Cushing's & Cancer: growth hormone

Showing posts with label growth hormone. Show all posts

Wednesday, April 24, 2013

Adult growth hormone deficiency – benefits, side effects, and risks of growth hormone replacement

Frontiers in Endocrinology, 04/24/2013

Reed ML et al. – Deficiency of growth hormone (GH) in adults results in a syndrome characterized by decreased muscle mass and exercise capacity, increased visceral fat, impaired quality of life, unfavorable alterations in lipid profile and markers of cardiovascular risk, decrease in bone mass and integrity and increased mortality.

The potential of GH to act as a mitogen has resulted in concern over the possibility of increased de novo tumors or recurrence of pre–existing malignancies in individuals treated with GH.

Though studies of adults who received GHRT in childhood have produced conflicting reports in this regard, long term surveillance of adult GHRT has not demonstrated increased cancer risk or mortality.

Read more: http://www.mdlinx.com/endocrinology/news-article.cfm/4588746/growth-hormone-adult-growth-hormone-deficiency#ixzz2RODfAgDb

Monday, September 10, 2012

8th Annual Convention for Adults with Pituitary Disorders

The confirmed convention dates for the 8th Annual Convention for Adults with Pituitary Disorders are Friday, April 19th, 2013-Sunday, April 21st, 2013 in Las Vegas, NV.

So far, they are looking at two hotels, either the SUNCOAST or TUSCANY.

More info as it becomes available.

Friday, April 20, 2012

Magic Foundation Cushing's Conference

Includes: Adult Growth Hormone Deficiency, Panhypopituitarism, Cushings and Acromegaly

July 19-22, 2012

Westin- Lombard

Chicago, Illinois

For immediate information please email or call our office: ContactUs@magicfoundation.org or (708) 383-0808.)

Speakers include:

Roberto Salvatori, M.D.
Ian E. McCutcheon, M.D.
Anthony P. Heaney, M.D., Ph.D.
Lawrence A. Frohman, M.D.
N. Karen Thames, Psy.D.
Mary Andrews

More information (PDF)

Monday, April 16, 2012

Day Sixteen, Cushing's Awareness Challenge

I wrote parts of this a few years ago, so all the "yesterdays" and "last weeks" are a little off...

Wow. That's about all I can say. Yesterday was possibly the best day of my life since I started getting Cushing's symptoms, and that was over 25 years ago. A quarter of a century of feeling exhausted, fatigued. A quarter of my life spent taking naps and sleeping.

Last week in this post I wrote in part:

I went to the endo yesterday. Nothing has changed for me. Nothing will. He wants me to take more cortef. I don't want to gain weight again. He looked up Provigil and it's not indicated for panhypopituitarism. So he won't prescribe it. My kidney surgeon probably won't let me take, anyway, but it was worth a try.

...

He did mention that in "only" 2.5 years maybe I can go back on growth hormone. I don't want to live like this another year let alone 2.5. But then, when I was on GH before it didn't help me like it helps most everyone else.

I'm tired of catering to a kidney that may or may not fail sometime anyway, tired of being so exhausted all the time. I feel like I've lost nearly half my life to this Cushing's stuff already.

So, yesterday I was supposed to go to a conference on web design for churches. My church sent me because they want me to spiff up their site and make them a new one for Christmas. I wanted to go because, well, I like learning new stuff about the web. I figured that I would learn stuff that would also be useful to me in others of my sites.

And I did!

But the amazing thing is this. My son had told me about a medication that was very similar to Provigil, that he had tried it while he was writing his doctoral thesis and it had helped him.

So, having tried the official doctor route and being rebuffed - again - I had decided to try this stuff on my own.

Just the night before I had written a response on Robin's wonderful blog that reads in part:

I hate this disease, too.

I was just talking to a friend today about how I'd try nearly anything - even if it ruined my one remaining kidney - to have a few days where I felt good, normal, where I could wake up in the morning rested and be able to have energy for the day.

I want to go out and have fun, to be able to drive for more than 45 minutes without needing to rest, to be have people over for dinner, whatever. I hate being restricted by my lack of energy.

My endo says to cheer up. In two and a half years I can try the growth hormone again. Whoopee. Didn't work the first time and maybe gave me, or contributed to, cancer growth. Why would I want to look forward to trying that again?

I want to feel good now. Today.

I hate that this disease kills but I also hate that it's robbed me of half my life already.

I wish doctors would understand that even though we've "survived", there's no quality of life there.

I hate Cushing's. It robs so much from so many of us. :(

As I said earlier, I have a history of daily naps of at least 3 hours a day. It cuts into everything and prevents me from doing many things. I have to schedule my life around these naps and it's awful.

A few years ago I went on a Cushie trip to Rockford. I've been there a few times and it's always so much fun. But this first year, we were going to another Cushie's home for barbecue. I didn't drive, I rested in the back of the car during the drive. We got there and I managed to stay awake for a little while. Them I put my head down on the dining room table and fell asleep. Our hostess kindly suggested that I move over to the sofa.

So, I have a long history of daily naps, not getting through the day, yadda, yadda.

So, I was a little nervous about yesterday. I really wanted to go to this conference, and was afraid I'd have to go nap in my car.

I got up at 5:30 am yesterday. Before I left at 7:15, I took my Cortef and then I took my non-FDA approved simulated Provigil. (Although it's not FDA approved, it is not illegal to possess without a prescription and can be imported privately by citizens)

I stayed awake for the whole conference, went to a bell rehearsal, did Stacey's interview, had dinner and went to bed about 10:30PM. NO NAP! I did close my eyes a little during the 4:00PM session but it was also b-o-r-i-n-g.

I stayed awake, I enjoyed myself, I learned stuff, I participated in conversations (completely unlike shy me!).

I felt like I think normal people feel. I was amazed. Half my life wasted and I finally (thank you Michael!) had a good day.

My kidney doctor and my endo would probably be appalled but it's about time that I had some life again! Maybe in another 25 years, I'll take another pill. LOL

Well, the energy from the Adrafinil is a one day thing. I felt great on Thursday. Friday and Saturday I slept more than usual. Saturday, today, was one of those days where I sleep nearly all day. Maybe if I took the drug more it would build up in my system, maybe not. But it was still worth having that one day where I felt what I imagine normal to be.

While I was being a slug today, my husband painted the entire house.

I'm not sure if I would have been this tired today or if I was somehow making up for the nap I didn't get on Thursday. Whatever the case, I'm glad that I had the opportunity to try this and to experience the wonderful effects, if only for one day.

Information from a site that sells this:

Alertness Without Stimulation

Adrafinil is the prototype of a new class of smart drug - the eugeroics (ie, "good arousal") designed to promote vigilance and alertness. Developed by the French pharmaceutical company Lafon Laboratories, adrafinil (brand name, Olmifon) has been approved in many European countries for treating narcolepsy, a condition characterized by excessive daytime sleepiness and other unusual symptoms.

