Authors: Rita Baron-Faust,Jill Buyon
The Autoimmune Connection: Essential Information for Women on Diagnosis, Treatment, and Getting On With Your Life (25 page)
Sjögren’s doesn’t directly affect reproduction, but some of the antibodies associated with it can cause problems.
Forty percent or more of women with Sjögren’s have antibodies to
SSB/La
, also associated with lupus. These antibodies to normal cellular components
can be harmful to a growing fetus and can lead to cardiac, skin, or blood-related problems, which are all grouped under the term
neonatal lupus
. If you are pregnant and have Sjögren’s, you need to have your serum (the clear part of the blood) tested for the presence and amount of these antibodies with a test called an (ELISA, see
pages 73
and
355
).
Sjögren’s patients who have antibodies to SSA/Ro and/or SSB/La can face the prospect of have a child with a condition called
neonatal lupus
(see
page 89
). Happily this is a rare problem. The name
neonatal lupus
is misleading since the mother may not have lupus at all and the baby doesn’t either. The condition is actually related to the presence of these antibodies. The most common problems associated with these antibodies include injury to the heart, skin, liver, and blood cells. The good news is that except for the heart problem the other features are transient and disappear when the antibodies are cleared from the child’s circulation at about six to eight months of age. The most serious problem involves the heart, called
heart block
. This occurs in one of 50 women with these autoantibodies.
If you are found to have antibodies to either
Ro
or
La
, your pregnancy is managed just as in women with lupus who have these antibodies.
Women with Sjögren’s may also have
antiphospholipid antibodies
. These antibodies are related to
antiphospholipid syndrome
(see
pages 347
to
362
). These antibodies may predispose women to form clots in the placenta, hampering blood flow to the fetus, and are associated with recurrent miscarriages (most often during the second trimester). Women found to have these antibodies are prescribed blood thinners, such as aspirin or heparin. Pregnancies in women with Sjögren’s found to have these antibodies are managed the same way as in women with antiphospholipid syndrome.
The major gynecological issue facing you with Sjögren’s syndrome is vaginal dryness and painful intercourse. However, not all vaginal dryness that occurs in women with autoimmune diseases is related to Sjögren’s.
Vaginal lubrication does not come from moisture-producing glands but mostly from fluid that’s passed from the bloodstream through the vaginal walls. “So dryness that occurs in Sjögren’s may be due to autoimmune effects on the blood vessels and the circulation in the vaginal area,” explains
Lila E. Nachtigall, MD, professor of obstetrics and gynecology at the New York University School of Medicine. Other autoimmune diseases, such as lupus and diabetes, can affect circulation and vaginal secretions; the stress of any chronic illness may also reduce vaginal moisture.
Before menopause, estrogen helps stimulate the normal growth and development of vaginal cells, as well as vaginal secretions. As estrogen levels drop in the years before and after menopause, vaginal tissues gradually begin to thin and atrophy, producing fewer secretions (surgical menopause, removal of the ovaries, causes a more rapid onset of vaginal dryness).
“Since Sjögren’s is most often diagnosed in women age 40 and over, some cases of vaginal dryness may be blamed on aging,” remarks Dr. Nachtigall. Low estrogen levels occur during other times of life, such as during breast-feeding, and lead to vaginal dryness. Primary ovarian insufficiency (premature ovarian failure) also causes dry eye and dry vagina (see
page 231
). Other causes must be ruled out before attributing the problem to Sjögren’s.
You and your partner should be reassured that this is a physical problem and not related to any failure of sexual arousal, stresses Dr. Nachtigall. Lubricants can make sex more comfortable. These are different from “personal moisturizers.” Lubricants are designed for use during sexual activity. “The ideal lubricant is odorless, tasteless, colorless, water soluble, and of a consistency that allows it to remain in the vagina. Never use oil-based products like petroleum jelly. They will interfere with the vagina’s natural self-cleansing mechanism,” she explains. Lubricants include
KY Jelly
and
Astroglide
.
Vaginal moisturizers
are designed for regular use to relieve dryness and irritation and to attract liquid to the dry vaginal tissues. Moisturizers include
Replens
(containing
pilocarpine
, which adheres to vaginal tissues),
Feminease
(containing
Yerba santa
, made from an aloe-like plant), and
Vagisil Intimate Moisturizer
. Both lubricants and moisturizers have an acidic pH that helps prevent vaginal infections and are nonhormonal. Replens is applied three times a week.
