March 14, 2007 Cushing's Help and Support/Newsletters

Figure 1. Appearance of the Patient

The patient's facial appearance shows some broadening of the nose and supra orbital ridges (left). At right, the patient's large hands are shown.

How Should a Patient with Suspected Pituitary Disease Be Worked Up?

The above scenario is increasingly common as a result of the advent of powerful imaging techniques such as MRI and computerised tomography scanning, which identify “coincidental” pituitary abnormalities in a significant minority of the adult population. Nonetheless, when such lesions are identified they warrant further characterisation.

The clinician confronted with such a case should ask the following questions:

Is there evidence of over secretion of pituitary hormone(s)?
Is there evidence of deficiency of pituitary hormones?
Is there evidence of pressure on structures surrounding the pituitary fossa?

The commonest cause of excess pituitary hormone secretion is a prolactinoma. It usually presents with galactorrhoea, oligo- or amenorrhoea, and hirsutism in premenopausal women and with hypogonadism in men. Cushing disease and acromegaly are less common and gonadotrophin-secreting adenomas and thyrotrophinomas are rare. Mild hyperprolactinaemia is commonly found in association with large pituitary tumours and is usually due to distortion of the pituitary stalk. This “disconnection” syndrome must be distinguished from a true prolactin-producing adenoma, as the treatment of the latter (with dopamine agonist drugs) is radically different from that of other types of pituitary adenomas.

Hypopituitarism can present with features of hypogonadism (amenorrhoea, loss of body hair, loss of libido and impotence), hypothyroidism, and hypoadrenalism. The latter, in addition to symptoms of hypocortisolism (tiredness, dizziness, fatigue) may also be associated with loss of ability to tan and generalised hypopigmentation.

Expansion of a pituitary mass superiorly can compress the optic chiasm, thus giving rise to bitemporal hemianopia. Lateral extension can compress cranial nerve III, IV, or VI. Occasionally pituitary tumours can bleed or infarct to cause pituitary apoplexy (sudden headache, photophobia, cranial nerve palsies, and collapse due to hypoadrenalism and in some cases hypoglycaemia). Investigations include pituitary function tests, formal visual field assessment, and in some cases further more detailed imaging.

Despite the absence of spontaneous symptoms, the patient admitted to increasing hand and shoe size when specifically asked, associated with a hoarse voice of three years duration. She had also suffered from frontal headaches as well as tingling of the right index finger. Previously, she had surgery for temporomandibular joint dysfunction.

On closer inspection, there was a suggestion of some broadening of the nose and prominence of the lips, rather large hands, and increased skin thickness (Figure 1). Visual fields were normal and Tinel's sign was positive. Blood pressure (BP) was 160/96 mm Hg. Blood tests showed normal urea, creatinine and electrolytes, fasting glucose of 6.6 mmol/l (normal range, <5.6 mmol/l), prolactin 330 imu/l (normal <550 imu/l), and thyroid stimulating hormone (TSH) of 1.4 mIU/l (normal 0.3–4.7 mIU/l) with free T4 of 16 pmol/l (normal 11–23 pmol/l).

What Is the Reason for the Tingling of the Right Index Finger?

The sensory disturbance in the distribution of the median nerve is typical of right carpal tunnel syndrome (CTS). CTS typically presents as pain in the medial three fingers radiating into the arm, worsening during the night.

Thickening of tendons or synovitis in the carpal tunnel area causes CTS. The history, in this patient, is typical of CTS and is characterised by pain, tingling, and numbness in the median nerve distribution. This patient does not have hypothyroidism (normal thyroid hormone and serum TSH levels) or diabetes mellitus (although she has impaired fasting glycaemia), was not pregnant or obese, and did not have a history or clinical manifestations of rheumatoid arthritis. The cause could be idiopathic, but the other features in the history and examination point towards endocrinopathy as being the underlying aetiology. The diagnosis of CTS can be confirmed by an electromyogram.

Is the Combination of High Blood Pressure and High Fasting Glucose Levels Common?