Non-narcoleptic users generally find that adrafinil gives them increased energy and reduces fatigue, while improving cognitive function, mental focus, concentration, and memory. It has been reported that quiet people who take adrafinil become more talkative, reserved people become more open, and passive people become more active.

Of course, many stimulant drugs, ranging from caffeine to methamphetamine, are known to produce similar alerting/energizing effects. Adrafinil has been described by some users as a "kinder, gentler" stimulant, because it provides these benefits but usually with much less of the anxiety, agitation, insomnia, associated with conventional stimulants.

Adrafinil's effects are more subtle than those of the stimulants you may be used to, building over a period of days to months. They appear to be based on its ability to selectively stimulate 1-adrenergic receptors in the brain.2 These receptors normally respond to norepinephrine (noradrenaline), a neurotransmitter linked to alertness, learning, and memory. This is in contrast to conventional stimulants, which stimulate a broader spectrum of brain receptors, including those involving dopamine. Its more focused activity profile may account for adrafinil's relative lack of adverse side effects.

There's more info about Adrafinil on Wikipedia

It's interesting that that snipped report that people become more talkative. I reported that in the original post, too, even though I didn't realize that this was a possibility.

A good quote that I wish I could relate to better:

"Time is limited, so I better wake up every morning fresh and know that I have just one chance to live this particular day right, and to string my days together into a life of action and purpose."

Lance Armstrong (1971 – )
Cyclist, seven-time Tour de France champion and cancer survivor

New stuff starts here:

Awhile ago I went to a handbell festival. I took a bit of adrafinil on the main day to try to stay awake for the whole day. It didn't seem to keep me as on as it did before. I can't be used to it already. Maybe I'm just that much more tired than I was before.

Our son lives in New York and every few years he gives us tickets to see a Broadway show. A couple years ago we took the train to NY to see Wicked. Usually my DH wants to go out and see sights while we're there. I usually want to nap.

This time we got up on Saturday morning, went out for breakfast. I wanted to take in the whole day and enjoy Wicked so I took some Adrafinil. We got back to the hotel and got ready to go to a museum or other point of interest.

But, DH wanted to rest a bit first. Then our son closed his eyes for a bit...

So, I found myself the only one awake for the afternoon. They both work up in time for the show...

Sigh It was a great show, though.

This last Christmas I was going to get my son some Adrafinil as a gift. The original place we bought it didn't have any more stock so I tracked it down as a surprise. He was going to give me some, as well, but couldn't get it from the original source, either. So he found something very similar called Modafinil. GMTA!

Saturday, April 14, 2012

Day Fourteen, Cushing's Awareness Challenge

And today, we talk about pink jeeps and ziplines...

How in the world did we get here in a Cushing's Challenge? I'm sliding these in because in Day Twelve I linked (possibly!) my growth hormone use as a cause of my cancer - and I took the GH due to Cushing's issues. Clear? LOL

I had found out that I had my kidney cancer on Friday, April 28, 2006 and my surgery on May 9, 2006. I was supposed to go on a Cushie Cruise to Bermuda on May 14, 2006. My surgeon said that there was no way I could go on that cruise and I could not postpone my surgery until after that cruise.

I got out of the hospital on the day that they left for the cruise and realized that I wouldn't have been much (ANY!) fun and I wouldn't have had any.

An especially amusing thread from that cruise is The Adventures of Penelopee Cruise. Someone had brought a UFC jug and decorated her and had her pose around the ship. The beginning text reads:

Penelopee had a lovely time on Explorer of the Seas which was a five day cruise to Bermuda. She needed something to cheer her up since her brother, Tom, went off the deep end, but that's another story!

Penelopee wanted to take in all of the sights and sounds of this lovely vessel. Every day she needed to do at least one special thing. Being a Cushie, she didn't have enough spoons to do too much every day.

On the first day, she went sunning on the Libido deck......she didn't last too long, only about 10 minutes. Goodness, look at her color! Do you think maybe her ACTH is too high?

Although I missed this trip, I was feeling well enough to go to Sedona, Arizona in August, 2006. I convinced everyone that I was well enough to go off-road in a pink jeep, DH wanted to report me to my surgeon but I survived without to much pain and posed for the header image.

In 2009, I figured I have “extra years” since I survived the cancer and I wanted to do something kinda scary, yet fun. So, somehow, I decided on ziplining. Tom wouldn’t go with me but Michael would so I set this up almost as soon as we booked a Caribbean cruise to replace the Cushie Cruise to Bermuda.

Each person had a harness around their legs with attached pulleys and carabiners. Women had them on their chests as well. In addition, we had leather construction gloves and hard hats.

We climbed to the top of the first platform and were given brief instructions and off we went. Because of the heavy gloves, I couldn’t get any pictures. I had thought that they would take some of us on the hardest line to sell to us later but they didn't. They also didn’t have cave pictures or T-Shirts. What a missed opportunity!

This was so cool, so much fun. I thought I might be afraid at first but I wasn’t. I just followed instructions and went.

Sometimes they told us to break. We did that with the right hand, which was always on the upper cable.

After the second line, I must have braked too soon because I stopped before I got to the platform. Michael was headed toward me. The guide on the end of the platform wanted me to do some hand over hand maneuver but I couldn’t figure out what he was saying so he came and got me by wrapping his legs around me and pulling me to the platform.

After that, no more problems with breaking!

The next platform was very high – over 70 feet in the air – and the climb up was difficult. It was very hot and the rocks were very uneven. I don’t know that I would have gotten to the next platform if Michael hadn’t cheered me on all the way.

We zipped down the next six lines up to 250-feet between platforms and 85-feet high in the trees, at canopy level. It seemed like it was all over too soon.

But, I did it! No fear, just fun.

Enough of adventures - fun ones like these, and scary ones like transsphenoidal surgery and radical nephrectomy!

Friday, April 13, 2012

Day Twelve, Cushing's Awareness Challenge

Today's Cushing's Awareness Challenge post is about kidney cancer (renal cell carcinoma). You might wonder how in the world this is related to Cushing's. I think it is, either directly or indirectly.

I alluded to this in Day Nine when I said:

I finally started the Growth Hormone December 7, 2004.
Was the hassle and 3 year wait worth it?
Stay tuned for Day 12, April 12, 2012 when all will be revealed.

So, as I said, I started Growth Hormone for my panhypopituitarism on December 7, 2004. I took it for a while but never really felt any better, no more energy, no weight loss. Sigh.

April 14 2006 I went back to the endo and found out that the argenine test that was done in 2004 was done incorrectly. The directions were written unclearly and the test run incorrectly, not just for me but for everyone who had this test done there for a couple years. My endo discovered this when he was writing up a research paper and went to the lab to check on something.

So, I went off GH again for 2 weeks, then was retested. The "good news" was that the argenine test is only 90 minutes now instead of 3 hours.

Wow, what a nightmare my argenine retest started! I went back for that Thursday, April 27, 2006. Although the test was shorter, I got back to my hotel and just slept and slept. I was so glad that I hadn't decided to go home after the test.

