Merck Manual: Euthyroid Sick Syndrome

Link
Asking your doctor
to explain this
should be fun.

Why is health care so hazardous? What needs to be done to improve safety?

Statement of Lucian Leape, M.D.
Member, Quality of Health Care in America Committee
Institute of Medicine
Adjunct Professor, Harvard School of Public Health

Concerning Patient Safety and Medical Errors

Before the
United States Senate
Subcommittee on Labor, Health and Human Services, and Education

January 25, 2000

"Good morning, Mr. Chairman and Senator Kennedy, and members of the committee. My name is Lucian Leape and I am a faculty member at the Harvard School of Public Health. I practiced as a pediatric surgeon for much of my career, but in recent years have focused my attention on research into medical errors. I am here today representing the Institute of Medicine's Committee on the Quality of Health Care in America which recently released the report To Err is Human: Building a Safer Health System.

In my testimony today, I will address two questions: 1) Why is health care so hazardous? 2) What needs to be done to improve safety?

Why is health care so hazardous?

Findings from several studies of large numbers of hospitalized patients indicate that each year a million or more people are injured and as many as 100,000 die as a result of errors in their care. This makes medical care one of the leading causes of death, accounting for more lost lives than automobile accidents, breast cancer or AIDS. While these findings are not new, and some hospitals have improved their error reduction activities, clearly a much greater effort is needed to make health care safe.

No physician or nurse wants to hurt patients, and doctors, nurses, and other health workers are highly trained to be careful and take precautions to prevent mistakes. They are held and hold themselves to high standards. Paradoxically, it is precisely this exclusive focus on the individual's responsibility not to make mistakes, reinforced by punishment, that makes health care so unsafe.

The reason is that errors are seldom due to carelessness or lack of trying hard enough. More commonly, errors are caused by faulty systems, processes and conditions that lead people to make mistakes. They can be prevented by designing systems that make it hard for people to do something wrong and easy to do it right. Safe industries, such as aviation, chemical manufacturing, and nuclear power, learned this lesson long ago. While insisting on training and high standards of performance, they recognize these are insufficient to insure safety. They also pay attention to factors that affect performance, such as hours and work loads, work conditions, team relationships, and the design of tasks to make errors difficult to make. They create safety by design. Health care must do likewise.

Approaches that focus on punishing individuals instead of changing systems provide strong incentives for people to report only those errors they cannot hide. Thus, a punitive approach shuts off the information that is needed to identify faulty systems and create safer ones. In a punitive system, no one learns from their mistakes."



Link

Wikipedia: Congenital hypothyroidism, PAX8

Congenital hypothyroidism is the most common preventable cause of mental retardation. Few treatments in the practice of medicine provide as large a benefit for as small an effort.

Congenital hypothyroidism

PAX8

Ultrasound Images of Thyroid Dysgenesis and More

Link
Osler didn't have this fancy technology; doctors should be able to tell if half of something isn't there by sight and touch.

ICD Codes for Thyroid Disorders

http://www.icd9data.com/2009/Volume1/240-279/240-246/
Thyroid disorders
http://www.icd9data.com/2009/Volume1/240-279/240-246/243/default.htm
Congenital hypothyroidism
Myxedema

Resource: Werner and Ingbar's THE THYROID

Werner and Ingbar's THE THYROID is online at Google Books. This link leads to the chapter on Hypothyroid conditions.

BMJ - Genetics of Congenital Hypothyroidism

From the abstract:

Journal of Medical Genetics 2005;42:379-389; doi:10.1136/jmg.2004.024158
Copyright © 2005 by the BMJ Publishing Group Ltd.
REVIEW
Genetics of congenital hypothyroidism
S M Park1, V K K Chatterjee2

1 Department of Clinical Genetics, Addenbrooke’s Hospital, Cambridge, UK
2 Department of Medicine, University of Cambridge, Addenbrooke’s Hospital

Correspondence to:
Correspondence to:
Dr S M Park
Department of Clinical Genetics, Box 134, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, UK; soo-mi.park@addenbrookes.nhs.uk
Congenital hypothyroidism is the most common neonatal metabolic disorder and results in severe neurodevelopmental impairment and infertility if untreated. Congenital hypothyroidism is usually sporadic but up to 2% of thyroid dysgenesis is familial, and congenital hypothyroidism caused by organification defects is often recessively inherited. The candidate genes associated with this genetically heterogeneous disorder form two main groups: those causing thyroid gland dysgenesis and those causing dyshormonogenesis. Genes associated with thyroid gland dysgenesis include the TSH receptor in non-syndromic congenital hypothyroidism, and Gs and the thyroid transcription factors (TTF-1, TTF-2, and Pax-8), associated with different complex syndromes that include congenital hypothyroidism. Among those causing dyshormonogenesis, the thyroid peroxidase and thyroglobulin genes were initially described, and more recently PDS (Pendred syndrome), NIS (sodium iodide symporter), and THOX2 (thyroid oxidase 2) gene defects. There is also early evidence for a third group of congenital hypothyroid conditions associated with iodothyronine transporter defects associated with severe neurological sequelae. This review focuses on the genetic aspects of primary congenital hypothyroidism.

