1. A Breast Assessment and Diagnostic Service (operated in partnership with the BC Cancer Agency)

A team consisting of radiologists, radiology technicians, surgeons, nurses and support staff provides assessment, diagnosis, treatment, follow up, consultation and counselling for women with breast abnormalities. The goal of the program is to ensure that women who have an abnormal mammogram result, or who have detected a breast abnormality receive a diagnosis as soon as possible. This is accomplished through a variety of possible diagnostic procedures, ranging from ultrasound to steriotactic core biopsy or open biopsy. Biopsy procedures are done using local anaesthesia, in a procedure room. A significant amount of supportive care, education and counselling are provided by the nurses working in the program. Approximately 80% of women referred because of breast lumps or other problems will know their diagnosis by the end of their first visit. About 4% of women referred to the program require surgical referrals or referrals to the BC Cancer Agency for treatment of breast cancer. The Vancouver Centre for the Screening Mammography Program of B.C. is co-located at the Women’s Health Centre.

Referrals to the Breast Assessment and Diagnostic Service can be made by calling (604) 875-3705.

2. Breast Health Provincial Outreach Service

This service aims to assist communities throughout BC in establishing diagnostic services for women with breast abnormalities. This includes sponsoring a two week educational program for Family Physicians from throughout the province, who wish to upgrade their knowledge and skills in the area of breast health in order to provide a higher level of care in their home communities.

For further information regarding the Family Practice Breast Fellowship Program please call Dr. Karen Kruse at (604) 875-2952.

3. The Breast Implant Centre

This component offers information, support groups and supportive counselling for women or health care providers with questions or concerns about breast implants. The Centre can provide current information regarding implants through its collection of articles, books and videos.

The Breast Implant Centre can be reached at (604) 875-3225.

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My purpose here is to put the benefits and risks of raloxifene into both a scientific and a practical perspective . My point of view is created by a complex interaction of my nearly menopausal status, my family history of both osteoporosis and breast cancer, my work as a physician who specializes in the treatment of people with osteoporosis and my work as a scientist on the actions of progesterone and on women’s hormone-related quality of life.

Raloxifene is a non-hormonal medication designed to act like estrogen in some parts of the body and to antagonize estrogen’s actions in other parts. Raloxifene decreased spinal fracture rates by 30% compared with placebo over three years in a study of 6,828 menopausal women with low initial bone density or previous spine fracture (1). Raloxifene also decreased the rates at which women got breast cancer over three years by about 65% in menopausal women with low bone density and probably lower than average risk for breast cancer (2). In the near future, raloxifene will also likely be indicated in Canada for treatment of osteoporosis in menopausal women and for the prevention of breast cancer in menopausal women at increased breast cancer risk. Depending on the results of trials currently in progress, it may also be used to prevent heart attacks and as breast cancer adjuvant therapy (to prevent breast cancer recurrence or the development of a second new breast cancer). Therefore, at first glance, raloxifene sounds like the answer to menopausal women’s prayers. Is it?

What led to the creation of raloxifene?

Before answering that question, let’s think about why raloxifene was created. Raloxifene was designed to be one-stop shopping, menopausal “hormone replacement therapy ” (sometimes called “HRT” (. I put “HRT” into quotation marks because I can barely make myself write it. The word “replacement” means that menopausal estrogen levels require fixing before a woman could become normal. That is just plain wrong! Consequently, although it is unfortunately standard language, when I hear someone say “HRT” I experience a wave of anger and disgust. I feel the same way when someone calls me a girl! Both are profound “put downs” for women.

You ask, “But you’re a doctor and you know some women have awful night sweats or a miserable time. How do you help those women if you reject ‘HRT’?” I do treat them, but, what I recommend or prescribe isn’t “replacement ” of something deficient, it’s specific therapy for a specific problem. A better term is “ovarian hormone therapy “(OHT for short). I believe that sound reasons for taking OHT include sleep-disturbing night sweats, early menopause (before age 40, or surgical menopause in a menstruating woman) and low bone density or fractures in a menopausal woman (3). Those of us lucky enough to have none of those should rejoice in our menopause!

Raloxifene was designed to do all the good things estrogen does. It was crafted to correct “estrogen deficiency” and the “problems” this is assumed to cause including osteoporosis, heart attacks, Alzheimer’s disease, dementia and all the other horrible things we fear about aging. I believe that menopause is an inevitable and normal (but not always a pleasant) part of our life cycle as women. After 30-35 years of cyclic, high ovarian hormone production I believe that we need a break. High estrogen levels cause all cells to proliferate (grow), require the body to store energy and demand attention from every organ system in the body. Progesterone interacts with all the cells that estrogen does and slows the growth rate of cells. It is unique in increasing the rate of breathing, raising the core temperature and therefore increasing the metabolic rate as well as stimulating the growth of osteoblast cells that build bone. It seems to me that these demands created by high levels of ovarian hormones are necessary and appropriate during reproductive adulthood but are not needed and may even be detrimental as we age.

Yes, we do lose bone, and we start losing it during the perimenopause when we are still having periods and our estrogen levels are higher than average (4). All of the evidence says to me that women who have built dense, strong bones in childhood and the teen years, and who keep their bones strong until perimenopause can lose the usual amount of bone density during the menopausal transition and not be at increased risk for osteoporosis. That means that preventing bone loss at menopause is important only if the bone density is already low.

What about heart disease? Don’t we know it increases after menopause and becomes a leading killer of women?

My 20 year old son’s response to that question was,”The doctors probably couldn’t figure out why elderly women died so they just wrote that their hearts failed!” Yes, heart disease does increase in older women. But why blame menopause or the normal decrease in estrogen levels when there is no increase in heart disease rate either at menopause (5) or related to hormone levels? Heart disease increases gradually after age 35 in all of us and more rapidly if we have genetic or lifestyle risks. The good news is that we have lots of things we can do to prevent heart disease. These include making sure we don’t have, or are getting treatment for, high blood pressure, abnormal lipid levels or diabetes. We can also exercise regularly, avoid becoming overweight (6), and not use cigarettes. There are no good scientific grounds to believe that estrogen therapy would prevent heart attacks unless the randomized, controlled trial which is now in progress as the “Women’s Health Initiative” in the U.S.A. eventually shows it. A randomized, double blind placebo-controlled study was recently published showing no OHT-related prevention of more heart attacks in women with existing heart disease (7). That study, called HERS for short, involved 2763 women aged 65-80 with coronary heart disease who were randomized to conjugated equine estrogen (CEE, Premarin 0.625 mg) and medroxyprogesterone acetate (MPA, Provera 2.5 mg) daily or identical placebos (containing no active medicine) for four years. The main study outcomes were death from heart disease, or new heart attack. This study showed no difference in either outcome with OHT when compared to the placebo group (7). The HERS results confirmed early randomized placebo controlled trials of high dose CEE treatment in men with heart disease by showing, not only no heart disease prevention, but also increased death and serious diseases related to abnormal blood clotting (8,9).

Back to the creation of raloxifene

It was made not only to do the good stuff we believe estrogen does (prevent bone loss, prevent heart attacks) but also to not do any of the bad things. Creation of a compound that acts against estrogen acknowledges that it is linked to abnormal vaginal bleeding and endometrial cancer and to breast cancer. What is interesting is that progesterone’s natural job is to counterbalance the proliferation (or cancer-promoting) effects of estrogen. Maybe we don’t need a designer “HRT” to do that?

Old epidemiological studies in two different groups of women indicate that women who had chronically non-ovulatory cycles (meaning that little or no progesterone was produced) and whose estrogen levels were normal or high were at increased risk for breast cancer (10,11). We also know that progesterone applied as a cream to the breast in a random, double blind study decreased the breast cell proliferation caused by normal or high levels of estrogen (12). Perhaps, changing the focus from “estrogen deficiency” at menopause to “progesterone deficiency” before menopause would be helpful!

Human studies using raloxifene

I consider raloxifene to be important because it prevents both osteoporotic fracture and breast cancer. That raises the question, “Why shouldn’t all menopausal women take raloxifene?” Every medication has unwanted adverse effects as well as real personal and dollar costs. Therefore, before we can adequately consider who should take raloxifene we must review its side effects and cost.