Although menopausal vaginal atrophy is somewhat worse in the Sjögren’s patient, it does respond to local estrogen therapy, either as a cream or a slow-release ring (
Estring
,
estradiol
made from yams) or a suppository,
Vagifem
(
estradiol
, also synthesized from yams), which release a small continuous dose of estrogen to vaginal tissues.
You may also want to ask your gynecologist about prescription
ospemifene (Osphena)
, a
selective estrogen receptor modulator (SERM)
approved to combat
postmenopausal vaginal dryness and painful sex. SERMs are estrogen
agonists
, compounds that act on estrogen receptors to produce estrogen-like actions in various tissues in this case, preventing atrophy of vaginal tissues. However, like estrogen, they can also affect the lining of the uterus and increase the risk of blood clots. So you need to discuss the risks and benefits with your doctor. Osphena is taken as a pill once a day.
27
Dry eye can be a component of menopause, so you need to mention it to your gynecologist, as well. “I think it’s very critical for women to recognize that Sjögren’s can affect nearly every system in their body. Lung problems can cause shortness of breath; there may be nerve problems, which a woman may not connect to her Sjögren’s,” stresses Dr. Smith. “Women need to communicate to their physicians when they have problems or changes, because if they don’t there’s no hope of those problems being addressed.”
But the problems of Sjögren’s are not unsurmountable.
“I wouldn’t say I ‘enjoyed’ the challenge. But I’m up for the challenge. Sjögren’s syndrome has been a life-changing experience, that’s for sure,” says Venus Williams of living with Sjögren’s—on and off the tennis court.
2
“I don’t like being defeated by anything. It makes me creative, that’s for sure. You have to figure out ways to win when you don’t feel well. You have to find different avenues in order to get your top health level, and you have to be tough. You can’t make any excuses, even though you have one of the biggest excuses available. It’s a roller coaster, but thankfully I’ve enjoyed roller coasters since I was a child.”
1
. Rhoden WC. Venus Williams pushes back hard, at the twilight.
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, August 24, 2013, F5.
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. Ain M, Venus Williams bares all.
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. Sullivan DA, Sullivan BD, Evans JE, et al. Androgen deficiency, meibomian gland dysfunction, and evaporative dry eye. See comment in PubMed Commons below.
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. Maddali Bongi S, Del Rosso A, Orlandi M, et al. Gynaecological symptoms and sexual disability in women with primary Sjögren’s syndrome and sicca syndrome.
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. Birnbaum J. Peripheral nervous system manifestations of Sjögren’s Syndrome: clinical patterns, diagnostic paradigms, etiopathogenesis, and therapeutic strategies.
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. Mengshoel AM, Norheim KB, Omdal R. Primary Sjögren’s syndrome: fatigue is an ever-present, fluctuating, and uncontrollable lack of energy.
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. Foulks GN, Forstot SL, Donish PC, et al., Guidelines for the management of dry eye associated with SjÖgren disease.
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. Jonsson R, Theander E, Sjöström B, Brokstad K, Henriksson G. Autoantibodies present before symptom onset in primary Sjögren syndrome.
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. Shiboski SC, Shiboski CH, Criswell LA, et al. American College of Rheumatology classification criteria for Sjögren’s syndrome: a data-driven, expert consensus approach in the Sjögren’s International Collaborative Clinical Alliance Cohort.
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. Schaumberg D, Buring JE, Sullivan DA, Dana MR. Hormone replacement therapy and dry eye syndrome.
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. Smith JA, Vitale S, Reed GF, et al. Dry eye signs and symptoms in women with premature ovarian failure.
Arch Ophthalmol
. 2004;122(2):151–156. doi:10.1001/archopht.122.2.151.
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. Phadatare SP, Momin M, Nighojkar P, et al. A comprehensive review on dry eye disease: diagnosis, medical management, recent developments, and future challenges.
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. Information on Restasis (cyclosporine ophthalmic emulsion) 0.5%.
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.