Abbreviations: ERSD, endoplasmic reticulum storage disease; NIS, sodium iodide symporter; PHP, pseudohypoparathyroidism; PPHP, pseudopseudo-hypoparathyroidism; PTH, parathyroid hormone; TPO, thyroid peroxidase; TRH, thyrotropin releasing hormone; TSH, thyroid stimulating hormone (thyrotropin)

Keywords: congenital hypothyroidism; candidate gene

Link to abstracthttp://jmg.bmj.com/cgi/content/abstract/42/5/379



Link to pdf

Hypothyroid and Alzheimer's - a connection?

Hypothyroid can not only cause dementia; this study suggests it is linked to Alzheimer's disease too.
http://pt.wkhealth.com/pt/re/clen/abstract.00003033-200012000-00012.htm;jsessionid=KBLSHYLsQBp2mqrqJ8Ttm4tsQXLVfpLc6kcfNyXXPVyXXGlL1YQT!-444506849!181195629!8091!-1
Given reliance on flawed American Thyroid level testing rather than on how the patient feels, prompt and appropriate treatment may not be delivered.

Peatfield was a general practitioner in the British National Health service who came to America and trained at the Broda Barnes Institute. He returned to England and started a thyroid private practice. His book summarizes over 25 years of clinical diagnosing and treating thyroid illness. One section of the book is devoted to the question, "Why thyroid blood tests can be unreliable".

Here is what Dr. Peatfield says:

"Anxiety in the medical establishment about rules and dogma has led to a slavish reliance on blood tests, which are often unreliable and can actually produce a false picture of the true situation"

"I have sadly come across very few doctors who can accept the fact that a normal, or low TSH, may still occur with a low thyroid."

"as a result of this test (TSH), thousands are denied treatment"

Peatfield lists several reasons why thyroid blood tests are flawed:

1) They measure hormone levels in the blood. What we really want to know is tissue levels, not blood levels.

2) The blood tests do not measure cellular receptor hormone resistance.

3) The blood tests do not measure conversion block. Some patients cannot convert their inactive T4 to active T3.

4) The thyroid tests do not account for adrenal insufficiency.

5) Paradoxical low TSH may occur with a low thyroid function.

These sentiments are shared by the teachings of Broda Barnes MD, and the Broda Barnes Foundation. However, Peatfield's book elaborates beyond the classic teachings of Broda Barnes by including chapters on the adrenal as well as a chapter on iodine supplementation. I found this book excellent, and it belongs in every medical library dealing with thyroid disease.

http://www.amazon.com/review/RSKEFGC2G8IZO

Thyroid Transcription Factors and Congenital Hypothyroidism

THYROID TRANSCRIPTION FACTORS AND CONGENITAL HYPOTHYROIDISM

Introduction
Primary congenital hypothyroidism (CH) is the most frequent endocrine-metabolic disease in infancy, with an incidence of about 1/3-4000 newborns. In about 85% of the cases, CH is caused by an alteration in the morphogenesis of the thyroid (thyroid dysgenesis, TD) (2). In 5-16% of cases TD it is associated with other major birth defects, mostly cardiac (Table 1) (3).
Most of the critical events in thyroid morphogenesis take place in the first 60 days of gestation in man or the first 15 days in mice. For this reason, thyroid developmental abnormalities result from morphogenetic errors during this period.
The regulation of formation, migration and proliferation of the thyroid gland are still largely unknown. Several genes, including those encoding thyroid specific transcription factors (TITF1, TITF2, PAX8), thyrotropin (TSH) and its receptor (TSHR), and/or other genes, have been demonstrated to play a role (1). Alterations in any of these genes can be responsible for thyroid dysgenesis.
Mutations in the genes involved in thyroid development give rise to animal models with TD, and mutations in the same genes have been identified also in a small number of patients with congenital hypothyroidism associated with TD.

