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So, what IS Amyloidosis?[edit]

One of the things I like(d) about Wikipedia is that even laymen can look up things like "Amyloidosis" and get an idea of what it is without having to deal with the jargon of that specific area.

However, this article is incomprehensible. Someone please make it comprehensible.

Seconded. I have no idea what the heck I just read, or what the disease affects, say nothing of what it does. I got more information from the article on Robert Jordan about the disease... 23:29, 29 April 2007 (UTC)
Unfortunately true. I had a long battle over at Hilbert space about making the intro paragraph comprehensible to a layperson, but to no avail.
This one seems to have a similar problem: someone who already understands it would find it to be a fine article, but for someone who doesn't know what's going on, it's pretty useless.
I'll have to see if I can find the appropriate tag to get an expert in to explain it.
*Septegram*Talk*Contributions* 17:30, 7 June 2007 (UTC)

I am an intelligent person and all it does it explain scientifically what is going on. It is quite uninformative for someone who wants to know the basics of the disease. All it did was leave questions unanswered and my head spinning. This is the worst article I've ever seen on here. The problem is that this is a rare disease and there are few who understand it, including many doctors. I will refer this to an internist that I know who is great at writing. (talk) 16:40, 1 February 2014 (UTC)Carolyn Smith

What it isn't?[edit]

"CJD, Alzheimer's and diabetes are almost never referred to as amyloidoses. However, all of these diseases, as well as some other disorders, are considered to be types of proteopathy, in which structurally aberrant proteins accumulate in certain cells and tissues."

I hav no clue why these diseases wouldn't be referred to as amyloidoses. I'm reading through the whole article after that, just to see why they might not fit, but my impulse is to snip. 08:08, 8 May 2007 (UTC)

This article is Terrible[edit]

Completely incomprehensible with loads of spurious detail and no overview at all-the opening sentence, is laden with medical jargon and factually wrong to boot. This needs a complete rewrite. I will do this when I've got time-possibly this weekend.FelixFelix talk 14:04, 13 July 2007 (UTC)

Thanks, Felix. When it's readable to a normal mortal, please feel free to yank the template I added.
*Septegram*Talk*Contributions* 16:43, 13 July 2007 (UTC)

It's a start[edit]

Next is sorting out the organ specific amyloidoses and then referencing and expanding. Perhaps a bit on biopsy to go with the histology section, and a table of all the precursor proteins. Also a section on clinical features of the systemic amyloisoses before the organ specific ones, perhaps. Hopefully it's all becoming a bit clearer, due to drastic simplification.FelixFelix talk 22:20, 14 July 2007 (UTC)

Mortality Rate?[edit]

Is it fatal? what percentage of people die from it. Robert Jordan is one of my favorite authors, so I am really quite concerned.

Yep, they do-the mortality depends on what type they have and whether they get treatment for the underlying cause or not.FelixFelix talk 20:23, 26 July 2007 (UTC)
RJ's gettin past it i think, he's helping test a new drug that is showing excellent results. his lamba light chains are within normal range now, but he's still dealing with it, but with less struggle than normal —The preceding unsigned comment was added by (talk) 14:23, August 23, 2007 (UTC)
Yes, it is fatal. It doesn't necessarily progress as fast as some cancers do but many cases are fairly asymptomatic until it's too late. While a patient might otherwise be able to get a heart or lung (or other organ) transplant, the doctors will not do an organ transplant in an amyloidosis patient until certain conditions are met. The patient must have free light chains lab results that are within normal parameters and bone marrow biopsies must also indicate that the disease has been sufficiently suppressed. If the patient is too ill to withstand the level of chemotherapy necessary to bring the condition within "normal" parameters, he or she may never qualify for the organ transplant and their condition will just continue to degrade until they expire. There is no "silver bullet" drug; there are a host of treatments that may be offered, but often times several years pass and several different treatment protocols are attempted before a good response to treatment is achieved - if it is ever achieved. While we do not refer to it as "remission", there are some who have had good, "durable responses" who have survived fifteen or twenty years after a successful treatment. But even those patients are strongly advised to return to their treatment center for an evaluation at least once per year. HDM/SCT (high dose melphalan with stem cell transplant) can only be done a maximum of two times, so if that was the treatment that brought the patient within good/reasonable parameters and they've had HDM/SCT twice already, if their blood work or bone marrow biopsy indicates that the disease is on the rise again, they'll have to find another treatment that will hopefully work. Once a patient has been diagnosed with amyloidosis, they will almost assuredly die from it eventually; it's just a matter of time. Unless of course, they get hit by a car first or something like that! And if the patient undergoes much chemotherapy, he or she may be fairly immunocompromised and at risk for other major health issues. Zapriori (talk) 00:30, 11 March 2010 (UTC)