Hypertension associated with problems with glucose metabolism is a common feature usually seen in people with the metabolic syndrome. Less commonly, it can be seen in endocrine diseases like Cushing syndrome and acromegaly. The reason for hypertension and hyperglycaemia in Cushing syndrome is due to the excess glucocorticoid levels whereas in acromegaly, it is due partly to the direct action of excess growth hormone (GH) on sodium retention and increased insulin resistance, respectively [1].

What Is the Next Step?

The symptoms of increasing soft tissue size, CTS, hypertension, hyperglycaemia, and temporomandibular joint dysfunction make acromegaly a possible diagnosis (Box 1). The duration of symptoms as well as the previous surgery for temporomandibular joint dysfunction suggests that the disease has been active for at least three years [2]. The usual (in 98% of cases) cause of acromegaly is a GH-secreting pituitary adenoma, usually a macro-adenoma (>1 cm). Other rare causes are pituitary carcinoma or GH-releasing hormone tumours.

Box 1. Symptoms and Signs of Acromegaly

Symptoms due to direct effect of the tumour

Headache
Visual impairment
Hypopituitarism
Hyperprolactinaemia

Symptoms due to GH excess

Soft tissue enlargement
Headache
Increased skin tags
Increased sweating
Acanthosis nigricans

Cardiovascular features

Hypertension
Biventricular hypertrophy
Diastolic dysfunction at rest and systolic dysfunction on effort
Endothelial dysfunction

Metabolic and other endocrine features

Impaired fasting glycaemia
Impaired glucose tolerance
Type 2 diabetes mellitus
Insulin resistance
Dyslipidaemia
Multinodular goitre
Hypercalciuria
Hyperparathyroidism

Musculoskeletal features

Joint stiffness
Arthropathy and osteoarthritis
Carpal tunnel syndrome
Osteopenia

Respiratory disease

Upper airway obstruction and snoring
Macroglossia
Obstructive sleep apnoea
Thickened vocal chords and hoarse voice

Neoplastic disease

Colorectal polyps and cancer
Probable breast, prostate, and thyroid cancer

Baseline GH levels are of limited value in diagnosing acromegaly since GH is normally secreted episodically, and high levels can also be seen in pregnancy, puberty, in response to pain, stress, malnutrition, and after a prolonged fast. The diagnosis can be confirmed by measuring GH levels in response to an oral glucose tolerance test (OGTT) (Box 2 outlines the protocol for OGTT to diagnose acromegaly). Insulin-like growth factor 1 (IGF 1) is a protein modulated by GH and produced in many body tissues, primarily in the liver. Serum levels of IGF 1 are fairly stable throughout the day and correlate closely with mean GH serum concentration.

Box 2. Protocol for Oral Glucose Tolerance and GH Suppression Test for Diagnosis of Acromegaly

Fast the patient from midnight.
Insert venous cannula prior to basal sample.
Administer oral 75 grams glucose at time 0 (just prior to basal blood sample) and collect blood samples for GH and glucose at 30-minute intervals up to 120 minutes.
Measure IGF 1 level with basal sample.

Further investigation and management of patients with suspected pituitary disease should be undertaken in specialised endocrine centres, to which such patients should be referred.

The patient's random GH level was 55 mu/l (0–20) along with an elevated IGF 1 level of 78 nmol/l (age-matched normal range being 12–44). She then proceeded on to an OGTT with glucose and GH level measurements; the results are outlined in Table 1.

Table 1. Oral Glucose Tolerance Test with Growth Hormone Results

The OGTT confirms failure of GH to suppress to levels below 2 mu/l (<1 mcg/l) as well as impaired fasting glycaemia and impaired glucose tolerance. Other tests of anterior pituitary function (prolactin, thyroid function tests, luteinising hormone, and follicle-stimulating hormone) as well as dynamic testing of adrenal reserve in response to synthetic ACTH (short synacthen test) were normal. MRI studies of the pituitary gland revealed a pituitary micro-adenoma (Figure 2).