All of the published studies currently providing new information about Raloxifene were designed, performed and paid for by the company that is marketing it. Therefore, it is wise to be skeptical. Raloxifene is a prime product of a very large multinational profit making pharmaceutical company. What we now know about Raloxifene’s side effects is far less than will eventually be known after it has been used for five or ten years by community women who are less selected and more variable than women who have taken part in the published studies.

Side Effects of raloxifene

Raloxifene side effects we now are sure about are thrombo-embolism (abnormal clotting of blood with/without clots moving through the circulation), hot flashes/night sweats and leg cramps. It is quite clear that Raloxifene is similar to estrogen in causing abnormal clotting in about one percent of women (significantly more than 0.3% on placebo, P = 0.002) (1). That risk may be much higher in women with a family or personal history of blood clotting, especially those who have had thrombophlebitis (inflammation of a vein caused by a blood clot obstructing flow) while taking the birth control pill or during pregnancy. Those women should not take raloxifene or oral estrogen. (Patch or gel estrogen probably has less blood-clotting effect and could possibly be used in low doses in women at moderate risk for thrombo-embolism).

The hot flash/night sweat side effect of raloxifene is noted in all human studies. Commonly women close to menopause want therapy to treat hot flashes. Most trials have excluded women from participation who experience troublesome hot flashes. None of the published studies really give a good idea about how severe these symptoms are, whether they get worse or better with longer use of raloxifene, whether they bother women a lot or a little. We do know that significantly more women randomly assigned to raloxifene than those assigned to placebo quit the studies before they were over (1).

Monitoring Women’s Experiences

In the raloxifene studies, as in most published studies the methods used to assess women’s hormone-related quality of life are inadequate. Studies report that they routinely “queried participants at every visit about adverse events” (2). That rather off-hand way of monitoring does not accurately assess the whole range of women’s experiences, would gather only the most severe symptoms, and only indicates whether they experienced any hot flashes or not. Furthermore, hot flashes are called a “non-serious adverse event”(1). What we really want to know is whether daytime hot flashes were frequent and severe or night sweats wakened women from sleep.

We do not know whether the 10% of women reporting hot flashes on raloxifene therapy were bothered by them. We do know that more women in the raloxifene group than the placebo group withdrew because of hot flashes (P < 0.001) (2).

Raloxifene does not increase vaginal bleeding, or cause stimulation of the endometrium (uterine lining) (12), in contrast to the rare but very serious endometrial cancer caused by its cousin, tamoxifen. Tamoxifen is the drug that is currently commonly used as adjuvant therapy for breast cancer. It was initially felt to have anti-estrogen effects on the endometrium but is now known to cause endometrial cancer (14).

Raloxifene also seems to cause little or no breast tenderness or pain, in contrast to approximately 20% who experience breast pain while taking estrogen therapy (15). About 13% of women on raloxifene, compared to 11% on placebo, experienced a flu-like syndrome and about 5% experienced some fluid retention or swollen feet compared with 4% of those on placebo. A few more women treated with raloxifene also developed diabetes mellitus, but the changes in fasting blood sugar levels were not different between groups.

Therefore, besides the serious risk for blood clotting problems, and an increase in night sweats, raloxifene appears to have few side effects.

What to do before beginning raloxifene

Before starting any new medication, I believe that it is important to keep a daily record of your experiences[2]. Two weeks or a month of record keeping before and after starting a new therapy will allow you to personally assess any changes, either positive or negative that are related to the new therapy.

What does Raloxifene cost?

It is currently priced at $54.02 for 24 tablets or $2.25/day (before dispensing fees) in Canada. That cost is substantially more than any estrogen preparation, than estrogen plus progesterone or the bisphosphonates which are used to treat osteoporosis. Unless health insurance plans or extended health insurance covers this, it is likely that many non-affluent women will be unable to afford raloxifene.

Who may want to take raloxifene?

First of all, it should be taken for a good reason. Because raloxifene is not appropriate for early menopause nor for treatment of night sweats, osteoporosis risk factors are the primary reason for its use. Important risk factors for osteoporosis and fracture include a family history of osteoporosis, past abnormal menstrual cycles, being chronically underweight, having used cigarettes in the past or currently smoking, chronic low exercise and low calcium and vitamin D intakes. A bone density measurement lower than one standard deviation below peak bone density (T score lower than -1) is another important osteoporosis risk factor.

Even if you have a good reason for menopausal therapy, what you choose to take depends on many factors. The first may include whether it is made in animals (as is Premarin), is chemically made or is “natural” (meaning identical to the hormone the body made before menopause, which is true of progesterone [Prometrium], and the estradiol preparations, Estrace, Estraderm, Vivelle or Estra Gel(. Another consideration is whether you prefer to have vaginal bleeding like menstrual cycles (or would much rather not]. Also, you may gag when taking any pills, or get a rash from patches or cremes. Finally, you may or may not have much money to spend on therapy.

You may choose estrogen and progesterone therapy for prevention of fractures, for example, because it is less expensive than raloxifene or the bisphosphonates (non-hormonal family of medications that decrease bone resorption and fracture – etidronate [Didronel, Didrocal], alendronate [Fosamax], or the soon-available risedronate [Actonel]).

You may also choose ovarian hormone therapy because, besides osteoporosis risk, you need something that will treat night sweats. If you are at risk for osteoporosis and are experiencing night sweats, but you have had blood clots and therefore should not take estrogen or raloxifene, you may decide to take a bisphosphonate combined with progesterone. The bisphosphonates prevent fracture.

Progesterone treats hot flashes (16) and increases bone formation (17). You can combine any of the bisphosphonates with progesterone (medroxyprogesterone, Provera 10 mg/d, or oral micronized progesterone, Prometrium 100 mg , 3 at bedtime daily). Clinical works suggest the increase in bone density is greater with bisphosphonates plus progesterone than with bisphosphonates alone. Finally, if you have an increased risk for breast cancer as well as risks for osteoporosis, if you are several years after menopause and have minor or no hot flash symptoms, raloxifene may be the right treatment for you.

Overview

In summary, raloxifene was created to be a medication that acted like estrogen for the bones and heart and against estrogen for the uterus and breasts. It does not treat hot flashes and may make them worse and is quite costly at about $2.50/day. However, it causes minimal flow or breast tenderness symptoms. Large randomized controlled trial data show that it will both prevent spinal fractures and breast cancer (although the latter is not an approved use for it). Studies of raloxifene and heart disease are currently being conducted. The Raloxifene Use and The Heart (RUTH) trial is a large (10,000 women) randomized placebo-controlled study of heart disease prevention by raloxifene in women with existing heart disease or three risk factors (18). Although raloxifene therapy lowers total cholesterol and LDL cholesterol it has no significant effect on the good HDL cholesterol (19, 20, 21). Furthermore, a double-blind placebo-controlled study of raloxifene or high dose CEE and vascular disease in menopausal monkeys showed no vascular prevention (22).

Menopausal women in general do not need treatment

We need healthy, meaningful lives. But if we have a need to prevent osteoporosis and if our risks for breast cancer are increased, it is appropriate to consider raloxifene.

Jerilynn Prior is a Professor of Endocrinology at the University of British Columbia and an internationally known expert on women’s health.