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. Rand AL, Asbell PA. Nutritional supplements for dry eye syndrome.
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. Kamiya K, Nakanishi M, Ishii R, et al. Clinical evaluation of the additive effect of diquafosol tetrasodium on sodium hyaluronate monotherapy in patients with dry eye syndrome: a prospective, randomized, multicenter study.
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. Lau OCF, Samarawickrama C, Skalicky SE. P2Y
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. Schmidt TA, Sullivan DA, Knop E, et al. Transcription, translation, and function of lubricin, a boundary lubricant, at the ocular surface.
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2013;131(6):766–776. doi:10.1001/jamaophthalmol.2013.2385.
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. Murphy R. OSD: help is on the way.
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. Ono M, Takamura E, Shinozaki K, et al. Therapeutic effect of cevimeline on dry eye in patients with Sjögren’s syndrome: a randomized, double blind clinical study.
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. Cummins MJ, Papas A, Kammer GM, Fox PC. Treatment of primary Sjögren’s syndrome with low-dose human interferon alfa administered by the oromucosal route: combined phase III results
. Arthritis Rheum (Arthritis Care Res)
. 2003;49(4):585–593. doi:10.1002/art.11199.
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. Carubbi F, Cipriani P, Marrelli A, et al. Efficacy and safety of rituximab treatment in early primary Sjögren’s syndrome: a prospective, multi-center, follow-up study.
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2013;15:R172. doi:10.1186/ar4359.
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. Devauchelle-Pensec V, Xavier M, Jousse-Joulin S, et al. Treatment of primary Sjögren’s syndrome with rituximab.
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. 2014;160(4):233–242.
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. Gottenberg JE, Ravaud P, Puéchal X, et al. Effects of hydroxychloroquine on symptomatic improvement in primary Sjögren syndrome. The JOQUER randomized clinical trial
. JAMA
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27
. Osphena.
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.
Vanishing Hormones—Type 1 Diabetes, Addison’s Disease, Primary Ovarian Insufficiency, and Other Endocrine Problems
I had all the symptoms: the blurry vision, the enormous thirst, the ravenous appetite, and I would feel the deep, deep fatigue. But I didn’t recognize them as diabetes. I was going through a divorce at the time and single motherhood, so not feeling “well” felt normal. So I missed the warning signs. Fortunately, I didn’t have any damage. I had been diagnosed with another autoimmune disease, sarcoidosis, in 1973 and I was seeing a doctor every month to monitor my lungs for nodules. So the diabetes was found with a routine blood test. I didn’t think about the symptoms or report them to the doctor until after he noticed the high glucose level and started asking me questions. It seemed so obvious after we got the blood test results, but it was so easy for me to overlook.
M
ARY
K
AY
, 67
Our bodies need fuel in order to run smoothly. We get that fuel from the carbohydrates and proteins we eat, which are converted to glucose and transported into cells by the hormone insulin. Normally the body keeps levels of blood glucose tightly regulated. But in diabetes that delicate balance is upset.
According to the American Diabetes Association (ADA), there are four categories of diabetes:
Type 1 diabetes, or insulin-dependent diabetes mellitus
(once called
juvenile-onset diabetes
), is strongly genetic and usually results from an autoimmune attack on the insulin-producing
beta
(or
islet
) cells in the pancreas that leads to insulin deficiency. Lack of insulin causes blood glucose to soar, wreaking havoc on the body.
Type 2, or non-insulin-dependent diabetes mellitus
, is a metabolic disorder frequently brought about by obesity, causing the body to gradually lose its ability to use insulin properly. Once termed
adult-onset diabetes
, an epidemic rise in obesity has increased its occurrence among children.
Gestational diabetes
is an often transient form of diabetes that arises during pregnancy, in which the body temporarily loses responsiveness to insulin. It usually resolves shortly after delivery, but the risk to develop type 2 diabetes in the future remains elevated. Other types of diabetes result from genetic defects in insulin action, pancreatic disease, or are drug- or chemical-induced.
1
Over 29 million American have diabetes,
2
and more than 347 million people are affected worldwide.
3
Ten percent have type 1 diabetes, which usually arises in early childhood or before age 30. Most people with diabetes have type 2, which typically occurs after age 40 and is related to obesity. However, later in life the two forms of diabetes often merge.
