: -0.83, hip: -1.87, and radius -3.54.
 Should her therapy be changed?

Questions answered by Harvey S. Marchbein, MD

Osteoporosis Ask the Expert

I am a 45 year old white female that was just diagnosed with 	osteoporsis. (-3.9 below the mean, which I'm told is severe). I had a hysterectomy at age 28 with no estrogen supplements. 	Because of cancer in my immediate family, estrogens are out of the question now. I am currently take Evista along 	with 1500 mg calicum w/vitiman D.

Depending upon the cancer and who in the family had the cancer (in addition to what year this information was imparted) this may or may not still be true. Unfortunately, Evista is not approved for osteoporosis and is no better than low dose estrogen or low dose Fosamax, so many experts would consider this insufficient therapy for your osteoporosis.

I have a t-5 compression that is 10yr old but is giving me 	alot of pain in the form of spasms. My doctor wants to do a nerve block but I insisted on therapy, hot packs , 	ultra sound and stim. My therapist wants me to do upper back exercises on the machines. Two doctors have told me 	to do nothing but walk. I'm confused and scared to even pick up my grandchild in case I should break a bone. How 	careful do I have to be? I'm afraid to do anything. Please help. Thank you, debbie

Many therapies can have similar, positive effects. Keeping that in mind, we always try to do the least invasive treatments fo a particular situation. Your questions might be best answered by a rheumatologist with a special interest in osteoporosis or an Osteoporosis Clinic at a University Hospital. they are somewhat too specific for this forum.

Does having twins at age 39 predispose the mother to osteoporosis? 	(I had my first child at age 25).

If appropriate calcium intake was observed and the patient has no other predisposing factors, the answer is *no more than any other 39 year old*.

Your case has too many variables and too little specific information for exact therapeutic recommendations, but some comments should be made.

I am a 45 year old who consumes little to no dietary calcium, 	and I have a strong family history of osteoporosis.

That is one thing that you can easily do and needs to be corrected immediately. Vitamin D is also needed in adequate amount.

My gynecologist did an osteoscan at my request this past 	August. I was diagnosed with osteopenia.

There is a great range of difference between osteopenia just over the cutoff for normal and osteopenia just below the cutoff for osteoporosis. In that we don't know what you were 2 or 5 or 15 years ago, a urinary NTX might be helpful to delineate the amount of bone loss you are currently experiencing.

All I have been able to find out in relation to the results 	is the bone loss is "moderate". I am having no menopausal symptoms and do not know whether I should begin 	hormone replacement therapy.

If you get regular periods and have no menopausal symptoms, then your aren't menopausal. Perimenopausal might be a better term. Birth control pills, recently shown to have no increased risk of breast cancer, may be a viable option.

When I consulted with my doctor, I expressed concern about 	breast cancer because I have cystic breasts.

No relationship has conclusivley been shown between cystic breasts (a subjective diagnosis in many) and breast cancer.

He told me that if I got cancer I would either live or die, 	but I did not want to get osteoporosis. He gave me a bag full of Premarin and told me to come back in a year.

If you get regular periods and are not menopausal, I'm not sure why one would be taking Premarin. If hormones are indicated, oral contraceptives, as noted above, might be more appropriate.

I did not start taking the hormones because I don't know 	what to do. How fast do the bones lose bone mass?

Depends upon the person. There are many medical conditions that may accelerate it as well as certain drug therapies that can predispose to it.

Would I possibly be a candidate for an osteoporosis drug 	since I am premenopausal and still have regular periods? If so, what drugs are available.

It appears that with certain inconsistencies in the history and treatment recommendations, a visit to an osteoporosis expert might be a good idea to delineate your possiblities as a perimenopausal patient.

Although I am 52 yrs old and pre-menopausal, a Dexa scan 	revealed osteopenia in my hip and low density in my spine. I've been placed on 5 mg. Fosamax and Arthrotec for 	occasional back pain in my hip and leg. My gyn. says that although my periods are irregular, I'm still producing 	more estrogen than could be gotten from HRT. My question is, at what point would HRT benefit me more than Fosamax 	, if at all?

Approximately 82% of women will be able to build bone with ERT/HRT but it is difficult to quantify how much good your estrogen is doing. A urinary NTX can be done to evaluate current bone loss to see if these changes may be, in part, due to recent bone loss as opposed to long term lower levels.

How bad is a reading of -.83 (spine) and -1.23 (hip) compared 	with women in my age group?