GI manifestations[edit]

doi:10.1111/j.1572-0241.2007.01669.x reviews the manifestations of amyloidosis on the digestive tract. JFW | T@lk 09:22, 16 December 2007 (UTC)

AL amyloidosis[edit]

Review of AL doi:10.1111/j.1365-2141.2007.06936.x by the people from the UK amyloidosis centre. JFW | T@lk 10:46, 24 January 2008 (UTC)

That link didn't work when I tried it, JFW. Nbauman (talk) 12:04, 24 January 2008 (UTC)


Since the amyloidologists like to classify amyloidosis on the basis of the type of amyloid, and the pathologists like to classify based on disease process, I've included a brief table of types of amyloid, which are referred to elsewhere, I know, but I think this is a bit neater. The systemic amyloidosis part needs more work, and I think some more info on pathogenesis, clinical correlartion & prgnosis would be useful. If I get time, I'll do it, but if someone else wants to, feel free. Mattopaedia (talk) 06:54, 6 March 2008 (UTC)

Although it's a nice looking table-I really don't see what this adds at all, apart from making the article more confused-it randomly mentions some amyloid proteins that are already classified sensibly , and others which aren't really amyloid proteins at all (which are also mentioned). I really want to remove this, but I thought I'd raise it here first.FelixFelix talk 10:56, 8 March 2008 (UTC)
Sorry Felix, perhaps I wasn't being clear in my comments above, so I'll try to be clearer, because I believe the table will ultimately be of value to the article.
  • This article is, to me, not a clear representation of the disorder, & needs improving. That's what I've set out to do. I'm a busy man, so I'm not going to do it all at once. I will help it evolve as my time allows. I notice you've made a lot of edits here. Perhaps you feel this is your "baby" and don't want some stranger fiddling with it. I know the sense of pride one gets from producing an article that seems like a wondrous piece of work. But this has to grow, so please, give it a chance. I don't want to disfigure your work, only enhance it.
  • I'm sure you know there are two common methods of classifying the amyloidoses -1.) On the amyloid type, and; 2.) On the clinical manifestation of the amyloid type. There is, of course, a combination of these two, also commonly used. I believe this needs to be indicated in the article.
  • Clinically, Systemic Amyloidosis is an entity that is subclassified into the primary and secondary amyloidoses. Localised amyloidosis is often considred seperately, but it can be AL-type, which makes it (in many cases) to be a primary amyloidosis.
    • Primary amyloidoses are associated with immunocyte dyscrasias & are the most common type.
    • Secondary amyloidoses occur as a result of some underlying chronic inflammatory or destructive process.
I believe the classification as it stands in the article does not clearly convey this, and my intention is to re-write so that it does.
  • My aim is to create an article that gives some consideration to the above points.
I disagree that the list of amyloid proteins is "random." You will notice that the list starts with primary (AA) then the more common secondary types, which, I believe, I have ordered by prevalence.
I disagree that the tabled proteins are already classified sensibly. There is scant consideration to the vagaries of classifaction I have outlined above.
I disagree with your assertion that some "aren't really amyloid proteins at all." Although there is controversy surrounding the definition of amyloid, I believe that any extracellularly deposited protein which has a β-pleated sheet configuration and which demonstrates green birefringence is generally accepted to be an amyloid protein. All of the proteins I have listed fit this classification.
On a personal-style note, I found your edit comment of "uugh!" somewhat offensive. Add that to the style of comment you've written above, and it makes your input here seem to me to be flippant and disrespectful of the time and effort of a medical colleague, who, like yourself, has an interest in providing good-quality free & readily accessible information. Whilst I thank you for your interest in my edits, I will respectfully request that your responses be more considered. Maybe I'm being oversensitive, I don't know, but it pays to be nice. Have a good day!
Mattopaedia (talk) 02:01, 11 March 2008 (UTC)
Fair enough, if you want to put time and effort into improving this article, that's great. I won't get in your way, but if I don't like the end result, I won't be backward about coming forward. And if you find my edits and edit summaries flippant and disrespectful, then sorry, I do think you are being oversensitive.FelixFelix talk 14:22, 11 March 2008 (UTC)