References

1. Ettinger B, Black DM, Mitlak BH, Knickerbocker RK, Nickelsen T, Genant H, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: Results from a 3-year randomized clinical trial. JAMA 1999; 282:637-645.
2. Cummings SR, Eckert S, Krueger KA, Grady D, Powles TJ, Cauley JA, et al. The effect of raloxifene on risk of breast cancer in postmenopausal women. Results from the MORE randomized trial. JAMA 1999; 281:2189-2197
3. Prior JC. Menopause. In: Gray J, Johnson G, editors. Therapeutic Choices. Ottawa, Ontario, Canada: C.K. Productions, 1995:468-477.
4. Prior JC. Perimenopause: The complex endocrinology of the menopausal transition. Endocr.Rev. 1998; 19:397-428.
5. Matthews KA, Meilahn E, Kuller LH, Kelsey SF, Caggiula AW, Wing RK. Menopause and risk factors for coronary heart disease. N.Engl.J.Med. 1989; 321:641-646.
6. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B, Monson RR, et al. Prospective study of obesity and risk for coronary heart disease in women. N.Engl.J.Med. 1990; 322:882-890.
7. Hulley S, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. J.Am.Med.Assoc. 1998; 280:605-613.
8. Coronary Drug Project Research Group. Coronary drug project: initial findings leading to modifications of its research protocol. J.Am.Med.Assoc. 1970; 214:1303-1313.
9. Coronary Drug Project Research Group. Coronary drug project: findings leading to the discontinuation of the 2.5 mg/day estrogen group. J.Am.Med.Assoc. 1973; 226:652-657.
10. Coulam CB, Annegers JF, Kranz JS. Chronic anovulation syndrome and associated neoplasia. Obstet.Gynecol. 1983; 61:403-407.
11. Cowan LD, Gordis L, Tonascia JA, Jones GE. Breast cancer incidence in women with a history of progesterone deficiency. Am.J.Epidemiol. 1981; 114:209-214.
12. Chang KJ, Lee TTY, Linares-Cruz G, Fournier S, de Lignieres B. Influence of percutaneous administration of estradiol and progesterone on human breast epithelial cell cycle in vivo. Fertil.Steril. 1995; 63:785-791.
13. Fugere P, Scheele WH, Srikanth KR, Anglin G, Strack TR, Nauden AB, et al. Raloxifene does not stimulate the uterus in postmenopausal women as compared to continuous combined hormone replacement therapy following 24 months of treatment. Fertil Steril 1999; 72:S182-S182 Abstract.
14. DiSaia PJ. Hormone-replacement therapy in patients with breast cancer. A reappraisal. Cancer 1993; 71:1490-1500.
15. Prince RL, Smith M, Dirk IM, Price RI, Webb PC, Henderson NK, et al. Prevention of postmenopausal osteoporosis: a comparative study of exercise, calcium supplementation, and hormone-replacement therapy. N.Engl.J.Med. 1991; 325:1189-1195.
16. Paterson MEL. A randomized double-blind cross-over trial into the effect of norethisterone on climacteric symptoms and biochemical profiles. Br.J.Obstet.Gynaecol. 1982; 89:464-472.
17. Prior JC. Progesterone as a bone-trophic hormone. Endocr.Rev. 1990; 11:386-398.
18. Barrett-Connor E, Wenger NK, Grady D, Mosca L, Collins P, Kornitzer M, et al. Hormone and nonhormone therapy for the maintenance of postmenopausal health: the need for randomized controlled trials of estrogen and raloxifene. J.Women’s Health 1998; 7:839-846.
19. Delmas PD, Bjarnason NH, Mitlak BH, Ravoux A-C, Shah AS, Huster WJ, et al. Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women. New England Journal of Medicine 1997; 337:1641-1647.
20. Draper MW, Flowers DE, Huster WJ, Neild JA, Harper KD, Arnaud CD. A controlled trial of raloxifene (LY139481) HCL: impact on bone turnover and serum lipid profile in healthy postmenopausal women. J Bone and Mineral Research 1996; 11:835v840.
21. Khovidhunkit W, Shoback DM. Clinical effects of raloxifene hydrochloride in women. Ann.Int.Med. 1999; 130:431-439.
22. Khovidhunkit W, Shoback DM. Clinical effects of raloxifene hydrochloride in women. Ann.Int.Med. 1999; 130:431-439.
23. Clarkson TB, Anthony MS, Jerome CP. Lack of effect of raloxifene on coronary artery atherosclerosis of postmenopausal monkeys. J.Clin.Endocr.Metab. 1998; 83:721-726.

The post Consider Raloxifene appeared first on BC Diabetes Foundation.

The first was the Gerald S. Wong Award earned for his exceptional efforts in assisting individuals with diabetes. The second was the Distinguished Service Award. He was chosen by his peers to receive this award for his contributions to the field of endocrinology.

Dr. Dawson has been a director of the B.C. Endocrine Research Foundation since it began over two and a half years ago. He has been involved with the Canadian Diabetes Association for many years and was a leader in educating general physicians about diabetes. As a MD and a PhD Dr. Dawson is very committed to research and education while maintaining his medical practice.

The post Congratulations to Dr. Keith Dawson appeared first on BC Diabetes Foundation.

Overactivity of the thyroid gland is called hyperthyroidism or thyrotoxicosis. Individuals with this condition may experience a number of symptoms including fatigue, weight loss, tremor, palpitation, sweating, heat intolerance, itch, frequent bowel movements, disturbance of menstrual function, weakness, skin rash or eye symptoms such as pressure, or double vision. There are two common blood tests ordered by family doctors to confirm the presence of hyperthyroidism. The first blood test is TSH (thyroid stimulating hormone). TSH is the signal sent by the pituitary gland to stimulate the thyroid gland. In nearly all cases of hyperthyroidism the TSH is very low or undetectable. The normal range for TSH is 0.3-5.5. The second test is the free T4 (thyroxine). This is the measurement of the amount of free thyroid hormone secreted by your thyroid hormone that is circulating in the blood. The normal range for free T4 is between 10-20.

There are four main causes of hyperthyroidism.

1. Graves Disease (diffuse toxic goitre). This condition is caused by overactivity of the immune system (autoimmunity) in which the body produces an antibody that stimulates the thyroid gland to overwork. The reasons why the immune system becomes overactive are unknown, though there is a genetic susceptibility (much more common in Chinese and South Asians) and appears to be more common following traumatic life events such as immigration, divorce or bereavement. Graves Disease does not get better on its own and therefore requires treatment. These treatments are discussed on below.

Graves Disease may also affect the eyes with a condition called Thyroid Orbitopathy – this is associated with prominence, swelling, double vision and tearing. Rarely the eye problem may be serious and require special treatment at the Thyroid Orbitopathy Clinic and the Vancouver General Hospital Eye Care Centre (phone (604) 875-4555). The skin of the lower legs may also rarely be affected with a thickening called myxedema – this too requires special treatment by a dermatologist. Treating the overactivity of the thyroid associated with Graves Disease has no effect upon either Thyroid Orbitopathy or myxedema.

2. Sub-acute (painful, viral) thyroiditis. This condition is caused by viral infection. Common viruses known to cause this problem are the influenza virus, adenoviruses and Coxsackie B virus. These are usually transmitted by droplet in the air and not by physical contact. The inflammation caused by the virus often produces pain and swelling in the thyroid gland (discomfort in the front of the neck which may radiate to the throat or ears). This pain usually responds to anti-inflammatory medication such as ibuprofen. The inflammation releases stored thyroid hormone producing hyperthyroidism. The symptoms of overactive thyroid may last up to 3-4 weeks but settle without specific treatment. A medication to slow the heart beat and reduce tremor (propranolol) is sometimes used. In up to 40% of cases the thyroid gland may become transiently underactive (hypothyroidism) during the recovery phase and may require treatment with replacement thyroid hormone (synthroid or eltroxin) for 6 to 12 months.

3. Silent thyroiditis (painless or postpartum thyroiditis). This condition, like Graves Disease, is also caused by the immune system but instead of there being an antibody that stimulates the thyroid gland to increase production of thyroid hormone, inflammation of the thyroid gland leads to the release of stored thyroid hormone. The natural history of silent thyroiditis is very similar to sub-acute thyroiditis described above (individuals first have overactivity then normal activity followed occasionally by underactivity of the thyroid gland), but is not associated with pain in the neck. This condition gets better without specific treatment. Silent thyroiditis occurs in up to 20% of women in the first year after childbirth and may recur with subsequent pregnancies.

4. Toxic multinodular goitre. This is a common cause of hyperthyroidism in older populations. The susceptibility to this condition is familial but the genetics are not clearly understood. In this condition one or more lumps in the thyroid gland grow slowly over many years and eventually produce an excessive amount of thyroid hormone. This condition does not get better on its own and therefore requires treatment. The commonest treatment is radioactive iodine which is described below. Surgical treatment with removal of most of the thyroid gland is also a valid option.

OTHER THYROID TESTS

You may be asked to undergo a study in the Nuclear Medicine Department at Vancouver Hospital which is situated in the Laurel Pavilion, 899 W12th Avenue on the ground floor. The phone number is (604) 875-4611 and the fax (604) 875-5009. This test will usually involve drinking a small amount of clear fluid containing a trace amount of radioactive iodine and then returning there 4 and 24 hours later for a measurement of the radioactivity in the thyroid gland. Alternatively, you may receive an injection of a different radioactive isotope, pertechnetate, (also in trace amounts) and a picture of the thyroid gland taken within 20 minutes. Other Nuclear Medicine departments also offer these tests.