The interpretation is as follows: 0 to -1.00 is normal; -1.01 to -2.5 is osteopenia; less than -2.5 is osteoporosis of varying degrees. The spine is normal and the "hip" is "early" osteopenia. This may have been present for many years and may not, as noted above, represent recent loss. By the way, did you mean "in your age group" to mean that this is what the bone density result said? If so, the interpretation is different. The standard deviations noted above are for comparisons to 20-30 year olds (this is standard).

Harvey S. Marchbein, M.D. FACOG, FACS
 Great Neck, New York

Questions answered by Harvey Marchbein, MD

I am 59 and have been diagnosed with osteoporosis. I had 	a total hysterectomy at age 42 and was unable to tolerate hormone replacement drugs at that time. So this diagnosis 	(through a bone scan) is not a surprise. There is a history of cancer, both male and female in my family. My primary 	care physician is recommending Climara patch as treatment, along with calcium I am already taking. I am worried 	about taking hormone replacement - mainly with the risk of breast cancer. Are there any better or safer treatment 	options - such as Evista or Fosomax? The research on both drugs seems to be good. Is one better than the other? 	Thank you very much for your response.

ERT has been questionably implicated in an increase in breast cancer but, from studies of HRT, there is no consensus as to whether or not hormones increase the of breast cancer. Many studies do show an increase but also show breast cancer being diagnosed at an earlier stage with a higher cure rate. The are many other advantages of ERT including reduction in heart disease, reduction in Alzheimer's disease, reduction in colon cancer and reduction is vision loss associated with macular degeneration.

Evista is not recommmended for the treatment of osteoporosis but rather for the prevention of osteoporosis. With a diagnosis of osteoporosis already, this would not be a first choice. ERT by patch is highly recommended but approximately 18% of women are gentically incapable of increasing bone density with estrogen and need medications such as Fosamax. An option for many would be starting ERT and doing a urinary NTx pre treatment and 3 months later. This test measures bone turnover and with adequate decrease after 3 months of therapy, it is reasonable to assume that bone density will increase.

How much calcium should you take as a supplement?

Depending upon the age of the individual, this varies. Calcium can be taken in appropriate foods and or supplements. Nutritionists point out that the body will not absorb more than 500-600 mg at one time, so larger amounts (1000 mg) will have to be split into smaller doses (500-600 twice a day). Teenagers need about 1500 mg per day. Adults need about 1000 mg per day. After menopause, 1000 mg per day if on hormones, 1200-1500 mg per day if not. After age 65, 1200-1500 mg per day. This presumes there are no medications or medical problems that would accelerate bone loss. In addition, Vitamion D 400IU per day until age 65, when many experts recommend 800IU per day. These same experts also feel that after age 65, at least half of the requirements should be by supplement, not just food.

Is it appropriate to compare DEXA results from say "Hologic" 	with results from "Lunar"?

It is difficult to compare DEXA results from machines from the same company much less from different companies. Another problem is what set of normals each practitioner uses. The T scores will vary depending upon the company, the machine and the updated (or not) set of normals upon which comparisons are drawn.

After having radiation theraphy in 1970, I had a pituitary 	tumor removed in 1974 (I was 29 years old then, I am 53 years old now).

I had my periods by hormone treatment (Premarin and Provera) 	all these years. Aproximately two years ago my periods became irregular (somethimes just dark spotting and others 	very light bleeding). My doctor put me on PREMPRO, supposedly to stop the periods completely. I took PREMPRO for 	several months, but I still bleed (dark spotting and very light bleeding) almost every month at different times 	of the month. I went back, and I was given a prescription for PREMPHASE this time. Well, I took PREMPHASE for several 	months and the same thing happened. A week ago I went back to the doctor and this time I was instructed to take 	a doble dosage of PREMARIN (1.25mg daily, PREMPHASE has .625mg) for the rest of the month of December, then in 	January to start with 10mg of PROVERA, days 1-14, and 1.25mg of PREMARIN from day 15-to the end of the month. The 	same day I took this double dosage I started cramping, and then bleeding. I stopped taking the double dosage, and 	decided to take just the regular PREMPHASE dosage.

At the last appointment (when the doctor asked me do do the 	double dosage), she indicated that if the above therapy (double dosage) didn't work, she would take me completely 	out of the hormones. My main concern is osteoporosis. If I stop the hormones now, could I develop osteoporosis?

If one were to be a responder to estrogen with respect to bone formation, discontinuation would tend to decrease bone overall.