More on classification[edit]

Now, I've had a closer look at the classification info in this document, and it was a reasonable departure from my understanding of its classification. So I've read Robbins Pathology, Harrisons Internal Medicine & Cecil Medicine, and all of them describe the classification essentially as I've put it (which is why I made these changes - I'm more inclined to believe thos texts, & would like wikipedia to be as credible). Again, I went with another table, because I feel it gives the reader q quick overview, and they can then go on to read more if they desire, rather than having to scroll through screens of prose. I've made no changes to the section on localised amyloidosis, only because I haven't had the time to look closely at it yet. In due course, I shall. There should be something written on pathogenesis, clinical presentation, prognosis and treatment. Cheerio! Mattopaedia (talk) 05:07, 11 March 2008 (UTC)

Is this a prion disease?[edit]

Hi, Is Amyloidosis a prion disease? Could it be diet-related? Thanks, Bennie —Preceding unsigned comment added by (talk) 18:18, 17 May 2008 (UTC)

John Smith[edit]

Who is John Smith? (talk) —Preceding comment was added at 21:33, 11 July 2008 (UTC)

Primary Systemic Amyloidosis Clinically Confined to the Heart.[edit]

Diagnosis: Primary Systemic Amyloidosis Clinically Confined to the Heart. Diagnosis made May, 1994- Jefferson University Hospital- Philadelphia, Pa., USA. Diagnosis confirmed -Mayo Clinic, Rochester, Minn. , USA - June, 1994. Diagnosis confirmed - Boston University Hospital, Boston, Mass., USA - July, 1994. AL. Lambda Light Chains. Treatment: Autologous Bone Marrow Transplant with Stem Cell Rescue - August 1994 - Boston University Medical Center Hospital (#2, tip of the hat, Lou - #1) Prognosis: They don't call me "THE CHOSEN ONE" for nothing. As for "Clinically Confined to the Heart" its more like "THE ONLY ONE" - 14+ years later. —Preceding unsigned comment added by Jrhelwig (talkcontribs) 23:44, 22 November 2008 (UTC)

Is amyloidosis the leading cause of death in supercentenarians?[edit]

On BBC Radio Four in August 2009, there was a programme on supercentenarians (broadcast on August 12 at 9 p.m., 2009). To accompany the programme, there was an article in the Radio Times for August 8-14, which claimed that amyloidosis is the leading cause of death of supercentenarians. The article also claimed that this has a similar aetiology to Alzheimer's disease, but does not affect the brain. Is this accurate? I know that the "Radio Times" is hardly the Lancet or the New England Journal of Medicine or the British Medical Journal and does make errors on occasion, but if any one find a reliable source for this claim, it would be good if it could go in the article here. It would also be a good way of linking this article to the article on supercentenarians. ACEOREVIVED (talk) 21:20, 4 October 2009 (UTC)

What are the symptoms of amyloidosis?[edit]

This article needs symptoms. (I'm diagnosing this article as lacking symptoms). I'd fix it but I'm not a doctor or expert like you probably are who is reading this. :)--Tomwsulcer (talk) 15:56, 5 October 2009 (UTC)

Symptoms, Treatments, Lay v. Medical Specialist Content, etc.[edit]

I'm usually interested in the grammar, spelling, polish, etc. of web pages in general and Wikipedia in particular, but have a vested interest in conveying accurate information about amyloidosis to the general public. I agree that this page needs work but am not here to criticize, only to try to improve it.

I have attended a significant number of patient support group meetings and know that patients and their families and friends are often scared and bewildered by such a diagnosis because they most likely have never heard of it before, the treatment options may seem very serious, the diagnosis may have been made later than it should have been, and it seems to be a difficult disease to comprehend particularly for lay persons. Newly-diagnosed patients often are so distressed by the seriousness of the disease that they don't understand the explanation they may have heard thus far, and may misunderstand what was said to them, what the disease is and what the treatments even try to accomplish. It may be difficult for some medical specialists to convey their understanding of the disease to lay persons as well.