TREATMENT OF THE OVERACTIVE THYROID GLAND

The conditions of Silent and Sub-Acute Thyroiditis, described above, get better on their own and do not require specific treatment. Symptomatic treatment with propranolol to slow the heart beat or reduce shaking and antib-inflammatory medication b(or prednisoneb) for pain may be required temporarily.

1. Antithyroid medication. This treatment is used almost exclusively for Graves Disease. Antithyroid medication in Canada comes in two forms: methimazole “Tapazole” and propylthiouracil “PTU”. In other parts of the world carbimazole, a very close relative of methimazole, is often used. Tapazole is used in most cases except during pregnancy when PTU is preferred (PTU is generally regarded as safe in pregnancy providing doses of 300 mg per day are not exceeded). All three medications work in the same manner, by interfering with the production of thyroid hormone within the thyroid gland. These medications take 4 to 6 weeks to reach full effect and then remain effective as long as the medication is taken. The initial dose will be decided upon by the doctor and will then be adjusted periodically (usually every 1 to 3 months) based on the results of the free T4 level in the blood. Usually the aim is to bring the free T4 level between 15 and 20. Typically treatment is given for a year and in the usual case the dose is gradually reduced as the thyroid gland shrinks during treatment and therefore less medication is required. After 12 months of treatment the medication is stopped and providing the patient feels well the free T4 level is remeasured 3 months later. In 50% or more of the cases the hyperthyroidism will not recur. In a large minority however, the condition does recur. It is difficult to predict which patients will have a recurrence but those who have a big thyroid gland at the beginning of treatment or who are very overactive or have been overactive for a number of years are more likely to recur. If recurrence occurs then the doctor usually recommends the second therapy – radioactive iodine discussed below.

Antithyroid medication has three side effects – the first two common and easily treated and the third rare and potentially serious. All resolve with cessation of treatment. Excessive dosing of the thyroid hormone may can cause underactivity of the thyroid gland (hypothyroidism) which may be manifest as weight gain, fatigue, puffiness around the face, cold intolerance – most are quite the opposite to the symptoms of hyperthyroidism. If you feel that your thyroid is going low you should have your free T4 tested even if this is not one of the scheduled tests.

The second side effect is a skin rash. This occurs in about 10% of patients and typically appears as “hives” and may be itchy. This rash does usually not go away unless the medication is stopped. Usually radioactive iodine is recommended should this occur, although in some cases the other antithyroid medication can be tried, though the chances of recurrence of the rash are very high.

The third side effect is extremely rare and potentially life-threatening if it is not recognized and treated appropriately – it occurs in less than 1 in 1,000 cases. This complication is called agranulocytosis and is a very low white blood cell count. White cells are involved in preventing infection. People with agranulocytosis develop high fevers, chills and often have a sore throat. If these symptoms occur you should see you family doctor immediately who will order a complete blood count (CBC). All of these side effects will disappear with cessation of the therapy.

2. Radioactive iodine. This treatment is used for either Graves Disease or toxic multinodular goitre (or for solitary toxic adenoma, a rare condition not discussed elsewhere). Iodine is incorporated into thyroid hormone being produced in the thyroid gland. If the incorporated iodine is radioactive the released gamma rays will damage the thyroid gland and lead inevitably to the destruction of the thyroid gland. For this reason radioactive iodine therapy (in a dose 100 times that used for the thyroid test mentioned above) is highly effective and need be given only once usually. Fewer than 10% patients require a second dose.

Because it leads to the destruction of the thyroid gland, thyroid function will eventually become low and will never recover. For this reason every individual who receives radioactive iodine should assume that he or she will eventually need to take replacement thyroid hormone (thyroxine) every day for the rest of his or her life. Most patients require replacement therapy within 6 months and almost every patient within 10 years.

Radioactive iodine is taken in a small glass of water, occasionally as a tablet and rarely by injection. It will not cause an individual to glow in the dark and will have completely left their system within 3-4 days. During that time an individual should not cuddle a baby closely to the neck. Other social activities may be maintained without risk or fear of contamination. Radioactive iodine must not be used if an individual is pregnant or may be pregnant. Women breast feeding must stop for 4 to 5 days after taking the treatment before resuming nursing.

3. Thyroid Surgery. For individuals with hyperthyroidism, surgery is reserved for difficult cases during pregnancy, for toxic multinodular goitre or toxic solitary nodule. Most individuals spend only 1 night in hospital post-operatively.

Dr. Tom Elliott is an active researcher and educator and the President of the BC Endocrine Research Foundation. He is also a busy physician treating individuals with endocrine disorders.

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The cover article on raloxifene by Dr. Jerilynn Prior presents a very well rounded discussion of the history and the use of raloxifene for treating osteoporosis and reducing the risk of breast cancer. Dr. Prior manages to put raloxifene in proper perspective as a therapeutic agent with respect to benefits, risks and cost.

Dr. Tom Elliott provides a comprehensive introduction to thyroid health problems. He discusses both hyperthyroidism and hypothyroidism, their diagnoses and treatment.

Both Dr. Prior’s and Dr. Elliott’s articles are excellent starting points for someone who needs some background in these areas. It is always helpful to know what questions to ask and what to expect if dealing with a health challenge and dealing with a physician.

We have also taken this opportunity to congratulate one of our directors, Dr. Keith Dawson for his recent awards for distinguished contributions to research and education in diabetes in Canada.

In addition, there is an article on the Breast Health Program at Children’s and Women’s Health Centre of BC. This is a short introduction for those who aren’t familiar with the program and contact numbers for those seeking more information.

I hope you enjoy this last issue of our current publication year. It has been a great first year and the response to the newsletter has been very positive. We look forward to continuing what we feel is a valuable tool for education.

The post From the Editor appeared first on BC Diabetes Foundation.

The launch was held at the Sassafras Room at Vancouver Hospital on July 29, 1999 and was well attended by the media. The first major coverage was an article in the Vancouver Sun that came out on August 16. I remember well that Monday morning because the foundation phone never stopped ringing and I was deluged by over fifty calls requesting the video. Subsequent articles have appeared in other publications and the orders continue to roll in. The response really has been overwhelming and reaffirms our belief that the video will play a major roll in assisting women and their doctors to understand the complex experiences that can occur at this time in a women’s life. As Dr. Prior said, “I’ve tried for at least five years to teach physicians about this change and have not been very successful. I decided to connect with women instead in hopes that doctors will catch up.”

Dr. Thomas Elliott, president of the B.C. Endocrine Research Foundation, attended the launch and made opening remarks. I had an opportunity to speak with Dr. Elliott afterwards and he had this to say. “I am really excited about the launch of this new video. I feel it will help greatly in the in the dissemination of important information relevant to every woman’s health.”

Dr. Penny Ballem, one of B.C.’s best-known women’s health experts spoke very highly of Dr. Prior’s work. “Jerilynn has slowly and methodically built her scientific evidence base. Changing dogma is difficult, especially for a woman in an area that has been primarily researched by men.”

The Daily Perimenopause Diary, 1990 is included with the video. Given the lack of accurate prospective, women-centred data about what the normal perimenopause is like, women need to be able to make sense of their own experiences. For this reason, Dr. Jerilynn Prior developed this diary as a way in which women can capture the whole range of their experiences: from vaginal bleeding to interest in sex, from breast tenderness to feelings of self worth. A portion of the video is devoted to helping women use this diary to better understand their own experiences.

Along with a better understanding women will also have a very detailed and structured tool for documenting and presenting this information to their doctors. The fact that estrogen levels appear to rise rather than fall during the perimenopause has immense therapeutic implications. It represents a full 180 degree turn in how women and physicians perceive and treat symptoms of the perimenopause. Rather than prescribing estrogen (a common solution in the past) which may simply compound the problems it is necessary to think in terms of the balance between estrogen and progesterone. When estrogen levels are high, cyclic progesterone therapy will bring the balance back to normal.

Although the experiences of perimenopause may be difficult, they will ease. Dr. Prior asserts, “We developed the video and diary to help women survive this confusing but normal stage of life.”

&mdash Dr. Eric Norman PHD

Dr. Norman is the Secretary of the B.C. Endocrine Research Foundation and Editor of the Quarterly Newsletter.