There has been a virtual epidemic of type 2 diabetes, fueled by soaring rates of obesity. However, the incidence of type 1 diabetes has also been increasing around the world, rising by as much as 4 percent a year, mostly among children, and it’s unclear why.
4
The most striking rise has been in Finland, which has the highest incidence of childhood type 1 diabetes in the world,
5
but all over Europe rates are expected to increase 60 percent by 2020.
4
In the United States, the incidence rose by 30 percent from 2001 to 2009 and is projected to keep increasing. Potential causes could be environmental, experts say, but most of the cases have been among genetically susceptible children.
6
While type 1 diabetes affects women and men about equally, it often clusters with other autoimmune diseases common in women, including
thyroid disease
,
celiac disease
,
pernicious anemia
,
Addison’s disease
,
myasthenia gravis
, and
vitiligo
.
The pancreas is part of the network of
endocrine
glands (including the thyroid, ovaries, and adrenal glands; see
pages 222
to
223
) that secrete hormones directly into the bloodstream.
As insulin-producing pancreatic
beta
cells are progressively destroyed by an autoimmune attack, the body produces less and less insulin and becomes less able to convert food into glucose and bring it into cells. As a result, glucose accumulates in the bloodstream. The blood vessel damage caused by high glucose leads to heart attacks, stroke, kidney disease, and blindness. Women with diabetes are at greater risk than nondiabetic women for cardiovascular disease (CVD). High glucose can also cause nerve damage, poor circulation, and tissue death in the legs, sometimes leading to amputations.
But high glucose may produce few or no symptoms in its early stage. The blurry vision and extreme thirst Mary Kay experienced only occur after blood glucose is greatly elevated. While type 1 diabetes can come on abruptly during childhood or adolescence, researchers now believe many middle-aged people thought to have type 2 diabetes actually have type 1 diabetes, but are misdiagnosed because they may not have a rapid progression to full-blown disease since the autoimmune destruction of beta cells often occurs more slowly. Type 1 diabetes is more common in Caucasians, while type 2 is more prevalent in African American, Latina, Native American, and Asian American women.
In type 1 diabetes, autoantibodies target not only the insulin-producing beta cells in the pancreas, but also proteins made by beta cells that sit on the cell surface, and even insulin itself. Other types of islet cells in the pancreas escape unharmed. Autoantibodies may be present years before symptoms of type 1
diabetes appear. In fact, 70 percent of people with type 1 diabetes screened for the national Diabetes Prevention Trial had one or more of the diabetes autoantibodies but no symptoms. As many as 70 to 80 percent of people newly diagnosed with type 1 diabetes have antibodies to islet cells; 80 to 95 percent have antibodies to a protein made by beta cells called
glutamic acid decarboxylase (GAD)
; two-thirds have antibodies to insulinoma antigen-2 (1A-2); and up to half have antibodies to insulin. Type 1 diabetes can come on gradually, but people with more antibodies may develop it more quickly.
There are a number of autoantibodies involved, but insulin and GAD appear to be the early targets of the attack in type 1 diabetes. The beta cells are destroyed, but they may actually be innocent bystanders of an immune attack on a virus that invades those cells.
You’ll recall that some viruses and bacteria may have the same shape as cells in the body, a phenomenon called molecular mimicry. A small area of the GAD protein on beta cells looks almost identical to a protein called
P2-C
on the
Coxsackie virus B
(one of a family of viruses that causes polio).
During an infection, T cells target an invading virus and destroy it. But once the infection is over, T cells on the prowl may see the GAD protein sitting on beta cells, think it’s a virus, and attack. Because viruses must first invade cells, some scientists believe they may change something about the islet cells that provokes a T-cell attack. The Coxsackie virus, as well as other enteroviruses (Coxsackie virus A and B, echovirus)
7
cytomegalovirus, adenoviruses, and viruses that cause mumps have all been implicated in type 1 diabetes.