Figure 2. MRI Studies of the Patient's Pituitary Gland

MRI of the pituitary gland showing a non-enhancing lesion occupying the bulk of the pituitary fossa (yellow arrow). The remaining normal pituitary is pushed to the left, as is the pituitary stalk. The optic chiasm can be seen just superior to the pituitary gland (white arrow).

Should Imaging Precede the Biochemical Investigations?

This patient's case highlights the dilemma clinicians are facing today as a result of the increasing use, availability, and precision of imaging techniques. She had a MRI scan previously that detected a pituitary tumour. Pituitary tumours that are detected coincidentally (so called “incidentalomas”) are not uncommon with reports of prevalence of up to 10% in adults. Given the limitations of diagnostic testing, biochemical screening requires sufficiently high pre-test probability to make it effective. Apart from the cost factor, an imaging-first principle in any field in medicine that relies on biochemical proof of disease leads to a cascade of tests and pursuit of false-positive results. Therefore, appropriate clinical evaluation should precede biochemical investigations, which then may need to be confirmed by imaging techniques [3].

Should This Patient Be Treated?

The pathologic effects of increased GH levels are progressive and are associated with increased morbidity and mortality. People with acromegaly have a 2- to 4-fold increase in mortality rate, mostly due to cardiovascular disease [4]. Many of the soft tissue overgrowth features as well as the increased cardiovascular risk can be reversed, at least partly for soft tissue and completely for cardiovascular disease, by appropriate therapy [5]. Appropriate therapy may also reduce or even prevent mass effects caused by tumour growth in the pituitary area. It is therefore important that diagnosis and treatment are instituted quite promptly.

What Treatment Modalities Are Available?

The underlying treatment strategy of acromegaly is to remove the pituitary tumour (especially macro-adenomas causing mass effects), normalise GH and IGF 1 levels whilst preserving normal residual pituitary function, and relieve symptoms. Medical, surgical, and radiotherapeutic means or, more commonly, some combination of the three can be used to try and achieve this. Currently five different modalities of treatment are available, although surgery remains the treatment of choice. Table 2 outlines the advantages and limitations of each modality.

Table 2. Advantages and Limitations of Different Modalities of Treatment for Acromegaly

In this patient, it was decided that it would be prudent to try and regress some of the soft tissue changes of acromegaly to minimise the risks of intubation during anaesthesia (although this approach is empirical and not widely practised). This was achieved by a somatostatin receptor analogue therapy, given every month. This reduced GH levels to 35 mu/l and IGF 1 levels to 56 nmol/l.

After four monthly injections of long-acting somatostatin receptor analogue therapy, the patient went on to have an endoscopic pituitary adenomectomy. Histology of the resected adenoma revealed a GH cell pituitary adenoma.

How Should Response to Surgery Be Assessed?

The currently accepted criteria for cure of acromegaly is a random or mean GH level of <5 mu/l or a nadir GH level of less than 2 mu/l during an OGTT and a serum IGF 1 level within the age-adjusted normal range [6]. The patient had an OGTT eight weeks after surgery as well as tests of anterior pituitary function. Nadir GH levels were 8.6 mu/l with a slightly raised IGF 1 level of 51 nmol/l, signifying partial resolution of acromegaly. Other anterior pituitary function tests were normal. Repeat MRI scan showed no definite target for further surgical intervention.

She was then started on somatostatin analogue therapy to achieve better GH level control. This reduced mean GH levels to 2.9 mu/l and normalised IGF 1 levels to 32 nmol/l. After discussion with the patient, it was decided not to proceed with radiotherapy since the acromegaly was well controlled with medical therapy and due to the high probability of hypopituitarism associated with radiotherapy. She remains asymptomatic and is under regular endocrine follow-up.