Approximately three months ago I attended an Osteoporosis 	Seminar, and at that time I was given a right heal bone density test, which the doctor indicated was OK at that 	time, even though I seem to be a high risk person (my mother developed osteoporosis, I take daily cortisone, synthroid, 	diuretic and potasium (DYAZIDE and SLOW-K), consume little milk products, and have very sedentary life - always 	tired, little energy).

It is unknown as to whether or not "OK" indicates normal bone or osteopenia without osteoporosis. The risk factors noted above are considerable.

Is there any other way that I could continue with my hormone 	therapy, to avoid developing osteoporosis?

Dr. Mischell, in California, is reported to use combination therapy in some patients, 5 days on and 2 days off. This helps some. A new HRT patch, Combipatch may also be helpful to some. Still others change from Prempro and Premphase to other estrogens and progesterones, including Estratab and Estrace (E) and Prometrium (P). There are other options in compounded medications including Bi-Est and Tri-Est from Women's International Pharmacy in Madison Wisconsin.

Another option is preventative therapy in patients with osteopenia in the form of Fosamax.

I am a 49 yr. old on HRT for 1 year and have been suffering 	from mild to severe chronic mid back pain for almost 3 yrs. My Gyn. Dr. thought it was due to osteoarthritis & 	that it might subside somewhat w/ HRT but it has not. I still get occasional hot flashes also. I was wondering 	if slightly higher doses than standard Prempro were ever used to alleviate either of these conditions. ( I am also 	seeing a Rhemetologist and have been diagnosed w/ osteoporosis and have just started taking extra calcium supp. 	plus Calcetonin spray as I have a sensitive stomach).

The only other advice the Rheumetologist has given is to 	take an exercise class (although I'm fairly active and not overwieght) and just take anti-inflamatorys (although 	even w/ buffers this still upsets my stomach at times..) Any suggestions?

Several points - 
 
 1) HRT has recently been shown to be somewhat helpful in the symptomatic relief of osteoarthritis.

2) Occasional hot flushes can be normal with adequate HRT but it might be appropriate to consult your physician about an Estradiol level. Depending upon the HRT used, the Estradiol level may be reflective of your supplemented estrogen level and indicate either adequate therapy or suboptimal therapy. Higher doses will not necessarily be more helpful with your osteoarthritis and higher doses are usually associated with higher risk rates and side effects. With respect to hot flushes, one may wish to consider herbal therapy, most notably Black cohosh. The major caveat is to be sure your liver chemistries are normal.

3) With respect to osteoporosis, depending upon the severity, estrogen can halt and/or reverse osteoporosis in about 82% of patients. Using urinary NTx (a chemical showing bone turnover - high NTx is not good and lower NTx 3 months after therapy is initiated can indicate response to therapy) may be helpful in delineating these patients who are estrogen "responders". For those who don't show lowering NTx, there is Fosamax (many with sensitive stomachs can take it although this is not universal). Fosamax is far superior to Calcetonin (*Miacalcin* - brand name) in efficacy and calcetonin is noted to be most effective at least 5 years after menopause but may still meet your needs. Didronel, an older medication, is making a comeback in some circles for patients sensitive to Fosamax who are less than 5 years from initiation of menopause.

4) For osteoarthritis and osteoporosis, exercise is extremely important. Stretching, aerobics and weight bearing exercises are crucial for maintainence of flexibility, cardiac conditioning and body strength. Exercise not only has these benenfits but, by increasing body strength and flexibility, aids in maintaining balance, which reduces falls.
    

I'm having trouble finding information on studies concerning 	Miacalcin for premenopausal women diagnosed with osteopenia (lumbar spine only). I'm a 42 year-old physical therapist 	who has been taking salmon-calcitonin via nasal spray since September 1997. How long should I remain on the Miacalcin? 	Are there any side effects? Can I start a low-estrogen birth control pill and continue taking the Miacalcin? I'm 	currently chewing 3 Tums 500 with meals for calcium and take 800 IU's of Vitamin D at bedtime; the only other medication 	I use is a Proventil inhaler before aerobic exercise for ex-induced asthma.

I would appreciate any information you could send my way!

Having no personal knowledge of the use of Miacalcin in premenopausal women with either osteoporosis or osteopenia, I performed a literature search and came across only one article in the first 60 stating that calcitonin had no effect on premenopausal osteoporosis. there is no mention at all of calcitonin for the prevention of osteoporosis. There is some data to suggest that premenopausal changes in BMD may not be significant. The DEXA results are not listed so the discussion will be in general.