Though I have some good knowledge of the disease, I am not a formal medical professional and cannot claim great medical accuracy in some descriptions or explanations in support group meetings. However, the medical staff at the BUMC Amyloidosis Research and Treatment facility does not seem to take exception to my comments.

I have been told some of the following factoids by medical staff or else have read it in printed materials provided by BUMC or various amyloidosis organizations. Things that lay persons and newly-diagnosed patients may do well to understand may include:

  • Amyloidosis affects approximately 8 persons per million, or somewhere between 2,000 and 3,000 persons diagnosed per year in the U.S.A.
  • We believe that amyloidosis may be under-diagnosed. A patient may be diagnosed with cardiovascular disease, for example, simply because it is far more common especially in the same age group that is affected by amyloidosis. Without a tissue biopsy or at the very least a cardiac echogram, the amyloidosis may not be correctly diagnosed.
  • Amyloidosis refers to a group of diseases, which other contributors have already made a good effort to describe.
  • Persons have made remarks regarding amyloidosis and Alzheimer's. It is my understanding that they are related diseases. Amyloidosis involves lambda- and kappa- free light chains while Alzheimer's involves beta free light chains. Amyloidosis can involve virtually any organ of the body except the brain (including the skin); Alzheimer's affects (perhaps) only the brain tissue.
  • My understanding of the disease (at least for Primary AL) is that it is originated in the bone marrow, that some regions of bone marrow seem to become rather "reprogrammed" to produce the proteins that the body cannot use and is not able to eliminate. The amyloid fibrils float around the bloodstream for awhile until settling into some organ or organs, where they begin to corrupt the qualities of the tissue. For example, the heart and lung tissue become thicker and stiffer, degrading the performance of those organs. The kidneys are affected by passing larger substances; protein leakage ("proteinuria") goes from a normal level of about 0.1 gram to an abnormal higher level of leakage of a gram or substantially more.
  • Patients I have met have had amyloidosis in tissue and organs including but not limited to kidneys, heart, lungs, pancreas, liver, thyroid, skin, larynx, eyes, tongue, gastrointestinal tract. If diagnosed early, it may be manifested in only one organ. If diagnosed later, other organs are likely to be involved. Some patients present particularly complicated cases in that they are not able to be categorized simply as Primary AL or AA or Familial, but seem to present as more than one such category, which may impact the ability to provide an effective treatment.
  • Even if a patient is diagnosed, there is no certainty that a particular treatment or set of treatments will result in a reduction of the disease. We do not consider there to be a cure for the disease at this time but only regard as "successful" treatments that create a lasting response that appears to have significantly stopped the production of amyloid fibrils and the imbalance of lambda and kappa free light chains. We may regard this as one would a remission of cancer. The amyloidosis may succeed in becoming productive again after some period of time.
  • If a medical professional (a GP, e.g.) detects something that could possibly be one of the amyloidosis variants, either a tissue biopsy and/or a blood serum free light chains test may be very helpful in shedding light on the situation. In the case of the tissue biopsy, the sample is usually sent to a laboratory that prepares the sample specimen with Congo Red stain and is inspected under polarized light for evidence of "apple green" birefringence. The blood serum free light chain test is a simple test to order that can indicate a gross elevation of either lambda or kappa free light chains, or simply indicate that the ratio of the two is not close to unity.
  • Treatments that I am aware of include high-dose intravenous melphalan with autologous stem-cell transplant. This is a somewhat newer treatment that has come into vogue in the past dozen years or so. The melphalan is administered over the course of two days and kills rapidly-dividing cells, the intentional target being the bone marrow in the attempt to destroy a sufficient amount of the corrupted bone marrow that is producing the amyloid. The adult stem cells are given to the patient a day or two after the second day of melphalan.
  • A treatment that has been used in the U.K and elsewhere for some years is referred to as "VAD", for Vincristine, Adriamycin (now called doxorubicin) and Dexamethasone, which is a steroid.
  • For patients who are unable to withstand high-dose IV melphalan treatment, oral melphalan is sometimes a treatment, sometimes also accompanied with dexamethasone.
  • A treatment that has become available within the past several years is a protease inhibitor, Velcade (bortezomib). The action of protease inhibitors is novel and interesting in that they are not a substance of a toxic nature as melphalan and vincristine are, for example.
  • Another treatment that has also had some success with some patients is Revlimid (lenalidomide, a derivative of thalidomide), an immunomodulator.
  • Some treatments have been combined to provide better efficacy. For example, it is not uncommon for dexamethasone to be used as part of a treatment of Velcade or Revlimid. Sometimes oral melphalan is also included in treatment, though its dosage is much lower than the high-dose IV melphalan.