7
Other immune system problems also contribute to type 1 diabetes—among them, not having enough
natural killer T cells (NK cells)
or the
T-regulator (T-reg)
cells that tell the NK cells which cells to target and which to ignore. In type 1 diabetes (and other autoimmune diseases), another step in giving instructions to NK cells also goes awry. T-cell receptors, which function kind of like TV antennae, need to pick up a signal from
antigen presenting cells (APCs)
to tell them which cells are foreign invaders and which aren’t. The APCs display bits of antigens on their surface within special molecules, kind of like hot dogs in a bun, explains Denise Faustman, MD, PhD, who heads the immunobiology laboratory at Massachusetts General Hospital. If the antigens are not properly displayed, or if the presentation process is somehow incomplete, the T cells never get the message to bypass the beta cells, she says.
No matter what triggers the attack, as beta cells are progressively killed off the pancreas produces less and less insulin. Insulin is critical to keeping the body’s cellular machinery running smoothly, fueling our cells. Think of insulin as a gas pump, and your cells as tiny cars. The “gas” is blood glucose, processed by the body from sugar in carbohydrates (all carbohydrates—whether doughnuts or fruits—are technically sugar). If the gas pump isn’t working properly, cells don’t get enough fuel and start to stall. The excess fuel in the pump backs up and spills over into the blood, and over time that high glucose can damage your blood vessels, your eyes, your kidneys, and your nerves. Insulin also helps the body store extra fuel as fat; to get badly needed fuel, the body taps into this reserve, and that’s why people with type 1 diabetes lose weight.
In young children, the destruction of beta cells and the loss of insulin can be dramatic, but in adults (especially older adults), it can occur more gradually. By the time type 1 diabetes is diagnosed in adults, the majority of the insulin-producing cells have been destroyed. While there’s no way at present to reverse that loss, researchers say it may one day be possible to regrow beta cells or trigger their regeneration (see
pages 212
to
213
).
Although the disease can run in families, 85 percent of people who develop it have no family history of type 1 diabetes (although family members may have other autoimmune diseases). The risk for people with a parent or sibling with type 1 diabetes is about 6 percent; the risk is 30 percent among identical twins. Even nonidentical twins or siblings have a greater risk of getting type 1 diabetes than people without a family history. More than a half-dozen genes are associated with the disease; some are more common among specific ethnic groups (such as Scandinavians), making them more vulnerable to environmental triggers, like viruses.
Mary Kay’s story continues:
I went into a diabetic coma a few months after I was diagnosed with diabetes in 1984. I think it was the result of a collision of medical events, including surgery that preceded it by six months, and an infection I developed afterward. The night before I went into the coma I had gotten the flu, and being newly diagnosed I wasn’t aware that dehydration and the flu are very dangerous for people with diabetes; it shoots your glucose level way, way up. So even though I had taken my insulin that day, because I was so sick
I got dehydrated. I developed ketoacidosis and went into a coma in my sleep. Fortunately, I was staying with a friend at the time, who noticed that my breathing was irregular the next morning and that I wouldn’t awaken. I was in a coma for nine days. If I had been home it might not have been noticed right away. I was a single mother with two small children; they were seven and nine at the time, and I don’t think they would have known to call 911. They know now. In fact, in the months following that, they did become quite frightened, and if I tried to sleep in on a Saturday morning, they would shake me and say “Mom, are you all right?”
In healthy people, the body carefully regulates the amount of glucose and insulin in the blood. When blood glucose becomes elevated (such as after eating), more insulin is produced to help remove it; when glucose falls, insulin secretion also drops. In people with diabetes, the body isn’t producing insulin, so glucose builds up in the blood instead of being transported into cells.
High blood sugar,
hyperglycemia
, causes intense thirst, dry mouth, and frequent urination. Some of the excess glucose leaks into the urine, and the excess glucose causes the kidneys to produce more urine, which can result in dehydration. Your doctor can detect glucose levels by dipping a specially treated paper into a urine sample. When cells don’t get enough glucose, the body starts breaking down fat to use for energy, which also produces weight loss.
As fats are broken down for energy by the liver, waste products called
ketones
are produced. If ketones build up faster than they can be excreted in urine, they begin to accumulate in the bloodstream, causing the blood to become acidic. This is called
diabetic ketoacidosis
, and it can come on suddenly with life-threatening consequences. In addition to the classic signs of hyperglycemia, ketoacidosis produces a fruity-smelling breath, shortness of breath, dry mouth, loss of appetite, nausea and vomiting, muscle weakness, dry flushed skin, blurry vision, and sleepiness. In severe cases, ketoacidosis can cause coma. (Symptoms are similar to
Addison’s disease
—see
pages 223
to
230
.)