Produced in co-operation with Biomedical Communications, UBC, “The Puzzle of Perimenopause” was funded by the B.C. Centre of Excellence for Women’s Health, which is located at B.C.’s Women’s Hospital and Health Centre. The B.C. Centre of Excellence is one of five Canadian research centres dedicated to improving women’s health.

The post The Puzzle of Perimenopause – an Educational Video appeared first on BC Diabetes Foundation.

Type 1 diabetes or insulin-dependent diabetes mellitus, is caused by the destruction of the beta cells, the cells in the pancreas which produce insulin. As insulin levels fall, blood sugar (glucose) rises. The destruction of the beta cells is mediated by the immune system. The trigger for this process is unknown but is felt to be related to viral infections and/or exposure to various antigens in the environment. By the time diabetes develops, fewer than 5% of the beta cells remain functional and within 5 years there is zero function. In the first year or two after diagnosis of diabetes the insulin requirement may decrease dramatically or even disappear. This is called an insulin “honeymoon” and is related to rejuvenation of some of the near-dead insulin secreting cells. Unfortunately, these “honeymoons” are shortlived, lasting 3-12 months.

The problem with diabetes is that if blood sugar is allowed to be significantly above normal for many years irreversible damage to the eyes, kidneys, nerves and blood vessels may result leading to significant disability or even death. If blood sugar can be kept close to normal throughout life, not only will you have very good quality of life but your life expectancy should be no different to people who do not have diabetes. The key to controlling diabetes is to learn to closely regulate diet, exercise, insulin administration and blood glucose testing.

Insulin

Insulin causes glucose to enter cells where it then provides energy for metabolism and growth. Insulin need only be present in fairly small amounts for this to occur sufficient to maintain life. However, if insulin levels are allowed to fall further the liver produces ketones which if allowed to accumulate cause acidosis, severe illness and even death. In the pre-insulin era (prior to 1922) all patients with your type of diabetes were dead within 12 months because of the overproduction of ketones. It is therefore necessary that small amounts of insulin be present in your blood at all times to prevent ketone production. This is achieved in clinical practice by giving 1 or more (usually 2) shots of long-acting insulin.

Long-acting insulins are called variously N (NPH), U (or ultralente), or L (lente). They typically enter the bloodstream after being injected into the skin at about 1 hour, peak at 4-10 hours and generally leave the system at around 14-20 hours. The dose of long acting insulin is generally adjusted so that your blood sugar is in the desirable range after periods of fasting or in the late afternoon before the evening meal.

Short-acting insulin comes in 2 forms – R (or regular, fast, soluble, clear, or Toronto) which enters the bloodstream after about 30 minutes, peaks at 2-4 hours and is gone by 6-8 hours and H (humalog) which enters the bloodstream at about 10 minutes, peaks at 45-90 minutes and is gone from the system in 3 to 4 hours. Short-acting insulin is generally given prior to a meal in doses sufficient to produce a normal sugar before the next meal (R) or 2 hours after the meal (H). The dose of short-acting insulin is adjusted based on a) the size and nature of the meal about to be taken, b) how high the blood sugar is prior to the meal, c) the expectation of exercise following the meal and d) presence or absence of illness (your insulin is generally slightly less effective and therefore you need higher doses). Because short acting insulin peaks generally after the stomach is empty and therefore peaks when there is little food to be absorbed, it is necessary to take snacks between meals. Therefore 3 snacks a day are generally necessary – between mid-morning, mid-afternoon and before bed. Without these snacks low blood sugar (hypoglycemia) may occur. Hypoglycemia is potentially very serious as sugar is the fuel of the brain. Without adequate fuel the brain works less well or may stop working completely. This may cause lack of concentration, decreased attention, confusion, seizures, coma or even death. Hypoglycemia is treated by consuming small quantities of sugar of highly refined carbohydrate.

Blood Glucose Testing

Blood glucose testing is necessary to determine the correct dose of insulin, the adequacy of the diet and the effects of exercise or illness upon blood sugar. Testing blood before each meal, at bedtime daily and at 3 a.m. once a week or so is ideal. In practice blood sugar may be tested less frequently but only once good blood glucose control is well established. Blood sugar may also be measured after meals, though it is difficult to control blood sugar swings after meals unless you take H insulin which currently is rather expensive and generally not indicated for most people with Type I diabetes. Blood sugar goals before meals should be 4-7 mmol/L (70-130 mg/dl). Bedtime goal should be 5-8 (90-145) and at 3 a.m. >3.5 (80). If you decide to test 2 hours after meals reasonable goals are <7 (125). Your physician will assess your longterm blood sugar control using a test called HbA1c. The level of HbA1c is a guide to blood glucose control over the previous 8-10 weeks. Values in people who do not have diabetes are 0.048-0.062. In people with Type I diabetes values < 0.073 are regarded as optimal, 0.073-0.080 as moderate, 0.081-0.090 fair and > 0.090 poor or compromised. It is well established that the risks of longterm complications of diabetes in patients with optimally controlled blood sugars are half those of patients with poorly controlled blood sugar.

Living with Diabetes

Over the periods of weeks and months you will learn to live with your diabetes. This will be a slow process of gradual adaptation and it will be tough but ultimately will bring rewards to you. Your physician and members of the diabetes care team will work closely with you to help you become master of your diabetes and lead a full and healthy life.

Insulin Adjustment

Once your diet and exercise program has become stabilized you will be in a position to consider adjusting insulin to produce sugars in the goal range. Before making any insulin adjustment you should have tested your blood sugar 4 times a day and once at 2-3 am during a minimum 4 day period. You should then calculate the average blood sugar at each time of day and compare those averages to your blood sugar goals. Flag any averages which are outside the goals and determine which outlier is the furthest from the goal. Then adjust the insulin dose that most likely affects that outlier blood sugar. For instance, if you are taking a shot of long-acting insulin at breakfast and bed and a shot of short-acting insulin with breakfast and dinner and your worst high blood sugar is at bedtime you should adjust your short-acting insulin before dinner. Adjust your insulin by increasing (or decreasing) the insulin by 10% rounding up or down as necessary. For example, if you had been taking 10 units of short-acting insulin before dinner you would increase it to 11. On the otherhand, if you were running low at bedtime you would decrease by 1 unit at least. On same insulin regime if you were high at breakfast but okay at 3 a.m. you would increase your bedtime long-acting; if you were high at lunch you would increase your short-acting before breakfast; if you were high at dinner you would increase your long-acting before breakfast. If you were high at 3 a.m. but okay at bed and breakfast you should probably not make any changes. An alternative to increasing your insulin would of course be decreasing your size of the most relevant meal i.e. the proceeding meal (or snack perhaps). You should not make any insulin adjustments if you have had any severe lows during the last several days or if your routine had been very unusual. Insulin adjustment is termed proactive. The intention is produce better blood sugars in the future rather than fixing them right now. See Fig1 and the analysis that follows below for an illustration of how you might record and analyze your blood sugars.

Fig 1 Blood Sugar Tabulation

Blood sugar targets: 5-8 before meals and bed, and more than 5 at 0300 hrs.

Example 1
	before b’fast	before lunch	before dinner	before bed	3 AM	Comments
Monday	8.9	13.4	4.2	11.4
Tuesday	12.1		8.8	9.8
Wednesday		10.2		7.6		at Canuck game
Thursday	6.8		7.9	7.2
Friday	9.4	14.6	11.6	10.8	14.5	spaghetti at mom’s
Saturday	10.8	8.4	5.4	10.2
Sunday	8.1	10.9		8.9
Averages	9.4	11.5	7.6	9.4	14.5
Example 2
	before b’fast	before lunch	before dinner	before bed	3 AM	Comments
Monday	13.6	8.6	3.8	13.4
Tuesday	18.7	9.6	6.6	4.4
Wednesday	10.4	8.8	21.6	17.0		cinnamon bun at Max’s
Thursday	15.8	19.7	4.3	10.3
Friday	9.1	12.7	7.1	13.3
Saturday	14.4	6.4	16.3	6.5
Sunday	12.9	8.4	4.9	2.8	14.0	swimming after dinner
Averages	13.6	10.6	9.2	9.7	14.0
Example 3
Monday	8.5	15.4	9.3	14.4
Tuesday	10.6	15.8	14.0	18.4
Wednesday	4.2	7.4	16.8	12.2
Thursday	18.6	16.4	15.8	5.3
Friday	3.5	11.1	2.9	12.8	4.8	training at Gold’s
Saturday	3.8	4.1	12.1	13.0		training at Gold’s
Sunday	2.2	12.8	5.3	7.7		training at Gold’s
Averages	7.3	11.9	10.9	12.0	4.8
Example 4
Monday	5.7	2.4	12.8	11.4
Tuesday	11.6	3.9	14.9	6.9	5.0
Wednesday	4.9	3.4	20.6	14.6
Thursday	8.6	3.1	13.7	9.0
Friday	14.8	5.5	15.0	8.5
Saturday	5.5	5.1	9.8	6.1
Sunday	8.1	2.1	14.2	7.0		LO11am mowing yard
Averages	8.5	3.6	14.4	9.1	5.0

Analysis of Fig. 1

Example 1: There are no lows, the numbers are fairly consistent and the average that is furthest from desirable is at lunchtime. Appropriate actions could be either increase short acting insulin before breakfast or reduce the size/type of breakfast or mid-morning snack.