DISCUSSION

Acromegaly is a rare condition with prevalence rates of 60 per million population. The condition can cause significant morbidity and mortality but may present with vague features; therefore a high index of clinical suspicion is warranted. The average delay in diagnosis after onset of the disease is about eight years. It can cause hypertension and disorders of glucose metabolism, which are increasing in prevalence, as well as soft tissue enlargement, which may take years to be noticed. The increasing use of imaging techniques has invented a new disorder—the incidentaloma. When incidentalomas are found in the pituitary, a thorough history and examination is required with relevant biochemical tests. The biochemical diagnostic criteria for acromegaly have changed over the past decade, bringing the GH diagnostic threshold to lower levels. The advent of better and more sensitive GH assays and better imaging have helped to diagnose more subtle forms of the disease, which would not have been picked up earlier, and may therefore hopefully reduce morbidity and mortality. Furthermore, newer treatment options, whilst expanding the therapeutic armour, also pose a challenge to the treating endocrinologist in deciding what best suits the patient.

Key Learning Points

Acromegaly is a rare but easily diagnosed condition that can cause significant morbidity and mortality.
Increasing use of imaging has led to an increase of incidental findings—the “incidentaloma”.
Symptoms of acromegaly may persist for many years before the diagnosis is made.
Newer modalities of GH assays and treatment have led to earlier diagnosis and may reduce symptoms and mortality.

References

Duncan E, Wass JA (1999) Investigation protocol: Acromegaly and its investigation. Clin Endocrinol (Oxf) 50: 285–293. Find this article online
Colao A, Ferone D, Marzullo P, Lombardi G (2004) Systematic complications of acromegaly: Epidemiology, pathogenesis, and management. Endocr Rev 25: 102–152. Find this article online
Aron DC, Howlett TA (2000) Pituitary incidentalomas. Endocrinol Metab Clin North Am 29: 205–221. Find this article online
Alexander L, Appleton D, Hall R, Ross WM, Wilkinson R (1980) Epidemiology of acromegaly in the Newcastle region. Clin Endocrinol (Oxf) 12: 71–79. Find this article online
Holdaway IM, Rajasoorya RC, Gamble GD (2004) Factors influencing mortality in acromegaly. J Clin Endocrinol Metab 89: 667–674. Find this article online
Melmed S, Casaneuva FF, Cavagnini F, Chanson P, Frohman L, et al. (2002) Guidelines for acromegaly management. J Clin Endocrinol Metab 87: 4054–4058. Find this article online

• From http://www.theeagle.com/stories/031007/health_20070310037.php

Saturday, March 10, 2007

Medical Edge: Stretch marks are treatable

By THE MAYO CLINIC
Special to the Eagle

Dear Mayo Clinic: Are there any effective nonsurgical treatments for stretch marks? - Chicago

Answer (from Dr. P. Kim Phillips, in dermatology at the Mayo Clinic in Minnesota): With many medical problems, doctors counsel a wait-and-see attitude in order to avoid interventions that may be painful, inconvenient and possibly unnecessary. The problem might go away by itself.

This is not the case with stretch marks, for which time is of the essence. They are most responsive to treatment before they are six weeks old. Even then, therapy might best be described as "mildly effective." Not every patient responds, and improvement, if it occurs, is often marginal.

Stretch marks develop in a variety of circumstances. Some involve a physical stretching of the skin (such as seen in weight lifters), substantial weight gain or adolescent growth spurts; areas of skin get stretched to the point that collagen and elastin fibers break down.

Other cases involve hormonal effects, such as from chronic steroid use or Cushing's syndrome. Sometimes, as in pregnancy, there is a physical component (stretching of the skin) as well as hormonal change.

Either way, a stretch mark is skin that has lost its elasticity - it cannot bounce back to its original form - and the resulting scarlike tissue is shiny, depressed, flaccid and thin compared to surrounding normal tissue. At first, the stretch mark may be pink, red or purple; later, it will fade to a color closer to the individual's natural skin tone, although it will be lighter. Its texture, however, will be unchanged.

One way to reduce the likelihood of a stretch mark's occurrence is to maintain a normal weight, which of course has numerous other benefits. And even though it is inevitable that a pregnant woman will put on weight over a relatively brief period, she can work with her obstetrician to minimize that gain by maintaining a proper diet and pursuing a suitable exercise program.