Friday I felt fine and drove back home, no problem. I picked up my husband for a biopsy and took him to an outpatient surgical center. While I was there waiting for the biopsy to be completed, I started noticing blood in my urine and major abdominal cramps. I left messages for several of my doctors on what I should do. I finally decided to see my PCP after I got my husband home.

When Tom was done with his testing, his doctor took one look at me and asked if I wanted an ambulance. I said no, that I thought I could make it to the emergency room ok - Tom couldn't drive because of the anaesthetic they had given him. I barely made it to the ER and left the car with Tom to park. Tom's doctor followed us to the ER and became my new doctor.

They took me in pretty fast since I was in so much pain, and had the blood in my urine. They thought it was a kidney stone. After a CT scan, my new doctor said that, yes, I had a kidney stone but it wasn't the worst of my problems, that I had kidney cancer. Wow, what a surprise that was! I was admitted to that hospital, had more CT scans, MRIs, bone scans, they looked everywhere.

My open radical nephrectomy was May 9, 2006 in another hospital from the one where the initial diagnosis was made. My surgeon felt that he needed a specialist from that hospital because he believed preop that my tumor had invaded into the vena cava because of its appearance on the various scans. Luckily, that was not the case.

My entire left kidney and the encapsulated cancer (10 pounds worth!) were removed, along with my left adrenal gland and some lymph nodes. Although the cancer (renal cell carcinoma AKA RCC) was very close to hemorrhaging, the surgeon believes he got it all. He said I was so lucky. If the surgery had been delayed any longer, the outcome would have been much different. I will be repeating the CT scans every 3 months, just to be sure that there is no cancer hiding anywhere. As it turns out, I can never say I'm cured, just NED (no evidence of disease). This thing can recur at any time, anywhere in my body.

I credit the argenine re-test with somehow aggravating my kidneys and revealing this cancer. Before the test, I had no clue that there was any problem. The argenine test showed that my IGF is still low but due to the kidney cancer I couldn't take my growth hormone for another 5 years - so the test was useless anyway, except to hasten this newest diagnosis.

So... either Growth Hormone helped my cancer grow or testing for it revealed a cancer I might not have learned about until later.

My five years are up now. My kidney surgeon *thinks* it would be ok to try the growth hormone again. I'm still a little leery about this, especially where I didn't notice that much improvement.

What to do?

Monday, April 9, 2012

Day Nine, Cushing's Awareness Challenge

Cushing's Conventions have always been special times for me - we learn a lot, get to meet other Cushies, even get referrals to endos!

As early as 2001 (or before) my pituitary function was dropping. My former endo tested annually but did nothing to help me with the symptoms.

In the fall of 2002 my endo refused to discuss my fatigue or anything at all with me until I lost 10 pounds. He said I wasn't worth treating in my overweight condition and that I was setting myself up for a heart attack. He gave me 3 months to lose this weight. Those 3 months included Thanksgiving, Christmas and New Years. Needless to say, I left his office in tears, again.

Fast forward 2 years to 2004. I had tried for awhile to get my records from this endo. He wouldn't send them, even at doctors' or my requests.

I wanted to go see Dr. Vance at UVa but I had no records so she would't see me until I could get them.

Finally, my husband went to the former endo's office and threatened him with a court order, The office manager managed to come up with about 13 pages of records. For going to him from 1986 to 2001 including weeks and weeks at NIH and pituitary surgery, that didn't seem like enough records to me.

In April of 2004, many of us from the message boards went to the UVa Pituitary Days Convention. That's where the picture above comes in. Other pictures from that convention are here.

By chance, we met a wonderful woman named Barbara Craven. She sat at our table for lunch on the last day and, after we learned that she was a dietitian who had had Cushing's, one of us jokingly asked her if she'd do a guest chat for us. I didn't follow through on this until she emailed me later. In the email, she asked how I was doing. Usually I say "fine" or "ok" but for some reason, I told her exactly how awful I was feeling.

Barbara emailed me back and said I should see a doctor at Johns Hopkins. I said I didn't think I could get a recommendation to there, so SHE referred me. The doctor got right back to me, set up an appointment. Between his vacation and mine, that first appointment turned out to be Tuesday, Sept 14, 2004.

Just getting through the maze at Johns Hopkins was amazing. They have the whole system down to a science, moving from one place to another to sign in, then go here, then window 6, then... But it was very efficient.

My new doctor was wonderful. Understanding, knowledgeable. He never once said that I was "too fat" or "depressed" or that all this was my own fault. I feel so validated, finally.

He looked through my records, especially at my 2 previous Insulin Tolerance Tests. From those, he determined that my growth hormone has been low since at least August 2001 and I've been adrenal insufficient since at least Fall, 1999 - possibly as much as 10 years! I was amazed to hear all this, and astounded that my former endo not only didn't tell me any of this, he did nothing. He had known both of these things - they were in the past records that I took with me. Perhaps that was why he had been so reluctant to share copies of those records. He had given me Cortef in the fall of 1999 to take just in case I had "stress" and that was it.

The new endo took a lot of blood (no urine!) for cortisol and thyroid stuff. I went back on Sept. 28, 2004 for arginine, cortrosyn and IGF testing.

He said that I would end up on daily cortisone - a "sprinkling" - and some form of GH, based on the testing the 28th.

For those who are interested, my new endo is Roberto Salvatori, M.D.
Assistant Professor of Medicine at Johns Hopkins

Medical School: Catholic University School of Medicine, Rome, Italy
Residency: Montefiore Medical Center
Fellowship: Cornell University, Johns Hopkins University
Board Certification: Endocrinology and Metabolism, Internal Medicine

Clinical Interests: Neuroendocrinology, pituitary disorders, adrenal disorders

Research Interests: Control of growth hormone secretion, genetic causes of growth hormone deficiency, consequences of growth hormone deficiency.

Although I have this wonderful doctor, a specialist in growth hormone deficiency at Johns Hopkins, in November, 2004, my insurance company saw fit to over-ride his opinions and his test results based on my past pharmaceutical history! Hello??? How could I have a history of taking GH when I've never taken it before?

Of course, I found out late on a Friday afternoon. By then it was too late to call my case worker at the drug company, so we had to appeal on Monday. My local insurance person also worked on an appeal, but the whole thing was just another long ordeal of finding paperwork, calling people, FedExing stuff, too much work when I just wanted to start feeling better by Thanksgiving.

As it turned out the insurance company rejected the brand of hGH that was prescribed for me. They gave me the ok for a growth hormone was just FDA-approved for adults on 11/4/04. The day this medication was approved for adults was the day after my insurance said that's what is preferred for me. In the past, this form of hGH was only approved for children with height issues. Was I going to be a ginuea pig again?

The new GH company assigned a rep for me, submitted info to pharmacy, and waited for insurance approval, again.

I finally started the Growth Hormone December 7, 2004.

Was the hassle and 3 year wait worth it?

Stay tuned for Day 12, April 12, 2012 when all will be revealed.

