Patient Develops Cyclic Cushing’s Syndrome Due to Lung Neuroendocrine Tumor

Posted on January 26, 2026 by MaryO

Tumors located outside the pituitary gland that produce the adrenocorticotropic hormone (ACTH) may cause, on rare occasions, cyclic Cushing’s syndrome — when cortisol levels show substantial fluctuations over time.

That finding, based on the case of a patient with ACTH-secreting lung cancer,  is found in the study, “Cyclic Cushing’s syndrome caused by neuroendocrine tumor: a case report,” which was published in Endocrine Journal.

Cushing’s syndrome is characterized by too much cortisol, either due to adrenal tumors that produce cortisol in excess, or because too much ACTH in circulation — resulting from ACTH-producing tumors — act on the adrenal glands to synthesize cortisol.

Cyclic Cushing’s syndrome (CCS) is a rare type of Cushing’s in which cortisol production is not steadily increased. Instead, it cyclically fluctuates, from periods with excessive cortisol production interspersed with periods of normal levels.

The fluctuations in cortisol levels over time pose difficulties for a definite diagnosis. Moreover, the precise mechanism underlying the periodic peaks of cortisol peaks are unknown.

Investigators now reported the case of a 37-year-old man admitted to the hospital due to repeated attacks of dizziness, weakness, and high cortisol levels for two weeks.

Repeated tests measuring the levels of cortisol in the blood and a 24-hour urine free cortisol (24 hUFC) assay confirmed a cyclic fluctuation of cortisol, with levels peaking three times and dropping twice (the standard rule for diagnosing CSC).

Upon hospitalization, he further developed high blood pressure and weight gain.

The patient underwent computed tomography (CT) scans, which revealed the presence of an ACTH-secreting tumor in the lungs, the likely cause of the patient’s Cushing’s symptoms. These type of tumors are called neuroendocrine tumors because they are able to release hormones into the blood in response to signals from the nervous system.

Additional scans detected tumors in the adrenal and pituitary glands, but further analysis revealed they were non-functioning tumors, i.e., as their name indicates, they didn’t release excessive ACTH. The thyroid gland also was positive for a tumor.

The patient underwent resection surgery to remove the tumor located in the lungs and nearby lymph nodes. After the surgery, the levels of cortisol in the blood and urine returned to normal, confirming the tumor as the source of the CSC.

The patient also received surgery to remove his thyroid tumor.

An analysis of the patient’s genomic DNA revealed a novel mutation in the PDE11A gene, which is linked to a rare form of ACTH-independent Cushing’s syndrome called primary pigmented nodular adrenocortical disease (PPNAD) type 2.

Whether the patient developed PPNAD, however, and the contribution of a potential PPNAD diagnosis to the CCS, requires further investigation. “To explore pathogenicity of the genetic mutation, we will still plan for a follow-up visit to this patient,” researchers wrote.

From https://cushingsdiseasenews.com/2019/01/24/patient-develops-cyclic-cushings-syndrome-due-to-lung-neuroendocrine-tumor/

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Myth: “You should be all better by now!

Posted on January 23, 2026 by MaryO

Myth: “You should be all better by now! You found out what was wrong, you got the surgery, it’s been quite some time, and you are STILL not better?! You SHOULD have gotten better by now!” Chronic illness follows the same pattern as normal illness. You get diagnosed, treated, and then go back to a state of recovery, eventually leading you back to a state of “normal health”.

Fact: Chronic illness is called chronic illness for a reason, because it is chronic! Wayne Dyer addresses this myth: We usually expect to follow a pattern that is characteristic of most illness. “The person has an illness and falls from the path of normal health. Then, comes a period of diagnosis and treatment followed by a period of convalescence (the general recovery of health and strength after illness). Finally, the person returns to good health again” (p. 251).

The person is supported, typically, by family, friends, neighbors, and their church community during the illness, treatment, and recovery, assuming that at some point the person will return to normal health and their assistance will no longer be needed (p. 251).

However, in the case of the chronically ill, a different cycle occurs. In the chronically ill, the person loses his normal health. He goes through a period of treatment and sometimes recovers. “But for a number of reasons, depending on the illness, the person does not return to a condition of normal health but continues in a fluctuating pattern of chronic ill health. The person may have periods when he feels better or worse, but at no time does he ever return to complete good health.” (p. 252).