Research has shown that tretinoin cream (Retin-A, Renova) may improve the appearance of recent stretch marks - those that are less than six weeks old - although it should never be used during pregnancy, as it might adversely affect the fetus. Tretinoin, when it works, helps to rebuild collagen, rendering the stretch mark more similar in appearance to one's normal skin. Once the mark is fairly well established - no longer reddish but light - it tends not to respond to this treatment.

Another option, which also is best used when the stretch mark is new but still has some effectiveness when it's older, is pulsed dye laser therapy. Used at wavelengths of light that are non-ablative (will not remove skin), the treatment remodels the dermis (the layer of skin just beneath the surface layer, the epidermis) by stimulating the growth of fibroblasts, cells that help produce the elastic tissues collagen and elastin.

Two leading options for older stretch marks are microdermabrasion and excimer laser therapy. Microdermabrasion uses mineral crystals blown onto the target tissue. This "polishing" gently removes the skin's topmost layer, which, when effective, results in new growth that is more elastic.

The excimer laser, a different system from the pulsed dye laser, does nothing for collagen or elastin growth. Instead, its aim is repigmentation by stimulating melanin production. If it works, the old and lighter scar is rendered similar in color to the surrounding skin, and therefore less visible.

Some individuals don't mind their stretch marks enough to seek treatment.

But for people who find them unsightly and unacceptable, help is available. They should work with a dermatologist or plastic surgeon to choose the most appropriate treatment. Factors to consider include age of the stretch mark, convenience of treatment (therapies differ in length and frequency of sessions) and cost (being cosmetic, these options are usually not covered by health plans).

Patients also need to be advised that treatment will, at best, be only partially effective. But for lots of people, that may be enough.

• To submit a question, write to medicaledge@mayo.edu or to Medical Edge from Mayo Clinic, c/o Tribune Media Services, 2225 Kenmore Ave., Suite 114, Buffalo, N.Y., 14207. For health information, visit www.mayoclinic.com.

• From http://www.azcentral.com/arizonarepublic/
arizonaliving/articles/0306metabolism0306.html#

Metabolism: Hero or villain?
Body's 'engine' gets too much weight-management blame, credit

Connie Midey
The Arizona Republic
Mar. 6, 2007 12:00 AM

Metabolism is not often - or at least not to any great extent - the weight-gain villain dieters accuse it of being.

Nor is it always the hero responsible for some people's ability to maintain a trim figure despite prodigious eating habits.

"People's metabolic rates can be different," says Valley physician Marshall Block of Endocrinology Associates, "but not so different that it accounts for the vast amount of obesity present in our society. Everyone pretty much agrees that the majority of obesity is due to excess caloric intake, not to a decrease in metabolic rates."

For a subject so much a part of everyday conversations about weight management, metabolism and claims about amping up its power continue to confound us.

Block defines it as "the sum of all the chemical reactions that occur inside the body to either create energy or use energy and make the products that the body needs to function."

Think of metabolism as your body's engine - one that never shuts down - and food as the fuel.

Calories from the food you consume provide energy for everything your body does, and they burn at a pace determined in part by your activity level, muscle-to-fat ratio and basal metabolic rate.

Basal metabolism is expressed in the number of calories needed for basic functions performed even while you're at rest: breathing, circulating blood, growing and repairing cells, maintaining organ function and so on.

These basic needs account for about 60 to 75 percent of the calories you burn each day, a number that remains fairly consistent. It's the number of calories you'd use if you stayed in bed all day.

Eating and processing food burns about 10 percent of calories expended daily, with physical activities responsible for the rest. Take in more calories than you burn, and the excess is stored as fat.

Yes, out-of-whack metabolism could be behind the five or 10 pounds that caught up with you and now won't let go, says Tosca Reno, author of The Eat-Clean Diet (Robert Kennedy Publishing, 2006, $16.95, paperback).

"But it's probably out of whack because we did it to ourselves," she says from her home near Toronto. "We're sort of globally responsible for trashing our metabolism."