Read Dr. Barbara Craven's Guest Chat, October 27, 2004

Thanks for reading :)

Saturday, April 7, 2012

Day Seven, Cushing's Awareness Challenge

Sleep. Naps. Fatigue. I still have them all. I wrote on my bio in 1987 after my pituitary surgery "I am still and always tired and need a nap most days. I do not, however, still need to take whole days off just to sleep."

That seems to be changing back, at least on the weekends. Last weekend, both days, I took 7-hour naps each day and I woke up tired. That's awfully close to taking a whole day off to sleep again.

In 2006, I flew to Chicago, IL for a Cushing's weekend in Rockford. Someone else drove us to Lake Geneva, Wisconsin for the day. Too much travel, too Cushie, whatever, I was too tired to stay awake. I actually had put my head down on the dining room table and fallen asleep but our hostess suggested the sofa instead.

This sleeping thing really impacts my life. Between choir rehearsals, I come home for a 45-minute nap. Sometimes, during adult choir rehearsals, I start to nod off anyway.

I only TiVo old tv shows that I can watch and fall asleep to since I already know the ending.

Maybe now that I'm more than 5 years out from my kidney cancer I can go back on Growth Hormone again. My surgeon says he "thinks" it's ok. I'm sort of afraid to ask my endo about it, though. I want to feel better and get the benefits of the GH again but I dont want any type of cancer again and I certainly can't afford to lose another kidney.

I'm feeling so old and weary today...

Thursday, January 19, 2012

GH replacement therapy associated with development of diabetes

Posted on EndocrineToday.com

Luger A. Diabetes Care. 2012;35:57-62.

The incidence of diabetes was increased in patients with growth hormone deficiency who were on growth hormone replacement therapy, according to researchers in Europe.

The researchers selected patients from KIMS — Pfizer International Metabolic Database. Patients were selected if they had severe adult-onset GH deficiency that was confirmed with a GH stimulatory test and naive to GH treatment. Patients with a history of Cushing’s disease or acromegaly or with diabetes at baseline were excluded.

The study included data from 5,143 patients. Plasma glucose, HbA1c values, lipid and insulin-like growth factor I concentrations and serum IGF-I measurements were obtained.

Five hundred twenty-three patients developed diabetes after a median of 1.7 years. Patients who developed diabetes were older, had higher BMI, waist circumference, waist-to-hip ratio and triglyceride concentrations. They also had higher systolic and diastolic blood pressure and lower HDL cholesterol.

The incidence of diabetes was 2.6/100 patient-years, decreasing from 4.1/100 patient-years during the first year of GH replacement therapy to 1/100 patient-years after more than 8 years of treatment. The overall observed cases/expected cases ratio was 6, decreasing from 10.8 in the first year of treatment to 1.9 after 8 or more years of treatment.

Sex, BMI, attained age during follow-up, years between pituitary diagnosis and GH treatment start and years since first treatment were significantly associated with diabetes occurrence. There was no significant association with GH dose. In patients who did not develop diabetes, plasma glucose concentrations increased from 84.4 mg/dL to 89.5 mg/dL, and HbA1c levels increased from 4.74% to 5.09% after 6 years of treatment.

“Despite widely demonstrated benefits of growth hormone replacement treatment in adult growth hormone deficiency, a marked increase in the risk of developing diabetes must be considered,” the researchers wrote. “All patients, but particularly those with an adverse risk profile, should be carefully followed regarding parameters of glucose metabolism.”

From http://www.endocrinetoday.com/view.aspx?rid=91303

Sunday, January 1, 2012

Red alert: Hypertension on the prowl

The family of Mr. Adulphus Opara of Umunokwu in Okwuato, Aboh Mbaise Local Government Area of Imo State was shocked to its nerves as the man slumped from the chair on which he was sitting and cuddling his little daughter who was just less than five months. Scampering and running up and down, all efforts by family members to revive their breadwinner were too little and too late as he died that sunny Saturday afternoon. It was later revealed by doctors at a private hospital that Adolphus died of hypertension attack.

The case of Adolphus is just one out of the numerous complaints of the havocs wreaked by untreated or unchecked hypertension. Medical experts say it has sent so many victims to their untimely grave.

Dr. Francis Duru, a physician and senior lecturer in Human Anatomy, College of Medicine, University of Lagos Teaching Hospital (LUTH), Idi Araba, described hypertension as a silent killer and the major cause of most sudden deaths in Nigeria. He said high blood pressure is when one’s BP is consistently above 140/90 mmHg.

According to him, “Normal blood pressure is when your blood pressure is measured at 120/80 mmHg most of the time. If your blood pressure is consistently above 140/90, then the person has hypertension or is hypertensive. Untreated hypertension can lead to many health complications and the worst of all is sudden death.”

MedicinePlus, a medical publication, defines hypertension or high blood pressure as a cardiac chronic medical condition in which the systemic arterial blood pressure is elevated. What that means is that the heart is having to work harder than it should to pump blood around the body. Blood pressure involves two measurements, systolic and diastolic. Normal blood pressure is 120/80 mm/Hg.

The first figure is the systolic blood pressure, the pressure there is in the arteries when your heart is contracting. The second, or lower figure, is the diastolic blood pressure, which is the pressure in your arteries between heartbeats. High blood pressure is anything above 140/90 mm/Hg. Hypertension is the opposite of hypotension. Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorised as “primary hypertension,” which means high blood pressure with no obvious medical cause.

The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system. MedicinePlus added: “Persistent hypertension is one of the risk factors for stroke, myocardial infarction, heart failure and arterial aneurysm, and is a leading cause of chronic kidney failure. Moderate elevation of arterial blood pressure leads to shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment may prove necessary in patients for whom lifestyle changes prove ineffective or insufficient.”

The American Heart Association, in one of its recent reports, made it known that the World Health Organisation (WHO) attributes hypertension, or high blood pressure, as the leading cause of cardiovascular mortality. The World Hypertension League (WHL), an umbrella organisation of 85 national hypertension societies and leagues, recognised that more than 50% of the hypertensive population worldwide are unaware of their condition. To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated May 17 of each year as World Hypertension Day (WHD). Over the past three years, more national societies have been engaging in WHD and have been innovative in their activities to get the message to the public. In 2007, there was record participation from 47 member countries of the WHL. During the week of WHD, all these countries – in partnership with their local governments, professional societies, nongovernmental organisations and private industries – promoted hypertension awareness among the public through several media and public rallies.

Causes and risk factors

Although Duru noted that there were several causes of hypertension, he still insisted that there were instances when it had no direct link or cause. He said: “Medically, we have causes, incidences and risk factors that are associated with hypertension. I am talking about factors that can cause or lead to hypertension. In this case we have issues like the level of water or salt in a person’s body; ability or inability of some organs like the kidneys or blood vessels to function at optimum levels; life history, that is, does hypertension run in your family? lifestyle, that is, the type of food you eat; lack of exercises and always being in a noisy place or being in a state of anxiety all the time. Let me also quickly add that excessive smoking and over-indulgence in alcohol can lead to hypertension.”