In this review we will briefly describe the role of thyroid transcription factors and their involvement in the pathogenesis of TD.

NKX2-1/TITF1
NKX2-1, also known as TITF1 (Thyroid Transcription Factor–1) is a homeodomain transcription factor that was initially identified in a rat thyroid cell as a nuclear protein able to bind to specific sequences in the Tg promoter. TITF1 belongs to the Nkx2 class of transcription factors and is encoded by a gene, located on chromosome 14q13 (Table 1). The gene is formed by at least 3 exons and encodes for 42 kDa protein that is phosphorylated. During human development, the gene is expressed in the ventral diencephalon and in the telencephalon; in the lung bud and in the thyroid primordium (1, 4).
Studies in mice demonstrated that Titf1 is required for the survival and subsequent differentiation of the cells.

Link

Interesting... this is not a rare disorder. If an endocrinologist who mainly treats children cannot recognize this in adults, how will s/he recognize it in the young persons in his/her care?

Congenital Hypothyroidism - Diagnostics and Treatment

THYROIDAL CONGENITAL HYPOTHYROIDISM

B1. Ontogeny of the Thyroid Gland

The thyroid gland is the first endocrine gland to appear during embryonic development. The gland develops from a median endodermal thickening in the floor of the primitive pharynx. This placode (median anlage) develops into a diverticulum that grows caudally. By seven weeks of gestation, the human thyroid gland has usually reached its final site in the neck. Experiments with knock-out mice show that the transcription factors NKX2.1, FOXE1 and PAX8 are crucial for thyroid development. [76] Hypoplasia caused by inactivation of the TSH receptor is a later phenomenon.[77]

Defects in NKX2.1

The transcription factor NKX2.1 (TTF-1) is a member of a protein family essential for developmental processes. The NKX2.1 gene is localized on chromosome 14q13 and is expressed in thyroid, lung and several structures of the forebrain. Mice missing the NKX2.1 gene are stillborn, lack the thyroid gland, the pituitary gland, lung parenchyma, and show extensive defects in brain development.[78] Mutations in the NKX2.1-gene are not a frequent cause of CH but result in a syndrome combining a variable degree of congenital hypothyroidism, choreoathetosis, muscular hypotonia and pulmonary problems. [79] [80] [81] [82] The unfavorable outcome of these patients probably does not reflect the hypothyroid state but is most likely due to impaired NKX2.1 expression in the central nervous system. In mice NKX2.1 haploinsufficiency results in hypothyroidism caused by the concomitant reduced expression of the TSH-receptor. [83] Hypothyroidism can range from thyroid agenesis with severe hypothyroidism to a moderate hypoplastic gland with mild hypothyroidism to complete euthyroidism.

Thyroidmanager.org - U of Chicago course

Lyme Disease Conflicts of Interest Uncovered

http://www.cdc.gov/mmwr/preview/mmwrhtml/figures/R807A2F1.GIF
Note: Deer ticks carrying Lyme Disease do not turn back at the US border.

Patient advocates and physicians concerned with the treatment of chronic Lyme disease finally had their voices heard at a July 30 2009 hearing mandated by a legal settlement between Connecticut's Attorney General and the Infectious Diseases Society of America (IDSA). More than a year after an investigation by Atty. Gen. Richard Blumenthal into the 2006 IDSA Lyme Guidelines' development revealed conflicts of interest by members of the IDSA guidelines' panel, a new panel heard testimony on whether the guidelines required revision. Insurance companies use the current highly restrictive treatment guidelines to deny patients reimbursement for medical care. "This dialogue would not have happened without the strong vision and leadership of the CT Attorney General Richard Blumenthal, who investigated this controversy, uncovered the facts, and called for this review," said Diane Blanchard, Co-President of Time for Lyme. "We hope it sets the stage for further dialogue."

Link
Webcast - available through August 2010

Could it be that evidence of use of a "flawed" test has been hushed up and permitted at "world class" Canadian hospitals to shore up denial of insurance claims in the USA? Cdn "national security" Lyme tests.
Discussion

"You may never need another thyroid test again"

Listening to the patient. Empirical medicine. Sir William Osler would approve....

From the page:
“These blood tests – they don’t work for you. They didn’t help you over the last 15 years you’ve been having problems, even when your problems became worse over the last two. It is because these thyroid antibodies variably bind up the hormones you have. There is no way to tell how much thyroid hormone you need based upon blood tests.”

Michelle’s eyes were rolling back into her head and her mouth was sagging open.

