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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.
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. 71.93.201.164 ( talk) 16:40, 1 February 2014 (UTC)Carolyn Smith
"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."
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)
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)
Is it fatal? what percentage of people die from it. Robert Jordan is one of my favorite authors, so I am really quite concerned.
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)
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)
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)
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)
Hi, Is Amyloidosis a prion disease? Could it be diet-related? Thanks, Bennie —Preceding unsigned comment added by 66.57.189.224 ( talk) 18:18, 17 May 2008 (UTC)
Who is John Smith? 128.208.1.225 ( talk) —Preceding comment was added at 21:33, 11 July 2008 (UTC)
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.
http://sites.google.com/site/curedofamy/ —Preceding unsigned comment added by Jrhelwig ( talk • contribs) 23:44, 22 November 2008 (UTC)
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)
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)
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:
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)
"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."
http://www.amyloidosis.org/whatisit.asp
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)
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)
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)
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
B) Subsection classification:
C) other
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.
5.80.198.100 ( 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)
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)
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)
Given that this ( amyloid purpura) is very far from common (15% according to the ref on that WL) it's perhaps not appropriate to have this image so prominent. Perhaps it should be under signs and symptoms? Thoughts? - Snori ( talk) 03:19, 15 April 2019 (UTC)
Hello, we are a group of medical students from Queen’s University. We are working to improve this article over the next month and will posting our planned changes on this talk page. We look forward to working with the existing Wikipedia medical editing community to improve this article and share evidence. We welcome feedback and suggestions as we learn to edit. Thank you. Jan2020-med2024 ( talk) 20:17, 23 November 2020 (UTC)
Croissanttabletennis ( talk) 17:24, 4 December 2020 (UTC)
Thank you for the feedback! Croissanttabletennis ( talk) 17:39, 4 December 2020 (UTC)
References
Targeted sentence: “In ATTR, liver transplant is a curative therapy because mutated transthyretin which forms amyloids is produced in the liver.[7] ”
Proposed Changed: Management of ATTR amyloidosis will depend on its classification as wild type or variant. [1] Both may be treated with tafamidis, a low toxicity oral agent that prevents destabilization of correctly folded protein. [1] Studies showed tafamidis reduced mortality and hospitalization due to heart failure. [1] Previously, for variant ATTR amyloidosis, liver transplant was the only effective treatment. [1] However, newer therapies including diflunisal, an anti-inflammatory drug, and inotersen and patisiran, drugs which prevent misfolded protein formation, have shown early promises in slowing disease progression. [1] The latter two drugs have shown their benefit in neurological impairment scores and quality of life measures. [1] However, their role in cardiac ATTR amyloidosis is still being investigated. [1]
Rationale for proposed change: This sentence was outdated: The supporting reference is from 1997 and management has evolved since then. Newer agents have emerged that have demonstrated effects on slowing disease progression.
Area of controversy: There is some ambiguity on this topic as some of the information regarding management with medication is still being uncovered. When proposing changes, I tried to make it clear that these are early promises.
This sentence is incomplete: The sentence does not differentiate between wild type and variant type ATTR amyloidosis which have some differences in management. Also, it did not specifically describe the benefits of treatment including the mortality and quality of life. KarnPuri22 ( talk) 18:39, 4 December 2020 (UTC)
References
I propose the following addition to the Amyloidosis#pathology section: Proposed addition: The vast majority of proteins that have been found to form amyloid deposits are secreted proteins, so the misfolding and formation of the amyloid occurs outside cells, in the extracellular space. [1] There is currently no evidence of any structural or functional similarities between the different types of proteins vulnerable to misfold into amyloid. [1] Thirty-seven proteins have been identified as being vulnerable to amyloid formation, and only four are cytosolic. [1] One third of amyloid disease is hereditary, in which case there is normally an early age of onset. [1] Half of amyloid-related diseases are sporadic and have a late age of onset – in these cases, the protein aggregation is due to a progressive loss of the body’s ability to regulate protein formation, with aging. A small number of amyloid disorders occur as a result of medical treatment. [1]
Rationale for proposed change: I propose adding the above text to give readers more context about the origin of amyloidosis in terms of risk factors – I think it could be helpful to someone who’s just been diagnosed with amyloidosis to know that there is often little rhyme or reason to who gets the disease, in case they’re having feelings of guilt or fears around risk factors they could have been exposed to. Also, I talked a little bit about where things happen spatially, which I hope could be helpful for people trying to visualize these processes, as histological processes are often hard to picture or conceptualize.