He added: ‘“You can easily become hypertensive when you reach the stage of adult age because one’s blood vessels are stiffer as one reaches old age. This leads to HBP. I can also tell you that high blood pressure increases your chances of having a stroke, heart attack, heart failure, kidney disease, and early death. I must also state it here that there are some conditions of health one will find oneself and one will surely expect to be hypertensive. For instance, some pregnant women are usually hypertensive especially from the sixth month until they put to birth. Diabetic patients are sometimes hypertensive although there is no causal relationship between hypertension and diabetes.

People who are obsessed are at risk of suffering from hypertension just as chronic kidney diseases and poor conditions or disorders of the adrenal glands can as well lead to hypertension.” The LUTH medical expert revealed that wrong or too much application of some drugs could also lead to hypertension. “Wrong application or continuous administration of some medications such as birth control pills, diet control pills, cold medications, etc are other ways by which hypertension can hit at a person”, he warned. Meanwhile, Duru noted that there were some instances when hypertension had no cause or trace and it is described as essential hypertension.

Symptoms

Most medical experts agree that hypertension, in most cases, has no external symptoms. To this effect, Duru said: “You can now see why we call hypertension a silent killer. It is a silent killer because it gives no sign, no symptom and no warning before it strikes. I must comment here that most Nigerians are suffering from hypertension without knowing it. This is why we also recommend that people should go for BP check regularly to confirm their status. Based on these facts, so many Nigerians develop sicknesses like heart diseases, kidney failures and other complications without any prior knowledge that all their problems started from untreated or unchecked hypertension.

It is also important to note that a hypertensive patient can live his normal life if he abides by medical advice and that means taking his drugs.” ADAM Medical Encyclopedia listed certain conditions as symptoms of hypertension. According to its report, “If you have a severe headache, nausea or vomiting, bad headache, confusion, changes in your vision, or nosebleeds you may have a severe and dangerous form of high blood pressure called malignant hypertension.” The publication recommended that there should be several checks before it could be ascertained that one has hypertension. It noted that: “Your health care provider will check your blood pressure several times before diagnosing you with high blood pressure. It is normal for your blood pressure to be different depending on the time of day. Blood pressure readings taken at home may be a better measure of your current blood pressure than those taken at your doctor’s office.”

Among the tests to be taken to confirm whether or not one has hypertension, according to Duru, are physical examinations to look for bad conditions of the heart or diseases severely affecting it, poor state or damage of the eyes, as well as other bad physical changes in your body. In this case, tests that enable doctors to handle the situation well include: cholesterol level; level of heart disease like echocardiogram or electrocardiogram; level of metabolic panel/ urinalysis or ultrasound of the kidney and this is when the case has become a chronic one.

Types

A widely posted medical material stated: “A blood pressure is usually classified based on the systolic and diastolic blood pressures. Systolic blood pressure is the blood pressure in vessels during a heartbeat. Diastolic blood pressure is the pressure between heartbeats. A systolic or the diastolic blood pressure measurement higher than the accepted normal values for the age of the individual is classified as pre hypertension or hypertension. Hypertension has several sub-classifications, including hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly.

These classifications are made after averaging a patient’s resting blood pressure readings taken on two or more office visits. Individuals older than 50 years are classified as having hypertension if their blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Hypertension is also classified as resistant if medications do not reduce blood pressure to normal levels.”

Accelerated hypertension – this is associated with headache, drowsiness, confusion, vision disorders, nausea, and vomiting. These symptoms are collectively called hypertensive encephalopathy. Hypertensive encephalopathy is caused by severe small blood vessel congestion and brain swelling, which is reversible if blood pressure is lowered.

Secondary hypertension– some additional signs and symptoms suggest that the hypertension is caused by disorders in hormone regulation. Hypertension combined with obesity distributed on the trunk of the body, accumulated fat on the back of the neck (“buffalo hump”), wide purple marks on the abdomen (abdominal striae), or the recent onset of diabetes suggests that an individual has a hormone disorder known as Cushing’s syndrome. Hypertension caused by other hormone disorders such as hyperthyroidism, hypothyroidism, or growth hormone excess will be accompanied by additional symptoms specific to these disorders. For example, hyperthyroidism can cause weight loss, tremors, heart rate abnormalities, reddening of the palms, and increased sweating.

In pregnancy–Hypertension in pregnant women is one symptom of pre-eclampsia. Pre-eclampsia can progress to a life-threatening condition called eclampsia, which is the development of protein in the urine, generalised swelling, and severe seizures. Other symptoms indicating that brain function is becoming impaired may precede these seizures such as nausea, vomiting, headaches, and vision loss.

In children –Some signs and symptoms are especially important in newborns and infants such as failure to thrive, seizures, irritability, lack of energy, and difficulty breathing. In children, hypertension can cause headache, fatigue, blurred vision, nosebleeds, and facial paralysis. Even with the above clinical symptoms, the true incidence of paediatric hypertension is not known. In adults, hypertension has been defined due to the adverse effects caused by hypertension. However, in children, similar studies have not been performed thoroughly to link any adverse effects with the increase in blood pressure. Therefore, the prevalence of paediatric hypertension remains unknown due to the lack of scientific knowledge.

Essential hypertension– this is the most prevalent hypertension type, affecting 90–95% of hypertensive patients. Although no direct cause has been identified, there are many factors such as sedentary lifestyle smoking, stress, visceral obesity, potassium deficiency (hypokalemia), obesity (more than 85% of cases occur in those with a body mass index greater than, salt (sodium) sensitivity, alcohol intake, and vitamin D deficiency that increase the risk of developing hypertension. Risk also increases with aging, some inherited genetic mutations, and having a family history of hypertension. An elevated level of rennin, a hormone secreted by the kidney, is another risk factor, as is sympathetic nervous system over activity.

Secondary hypertension–By definition, this results from an identifiable cause. This type is important to recognise since it’s treated differently to essential hypertension, by treating the underlying cause of the elevated blood pressure. Hypertension results in the compromise or imbalance of the path physiological mechanisms, such as the hormone-regulating endocrine system, that regulates blood plasma volume and heart function.

Treatment

According to an ADAM Medical Encyclopedia research work, “The goal of treatment is to reduce blood pressure so that you have a lower risk of complications. You and your health care provider should set a blood pressure goal for you. If you have pre-hypertension, your health care provider will recommend lifestyle changes to bring your blood pressure down to a normal range. Medicines are rarely used for pre-hypertension. You can do many things to help control your blood pressure, including: Eat a heart-healthy diet, including potassium and fibre, and drink plenty of water.

Exercise regularly — at least 30 minutes of aerobic exercise a day. If you smoke, quit – find a programme that will help you stop. Limit how much alcohol you drink — one drink a day for women, two a day for men. Limit the amount of sodium (salt) you eat — aim for less than 1,500 mg per day Reduce stress — try to avoid things that cause you stress. You can also try meditation or yoga. Stay at a healthy body weight — find a weight-loss program to help you, if you need it.