Example 2: There are no lows, the numbers are somewhat consistent, and the average that is most out of range is breakfast. Appropriate action would be to increase evening long acting insulin and test once or twice at 0300 hrs in the following week to make sure there are no lows at that time.

Example 3: Although none of the averages are out of range, the 3 consecutive breakfast lows following training the night before are dangerous. This was despite bedtime readings on the same nights being high. Appropriate action would be to decrease evening long acting on training nights.

Example 4: Lunch readings are consistently low. There was one mild low at 1100 hrs as well. Decrease breakfast short acting insulin or take a bigger breakfast or mid-morning snack.

“One-off” high blood sugars

The notion of “fixing the blood sugar right now” is best tackled by using a “sliding scale”. This refers to taking extra short acting insulin at any one time of day to nominally lower your blood sugar into the goal range. For instance if it is breakfast time and your blood sugar is 12 (goal 4-7) and you normally take 8 units of short acting for breakfast you may decide to take an extra 2 units to do so. There is no perfect sliding scale for every person with diabetes. One very conservative approach to sliding scale follows:

“One-off” high blood sugars

An alternative to taking extra insulin if your sugar is above your glycemic goal would be to do a short amount of exercise. It is fairly simple to learn how much exercise is required to bring your blood sugar down. For instance, on a stationary bicycle for 10 minutes may drop the blood sugar anywhere between 1-4 mmol?L. The virtue of exercise over sliding scale insulin is that you will never suffer from rebound phenomenon. Rebound phenomenon is where you take more insulin than is desirable, then go low and then the blood sugar bounces up as your body struggles to produce glucose. The body’s tendency to prevent hypoglycemia is called counter-regulation and involves the secretion of a number of hormones including glucagon, adrenaline, cortisol and growth hormone. The rebound effects from counter-regulation may last for up to 24 hours after a severe low blood sugar.

“Rules” of Insulin Adjustment

Before you follow the rules below you must be testing frequently and following your meal and exercise plan closely. Generally only one insulin should be changed at a time. Increase or decrease insulin by 10% (or by1 unit if 10% is less than 1 unit). The rules below pertain to individuals taking regular short acting insulin. If you take ultra short acting insulin the rules are slightly different – these are appended later.

Lows

Lows always take precedence over highs. Even if you are high some or a lot of the time, If you have lows that are occurring consistently you must avoid them first. If lows are due to exercise, consider only changing an insulin dose (or increase meal or snack) for that specific day or time of day only.

• Breakfast lows: decrease evening long acting insulin
• Lunch lows: decrease breakfast short acting insulin (or increase breakfast or mid-morning snack)
• Dinner lows: decrease morning long acting insulin (or increase lunch or mid-afternoon snack)
• Bedtime lows: decrease dinner short-acting insulin (or increase dinner or evening snack)
• 0300 hrs lows: decrease evening long-acting insulin or take evening long acting insulin later (at bedtime if you are taking it before dinner)

Highs

Always consider dietary adjustments. If highs are one-off, consider exercising your blood sugar down or using a sliding-scale (see below).

• Breakfast highs: increase evening long-acting insulin (but check your 0300 hrs test before doing so)
• Lunchtime highs: increase breakfast short-acting insulin (or decrease breakfast or mid-morning snack)
• Dinner highs: increase morning long-acting insulin (or decrease lunch or med-afternoon snack)
• Bedtime highs: increase dinner short-acting insulin (or decrease dinner or evening snack)
• 0300 hrs highs: no action necessary if breakfast sugar OK (and HbA1c OK), otherwise talk to MD

Ultra-Short-Acting Insulin

Humalog (lispro) is a form of ultra-short-acting insulin that has been modified so that it is absorbed quicker in to the blood stream after subcutaneous injection. In general terms, one unit of Humalog has the same blood glucose lowering effect as one unit of regular (short acting) insulin. After subcutaneous injection it begins to be absorbed within 10 minutes. It reaches its peak effect between 1 and 2 hours and disappears by 4 to 5 hours. Because Humalog is very short acting, between meal snacks are usually not necessary. The likelihood of gaining weight with Humalog therapy is therefore smaller than with regular insulin in a multiple daily dosing schedule. Though I never encourage my patients to miss meals, the chances of severe hypoglycemia when you miss a meal (and of course don’t take Humalog) is much lower than with conventional insulin schedules. This quicker onset and shorter duration of action has some major advantages. The first is that you need not wait after taking your injection to eat. In fact, if you delay eating you run the risk of severe hypoglycemia. If you are forgetful or if there is a chance that you will not eat as soon as expected, it is acceptable to take Humalog after you eat. For the average size meal most people require 2-6 units. You need to experiment to see how much you need based on your body size, how much carbohydrate/starch there is in the meal you are going to eat etc. You should always test before taking your Humalog and give yourself extra sliding scale Humalog if your sugar is higher than your pre-meal target (usually in the range of 5-8). The best way to tell whether you take the ideal amount of Humalog is to test your blood sugar 1-2 hours after you eat. A reasonable target for sugar at this time is 9-10. If your sugar is lower than this you took too much; if it is higher you took too little. The alternative of course is you either ate too little or too much or made poor food choices.

Although using Humalog according to the above recommendations means more testing, it will lead to fewer hypoglycemic reactions, particularly severe hypoglycemic reactions. It will lead to improved HbA1c and ultimately will lead to better quality of life in the short term and fewer complications in the long term.

All patients taking Humalog need to take 2 daily shots of long-acting insulin. The long-acting insulin will be either NPH (N), lente (L), or ultra-lente (U). The best times to take your long-acting insulin is at lunchtime and at bedtime. The advantage of this is that the long-acting insulin typically peaks between 6 and 8 hours – this will be around 5-6 am for the bedtime N and at dinner time for the lunchtime N. The body is resistant to hypoglycemia at 5-6 am and of course your eating at dinner time. The dose of long-acting insulin is adjusted according to the blood sugar before meals. Thus, if the pre-meal breakfast sugar is too high you should probably increase your bedtime long-acting. Before doing so it is wise to test at 3 am to rule out the possibility that your morning high is not due to an asymptomatic early morning low followed by a rebound high. By the same argument, a high blood sugar at lunchtime may mean you need to increase your bedtime long-acting, though if your 2 hour post breakfast is too high then the correct adjustment would be to increase your breakfast Humalog not to increase your bedtime N. Remember you judge your dose of Humalog based on the 2 hour post meal reading. Similarly, a good 2 hour post lunch reading accompanied by a high pre-dinner reading should mean you increase your lunchtime long-acting. Similarly, a good 2 hour post dinner reading accompanied by a high bedtime reading should lead to an increase in the lunchtime long-acting.

A typical insulin schedule using Humalog schedule therefore contains a shot of Humalog before each meal and two shots of long-acting insulin, usually at lunchtime and bed. Most patients following this schedule successfully take roughly 50% of their insulin as Humalog at 50% is long-acting.

Traveling and Humalog

Continue to take your 2 shots of long-acting insulin 12 hours apart whether or not this falls at typical lunchtime or bedtime (this won’t be the case when you cross major time zones). Give yourself Humalog whenever you eat (this is usually frequent on long flights). If you find you are running high between meals give yourself small extra doses of Humalog (say 1-2 units). When you get to your destination gradually adjust your 2 shots of long-acting to conform to the local lunchtime and bedtime. Within a day or two you will be stable.