Presuming there are no other predisposing factors for osteoporosis, the birth control pill option mentioned is an excellent one if approved by your physician and the literature supports this.

In patients with adequate weight bearing exercise, adequate Calcium (1000-1500mg per day depending upon BMD status - maximum dose 500-600mg per dose - therefore 2-3 doses per day) and adequate vitamin D (400IU is recommended for the average person person under 65) miold osteopenia may be their norm and may not represent a loss.

The literature confirms the less than acceptable response from calcitonin for the treatment of osteoporosis (not osteopenia), and with that, best effect after 5 years of menopause (not premenopausal).

Please, send me your information about the need of calcium 	supplements in a woman who is entering in menopause,except of HRT and the role of these in renal stones formation. 	Thank you.

 is a wonderful site to answer your questions. The usual recommendation is 1000-1200mg daily of calcium usually taken in split doses of no more than 500-600mg per dose. This can also be accomplished with food rich in calcium. In menopause, calcium intake needs to be higher in patients not on HRT (1200-1500mg) whereas pateints on HRT need less (1000-1200mg) per day. Vitamin D in adequate amounts is also needed (400-800IU per day). Renal stones do not seem to be related to calcium intake (New England Journal of Medicine, 1993).

I am 60 yrs. young. Back in the 70's I tried the "pill" 	and after 6 months I landed in the hospital with a blood clot in the calf of my leg. Was put on Hefferin and then 	cumadin. A year ago my physician put me on fosomax with a calcium supplement. I followed directions. Stay upright, 	etc. 6 months later I had a large kidney stone in right kidney . Had the stone smashed, they classified it as a 	calcium stone. I am afraid to take the foxomax again. My sisters all have osteoarthritis so I probably will have 	it too. Is there anything else on the market? Or do I just keep on exercising and hope for the best. Thank you.

There is much debate at present about whether or not a patient with a previous thrombophlebitis (blood clot) can be on hormone replacement therapy.

There is no evidence that either Fosamax or Calcium supplementation causes kidney stones.

No information provided would cause me to change the therapy. If a change were desired, there are (presuming you are on Fosamax for osteoporosis and not osteopenia (less bone loss than osteoporosis)) some choices but they have been shown to be less effective....Miacalcin nasal spray and Didronel oral medication. (Both HRT and Evista have been associated with a 2-3 fold increase in thrombophlebitis - and this relates to my first point.) Adequate calcium supplementation, Vitamin D and exercise are all important parts of the program to maintain and hopefully build bone. the medications discussed increase the effectiveness of the entire process.

One last point...there are always new medications the horizon.

There are 3 questions here asked by the same person.

 Question 1. Between AP Dexa, Lateral Dexa and QCT which is the advisable 	modality and why, please. Question 2. Considering T scores, 2.5 SD below the mean indicates Osteoporosis. After 	a certain age then would not the mean also lie then in the osteoporotic range. Question 3. In reporting QCT are 	T scores also given and their significance.

Three important questions.
 1. Lateral DEXA is of limited value because of the many technical difficulties involved in this measurement. Too often only 1 or 2 vertebrae can be included in the analyses reducing both accuracy and precision.
 QCT is a very good technique that allows simultaneous measurement of vertebral body cortical bone, cancellous bone and combined cortical and cancellous bone. It is the only true measure of volumemetric density (gm/cc), and the only true measure of cancellous bone. This technique has limitations related to expense, radiation exposure, and precision. Newer CT technologies have reduced most of these limitations. As CT is replaced by PET scans and MRI more radiology departments will have more time available on their CT instruments and we may see a resurgence of this technology. AP DEXA is the most standard approach to spine BMD and there is most data avaialble for relating BMD to fracture risk and for serial measurements. The accuracy and precision is excellent. The only drawback relates to the inclusion of posterior elements of the veretbra in the analyses and not just the vertebral body. AP DEXA may be influenced adversely by aortic calcification and osteophytes.

2. The T score relates to the mean of healthy, premenopausal women. As bone density decreases with age increasing numbers of women will indeed have osteoporosis by this T score definition. The mean would probably not reach -2.5 (with spine or hip DEXA) until about age 90 and above. When considering whether or not the osteoporosis is only on the basis of age you should also evaluate the Z score. This relates the subject to others of the same age, gender, and ethnicity. If Z score is -2.0 or lower there should be increasing suspicion that the bone loss is not simply on the basis of age.

3. T scores are available for QCT and they have the same significance as T scores with other bone density modalities.