There are many different medicines that can be used to treat high blood pressure but must be prescribed by well-qualified physician. Often, a single blood pressure drug may not be enough to control your blood pressure, and you may need to take two or more drugs. It is very important that you take the medications prescribed to you. If you have side effects, your health care provider can substitute a different medication. Most of the time, high blood pressure can be controlled with medicine and lifestyle changes.

Effects

It has been gathered through various medical work that a patient is at risk and may likely suffer from complications when BP is not treated or controlled. The ADAM Medical publication warned that the following poor conditions of health might result as an evidence of poor treatment: Bleeding from the aorta, the large blood vessel that supplies blood to the abdomen, pelvis, and legs. Chronic kidney disease, heart attack and heart failure, poor blood supply to the legs, stroke and problems with the vision.

Here Duru was of the view that most of the sudden death now recorded in Nigeria was as a result of untreated hypertension. ‘ I have explained earlier that most Nigerians are hypertensive without knowing it. In other words, they carry on their daily activities or life style without undergoing the tests and living the medically prescribed way a hypertension victim suppose to observe’. ‘ The effect’, he explained, ‘is that the patient might likely be attacked or hit by stroke, kidney failure or heart attack which leads to instant death. You know I described it as a silent killer and this is exactly what I mean.

So many Nigerians have been killed by heart failure resulting from hypertension. In some instances the person slumps at home, on the road, in the office or anywhere as the case might be. At some other time, the victim goes to bed and does not wake up. When we experience such situations, some us, in the usual Nigerian way, blame it on the wicked landlord, the envious next door neighbour or a witch or wizard in the village.’

Prevention

Doctors have unanimously agreed that hypertension has no permanent cure. At best, it can be managed or controlled. Duru explains further. He said: ‘first, for now, there is no permanent cure for hypertension, medically speaking. As a Christian, I believe in miracles but in medical terms, it is yet to be proved that hypertension has any known permanent cure. If you a victim, it means that you have to be on drugs all the days of your life. And such a patient must be ready to go for BP check regularly. He has to abstain from certain behaviour like too much salt in-take, smoking, taking more than two bottles of beer daily and he must watch his weight and do regular exercises.

I am aware the trado-medicine people usually come up with so many claims but they are also not bold enough to submit their claims to empirical proves or thorough laboratory tests.’ A medical sponsored by the American National Heart, Lung and Blood Institute reported that the prevention depends on so many factors: It wrote thus: ‘ The degree to which hypertension can be prevented depends on a number of features including current blood pressure level, sodium/potassium balance, detection and omission of environmental toxins, changes in end/target organs (retina, kidney, heart, among others), risk factors for cardiovascular diseases and the age at diagnosis of pre hypertension or at risk for hypertension.

A prolonged assessment that involves repeated blood pressure measurements provides the most accurate blood pressure level assessment. Following this, lifestyle changes are recommended to lower blood pressure, before the initiation of prescription drug therapy. According to the British Hypertension Society, the process of managing pre hypertension includes lifestyle changes such as the following: Weight reduction and regular aerobic exercise (e.g., walking): Regular exercise improves blood flow and helps to reduce the resting heart rate and blood pressure. Reduce sodium (salt) in the body by disuse of condiment sodium and the adoption of a high potassium diet, which rids the renal system of excess sodium.

Many people use potassium chloride salt substitute to reduce their salt intake.’ In 2003 the American Heart Association recommended the following drugs for the treatment of hypertension: Potassium - is essential for the proper functioning of the heart, kidneys, muscles, nerves, and digestive system. Usually the food you eat supplies all of the potassium you need.

Bosentan - is used to treat Pulmonary Arterial Hypertension (PAH, high blood pressure in the vessels that carry blood to the lungs). Bosentan may improve the ability to exercise and slow the worsening of symptoms in patients with PAH. Tadalafil (Cialis) is used to treat erectile dysfunction (impotence; inability to get or keep an erection) in men. Tadalafil (Adcirca) is used to improve the ability to exercise in people with pulmonary arterial hypertension (PAH; high blood pressure in the vessels carrying blood to the lungs, causing shortness of breath, dizziness, and tiredness.

From http://www.sunnewsonline.com/webpages/features/icon/2012/jan/01/icon-01-10-2012-003.html

Thursday, November 10, 2011

Patients Diagnosed With Severe Adult GH Deficiency Using The Insulin Tolerance Test, Arginine Or Glucagon Stimulation Tests Share Similar Clinical Features

PDF (277.1 KB)

Authors

Andy Toogood, MD, FRCP¹, Georg Brabant, MD, PhD FRCP², Dominique Maiter, MD, PhD³, Björn Jonsson, PhD⁴, Ulla Feldt-Rasmussen, MD, PhD⁵, Maria Koltowska-Haggstrom, PhD⁶, Ase Krogh Rasmussen, MD, PhD⁵, Michael Buchfelder, MD⁷, Bernhard Saller, MD, PhD⁸, Beverly M K Biller, MD⁹

¹Department of Endocrinology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, B15 2TH, United Kingdom
² Experimental and Clinical Endocrinology, MedizinischeKlinik I, RatzeburgerAllee 160, D-23538, Lübeck, Germany
³Department. of Endocrinology, CliniquesUniversitaires Saint-Luc, Avenue Hippocrate, 54.74, 1200 Brussels
⁴Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden
⁵Department of Medical Endocrinology, Rigshospitalet, Copenhagen, 2100, Denmark
⁶KIMS Pfizer Endocrine Care, Specialty Business Unit, Pfizer Health AB, Sollentuna, 190 91, Sweden
⁷Department of Neurosurgery, University of Erlangen Nuernberg, Erlangen, 91045, Germany
⁸ Pfizer Endocrine Care Europe, Tadworth, United Kingdom
⁹Neuroendocrine Unit, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, United States

Abstract

Objective: To determine whether the ITT, arginine (AST) and glucagon stimulation tests (GST) identify patients who have similar features of GH deficiency using a diagnostic threshold of 3 μg/l.

Patients and Methods: 5453 tests were available from 4,867 patients registered in the KIMS database (49.9% females, ITT = 3111, AST = 1390, GST = 952). Comparisons were made for GH peak, BMI, lipids, waist circumference, waist:hip ratio and quality of life (QoL-AGHDA questionnaire).

Results. There were significant (p<0.0001) intra-individual correlations between the GH peaks for the ITT vs AST (r = 0.655), ITT vs GST (r = 0.445) and AST vs GST (r = 0.632). GH peaks in response to all tests were negatively correlated to the number of additional pituitary hormone deficiencies, and positively correlated to IGF-I SDS. BMI had a negative influence on all three tests.

Comparing GHD patients according to the diagnostic test used, most clinical variables did not differ between the groups. The only exceptions showing any difference were BMI being slightly higher in the AST and GST groups, triglyceride levels increased in the GST group, and IGF-I SDS was lower in the ITT and AST than in the GST group. Waist circumference was larger and quality of life was worse in the GST group than in the other groups.

