Tuesday, August 2, 2011

I Tossed Crispy’s Insulin in the Trash

Most diabetic cats require lifelong oral or injectable medication. For a few lucky cats (and owners), however, diabetes resolves. How does this happen?

My cat Crispy has terrible skin allergies. A few years ago, it got really really bad. She was chewing at her feet and the insides of her legs non-stop. I tried a hypoallergenic diet, but that made no difference. I would have liked to have tried antihistamines but Crispy is impossible to medicate. It’s embarrassing that I’m a veterinarian and I prescribe medications to cats all day, and yet I cannot medicate my own cat. I’ve tried flavored liquids, I’ve tried hiding pills in treats, I’ve had treats made up with the medication blended throughout the treat (she ate exactly one of them, and never ate another one, ever again). Omega-3 fatty acids are anti-inflammatory in some cats, and may help reduce skin inflammation when given daily. So I tried putting them on her food. She caught one whiff of them on her food and that was that. She absolutely refused to touch the food thereafter.

I could tell from the appearance of the skin problem that this type of allergic dermatitis would probably respond nicely to steroids. I’m not crazy about giving steroids to cats, but with skin allergies, you give steroids initially at a high-ish dose, and then you rapidly taper the dose down to the lowest dose that controls the signs. I was figuring 1 tablet of prednisolone twice daily for 5 days, then once daily for 5 days, then every other day thereafter. I was hoping that once I got down to the every other day dosing, it wouldn’t be too horrible. Well, several bite and scratch wounds later, I abandoned the process. Crispy will simply not allow herself to be orally medicated. Period.

I had to do something. Look at what she was doing to her leg!

As a last resort, I gave Crispy an injection of a long-acting steroid.

I know that this is done quite often by other veterinarians, but I rarely do it. Long-acting steroids have the potential for side effects. First of all, they are immunosuppressive. This is why we give them. If the immune system is causing problems, we want to dampen the immune response. With skin allergies, we want the steroids to get those inflammatory cells out of the skin, where they’re making the cat miserable. But, by suppressing the immune system, you put the cat at increased risk for developing opportunistic infections. Steroids are also antagonistic to insulin. Give for a prolonged period, they can induce a diabetic state in the cat. Steroids also cause retention of water. In most cats, it’s not a problem. For cats with heart disease (especially mild, undiagnosed heart disease), the increase in blood volume caused by the steroids may be enough to result in congestive heart failure. This is why I prefer pills to an injection. With pills, if adverse signs develop, you stop the pills, and the drug is out of the body is just a few days. With an injection, once you give it, you cannot take it back. Steroid injections can last anywhere from 3 weeks to perhaps 3 months! In Crispy’s case, I was left with few options, so I gave her a steroid shot, but at a reduced dose, and I monitored her carefully. Crispy’s skin cleared up immediately, and she had no worrisome side effects at all. Her skin looked great.

About two months later, the signs returned. Once again, I had the same dilemma: a skin problem in a cat who won’t allow me to medicate her. I tried a topical spray, but that didn’t help. She hated the sound that the spray bottle made, and the way it felt on her skin. As soon as she saw me coming, she’d run for the hills. That got me a bit depressed. Her legs started looking as bad as they did several months prior. Reluctantly, I gave her a second steroid shot. Within two weeks, her skin had healed up and the fur had started to grow back where she had licked and pulled it out. And then…

I noticed that the clumps of urine in the litter box were getting big. Really big. They were like cinderblocks! I knew Crispy was the culprit, because Crispy urinates in the back of the litter box, while Mittens urinates in the front. I also noticed that Crispy would often have clumping litter stuck to her feet. We call this “frosty paws”, and it is a sign that a cat is making a lot of urine. Fearing the worst, I brought her into my hospital for some routine blood tests, and my fears were confirmed: Crispy was diabetic.

Before I get to the good part, i.e. how the diabetes resolved, let me give everyone a little refresher course on diabetes in cats.

Diabetes 101

Diabetes is one of the most common endocrine (glandular) disorders in cats. While the exact cause of diabetes in not known, obesity, genetic predisposition, pancreatic disease, hormonal imbalances, and certain medications have all been incriminated. Diabetes occurs when the pancreas fails to produce adequate amounts of insulin, a hormone necessary for controlling blood glucose (sugar) levels. When food is digested, sugar enters the bloodstream. The body uses this sugar for energy, growth, and repair. Insulin is necessary for the sugar in the bloodstream to enter into tissue cells where it is needed – in muscles, for example. Without enough insulin, sugar accumulates in the bloodstream where it eventually gets filtered out into the urine. Large quantities of water accompany the sugar that is lost through the kidneys. Consequently, diabetics produce a large volume of urine. To avoid getting dehydrated, cats compensate for this fluid loss by drinking excessively. Because the sugar cannot get into their cells without insulin, they switch to using fat and protein as an energy source, and diabetic cats usually lose weight as a result. Overweight cats are more likely to be afflicted with diabetes.

Diabetes is usually easy to diagnose. Most cats are presented to the veterinarian with the classic signs of diabetes: excessive urination, excessive thirst, very good appetite, and weight loss. High levels of sugar in the blood and the presence of sugar in the urine allow for a straightforward diagnosis. Occasionally, the clinical signs can be misleading, and the blood and urine tests can be equivocal, making the diagnosis somewhat tricky. In these instances, some additional tests may be necessary before arriving at a definitive diagnosis.

Treatment of diabetes involves medication and special diets. The majority of feline diabetics receive insulin injections. Although some cat owners are distraught at the thought of administering injections and would prefer to give pills, in most cases, insulin injections are the best choice and are actually much easier to administer than pills. Crispy could not be pilled, but giving her insulin injections was the easiest thing in the world.