Even though we appear to have a wide variety of drugs to choose from for chemotherapy, I believe that we're barely scratching the surface of therapies and that far better therapies must be developed that do not have the wide-ranging, debilitating and high-risk side effects of current treatment options.

Regarding prion disease, it wouldn't surprise me if researchers are able to draw a connection between something like BSE and amyloidosis sometime in the next couple of decades. I think it's an interesting question. Better understanding of either of them may lend better understanding to the other. Funding for research is a bit of a sore subject for any of the rare diseases, so research progress is unfortunately apt to be much slower than with the much better-known diseases. It would be interesting to collect data on patients in regards to their diet to see whether vegetarians are as likely to contract amyloidosis as omnivores are. I am only aware of a handful of sites in the world that are actively participating in amyloidosis research. Some of the the treatments we currently have or are investigating for use on amyloidosis are fallout from other treatment programs such as Multiple Myeloma or various cancers.

Some of my initial research of amyloidosis on the web about five years ago initially led me to mistakenly believe that there was an inherent connection to Multiple Myeloma. It is not a given that an amyloidosis patient also has Multiple Myeloma. Some do; many do not. I hope that this Wikipedia article can help patients and families (and even some medical personnel who have little or no first-hand experience of amyloidosis) clarify this and other aspects of the disease.

Researchers that I either know or know of include Skinner, Seldin, Gertz, Comenzo, Dember, Sanchorawala and others. I hope that some of the folks in research can help us beef up the content and clarity of the page so that it is of use to patients, families and friends of patients and medical personnel as well.

Zapriori (talk) 12:18, 10 March 2010 (UTC)

Type AA Amyloidosis Prognosis[edit]

"SECONDARY AMYLOIDOSIS is caused by a chronic infection or inflammatory disease such as rheumatoid arthritis, familial Mediterranean fever, osteomyelitis, or granulomatous ileitis. The deposits in this type of the disease are made up of a protein called the AA protein. Medical or surgical treatment of the underlying chronic infection or inflammatory disease can slow or stop the progression of this type of amyloid."

I submit "Type AA" Amyloidosis is not "terminal" and not necessarily "usually fatal." --Remingtonhill1 (talk) 03:12, 1 May 2010 (UTC)


doi::10.1111/bjh.12286 - the British expert centre has estimated that the incidence is 0.8/100,000 most of which AL amyloid. This will require a secondary source for confirmation. JFW | T@lk 18:11, 11 March 2013 (UTC)

Pathology: protein fragments?[edit]

Is "protein fragments" an awkward way of expressing that some proteins are made of more than one peptide chain? Or do cells make other kinds of protein fragments? Monado (talk) 17:55, 4 May 2014 (UTC)

It's part of a big chunk of text added back in 2010 (diff) by someone who was apparently trying to simplify or avoid certain technical terms. The editor may not have been entirely comfortable in the English language, as well. While some of this editors' work has since been revised (reference to the spleen "exploding" has been replaced with rupturing, for instance), there's still a lot of editing needed.
There are a few things that the text could be trying to describe, depending on which particular amyloid disease the writer had in mind; it's certainly not clear. If they're thinking of light chain amyloidosis, for instance, then yes—they're describing a protein subunit (immunoglobulin light chain) that forms covalent links with other polypeptides (a total of two each of Ig heavy and Ig light chains) to make a complete antibody molecule. If they're thinking of familial amyloid polyneuropathy, then they're describing a transthyretin (TTR) monomer, which normally forms a non-covalent complex of four identical TTR units. If they're thinking of beta amyloid, it's a little tiny cleavage product that results when the gamma secretase protease cuts a piece off the amyloid precursor protein (APP). TenOfAllTrades(talk) 18:41, 4 May 2014 (UTC)

The page is confusing the category of diseases called "amyloidoses" with specific types of amyloidosis[edit]

The amyloidosis article is a bit of a mess right now. The article confuses the generic term amyoidosis with the various different specific types of amyloidoses. It seems to me that this article should be describing the category of diseases that encompass the amyloidoses and that specific information about the various types (light chain amyloidosis or AA amyloidosis or whatever) should be contained in their own articles. I'm not really sure about how to go about doing this....would appreciate any help.