She obviously needed more of an explanation. “Let’s try another analogy. When a traffic helicopter flies overhead, it sees all the cars on the road – and says, ‘There’s plenty of transportation to take people around the city.’ But what if a meter maid noticed they didn’t pay their parking tickets and put a red parking boot on some of them. They wouldn’t be able to go anywhere. In order to have enough transportation for the city – you might need twice as many cars. Unfortunately – there is no way to know how vicious that meter maid is – we just know that she is there. There is no way to know how much of a negative effect those thyroid antibodies are having, we just know that they are there. The presence of thyroid antibodies throws off every thyroid test, including the TSH.”

Michelle was exasperated. Slumping back in her chair, “Then how will I ever know how much medicine to be on?”

“You forgot, there is one more type of testing that will be most effective for you.” Michelle became interested again and leaned forward. “We should test the effect that thyroid hormones have on your body. With hormone resistance, it is often easier and more effective to test the function of the hormone, not the actual level. This idea isn’t new. In Type II Diabetes, we know there is insulin hormone resistance. We don’t check insulin levels – we check what it does by monitoring your blood sugar levels. There are many different types of thyroid hormone resistance. In addition to the Reverse T3 phenomenon and Thyroid Antibodies, some people are deficient of essential fatty acids or other vitamins, limiting thyroid hormone’s ability to get into the brain or other cells to have its full effect.9,10 We just have to check what thyroid hormone does in your body.

“Though active thyroid hormone is needed to lower cholesterol and blood pressure, to raise blood sugar when hypoglycemic, and to convert beta-carotene into Vitamin A, there is no specific blood test to show whether thyroid hormone is working properly or not. Dr. Broda Barnes, MD, PhD, who wrote one of the first books on hypothyroidism, ‘Hypothyroidism: the unsuspected illness,' described a simple temperature test using a mercury thermometer.11 Mercury thermometers are more accurate than digital ones, and because they are hard to find nowadays, I’ll sell one to you for a dollar (that’s all they cost me). Here is a handout to describe how to do the test.

“Lastly, I want you to take this sheet of paper that has ten, 10-point scales on it. I want you to write down the ten things most important to you. For the first line, fill in ‘Energy Level.' Zero will be where you can’t get out of bed, ten being where you are excited about travel and are planning a fun trip. If you are spending money you don’t have, you might be at a twelve. Please call me before they take away your credit cards.” Michelle smiled. “Fill in the other nine items with the things most important to you: weight, skin, and mood are three things you’ve already mentioned. Many people also put down constipation, hair growth/loss, nail quality, and cold/heat intolerance, menstrual periods, and libido. Lastly, there are checkboxes at the bottom for ‘Palpitations’ (sensations of your heartbeat) and ‘Anxiety.' If you feel like you have too much coffee or caffeine in your system, you might be getting too much medication. Every so often, scale yourself. If you are getting better – then we know you are on the right track.”

“I think I finally understand these tests, so what do we do now? You said I would have options in choosing my own care.”

Link

Sir William Osler tailored treatment for optimum patient wellness.

Mental status symptoms and thyroid

Illustration - low thyroid/hypothyroid/myxedema

If you look like the lady in this image and feel terrible -
but your doctor says you are endocrinologically "stable",
ask your doctor whether s/he treats lab tests - or people.

If your thryoid is not functioning well and your physician fails to recognize the source of your symptoms, you may be set for years of bad health and altered mental status.

Many psychiatric disorders and symptoms are related to thyroid hormones. Both underactive (hypothyroidism) and overactive (hyperthyroidism) thyroid hormone blood levels can trigger panic attacks. In approximately 1/3 of patients with depression, borderline personality disorder, panic disorder, bulimia, alcoholism in remission, and anorexia nervosa the pituitary gland does not properly increase blood levels of TSH when signaled to do so by the hypothalamus. This can cause "hypothyroidism" with "normal" blood values. "Normal" is a statistic referring to the middle 96% of the population - it does not mean that "normal" is normal or healthy for you. "Normal" cholesterol by the middle 96% technique includes cholesterol levels of 300, whereas the middle statistically is 220, and the goal is less than 200.

From Low thyroid and mental illness
Also see Thyroid and Schizophrenia
Hypothyroidism and Psychiatric Illness
Treatment of hypothyroidism
Myxedema Madness
Myxedema Madness PDF
Anxiety and Thyroid Disease
Anxiety and endocrine disease
Efficacy of T3
T3/T4 Combination in Bipolar
29 Medical Causes of Schizophrenia


Getting locked into a position due to outdated information can be fatal for doctor and patient.

More on this issue to come...