Insulin Adjustment Software

In collaboration with a young computer programmer who has diabetes and who is also my patient I have developed an insulin adjustment software that runs on IBM compatible computers. It is a DOS based program but does run very well on Windows or Windows 95/98. I would be happy to give you a copy of this software which will make specific suggestions about insulin adjustment. This software will automatically make the most appropriate suggestion.

Driving/Operating Machinery and Diabetes

If you have a severe low while you are driving or operating machinery there is a risk of injury or death to you or others. It is therefore your responsibility that this never happens. You should never drive a car without knowing what your blood sugar is within the last hour or so. If you have had a recent severe hypoglycemic reaction you should test immediately before driving. You should not drive with a blood sugar under 4.5 (under 6 if you have hypoglycemia unawareness, or recent severe low) and you should always carry snacks with you to treat yourself. If you are driving long distances you should stop every hour or two to test your blood sugar. If you have motor vehicle accident with a low blood sugar it is likely that the SuperIntendent of Motor Vehicles will temporarily rescind your driver’s licence. This will necessitate re-certifying through the Diabetes Centre and may cause you to lose your job if it requires driving.

International Travel and Insulin

There is no single or correct way to adjust insulin during long distance air travel, particularly when major time zones are being crossed. In general, the best approach is to continue taking your 1 or 2 shots of long-acting insulin so that you at no time produce ketones. It is best during this sort of travel to take a shot of short-acting insulin before each meal basing the dose on the same criteria mentioned above – size and nature of meal etc. In doubt it is safer to take frequent very small doses of short-acting insulin (taking extra insulin according to a sliding scale every few hours) rather than guessing and giving yourself too much insulin and running low.

Intercurrent Illness and Insulin

During intercurrent illness (colds, flu etc) your body will be less sensitive to insulin and you will therefore require more. The simplest approach is to take the usual amount of long-acting insulin, to test more frequently and to use the sliding scale mentioned above but to give 1 or 2 units more than you would usually give at any one time. Providing you test frequently and do not develop ketones (see below) and give yourself insulin the chances of a significant problem are very small.

Testing Urine for Ketones

You should purchase some ketostix or equivalent from the pharmacy. You should test your urine for ketones if you have 2 or more consecutive blood sugars over 15. If the high sugar is simply due to dietary indiscretion it is very unlikely you will have ketones but if you are feeling unwell then it is likely your body is producing ketones. Should ketones be present in anything other than trace amounts you should test your blood sugar every 2 hours and use a sliding scale of insulin adding an extra 2 units to each sliding scale increment (if you would normally take an extra 4 for a blood sugar of 14.1-16.0 take 6 units instead). If the blood sugar continues to rise and you continue to feel unwell or are vomiting you should go immediately to the nearest Emergency ward. You should also drink copious amounts of sugar-free liquids if you have ketones. You will not feel like eating in any case.

Ketones may also be produced by the body during starvation. This is in fact normal and providing your blood sugar is not over 10 these ketones can be safely ignored if you are starving (or fasting).

Diabetes and the Internet

There are innumerable websites for diabetes information. Some links to other diabetes websites are:

• www.toptenlinks.com
• www.diabetes.ca
• www.diabetes.org

Diabetes and Research

There is a large amount of research being carried out at the Vancouver Hospital and at other centres in Vancouver as well as many studies being done in other centres across Canada, North America and the Western World. There may be a number studies for which you are eligible. Please feel in no way obliged to participate in these studies as they are separate from the clinical relationship you have with me or your diabetes physician.

To facilitate research and education in the diabetes area (and other areas of endocrinology including thyroid, pituitary, women’s health, menopause and osteoporosis, cholesterol and lipid abnormalities) a charity of which Dr. Elliott is the president, the BC Endocrine Research Foundation was established in 1997. The Foundation is always looking for assistance be it either in time as a potential volunteer or financial support. You may discuss this with me at anytime.

Dr. Tom Elliott is an active researcher and educator and the President of the BC Endocrine Research Foundation. He is also a busy physician treating individuals with endocrine disorders.

The post Introduction to Type 1 Diabetes appeared first on BC Diabetes Foundation.

There is controversy in some circles about the value of treating women with gestational diabetes mellitus (GDM), a condition that occurs in about 5% of pregnancies. This article will describe evidence clearly demonstrating that treatment has been effective and that the current standard of regular screening and treatment aimed at normalizing maternal blood glucose levels should continue.

The concept of looking for a form of diabetes in pregnancy arose from the observation of high perinatal mortality in women who subsequently developed diabetes. Initial studies found a 4.3 fold increased perinatal mortality in untreated GDM compared with controls (ie., non-GDM). Since this finding there have been few prospective studies which have not included some form of therapy for all patients. Even with treatment, however, the majority of studies around the world have found an increased risk of adverse pregnancy outcomes with GDM.

Recent investigations have shown adverse perinatal outcomes with lowermaternal glucose values than would have been considered abnormal by the original Sullivan criteria. This led the Fourth International Workshop-Conference on Gestational Diabetes Mellitus to recommend lower values on the glucose tolerance test (Coustan-Carpenter) be used when diagnosing GDM. The association of GDM with adverse perinatal outcomes has been established beyond a reasonable doubt.Some people arguing for a trial examining no treatment in GDM, quote studies that show only minor complications. However, all diabetic patients in these trials received some treatment. Were the complications relatively minor because no treatment was needed or was it because the treatment given was moderately effective? This can best be answered by reviewing studies with minimal or no treatment, focusing on the most severe complications.

An important concept in all types of diabetes is that different levels of hyperglycemia (high blood sugar) are associated with different complications. Fasting glucose levels of 6.1 to 6.9 mmol are associated with an increased risk of macrovascular disease while values greater than 6.9 mmol carry an additional risk of microvascular complications including damage to the eyes (retinopathy), kidneys (renopathy), nerves (neuropathy) and blood vessels.

A direct relationship has been established between maternal blood glucose levels and perinatal mortality for all types of diabetes in pregnancy, including GDM. Patients with a mean glucose less than 5.6 mmol had a 3.8 percent perinatal mortality, compared to 16 percent when the mean blood glucose was 5.6 to 8.3 mmol and 24 percent for those greater than 8.3 mmol.

Studies focusing on GDM begin with those showing the relationship between an abnormal glucose tolerance test (GTT) and perinatal mortality in patients who were not treated. Perinatal mortality is generally 2 to 3.3 times greater in women with diabetes than in those without diabetes.

Several studies demonstrated that intensified treatment (ie., reduction) of blood glucose resulted in a marked reduction in mortality compared with previous pregnancies. Mortality was reduced from a range of 7.4 to 27.5 percent to 0 to 1.8 percent.In recent studies perinatal mortality remains at an increased level when tight glucose control was either not attempted or not achieved. A large maternity hospital in Kuwait treated GDM patients with insulin but found that the degree of patient monitoring and compliance was not as high as in many other centres.

The relative risk for total perinatal mortality was two (95% CI 1.2 to 3.7) and unexplained intrauterine deaths was 13.4 (95% CI 2.9 to 61.6) compared with controls. Another study used diet treatment for gestational diabetes if the preprandial (prior to a meal) glucose levels were 4 to 7 mmol and only started insulin when the values were greater than 7 mmol, which is much higher that currently recommended. The perinatal mortality in this study was 49.2/1000 compared to a background of 11.6/1000. While modern treatment approaches have resulted in normal perinatal mortality in recent studies, these studies demonstrate the danger of sub-optimal glucose control.

A number of studies show an increased risk of congenital malformations in GDM. Absolute risks range from 5.1 percent to 16 percent, all significantly higher than the corresponding control groups.

There is general agreement that there is an increased risk of macrosomia (abnormally large body) in GDM with its associated risks of birth trauma and operative delivery. The relative importance of hyperglycemia in the development of macrosomia in GDM has been challenged, with some believing that associated maternal age and obesity are major causative factors. A recent study clarifies this issue by finding that while maternal pregravid (before pregnancy) weight and weight gain during pregnancy were important determinants of birth weight in non-diabetics, these factors were not important if the mother had GDM.