Conclusions. This study demonstrates that the ITT, AST and GST produce similar GH peaks, are influenced by similar clinical factors and identify patients with similar features of GH deficiency at a diagnostic threshold of 3 μg/L.

Keywords

Growth hormone deficiency, ITT, stimulation tests, glucagon, arginine, clonidine, IGF-I

Show References

From http://aace.metapress.com/content/h4228513un4m6370/

Saturday, November 5, 2011

What Is the Best Approach for the Evaluation and Management of Endocrine Incidentalomas?

Key points include: Advances and more frequent use of diagnostic radiology have led to the increased prevalence of endocrine incidentalomas; Pituitary, thyroid, and adrenal incidentalomas must be assessed for dysfunctional hormone secretion and malignant potential; Inpatient management of endocrine incidentalomas should include consultation of endocrine or surgical teams in cases of dysfunctional or malignant lesions; Post-discharge instructions shouldclearly delineate timelines for repeat imaging, laboratory testing, and subspecialist follow-up.

by Darlene Tad-y, MD, Section of Hospital Medicine, University of Colorado Denver

Benign adrenal gland tumors.

Case

A 54-year-old man with a history of hypertension treated with hydrocholorothiazide and Type 2 diabetes mellitus is admitted with abdominal pain and found to have an incidental 2.1-cm left adrenal mass on CT scan of the abdomen. He denies symptoms of headache, palpitations, weight gain, or muscle weakness. His exam is significant for mildly elevated blood pressure. What is the best approach for evaluation and management of this incidental finding?

Overview

Incidentalomas are mass lesions that are inadvertently discovered during radiolographic diagnostic testing or treatment for other clinical conditions that are unrelated to the incidental mass. In recent decades, improvements in radiographic diagnostic techniques and sensitivity have led to increasing discovery of incidental lesions that are often in the absence of clinical signs or symptoms.¹ Three commonly discovered lesions by hospitalists are pituitary, thyroid, and adrenal incidentalomas.² The concerns associated with these findings relate to the potential for dysfunctional hormone secretion or malignancy.

Patients found with pituitary incidentalomas can be susceptible to several types of adverse outcomes: hormonal hypersecretion, hypopituitarism, neurologic morbidity due to tumor size, and malignancy in rare cases. Thyroid incidentalomas are impalpable nodules discovered in the setting of ultrasound or cross-sectional neck scans, such as positron emission tomography (PET) scans. Discovery of a thyroid incidentaloma raises concern for thyroid malignancy.³ The increased use of abdominal ultrasound, CT scans, and MRI has fueled the growing incidence of adrenal incidentalomas (AIs).

The discovery of an endocrine incidentaloma in the inpatient setting warrants a systematic approach that includes both diagnostic and potentially therapeutic management. A hospitalist should consider an approach that includes (see Table 1):

click for large version

Table 1. General inpatient approach to endocrine incidentalomas

Characterization of the incidentaloma, including clinical signs and symptoms, size, hormonal function, and malignant potential;
Immediate management, including medical versus surgical treatment; and
Post-discharge management, including monitoring.

Review of the Data

Pituitary incidentalomas. The prevalence of pituitary incidentalomas found by CT ranges from 3.7% to 20%, while the prevalence found by MRI approximates 10%. Autopsy studies have revealed a prevalence ranging from 1.5% to 26.7% for adenomas less than 10 mm, considered to be microadenomas. Broad categories of etiologies should be considered: pituitary adenoma, nonpituitary tumors, vascular lesions, infiltrative disorders, and others (see Table 2). The majority of pituitary adenomas secrete prolactin (30% to 40%) or are nonsecreting (30% to 40%). Adenomas secreting adrenocorticotropin hormone (ACTH, 2% to 10%), growth hormone (GH, 2% to 10%), thyroid-stimulating hormone (TSH, <1%), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) are much less common.2 Significant morbidity and premature mortality are associated with hyperprolactinemia, acromegaly (growth hormone excess), Cushing’s syndrome, and hyperthyroidism. Additionally, up to 41% of patients with macroadenomas were found to have varying degrees of hypopituitarism due to compression of the hypothalamus, the hypothalamic-pituitary stalk, or the pituitary itself.⁴

TABLE 2. DIFFERENTIAL DIAGNOSIS FOR PITUITARY INCIDENTALOMAS^2,4,14

Pituitary adenoma:

Secreting: prolactin, growth hormone, ACTH, glycopeptides (LH, FSH, TSH, a-subunit)
Nonsecreting

Non-pituitary tumors:

Germ cell tumors
Craniopharyngioma
Meningioma
Metastatic disease

Vascular lesions:

Aneurysms
Hamartomas
Infarctions

Infiltrative:

Sarcoidosis
Histiocytosis
Lymphocytic hypophysitis
Eosinophilic granulomas

Other:

Rathke’s cleft cyst
Anatomic abnormalities

ACTH=adrenocorticotropin hormone, GH=growth hormone, TSH=thyroid-stimulating hormone (thyrotropin), LH=luteinizing hormone, FSH=follicle-stimulating hormone

Recently, the Endocrine Society released consensus recommendations to guide the evaluation and treatment of pituitary incidentalomas, which are included in the approach outlined below.⁵ A detailed history and physical examination should be obtained with specific inquiry as to signs and symptoms of hormonal excess and mass effect from the tumor. Examples of symptoms of hormone excess can include:

Prolactin: menstrual irregularity, anovulation, infertility, decreased libido, impotence, osteoporosis;
Growth hormone: high frequency of colonic polyps and colon cancer (chronic excess);
TSH: thyrotoxicosis, atrial fibrillation; and
ACTH: hypertension, osteoporosis, accelerated vascular disease.

Symptoms related to the mass effect of the tumor include visual field defects and hypopituitarism related to the deficient hormone, including:

FSH/LH: oligomenorrhea, decreased libido, infertility;
TSH: hypothyroidism (weight gain, constipation, cold intolerance);
ACTH: adrenal insufficiency (hypotension, hypoglycemia, weight loss); and
ADH: polyuria, polydypsia.

The size and location of the pituitary lesion must be assessed. Lesions greater than 10 mm are considered macroademonas, and their size will affect their management. If the lesion was initially identified by CT scan, an MRI is recommended to better evaluate it.⁵ If the MRI locates the incidentaloma abutting the optic nerve or chiasm, then the patient should undergo a formal visual field examination.