According to Dyer (1990), “Unfortunately, family members, friends, and neighbors do not know how to respond to this unfamiliar pattern, and they usually shift their attention away from the chronically ill person as others with the more normal cycle of sickness occupy their attention” (p 252). At this point, the person with the chronic illness feels a lack of support, understanding, and help. This can lead to increased pain, depression, and anxiety.

It is very difficult for family members, such as spouses, to deal with the person with chronic illness. “Chronic illness can disrupt and pide a family, or it can provide the family with an opportunity to grow in understanding, patience, sacrifice, and love for one another” (Dyer, 1990, p. 256).

For the chronically ill person and his family, the friends, neighbors, and church can either be a source of support and help or elicit feelings of neglect, rejection, and misunderstanding. Most people help at the beginning of the illness, but then become confused when the person doesn’t get better, so they withdraw their attention (p. 256).

Here are some ideas for helping the chronically ill person and family:

• Discuss in some detail with the person how his illness is affecting him and his family and find out what his needs are

• Make short visits to not overtire or over stimulate the patient

• Send a card or make a short phone call to the sick person

• Look for ways to help with young children

• Send a small gift

• Avoid saying things to make the person feel pressured such as “I hope you can come back to church every Sunday now”

• Don’t ask, “What can I do to help?” People don’t like to have to ask for support. Express sensitivity and go ahead and do something (p. 258).

Reference: Dyer, W.G. (1990). Chronic Illness. In R. L. Britsch & T.D. Olson (Ed.), Counseling: A guide to helping others, volume 2, 250-259.

Please take the time to view this video on “Chronic Illness versus Normal Illness” and share with your loved ones:

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Insulin Resistance Unveiled: Cushing’s Disease in a Patient with Type 1 Diabetes Mellitus and Worsening Glycemic Control

Posted on January 22, 2026 by MaryO

Highlights

  • Coexistence of hypercortisolism secondary to ACTH-producing pituitary adenoma and type 1 diabetes mellitus.
  • Presentation of Cushing’s disease in individuals with type 1 diabetes mellitus.
  • Automated insulin delivery utilization in type 1 diabetes with comorbid refractory hypercortisolism.

ABSTRACT

Background/Objective

Type 1 diabetes mellitus is an autoimmune disease often characterized by endogenous insulin deficiency and often sensitivity to endogenous insulin administration. Cushing’s disease, though rare, should be considered as a cause of insulin resistance and increased insulin requirements in individuals with type 1 diabetes mellitus.

Case Presentation

A 21-year-old female with type 1 diabetes mellitus presented with steadily increasing insulin requirements via her hybrid closed-loop insulin pump. She subsequently developed hypertension, weight gain, violaceous striae, and cystic acne. Laboratory evaluation revealed unsuppressed cortisol of 16.6 μg/dL after a 1-mg dexamethasone suppression test, with a simultaneous adrenocorticotropin hormone level of 73.3 pg/mL. Pituitary MRI showed a 1.9 cm sellar mass with local invasion. She underwent transsphenoidal hypophysectomy. Postoperative cortisol was 8.9 μg/dL after intraoperative dexamethasone exposure. Residual hypercortisolism was confirmed, necessitating gamma knife radiation and pharmacologic treatment with a steroidogenesis inhibitor.

Discussion

We present a case of Cushing’s disease due to a corticotropin-secreting pituitary macroadenoma in a young woman with type 1 diabetes. Her initial presentation included rising insulin requirements, followed by overt hypercortisolism. Despite surgery, persistent hypercortisolism required further intervention with gamma knife radiation and osilodrostat. She experienced reductions in both weight and insulin needs, with normalization of cortisol levels on maintenance osilodrostat.

Conclusion

Cushing’s syndrome should be considered in the differential diagnosis of patients with type 1 diabetes and increasing insulin requirements. This case underscores the importance of regular review of automated insulin delivery data and consideration of endocrine causes of insulin resistance and increased insulin requirements in those with type 1 diabetes.