There is growing evidence that inadequately treated GDM has lifelong adverse effects. The incidence of Type 2 diabetes is increasing at all ages and there is a great deal of interest in identifying those at high risk. High maternal glucose levels during pregnancy increase the risk of adolescent obesity and impaired glucose tolerance, an association that is independent of maternal weight and type of diabetes. There has also been interest in the finding that small birth weight, but not large birth weight, is associated with an increased risk of Type 2 diabetes. Further analysis shows that this is only true for women who do not have diabetes during their pregnancy. For infants of diabetic mothers the curve is U-shaped with both small and large birth weights carrying a significantly increased risk of early Type 2 diabetes.

Treatment of GDM has been shown to result in improved outcomes. A number of studies have now shown that perinatal outcome is directly related to maternal glucose levels and that the attainment of maternal normoglycemia will result in outcomes no different from uncomplicated pregnancies.

One large, prospective, population-based study compared conventional with intense treatment of GDM. The intense group had significantly better outcomes including less macrosomia, fewer caesarian sections, shoulder dystocias (difficult labour), metabolic complications, special care nursing admissions and shorter length of hospital stays. Outcomes in the intense group were no different from the control population without diabetes.

Finally, there is the issue of cost. Analysis has found that three dollars are saved for every dollar spent in the diagnosis and treatment of GDM.

In conclusion, untreated GDM has severe short and long term complications and intense glycemic control can reduce the risk compared to that of non-diabetic controls. The value of treatment of GDM has been proven beyond a reasonable doubt and should remain the current standard of care.

Dr. David Thompson is the acting head of the Division of Endocrinology at University of British Columbia. He is an expert in gestational diabetes and maintains a medical practice as well as a research program.

References

1. Persson B., Hanson U.. Neonatal morbidities in gestational diabetes. Diabetes Care 1998; 21 (supplement 2) B1- B167.
2. Langer O., Is normoglycemia the correct threshold to prevent complications in the pregnant diabetic patient? Diabetes Reviews 1996; 4:2- 10.
3. Langer O., Rodriguez D., Xenakis E., Mc Farland M., Berkus M., Arredondo F.. Intensified versus conventional management of gestational diabetes. American Journal Obstetrics Gynecology 1994; 170:1036-1047.

The post Gestational Diabetes appeared first on BC Diabetes Foundation.

The DIGAMI (5) study examined only patients who had suffered a heart attack. One of the study groups had usual management of their diabetes while the other group had its average glucose levels lowered significantly. In contrast to the other studies the group with the lower glucose levels had a significantly higher survival rate which persisted for 3 years after the heart attack. Another study, the Wisconsin early diabetic retinopathy study, a prospective but not randomized cohort study, showed significantly more macrovascular disease in patients with poor glucose control compared to those with good glucose control. In general, outcomes after macrovascular events such as heart attack and stroke are related to the degree of glucose elevation – the higher the glucose the worse the outcome.

The Hypothesis

There are reasons to believe that good glucose control should be effective in decreasing the risk of macrovascular disease that begins at a lower glucose elevation than microvascular disease. A direct relation exists between the degree of glucose elevation and the incidence of macrovascular disease, this lower glucose threshold being the main reason for establishing the categories of impaired fasting glucose and impaired glucose tolerance. Since glucose reduction reduces microvascular complications one would expect this should also apply to macrovascular disease that begins at even lower glucose thresholds.

Why have research studies been unable to demonstrate this?

There are several possible explanations for this discrepancy.

1. The first one is that good glucose control is simply not very effective in preventing macrovascular complications. The explanation is counter-intuitive – if diabetes causes both micro and macrovascular disease why should treatment prevent one type and not the other?
2. Another explanation is that glucose levels must be reduced to normal in order to prevent macrovasacular complications. In all studies to date the best glucose control achieved was still only near normal. This explanation is plausible although it assumes a different dose response for micro vs macrovascular disease. A National Institute of Health study, with normal glucose levels in diabetics as one of the goals, is currently underway and may address this issue.
3. A third possibility is that good glucose control is necessary but not sufficient on its own, to reduce the macrovascular complications in diabetes. Atherosclerosis, the process that causes damage to large arteries, has several factors that cause its development. This is in contrast to microvascular disease where elevated glucose levels are the only causative factor. The known risk factors for atherosclerosis include smoking, hypertension, elevated cholesterol levels and damage to the lining of the arteries.

Diabetes and Risk Factors

Diabetes is known to worsen the effects of some of these risk factors. For example, the UKPDS showed that hypertension must be more tightly controlled in diabetes than in any other condition. Diabetes makes elevated cholesterol levels even more damaging by changing the chemical nature of the cholesterol particle in a way that makes it more toxic to blood vessel walls. This hypothesis proposes that by the time a person has had diabetes for several years, these other factors as well as glucose levels must be treated to achieve significant benefit.

This is similar to the findings in advanced microvascular complications. Diabetic patients with eye damage benefit more from laser therapy and good glucose control than from good glucose control alone. Patients with kidney damage require the addition of a class of drugs called ACE inhibitors, along with good glucose control, to prevent progression of the kidney damage. Additional evidence comes from the HOPE study and Hellman’s study on multiple risk factor management. These studies showed that diabetic patients with good control of blood pressure and cholesterol had fewer macrovascular events than the group which was not treated in such a manner.

Summary

The final answer will come from further research. We have started a study attempting to improve outcomes in patients with diabetes undergoing cardiac bypass surgery. Diabetic patients have approximately double the complication rate compared to people without diabetes having the same surgery. We are going to test the hypothesis that controlling all the metabolic risk factors discussed above – glucose, cholesterol, blood pressure and protecting the arterial wall – will significantly reduce complications. Not only could this benefit the patient but it may also reduce the average length of hospital stay and reduce the costs to the health care system. This project and others will, we hope, shed light on the relationship between blood sugar control and macrovascular disease. Regardless of the findings, however, it is still very important to control glucose levels in people with diabetes because of the dramatic benefit that this has on reducing the risk of microvascular complications.

Dr. David Thompson is the acting head of the Division of Endocrinology at University of British Columbia. He is an expert in diabetes and maintains a medical practice as well as a research program.

References

1. The Diabetes Care and Complications Trial Research Group. Effect of intensive diabetes management on macrovascular events and risk factors in the The Diabetes Care and Complications Trial. Am. J. Cardiol. 1995; 75: 984-903.
2. UKPDS (United Kingdom Prospective Diabetes Study);. Effect of intensive blood glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998;352:854-865.
3. UKPDS (United Kingdom Prospective Diabetes Study). Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837-853.
4. Ohkubo Y, Kishikawa H, Araki E, Miyata T, Isami S, Motoyoshi S, Kojima Y, Furuyoshi N, Shichiri M. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study. Diab Res Clin Pract 1995;28:103-117.
5. Malmberg K, Ryden L, Efendic S, Herlitz J, Nicol P, Waldenstrom A, Wedel H, Welin I. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): Effects on mortality at 1 year. J Am Coll Cardiol 1995;26:57-65.

The post Cardiovascular Disease and Diabetes appeared first on BC Diabetes Foundation.

The cover article on gestational diabetes is an excellent example of this. As if being pregnant doesn’t present enough challenges approximately one in twenty women will find themselves dealing with the symptoms of gestational diabetes during her pregnancy. Dr. David Thompson, a specialist in this field, presents an informative overview on this subject and provides convincing evidence that proper management of gestational diabetes is essential to the health of the fetus and the health of the mother.

The B.C. Endocrine Research Foundation is proud to be distributing the educational video and diary Dr. Jerilynn Prior has just released. It is called ‘The Puzzle of Perimenopause’ and presents information on the physiological, physical and emotional changes many women experience when their normal hormone levels begin to fluctuate. This can happen as early as the late thirties and continue on into the early fifties. We have provided an overview of the video and diary including the launch and some feedback from those who have followed Dr. Prior’s work.

Being young, especially being a teenager usually means that there are plenty of chores to do. Some youths have the additional responsibility of managing their diabetes. Type I diabetes (juvenile diabetes) has been getting a lot of press lately as research takes steps forward. In this issue Dr. Thomas Elliott, a diabetes expert provides an excellent introduction to type I diabetes, causes and management.

I have the pleasure of sharing some interesting recipes with you in the Food For Thought column. These are really fun recipes.

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