Ketoacidosis is usually triggered by a sharp drop in insulin (if you forget to take a dose of insulin), but it can also be brought on by illness or a major life stress (like a car accident), says Carol J. Levy, MD, CDE, an associate professor of medicine, endocrinology, diabetes and bone disease and director
of the Diabetes Center at Mount Sinai Hospital in New York City. “When you’re under stress, stress hormones tell the liver to release stored glucose (glycogen). But these hormones also block the effects of insulin,” she explains. If your insulin is low to begin with, a bout with the flu or extreme stress could bring on ketoacidosis, which requires immediate treatment with insulin and fluids. The risk of ketoacidosis is 50 percent higher in women, according to the ADA.
Sometimes diabetes can cause (or be associated with) menstrual irregularities, infertility, and pregnancy complications, and it is associated with primary ovarian insufficiency (previously referred to as premature ovarian failure) and an earlier menopause.
As high blood glucose damages blood vessels in the eye, fluid leaks from the tiny blood vessels behind the retina.
Diabetic retinopathy
is the most common cause of blindness in people aged 20 to 75. Often the first sign of a problem is a blurring of vision. This damage may be visible during a routine eye exam.
Diabetes also injures blood vessels in the legs, impeding circulation and causing pain (
intermittent claudication
) while walking. Women are 76 times more likely than men to suffer damage to small blood vessels in their extremities (
peripheral vascular disease, PVD
).
When blood supply to nerves is diminished, the nerves become damaged and don’t send out pain signals when there’s an injury. So a small cut you may not feel can become ulcerated. If diabetic ulcers go untreated, the tissue can die and become gangrenous, and the limb may need to be amputated.
As glucose accumulates in the bloodstream, it can damage large blood vessels, making it easier for fatty plaques to accumulate inside artery walls, narrowing key arteries and impeding blood supply to the heart. If those plaques rupture and form blood clots, it can completely block an artery, leading to heart attack and stroke. If you have diabetes, you’re three to four times more likely to suffer a heart attack and stroke than people without diabetes because the high glucose levels reduce the protective effects of estrogen on cholesterol and blood vessel flexibility before menopause.
You’re also at increased risk of bone loss and hip fracture, which studies suggest is partly due to a hormonal disruption and to lower levels of vitamin D and magnesium. You can also have an overactive
parathyroid gland
(see
pages 229
to
230
), which causes the body to leach calcium from the bones. So you may need regular bone density scans and possibly bone-building drugs.
Between 10 and 21 percent of women with diabetes develop kidney disease. Damage to kidney cells,
diabetic nephropathy
, is the most common reason for kidney dialysis (needed to help rid the body of waste products) or a kidney transplant.
Diabetes also causes skin problems, including fungal infections in the corners of the mouth and under the breasts and armpits. One of the common symptoms of diabetes is itching brought on by dry skin and poor circulation, especially in the lower legs. Women can develop a skin condition called
diabetic dermopathy
, which produces brown spots, especially on the legs. Atherosclerosis can also affect the skin when it narrows blood vessels in the legs, causing it to thin and feel cool; your toenails may thicken and become discolored, and your toes may feel cold. You can also suffer chronic vaginal yeast infections, gum disease, and infections of the tiny glands in the eyelid (
styes
).
Unexplained weight loss is also a symptom of exocrine pancreatic insufficiency (EPI), stemming from inadequate digestion of food and malabsorption of nutrients.
8
Other symptoms of EPI that can occur in diabetes include nausea, appetite loss, gas, bloating, abdominal pain, diarrhea, and
steatorrhea
(unabsorbed fat in the stools), oily, foul-smelling stools that float, which also occurs in celiac disease (see
page 270
). You can also have bone loss and vitamin deficiency (notably vitamin B
12
, calcium, and vitamin D), as well as muscle cramps, bone pain, and easy bruising. If you start to have these symptoms or GI problems along with your diabetes, it’s wise to see a pancreatic specialist, since EPI can arise in diabetes.
8