KEY WORDS

Type 1 Diabetes Mellitus
T1DM
Cushing’s disease
Insulin resistance
Insulin pump
Total Daily Dose
TDD

Introduction

Cushing’s syndrome occurs as the result of prolonged elevation in plasma cortisol which can lead to adverse effects including insulin resistance, hyperglycemia, hypertension, weight gain, immunosuppression, and neurocognitive changes. Cushing’s syndrome can occur due to exogenous exposure to corticosteroids or endogenous cortisol hypersecretion. The most common etiology of endogenous hypercortisolism is Cushing’s disease secondary to a corticotrophin-secreting pituitary tumor. In 90% of cases of Cushing’s disease, patients present with pituitary microadenomas, with only 10% of patients presenting with pituitary tumors >1 cm1.
Type 1 diabetes mellitus is an autoimmune condition characterized by T-cell mediated destruction of pancreatic beta cells with ultimate inability to produce insulin and subsequent insulin dependence2. Over the last decade, there has been significant advancement in diabetes management strategies and insulin delivery with creation of hybrid closed-loop insulin pump technology used in conjunction with continuous glucose monitoring systems to provide automated insulin delivery. Within the field of endocrinology, this has required a shift in both the interpretation of glycemic data, insulin utilization data, as well as a pivot to approaching titration of insulin pump settings. Assessment of total daily basal and total daily dose (TDD) in automated mode is of utmost importance when utilizing automated insulin delivery as the amount of insulin utilized can vary significantly in comparison to fixed quantities seen with use of manual mode in an insulin pump2,3.
Type 1 diabetes mellitus is typically characterized by relative insulin sensitivity, particularly early in the disease course. Patients can develop insulin resistance over time, particularly in the setting of comorbid obesity. However, we present a case of a young woman with type 1 diabetes mellitus presenting with steadily increasing insulin requirements followed by development of overt Cushing’s secondary to corticotropin-secreting pituitary macroadenoma. She was utilizing a hybrid-closed loop insulin pump technology with insulin pump download indicating diminished glycemic control despite a steady increase in total daily insulin requirements. This is only the third reported case of Cushing’s disease in a person living with type 1 diabetes mellitus4,5.

Case Presentation

A 21-year-old female with a history of type 1 diabetes diagnosed at age 11 in the context of admission for diabetic ketoacidosis initially presented to adult endocrinology for routine outpatient diabetes management. Type 1 Diabetes Mellitus was managed with automated hybrid-closed loop insulin pump technology (Tandem T-slim X:2 with Dexcom G6 continuous glucose monitoring system). Her hemoglobin A1c was 6.2% with a review of her continuous glucose monitoring system indicating time in range of 73% with 21% of blood glucose levels >180 mg/dL. At that time, she reported concerns regarding high insulin requirements despite an active lifestyle as she was running out of insulin for use in pump early. She was noted to have significant prandial insulin requirements with insulin to carbohydrate ratio of 1 unit for every 3.0-4.5 carbohydrates, raising concern for insulin resistance. Over the next 16 months, she had weight gain of 15.8 kg with elevation in blood pressure and worsening hyperglycemia. Review of her insulin pump downloads indicated a steady increase in her total daily insulin requirements of close to 30%, coupled with reduced time in range and increase in HbA1c.
On repeat physical examination, the development of cystic acne, trace pitting pedal edema, and purple violaceous striae on the abdomen, hips, and thighs were observed. She was also noted to have a new elevation of blood pressure to 162/101 mm Hg. She declined exposure to exogenous corticosteroids (including oral, topical or intra-articular formulations). Based on clinical examination and changes in insulin requirements, the decision was made to evaluate for hypercortisolism. Laboratory evaluation at that time revealed unsuppressed 08:00 AM cortisol level of 16.6 ug/dL after 1 mg of dexamethasone the evening prior. Dexamethasone level was confirmed to be more than adequate at 418 ng/dL (reference range for 8:00 AM level following 1 mg dexamethasone previous evening: 140-295 ng/dL). A simultaneous ACTH level was elevated at 73.3 pg/mL (reference range: 7.2-63.3 pg/mL). She was also noted to have midnight salivary cortisol levels of 0.646, 0.290, and 0.350 ug/dL on three consecutive evenings (reference range <0.010-0.090 ug/dL).
She then underwent MRI pituitary with and without gadolinium enhancement which revealed 1.8 x 1.9 cm enhancing sellar mass with invasion of the right cavernous sinus, extension around the right internal carotid artery, as well as posteriorly down the dorsal aspect of the clivus (Figures 1 and 2). As both hypercortisolism as well as type 1 diabetes mellitus have been implicated as etiologies for lower bone density with subsequent increased risk of osteoporosis later in life, bone densometry was also obtained for this patient. She was found to have low bone mineral density for her age with Z-score of the lumbar spine of -3.2, Z-score of the femoral neck of -2.3, and Z-score of the total hip of -2.8.