I've deleted the section on signs / symptoms because this is really meaningless when discussing the large number of diseases called amyloidoses. It seems that most of the signs/sx were talking about light chain amyloidosis, not the many other kinds that exist.

Wawot1 (talk) 16:33, 8 May 2014 (UTC)

Many recent edits seem to be making the confusion worse, not better...amyloidosis is not a single disease, but a category of diseases. Need to clarify this. Wawot1 (talk) 08:22, 15 November 2014 (UTC)

Peer Review[edit]

Hi, thanks for taking on this challenging article. It will be a great resource to those within and outside of the medical community. As noted above by another reviewer, I think it would be good to emphasize that amyloidosis is not one disease but encompasses a spectrum of diseases. Here are my comments based on the areas of focus you noted:

                           A) intro
  • Could delete “in medicine”
  • Maybe simplify lead and just say, “amyloids are insoluble proteins and can deposit in a number of organs or tissues, disrupting normal function.”
  • Might add a line at the end like- “Although they can affect almost every organ, amyloid typically deposit here x x…. leading to blank ….”

B) Subsection classification:

  • if you wanted you could break down the signs and symptoms section which is quite long and create organ system subheadings: heart, kidney, liver, etc or Create subsections based on AA, AL, etc (could give brief overview of these processes and link to more detailed articles)
  • Tighten up the proteolysis discussion in the pathogenesis section - some redundancy here. “This happens b/c the misfolded proteins become robust enough…” and “the reason they aggregate…” sentences basically say the same thing, just the later more sophisticated than the former.

C) other

  • If I were a lay reader, I wouldn’t understand AA vs AL amyloidosis, which is introduced somewhat abruptly in the signs and symptoms section. Maybe clarify those terms briefly in S/S section.
  • Pathogenesis section: create new sentence for: “proteases come and digest the misfolded fragments and proteins”

Jmtseng (talk) 23:47, 17 November 2014 (UTC)


I'm copying here an old stub named Amyloid degeneration which is now a redirect to the present page, since some of the content of the old stub might be relevant (source) to ==History== here:

Amyloid degeneration is a type of degeneration with the deposit of lardacein in the tissues. It indicates[disambiguation needed] impairment of nutritive function and is seen in wasting diseases. It is also sometimes called Abercrombie's disease, Abercrombie's syndrome, Virchow's syndrome, bacony disease, cellulose disease, hyaloid disease, lardaceous disease, waxy disease, and waxy degeneration. Its alternate names honour Scottish physician John Abercrombie and German physician Rudolf Ludwig Karl Virchow. (talk) 18:24, 1 July 2015 (UTC)


Looking at the current lede sentence;

"Amyloidosis is a rare disease that results from accumulation of inappropriately folded proteins."

Two complaints about this line. 1) It seems like it's ripped off from here. 2) I think Alzheimer's might technically count as an Amyloidosis (ref 1,2,3), in which case using the term "rare" seems wrong.

Anyone with more expertise on this than myself want to comment? NickCT (talk) 18:32, 27 October 2015 (UTC)