Indications for an inpatient surgical referral for treatment include: a lesion larger than 2 cm, evidence of mass effect such as visual field defects, neurologic compromise, opthalmoplegia, hypopituitarism, a tumor abutting the optic nerve or chiasm, pituitary apoplexy, and hypersecretion of hormones other than prolactin. Patients with prolactinomas warrant an inpatient endo-crinology consult and may need medical management with a dopamine agonist. Hormone replacement therapy can also be provided for patients with hypopituitarism.^2,5

For patients who do not meet the criteria for inpatient surgical therapy, follow-up management must be arranged at the time of discharge. Clinical, laboratory assessment, and an MRI should be scheduled six months after the initial finding of the incidentaloma with the patient’s PCP or with an endocrinologist.⁵

Thyroid incidentalomas. The prevalence of thyroid nodules based on ultrasound studies ranges from 19% to 46%, with autopsy studies estimating an incidence of approximately 50%.^2,6 Incidence of thyroid nodules also increases with age, as almost 60% of people over the age of 60 harbor a thyroid incidentaloma. The rate of malignancy in the general population has ranged between 8% and 24%; however, in the last decade, the rates have increased by 2.4 times as more sophisticated ultrasound techniques and liberal use of fine-needle aspiration (FNA) biopsies have detected subclinical disease.^7,8

Etiologies for incidental thyroid nodules can be divided into benign and malignant causes. Benign etiologies include thyroid cyst (simple or complex), multinodular goiter, and Hashimoto’s thryoiditis, while malignant causes include papillary, medullary, follicular, Hurthle cell, and anaplastic carcinomas, thyroid lymphomas, and rare instances of metastatic cancers.^2,3

Targeted history and physical examination helps to characterize the thyroid incidentaloma. Historical features, such as palpitations, weight loss, anxiety, new onset atrial fibrillation, or menstrual irregularities, coupled with tachycardia, tremors, proximal muscle weakness, and a palpable nodule aid in the diagnosis of hyperthyroidism. Findings such as a family history of thyroid cancer, symptoms of hoarseness or dysphagia, rapid growth of the nodule, environmental or history of head or neck irradiation along with physical findings of a hard, fixed nodule, or cervical lymphadenopathy increase the suspicion for malignancy.^2,7

The functionality of the nodule can be assessed by checking TSH, free T3, and free T4 levels. Suppression of TSH (< 0.1 mU/L) with elevated levels of free T3 and T4 indicates nodule production of excess thyroid hormone and warrants thyroid scintography. Thyroid scintography will identify the nodule as “hot” (hyperfunctioning) or “cold” (nonfunctioning).²

Regardless of the radiographic modality that initially identified the thyroid incidentaloma, a dedicated thyroid high-resolution ultrasound should be ordered to assess the size, multiplicity (single or multinodular), location, and character (solid, cystic, or mixed).⁷

Recommendations for proceeding to FNA to evaluate for malignancy differ among subspecialty societies. Generally, nodules larger than 1 cm or nodules smaller than 1 cm with risk factors for malignancy should be referred for FNA.^2,7

If diagnostic workup identifies a patient with hyperthyroidism due to an autonomously functional nodule or a nodule that may be at high risk for malignancy, it is appropriate to involve an endocrinologist and possibly a surgical subspecialist prior to discharge. Management of hyperthyroidism can include starting antithyroid agents (methimazole or propylthiouracil), radioactive iodine ablation, or referral for surgery.

Preparation for discharge of the patient whose incidentaloma is nonfunctional or does not appear to be malignant should include appointments to recheck thyroid hormone levels, including TSH as well as a thyroid ultrasound within one year of the initial discovery.

Adrenal incidentaloma. The prevalence of AIs found by CT of the abdomen ranges from 0.4% to 4%, while autopsy studies have found a prevalence of 1.4% to 9% with increasing prevalence with age.^2,9,10 The majority of AIs are benign and nonfunctioning adenomas, in the absence of known malignancy. Other differential diagnoses include Cushing’s syndrome, pheochromocytoma, adrenocortical adenoma, aldosteronoma, and metastatic lesions.

Because functioning adrenal incidentalomas may be clinically silent, any patient found with an AI must undergo biochemical workup as part of their evaluation to assess for pheochromocytoma, Cushing’s syndrome, and if he or she has a history of hypertension or hyperaldosteronism (Conn’s syndrome). Table 3 outlines the approach for characterizing adrenal incidentalomas.^2,11,12 An important point is that imaging studies are not useful in distinguishing a functioning versus nonfunctioning tumor but rather can help to discriminate malignant lesions.¹¹

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Table 3. Characterization of the adrenal incidentaloma^2,11

Inpatient surgical consult for resection is indicated if the patient is found to have pheochromocytoma, clinically apparent functioning adrenocortical adenoma, or a tumor size greater than 4 cm. Consultation with an endocrinologist is also recommended if biochemical tests are positive. If the diagnostic workup leads to suspicion for infection or metastatic disease, the patient should be referred for FNA.^2,12

For patients whose lesions do not require surgical resection, repeat CT scan of the abdomen is recommended six months from the initial finding. Hospitalists should also arrange for the patient to repeat biochemical testing, including an overnight dexamethasone test.^12,13

Back to the Case

The patient underwent biochemical testing and was found to have normal levels of plasma-free metanephrines, a plasma aldosterone, plasma renin activity ratio less than 20, and a serum cortisol level of 7 mg/dL after his overnight dexamethasone suppression test. The 24-hour urine collection for free cortisol revealed elevated levels of cortisol in the urine, and the ACTH level was low.

Endocrinology and endocrine surgery teams were consulted, and recommended surgical resection. After surgical resection of his tumor, the patient was started on glucocorticoid replacement and was discharged with a follow-up appointment with endocrinology.

Bottom Line

An inpatient approach to endocrine incidentalomas should include characterization of the clinical signs and symptoms, size, function, and malignant potential of the lesion. Based on this, inpatient surgical or medical management can be determined. Post-discharge management should include arrangements for surveillance testing and follow-up with appropriate subspecialists.

Dr. Tad-y is assistant professor of medicine and a hospitalist at the University of Colorado Denver.

KEY POINTS

Advances and more frequent use of diagnostic radiology have led to the increased prevalence of endocrine incidentalomas.
Pituitary, thyroid, and adrenal incidentalomas must be assessed for dysfunctional hormone secretion and malignant potential.
Inpatient management of endocrine incidentalomas should include consultation of endocrine or surgical teams in cases of dysfunctional or malignant lesions.
Post-discharge instructions should clearly delineate timelines for repeat imaging, laboratory testing, and subspecialist follow-up.

ADDITIONAL READING

Shirodkar M, Jabbour SA. Endocrine incidentalomas. Int J Clin Pract. 2008; 62:1423-1431.
Freda PU, Beckers AM, Katznelson L, et al. Pituitary incidentaloma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2011;96:894-904.
Iyer NG, Shaha AR, Silver CE, et al. Thyroid incidentalomas: to treat or not to treat. Eur Arch Otorhinolaryngol. 2010;267:1019-1026.
Zeiger MA, Siegelman SS, Hamrahian AH. Medical and surgical evaluation and treatment of adrenal incidentalomas. J Clin Endocrinol Metab. 2011;96:2004-2015.

References

From http://www.the-hospitalist.org/details/article/1380161/What_Is_the_Best_Approach_for_the_Evaluation_and_Management_of_Endocrine_Inciden.html