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Figure 1. MRI pituitary coronal image revealing sellar mass with invasion of the right cavernous sinus, extension around the right internal carotid artery.

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Figure 2. MRI pituitary sagittal image revealing 1.8 x 1.9 cm sellar mass.

She was evaluated by neurosurgery and underwent endoscopic trans-sphenoidal resection of pituitary macroadenoma. Pathology revealed immunoreactivity for neuroendocrine marker INSM1 (Insulinoma-associated protein 1) and adrenocorticotropic hormone. The lesion was negative for immunoreactivity for prolactin, growth hormone, thyroid-stimulating hormone, follicle-stimulating hormone, and beta-luteinizing hormone.
The cortisol level was 8.9 ug/dL on post-operative day 1. It is notable that she had received 10 mg of intravenous Dexamethasone intraoperatively, raising concern for residual tumor. On post-operative day 3, cortisol level was 4.1 mcg/dL with ACTH level of 94.5 pg/mL. Repeat random cortisol level was 16.3 mcg/dL with simultaneous ACTH level of 63.3 pg/mL. Upon being discharged home, a repeat 24-hour urinary free cortisol was obtained in the outpatient setting and found to be elevated at 464 ug/24 hours (reference range: 6-42 ug/24 hours), consistent with refractory hypercortisolism (Table 1, Figure 4). She was then initiated on osilodrostat, a steroidogenesis inhibitor approved by the FDA in 2020 for use in refractory Cushing’s disease after pituitary surgery. Osilodrostat works via inhibition of 11β-hydroxylase and aldosterone synthase to inhibit the production of cortisol and aldosterone6,7. She underwent ongoing up titration to a maintenance dose of osilodrostat 7 mg twice daily with additional insulin pump titrations over a 2-year duration. Urinary free cortisol was monitored as this is the gold standard for monitoring refractory Cushing’s and the preferred modality for monitoring cortisol levels in individuals on osilodrostat. Final repeat 24-hour urine free cortisol level normalized to 35 ug/24 hours and TDD of insulin via automatic insulin delivery system was lower than time of diagnosis of pituitary Cushing’s at 96 units per day despite having had a roughly 27 kg weight gain (Table 1, Figure 4).

Table 1. Weight trends as well as TDD of insulin listed along with glycemic parameters from automated insulin dosing system Tandem T-slim X:2 with automated mode utilizing Decom G6 CGM. 24-hour urine cortisol collection data included to highlight degree of hypercortisolism. Treatments denoted by asterisk in table include

Date Weight (kg) Total daily insulin dose (units/day) HbA1c (%) Time in range (%) Urine cortisol (mcg/24 hours); RR 6-42 mcg/24 hours
03/2021 72.7 99.25 6.2 73
06/2021 74.5 109.56 6.6 73
12/2021 80.0 117.17 6.9 62
05/2022 88.5 126.84 6.9 57
11/2022∗ – – – –
12/2022 93.8 124.15 7.0 61 464
01/2023∗∗ – – – –
02/2023 35
06/2023∗∗∗ – – – –
06/2023 100.4 122.76 7.0 54
07/2023 137
12/2023 100.9 130.34 6.8 48 48
08/2024 106 125 6.9 58 76
02/2025 100 96 5.8 76 42
∗
Transsphenoidal resection.
∗∗
Osilodrostat initiated.
∗∗∗
Gamma knife radiosurgery.

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Figure 3. MRI pituitary coronal image revealing right eccentric heterogenous enhancing sellar mass which is decreased in size. Redemonstrated residual tissue around the right carotid artery.