Perhaps the sentence can be rewritten and the word "rare" avoided? --My Core Competency is Competency (talk) 20:08, 27 October 2015 (UTC)
  1. It seems is an unattributed WikiPedia clone, we should probably get in touch with WMF-legal.
  2. Localised amyloid deposits ≠ amyloidosis
  3. It is pretty rare, sure we could specify, but I don't see why we would need to remove it.
CFCF 💌 📧 21:22, 27 October 2015 (UTC)
re "clone" - Scanning through their stuff it seems like most of what they have is attributed to the National Library of Medicine. Why do you think it's a clone of us, rather than us being a close of them?
re "amyloid deposits ≠ amyloidosis" - Really? So which amyloid deposit diseases count as amyloidosis? Where's the list? Why do some sources call Alzheimer's amyloidosis? NickCT (talk) 21:50, 27 October 2015 (UTC)
re "clone"—it looks like is lifting text from multiple Wikipedia articles without attribution, and claiming copyright on it. The first randomly selected medical articles I looked at (schizophrenia and lung cancer, compare: [1], [2]) do exactly the same thing: copying the lede from Wikipedia's articles and adding them to the bottom of their pages.
re "amyloid deposits ≠ amyloidosis"—yes, really. It's a semantic thing related to the way that physicians typically use the terms, rather than the straightforward "sensible" interpretation of what the terms perhaps "ought" to mean. And in any field, you'll find a few rebels who want to argue the point. (I don't think the rebels have reached critical mass in this particular field, to the point where Wikipedia should adopt their broader definition.) It's similar to how the word chemotherapy in most contexts is just presumed to mean chemotherapy for cancer treatment, even though the word's meaning is much broader. TenOfAllTrades(talk) 22:49, 27 October 2015 (UTC)
apparently it does seem to be (in regards to use of this Amyloidosis article term I agree w/ TenOfAllTrades)--Ozzie10aaaa (talk) 08:57, 28 October 2015 (UTC)
@TenOfAllTrades: - Good analogy to chemotherapy. One thing I'm still left wondering is how many "rebels" one needs before there's a critical mass. Clearly there are at least a few high-quality RS's which explicitly and specifically call things like Alzheimer's amyloidosis. I'm not sure the same applies to chemotherapy.
And how do we know that VisualMD is lifting from Wikipedia rather than vice versa? NickCT (talk) 13:19, 28 October 2015 (UTC)
Regarding terminology—I wouldn't say that the field has adopted a broader definition until it shows up in standard textbooks. (
Regarding VisualMD, it's pretty obvious from the structure of their pages. (Follow the links provided.) In all cases, the VisualMD site has a summary from somewhere else (not sure if they're creating them in-house or scraping them from some other site(s) or some combination of both), followed by a direct copy of the exact text of the Wikipedia article lede (including the bolding of alternate article titles) with the footnotes stripped. It strikes me as exceedingly implausible that on some of our more highly-watched and -edited medical articles someone could copy & paste in an entire lead section, and that they (or someone else) would subsequently, meticulously add ten or a dozen citations without altering a single word of the text. It's even more implausible that someone would do so while only copying the bottom half of the VisualMD page, and even more incredible that the VisualMD page would happen to be precisely created so that the bottom portion of their text would function as a standalone Wikipedia article lede. TenOfAllTrades(talk) 15:03, 28 October 2015 (UTC)
@TenOfAllTrades: - The "text book definition" standard seems reasonable.
Re VisualMD - Ah Ok. So it just seems very improbable that WP is stealing. Agreed. For a second I thought you might have some way to absolutely confirm which direction the thiefery was going.  ;-) NickCT (talk) 19:56, 28 October 2015 (UTC)
The claim is verifiable. Both NORD and Orphanet list it: Search for it at NORD and page at Orphanet. WhatamIdoing (talk) 18:31, 28 October 2015 (UTC)
@WhatamIdoing: - Which claim? NickCT (talk) 19:56, 28 October 2015 (UTC)
The claim that amyloidosis is a rare disease. WhatamIdoing (talk) 21:10, 28 October 2015 (UTC)
The first link doesn't seem to work. I don't see where it says it's rare in the second. Regardless, I guess I was more curious about whether Alzheimer's was an amyloidosis (because if it is, then "rare" clearly isn't true). I think TenOfAllTrades touched on the right point which is that Amlzheimer's doesn't meet the text book standard for amyloidosis. NickCT (talk) 14:52, 29 October 2015 (UTC)
Being a rare disease is a criteria for Orphanet inclusion. CFCF 💌 📧 15:48, 4 November 2015 (UTC)

Lancet Seminar December 2015[edit]

Lancet. 2015 Dec 21. pii: S0140-6736(15)01274-X. doi: 10.1016/S0140-6736(15)01274-X.
Systemic amyloidosis.
Wechalekar AD1, Gillmore JD2, Hawkins PN2.
--Nbauman (talk) 06:36, 17 February 2016 (UTC)

Now in print issue doi:10.1016/S0140-6736(15)01274-X JFW | T@lk 12:52, 24 June 2016 (UTC)

Cerebral Amyloid Angiopathy[edit]

While this is a separate entity, they are both often referred to as amyloid. Should there be a disambiguation?

Thanks. Streddy75 (talk) 13:17, 21 October 2016 (UTC)