Reno cites poorly spaced meals, out-of-control portion sizes and neglect of strength-building exercises as a few of the culprits. Serious metabolic and endocrine diseases that contribute to significant weight gain are uncommon, she says.

At his Valley offices, physician Block sees just one or two people a year with Cushing's syndrome, for example.

The syndrome, characterized by increased fat in the face, neck and upper body and thinning in the rest of the body, can account for 10 to 20 pounds in excess weight, he says. The condition requires medical treatment that may include surgery, radiation, chemotherapy or cortisol-inhibiting drugs.

The more commonly seen hypothyroidism, or underactive thyroid, slows metabolism and can cause weight gain, Block says. About 10 to 15 pounds is typical.

"For patients diagnosed with hypothyroidism, a lot of the weight gain is due to water retention, and as soon as you give them thyroid pills, that weight is lost," he says. "People who are 100 pounds overweight and blame their thyroid? They're in left field."

The solution is simple, but not as effortless or fast as suggested by people promoting what they call metabolism-revving pills, foods and programs, Block says.

"In order to lose one pound of fat, you need to burn approximately 3,500 calories," he says. "You can do that in one week by cutting 500 calories a day from your diet or exercising enough to burn 500 calories a day, or by (a balance of) both."

Reach the reporter at connie.midey@arizonarepublic.com or (602) 444-8120.

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Newest Bios:
To add or edit your bio, http://www.cushings-help.com/forms/bio.htm
Adrenal
Cathy Tia	Cathy had the left side of her pituitary gland removed and a BLA. Cathy has been through 2 cycles of IVF fertility treatment and the second one worked. She had a baby girl. Cathy updated her bio in March of 2007. She has another new 5mm tumour on the right side of her pituitary gland. She has Nelsons Syndrome after having both adrenals removed. They want to give her radiation and she's looking for suggestions.	Wellington, New Zealand

Not Yet Diagnosed Patients
Dawnell (hazleyes74)	Dawnell is not yet diagnosed with Cushing's but she has been diagnosed with PCOS, Chronic Fatigue Syndrome and Fibromyalgia so far. She has been prescribed Celexa for mild depression then Effexor XR and Toprol XL; and Relafen and flexeril.	Kingston Mines, Illinois
Grace (Fatnsassy)	Grace is not yet diagnosed with Cushing's but has had many symptoms over several years.	Ohio
Melanie (forskyla)	Melanie has been diagnosed with PCOS so far. She is seeing Dr Friedman.	California
Mindy (myndee11)	Mindy thinks she has Cushing's but her doctor isn't listening.	Tigard, Oregon
Oklahoma (Faith_Hope)	Oklahoma has had Cushing's symptoms for over 6 years.	Green Country, Oklahoma
Sonia (Sonia)	Sonia is not yet diagnosed with Cushing's but she has had about 5 Doctors tell her that she Cushing's however all labs come back normal then they drop her. She has seen 2 Endocrinologists and they will not do anything else. One in Florida and one in Tennessee at Vanderbilt.	Milton, Florida
Tracy (kiwibaitnz)	Tracy has been diagnosed with PCOS so far. She is taking Metformin for insulin resistance and has a thyroid problem, Auto immune thyroiditis (Hashimotos) and has taken thyroxine.	Whangarei, New Zealand / California

Pituitary Patients
Cathy Tia	Cathy had the left side of her pituitary gland removed and a BLA. Cathy has been through 2 cycles of IVF fertility treatment and the second one worked. She had a baby girl. Cathy updated her bio in March of 2007. She has another new 5mm tumour on the right side of her pituitary gland. She has Nelsons Syndrome after having both adrenals removed. They want to give her radiation and she's looking for suggestions.	Wellington, New Zealand
Judi (Cushie Judi)	Judi was first diagnosed with Cushing’s 1/12/06, MRIs now show possible masses in both the pituitary and adrenal glands.	Batavia, NY
Yvonne (Yvonne)	Yvonne was diagnosed with Cushing's when she was 17. She is currently going through a number of operations to sort out scars and skin which has been stretched.	Ayrshire, United Kingdom / Scotland

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