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Figure 4. Graphical representation of weight (kg), total daily dose of insulin (units per day), and 24-hour urine cortisol measurements (mcg/24 hours).

Due to ongoing hypercortisolism, repeat MRI pituitary with and without gadolinium enhancement was obtained and revealed residual disease in the right sella with right cavernous sinus involvement and extending posteriorly along the dorsal aspect of the clivus (Figure 3). She had subsequent consultation with neurosurgery at which time the decision made to proceed with single-fraction gamma knife stereotactic radiosurgery. She received additional treatment of gamma knife radiosurgery with dose of 18 Gy to target residual pituitary disease.

Discussion

We present, to our knowledge, the third reported case of Cushing’s disease due to a corticotropin-secreting pituitary adenoma in an individual with type 1 diabetes. Prolonged hypercortisolism, as seen in this case, is associated with obesity, hypertension, decreased bone density, insulin resistance, and decreased glucose control. Hypercortisolism is most commonly caused by chronic exogenous corticosteroid exposure however, endogenous hypercortisolemia should be considered as a potential etiology of worsening glycemia and insulin resistance in individuals with diabetes mellitus.
The coexistence of Cushing’s disease secondary to a corticotropin-secreting pituitary macroadenoma in an individualwith type 1 diabetes mellitus is exceedingly rare. Furthermore, only 10% of pituitary Cushing’s cases present with macroadenomas at the time of diagnosis. Several studies indicate that smaller lesions at the time of diagnosis and earlier diagnosis of Cushing’s disease are associated with reduced risk of disease recurrence6,7,8. In this case, a young female presented with a macroadenoma at the time of diagnosis and had residual post-operative hypercortisolism requiring gamma knife radiation and pharmacologic intervention with osilodrostat, a steroidogenesis inhibitor approved by the FDA in 2020 for use in refractory Cushing’s disease after pituitary surgery. Osilodrostat works via inhibition of 11β-hydroxylase and aldosterone synthase to inhibit the production of cortisol and aldosterone9,10. Of the two other reported cases of comorbid type 1 diabetes and Cushing’s disease, one individual presented with a macroadenoma at the time of diagnosis. This case occurred in a pediatric male with type 1 diabetes mellitus who was ultimately admitted to the hospital with worsening headaches in the setting of pituitary apoplexy. Prior to hospitalization, this individual showed numerous clinical stigmata of hypercortisolism.
Other contributors to increased insulin resistance, such as obesity, infection, stress, and concurrent glucocorticoids, should also be considered in the differential diagnosis when evaluating etiologies for unexplained changes in glycemic control. However, this case emphasizes the importance of considering the possibility of comorbid Cushing’s disease in persons with type 1 diabetes mellitus. This is imperative to mitigate the consequences of prolonged hypercortisolism and to potentially aid in earlier diagnosis. In this case, declining glucose control and increasing insulin requirements were noted prior to other overt clinical findings of hypercortisolism. Thus, this case also underscores the importance of steadfast evaluation of insulin dose requirements for individuals using continuous insulin infusion devices (particularly hybrid closed-loop automated insulin delivery [AID] systems). With growing emphasis on the review and utilization of the one-page ambulatory glucose profile, it is important to also review insulin pump settings and insulin delivery for those utilizing these systems as automated insulin delivery profile for total daily dose can change and should be reviewed at each visit.

Conclusion

In closing, this case emphasizes the importance of considering secondary endocrine disorders in those living with diabetes mellitus who experience sudden or unexplained changes in glycemic control and insulin requirements. Although rare, coexistence of type 1 diabetes and Cushing’s disease can occur. Prompt recognition and treatment of the underlying Cushing’s disease can lead to significant improvements in insulin sensitivity and glycemic outcomes. This report reinforces the need for multidisciplinary management of vigilant monitoring in patients with coexisting endocrine pathologies, particularly when advanced diabetes technologies are in use. Ultimately, it highlights the critical role of clinical suspicion and timely intervention in optimizing outcomes for complex endocrine cases.

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References

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Adrenal Diseases During Pregnancy: Pathophysiology, Diagnosis And Management Strategies

Posted on January 15, 2026 by MaryO

Am J Med Sci. 2014 Jan;347(1):64-73. doi: 10.1097/MAJ.0b013e31828aaeee.