Thank you! I appreciate your time and look forward to your feedback. REIJONES ( talk) 18:52, 4 December 2020 (UTC)
References
Original text: “Tissue can come from any involved organ, but in systemic disease the first-line site of the biopsy is subcutaneous abdominal fat, known as a "fat pad biopsy", due to its ease of acquisition versus biopsy of the rectum, salivary gland or internal organs. An abdominal fat biopsy is not completely sensitive, and sometimes, biopsy of an involved organ (such as the kidney) is required to achieve a diagnosis. For example, in AL amyloidosis only 85% of people will have a positive fatpad biopsy using Congo red stain. By comparison, rectal biopsy has sensitivity of 74–94%.”
Proposed change to text: A sample of tissue can be biopsied or obtained directly from the affected internal organ, but the first-line site of biopsy is subcutaneous abdominal fat, known as a “fat pad biopsy”, due to its ease of acquisition. An abdominal fat biopsy is not completely sensitive and may result in false negatives, which means a negative result does not exclude amyloidosis diagnosis. [1] [2] However, direct biopsy of the affected organ may still be unnecessary as other less invasive methods of biopsy can also be used, including rectal salivary gland biopsy, lip, or bone marrow biopsy which can achieve a diagnosis in up to 85% of people. [1]
Rationale for proposed change:
The article previously did not explain what was meant by “involved” organ, and lists the “rectum, salivary gland, or internal organs” as examples. I wanted to be more clear and specify that there is a difference between sampling the internal organ and sampling other tissue. I also provided an explanation for what it means when a test is not “completely sensitive” by explaining that false negatives may occur, which means that a diagnosis cannot be excluded yet. The article then states that the biopsy of the “involved” organ is required to achieve diagnosis, but then proceeds to give “rectal biopsy” as an example, yet the rectum is not related to the usual “involved” internal organs (i.e. rectal biopsy is not biopsy of the “involved organ”; it is another alternative to direct organ biopsy). I wanted to make it clear that direct organ biopsy (e.g. if you suspect the kidney has amyloid tissue, then you would sample the kidney) is often unnecessary as many less invasive diagnostic techniques exist. I also wanted to update the provided statistic using a more recent source. -- Jwoodly ( talk) 19:21, 4 December 2020 (UTC)
References
References
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
Jan2020-med2024 ( talk) 19:42, 4 December 2020 (UTC)
References
Original: “The three most common forms of amyloidosis are AL, AA, and ATTR amyloidoses. The median age at diagnosis is 64.[8]
In the western hemisphere, AL is the most prevalent, comprising 90% of cases.[14] In the United States it is estimated that there are 1,275 to 3,200 new cases of AL amyloidoses a year."
Changes:
Amyloidosis has a combined estimated prevalence of 30 per 100,000 persons with the three most common forms being AL, ATTR, and AA. The median age at diagnosis is 64.
[1]
[2]
AL has the highest incidence at approximately 12 cases per million persons per year and an estimated prevalence of 30,000 to 45,000 cases in the US and European Union. [2]
Rationale for proposed change: I changed the first sentence to include the combined prevalence of all types of amyloidosis. This is a good statistic to provide as it gives the reader an idea of how rare amyloidosis is. Also, I rearranged the order of the last two types of amyloidosis and placed ATTR before AA. This is important because it organizes the types of amyloidosis from most to least common and reflects the current understanding that AA has become rarer than the first two types due to advancements in treating chronic infectious diseases. The information for both changes come from two review articles published within the past 3 years from JAMA and Current Medical Research and Opinion, two highly reputable journals.
Next, I changed the two sentences about AL amyloidosis. The first sentence’s statistic regarding “90% of cases” was unfounded in the cited source. Furthermore, they provided an outdated statistic/source from 1997 for the incidence in the second sentence. I replaced these two sentences with a sentence that provided the prevalence and incidence from reputable sources updated within the past 3 years. The information for this sentence change comes from JAMA and Current Medical Research and Opinion. Jlowe24 ( talk) 22:35, 4 December 2020 (UTC)
References
Suggested Change #15
Original: Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein. [1]
Suggested Change: Outcomes in a person with AA amyloidosis depend on the underlying disease, organ(s) affected, and correlate with the concentration of serum amyloid A protein. [2]
Rationale: The updated reference helps to provide prognosis context in a more broad sense, as the original reference was focused on GI amyloidosis. This updated reference allows for the most recent prognosis summary for amyloidosis from a reputable source. It also emphasizes how prognosis can be greatly influenced by which organ(s) is affected.
Gajsiv ( talk) 23:55, 19 November 2021 (UTC)
Suggested Change #16
Original: People with ATTR have a better prognosis and may survive for over a decade. [3]
Suggested Change: People with ATTR, mATTR and wATTR have a better prognosis when compared to people with AL and may survive for over a decade. [4] [5] Survival time is not associated with gender or age, however, some measures of reduced heart function are associated with a shorter survival time. [6]
Rationale: The current sentence is incomplete as it is missing the context of a comparison group. Simply stating that people with ATTR have a better prognosis does not provide useful information unless it is compared to a different subtype of amyloidosis. To correct this we have added more information on subtypes and a comparison group to provide the needed context.