Type 1 and 2 (and 3) vs. IDDM and NIDDM

In humans, we classify the diabetes as Type 1 or Type 2. Type 1 diabetes is characterized by genetic susceptibility to diabetes as well as destruction of the beta cells, the pancreatic cells responsible for producing insulin. Type 1 diabetics cannot produce enough insulin to keep their blood sugar regulated, and are dependent on insulin treatment for control of the disease. People with Type 1 diabetes are therefore classified as having insulin-dependent diabetes mellitus (“IDDM”). Humans with Type 2 diabetes, on the other hand, usually have a combination of insulin resistance and beta cell dysfunction. Their beta cells produce insulin, but usually in inadequate amounts, and their bodies don’t recognize or react to the insulin in the proper way. In humans with Type 2 diabetes, control of the diabetic state is usually possible through diet, exercise, and oral drugs. In other words, most humans with Type 2 diabetes can be controlled without the need for insulin and are said to have non-insulin-dependent diabetes mellitus (“NIDDM”). If beta cell dysfunction and insulin resistance become severe, however, insulin may eventually be necessary. As such, humans with Type 2 diabetes can have IDDM or NIDDM.

In cats, it is very difficult to figure out whether a cat has Type 1 diabetes vs. Type 2. It is perhaps more accurate to classify feline diabetes as IDDM or NIDDM, based on their need for insulin to control the diabetes, rather than Type 1 or Type 2. At the time diabetes is diagnosed, about 70% of cats have IDDM, while NIDDM accounts for the remaining 30%.

And then there’s something we call Type 3 diabetes. Type 3 diabetes occurs when something within the patient is interfering with insulin, leading to glucose intolerance. Cushings' Disease (Hyperadrenocorticism) is the most common cause of type III diabetes in dogs. This is a disorder that occurs when too much of the hormone cortisol is released by the adrenal glands. Cortisol is the body’s own natural steroid. Cushing’s disease is rare in cats. In cats, the most common cause of type 3 diabetes is steroid (prednisolone or prednisone) therapy. Sometimes, this type of diabetes will often resolve after the drug is withdrawn.

Transient diabetes

A small percentage of diabetic cats – cats who developed their diabetes naturally, and not secondary to steroids, like Crispy – are revealed to be “transiently” diabetic, usually within a few weeks after the disorder is diagnosed and treatment has begun. In these cats, the high blood sugar, presence of sugar in the urine, and clinical signs resolve, and insulin treatment can be discontinued. How does this happen?
In normal cats, when the pancreas detects elevated levels of sugar in the blood stream, it responds by secreting insulin. Blood sugar levels will then drop, gradually returning to normal. Some cats, however, may have a hidden problem with their pancreas – a decreased number of beta cells, and an impaired ability to secrete insulin. They may appear clinically normal, but they’re actually on the “brink” of being diabetic. If they’re then given drugs that impair insulin function, or if they become overweight or obese, the cats become intolerant of carbohydrates and develop high blood sugar. In some of these cats, though, the high levels of blood sugar causes something called “glucose-induced desensitization”, a temporary, reversible state in which beta cell function becomes even further suppressed, and these cats become insulin-dependent diabetics. In this population of cats, if you lower the blood sugar by giving insulin and correct or control concurrent disorders, beta cell function may be restored, and they begin to release insulin again, and the cat returns to their subclinical state, i.e. they’re go back to being “on the brink” again. I’ve had cats like this in my practice. They were diabetic, and were being given insulin injections, and suddenly they have a hypoglycemic crisis – their blood sugar drops and they they get sick, often necessitating a trip to the emergency clinic. We drop their insulin dose, and soon discover that they actually no longer need the insulin. If this happens, it usually occurs within the first six months of the diagnosis. But not always. A patient of mine named Danny was diabetic and was receiving insulin for about five years, when his pancreas suddenly decided to start secreting insulin again.

With Crispy, after about 3 years of giving her four units of twice-daily insulin, I noticed that she never experienced any of the signs of diabetes at all.

No excessive thirst, no more cinderblocks of clumped urine in the litterbox, normal appetite, and (unfortunately) no weight loss. (She’s a fatty; a little weight loss would have done her good.) I decided to check her blood sugar and it was low. Not dangerously low, but definitely lower than normal, and she had no sugar in her urine. Most diabetics, even those that are pretty well-controlled, will have at least a trace amount of glucose in their urine. Crispy had zero. So, I weaned her insulin dose down from 4 units twice a day, to 3 units, to 2, then 1, then off. Her blood sugar stayed normal. It still is. I tossed her insulin and syringes away. It’s a great feeling, akin to throwing out your contact lens case and solution after Lasik surgery.

End of story?

So, is that it for Crispy and her diabetes? Well, I’m not sure. In a study, published in 1999, of 10 cats with transient diabetes, seven cats did not experience a recurrence of their diabetes. Three of the cats, however, had a recurrence of their diabetes, one six months later, one 14 months later, and one 3.4 years later. In the study, it was not possible to predict which of the transient diabetics were at higher risk of a relapse. Certainly, cats whose diabetes seems to have resolved should be considered to be susceptible to a recurrence of their clinical diabetes, and it would be important to avoid the circumstances that could promote a return to the diabetic state. That would include avoiding any medications known to antagonize the effectiveness of insulin, such as glucocorticoids and progestins, maintaining ideal body weight, and minimizing concurrent illnesses. I don’t know about maintaining her ideal body weight (no matter what I do, she seems destined to be three pounds overweight), but I certainly won’t be giving her steroids again.

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