Author information

Abstract

: Adrenal diseases-including disorders such as Cushing’s syndrome, Addison’s disease, pheochromocytoma, primary hyperaldosteronism and congenital adrenal hyperplasia-are relatively rare in pregnancy, but a timely diagnosis and proper treatment are critical because these disorders can cause maternal and fetal morbidity and mortality.

Making the diagnosis of adrenal disorders in pregnancy is challenging as symptoms associated with pregnancy are also seen in adrenal diseases. In addition, pregnancy is marked by several endocrine changes, including activation of the renin-angiotensin-aldosterone system and the hypothalamic-pituitary-adrenal axis.

The aim of this article was to review the pathophysiology, clinical manifestation, diagnosis and management of various adrenal disorders during pregnancy.

PMID:
23514671
[PubMed – in process]

From http://www.ncbi.nlm.nih.gov/pubmed/23514671

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A Letter To Patients With Chronic Disease

Posted on January 10, 2026 by MaryO

MaryO’Note:  Dr. Rob was interviewed by Robin (staticnrg) and Mary O’Connor (MaryO) October 2, 2008 on BlogTalkRadio Cushing’s Help

Listen to this interview here: http://www.blogtalkradio.com/cushingshelp/2008/10/03/robin-staticnrg-and-mary-oconnor-maryo-interview-dr-rob-1

July 14, 2010
by Rob Lamberts

Dear Patients: You have it very hard, much harder than most people understand.  Having sat for 16 years listening to the stories, seeing the tiredness in your eyes, hearing you try to describe the indescribable, I have come to understand that I too can’t understand what your lives are like.  How do you answer the question, “how do you feel?” when you’ve forgotten what “normal” feels like?  How do you deal with all of the people who think you are exaggerating your pain, your emotions, your fatigue?  How do you decide when to believe them or when to trust your own body?  How do you cope with living a life that won’t let you forget about your frailty, your limits, your mortality?

I can’t imagine.

But I do bring something to the table that you may not know.  I do have information that you can’t really understand because of your unique perspective, your battered world.  There is something that you need to understand that, while it won’t undo your pain, make your fatigue go away, or lift your emotions, it will help you.  It’s information without which you bring yourself more pain than you need suffer; it’s a truth that is a key to getting the help you need much easier than you have in the past.  It may not seem important, but trust me, it is.

You scare doctors.

No, I am not talking about the fear of disease, pain, or death.  I am not talking about doctors being afraid of the limits of their knowledge.  I am talking about your understanding of a fact that everyone else seems to miss, a fact that many doctors hide from: we are normal, fallible people who happen to doctor for a job.  We are not special.  In fact, many of us are very insecure, wanting to feel the affirmation of people who get better, hearing the praise of those we help.  We want to cure disease, to save lives, to be the helping hand, the right person in the right place at the right time.

But chronic unsolvable disease stands square in our way.  You don’t get better, and it makes many of us frustrated, and it makes some of us mad at you.  We don’t want to face things we can’t fix because it shows our limits.  We want the miraculous, and you deny us that chance.

And since this is the perspective you have when you see doctors, your view of them is quite different.  You see us getting frustrated.  You see us when we feel like giving up.  When we take care of you, we have to leave behind the illusion of control, of power over disease.  We get angry, feel insecure, and want to move on to a patient who we can fix, save, or impress.  You are the rock that proves how easily the ship can be sunk.  So your view of doctors is quite different.

Then there is the fact that you also possess something that is usually our domain: knowledge.  You know more about your disease than many of us do – most of us do.  Your MS, rheumatoid arthritis, end-stage kidney disease, Cushing’s disease, bipolar disorder, chronic pain disorder, brittle diabetes, or disabling psychiatric disorder – your defining pain –  is something most of us don’t regularly encounter.  It’s something most of us try to avoid.  So you possess deep understanding of something that many doctors don’t possess.  Even doctors who specialize in your disorder don’t share the kind of knowledge you can only get through living with a disease.  It’s like a parent’s knowledge of their child versus that of a pediatrician.  They may have breadth of knowledge, but you have depth of knowledge that no doctor can possess.

So when you approach a doctor – especially one you’ve never met before – you come with a knowledge of your disease that they don’t have, and a knowledge of the doctor’s limitations that few other patients have.  You see why you scare doctors?  It’s not your fault that you do, but ignoring this fact will limit the help you can only get from them.  I know this because, just like you know your disease better than any doctor, I know what being a doctor feels like more than any patient could ever understand.  You encounter doctors intermittently (more than you wish, perhaps); I live as a doctor continuously.

So let me be so bold as to give you advice on dealing with doctors.  There are some things you can do to make things easier, and others that can sabotage any hope of a good relationship:

  1. Don’t come on too strong – yes, you have to advocate for yourself, but remember that doctors are used to being in control.  All of the other patients come into the room with immediate respect, but your understanding has torn down the doctor-god illusion.  That’s a good thing in the long-run, but few doctors want to be greeted with that reality from the start.  Your goal with any doctor is to build a partnership of trust that goes both ways, and coming on too strong at the start can hurt your chances of ever having that.
  2. Show respect – I say this one carefully, because there are certainly some doctors who don’t treat patients with respect – especially ones like you with chronic disease.  These doctors should be avoided.  But most of us are not like that; we really want to help people and try to treat them well.  But we have worked very hard to earn our position; it was not bestowed by fiat or family tree.  Just as you want to be listened to, so do we.
  3. Keep your eggs in only a few baskets – find a good primary care doctor and a couple of specialists you trust.  Don’t expect a new doctor to figure things out quickly.  It takes me years of repeated visits to really understand many of my chronic disease patients.  The best care happens when a doctor understands the patient and the patient understands the doctor.  This can only happen over time.  Heck, I struggle even seeing the chronically sick patients for other doctors in my practice.  There is something very powerful in having understanding built over time.
  4. Use the ER only when absolutely needed – Emergency room physicians will always struggle with you.  Just expect that.  Their job is to decide if you need to be hospitalized, if you need emergency treatment, or if you can go home.  They might not fix your pain, and certainly won’t try to fully understand you.  That’s not their job.  They went into their specialty to fix problems quickly and move on, not manage chronic disease.  The same goes for any doctor you see for a short time: they will try to get done with you as quickly as possible.
  5. Don’t avoid doctors – one of the most frustrating things for me is when a complicated patient comes in after a long absence with a huge list of problems they want me to address.  I can’t work that way, and I don’t think many doctors can.  Each visit should address only a few problems at a time, otherwise things get confused and more mistakes are made.  It’s OK to keep a list of your own problems so things don’t get left out – I actually like getting those lists, as long as people don’t expect me to handle all of the problems.  It helps me to prioritize with them.
  6. Don’t put up with the jerks – unless you have no choice (in the ER, for example), you should keep looking until you find the right doctor(s) for you.  Some docs are not cut out for chronic disease, while some of us like the long-term relationship.  Don’t feel you have to put up with docs who don’t listen or minimize your problems.  At the minimum, you should be able to find a doctor who doesn’t totally suck.
  7. Forgive us – Sometimes I forget about important things in my patients’ lives.  Sometimes I don’t know you’ve had surgery or that your sister comes to see me as well.  Sometimes I avoid people because I don’t want to admit my limitations.  Be patient with me – I usually know when I’ve messed up, and if you know me well I don’t mind being reminded.  Well, maybe I mind it a little.

You know better than anyone that we docs are just people – with all the stupidity, inconsistency, and fallibility that goes with that – who happen to doctor for a living.  I hope this helps, and I really hope you get the help you need.  It does suck that you have your problem; I just hope this perhaps decreases that suckishness a little bit.

Sincerely,

Dr. Rob

Post Script: This post has generated a huge amount of conversation and interest (as witnessed by the large number of comments!).  I very much appreciate the dialogue it has spawned both here and across the web.  I’ve subsequently written follow-up posts explaining my thoughts in more detail – largely in response to the comments here.  One of them discusses in more detail my own experiences as a doctor and the second talks of the importance of  knowing and being known.  Reading these will give you a better picture of my thought process and perspective on this.Dr. Rob

From http://more-distractible.org/musings/2010/07/14/a-letter-to-patients-with-chronic-disease

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