References
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cite journal}}
: Check date values in: |date=
(
help)
"rectal salivary gland biopsy"
Looks like a missing or. S C Cheese ( talk) 15:59, 22 May 2021 (UTC)
Hello, we are a group of medical student’s from Queen’s University. We are working to improve this article over the next month and will posting our planned changes on this talk page. We look forward to working with the existing Wikipedia medical editing community to improve this article and share evidence. We welcome feedback and suggestions as we learn to edit. Thank you. MohamedGemae ( talk) 20:27, 15 November 2021 (UTC)
Suggested Change #1:
References
Suggested Change #2:
References
Suggested Change #3:
References
Suggested Change #4: proposed addition to Pathogenesis section
References
Suggested Change #5: "Diagnosis" section, "Classification" heading.
Abbr. | Amyloid type/Gene | Description | OMIM |
---|---|---|---|
Aβ2M | β2 microglobulin | Not to be confused with Aβ, β2m is a normal serum protein, part of major histocompatibility complex (MHC) Class 1 molecules. Haemodialysis-associated amyloidosis | |
Aβ | β amyloid/ APP | Found in Alzheimer disease brain lesions. | 605714 |
ATTR | transthyretin | Transthyretin is a protein that is mainly formed in the liver that transports thyroxine and retinol binding protein. A mutant form of a normal serum protein that is deposited in the genetically determined familial amyloid polyneuropathies. TTR is also deposited in the heart in wild-type transthyretin amyloidosis, also known as senile systemic amyloidosis. Also found in leptomeningeal amyloidosis. | 105210 |
APrP | prion protein | In prion diseases, misfolded prion proteins deposit in tissues and resemble amyloid proteins. Some examples are Creutzfeldt–Jakob disease (humans), BSE or "mad cow disease" (cattle), and scrapie (sheep and goats). A recently described familial prion disease presents with peripheral amyloidosis causing autonomic neuropathy and diarrhea. | 123400 |
APro | prolactin | Prolactinoma | |
ALys | LYZ | Familial visceral amyloidosis | 105200 |
ALECT2 | LECT2 | In LECT2 amyloidosis, the LECT2 protein deposits in the kidneys and various other tissues but only kidneys show signs or symptoms; these are typical those of kidney failure. | |
AL | amyloid light chain | AL amyloidosis / multiple myeloma. Contains immunoglobulin light-chains (λ,κ) derived from plasma cells. | 254500 |
AKer | keratoepithelin | Familial corneal amyloidosis | |
AIAPP | amylin | Found in the pancreas of people with type 2 diabetes. | |
AGel | GSN | Finnish type amyloidosis | 105120 |
AFib | FGA | Familial visceral amyloidosis | 105200 |
ACys | CST3 | Cerebral amyloid angiopathy, Icelandic-type | 105150 |
ACal | calcitonin | Medullary carcinoma of the thyroid | |
ABri
ADan |
ITM2B |
Cerebral amyloid angiopathy, British-type
Danish-type |
176500
117300 |
AApoA1 | APOA1 | Familial visceral amyloidosis | 105200 |
AANF | atrial natriuretic factor | Senile amyloid of atria of heart | |
AA | SAA | Serum amyloid A protein (SAA) is an acute-phase reactant that is produced in times of inflammation. | |
? | OSMR | Primary cutaneous amyloidosis | 105250 |
As of 2010, 27 human and 9 animal fibril proteins were classified, along with 8 inclusion bodies.
Fibril protein | Precursor protein | Target Organs | Systemic and/or localized | Acquired or hereditary |
---|---|---|---|---|
AL | Immunoglobulin light chain | All organs, usually except CNS | S, L | A, H |
AH | Immunoglobulin heavy chain | All organs except CNS | S, L | A |
AA | (Apo) serum amyloid A | All organs except CNS | S | A |
ATTR |
Transthyretin, wild type
|
Heart mainly in males, lung, ligaments, tenosynovium
|
S
|
A
|
Aβ2M |
β2-microglobulin, wild type
|
Musculoskeletal system
|
S
|
A
|
AApoAI | Apolipoprotein A I, variants | Heart, liver, kidney, PNS, testis, larynx (C
terminal variants), skin (C terminal variants) |
S | H |
AApoAII | Apolipoprotein A II, variants | Kidney | S | H |
AApoAIV | Apolipoprotein A IV, wild type | Kidney medulla and systemic | S | A |
AApoCII | Apolipoprotein C II, variants | Kidney | S | H |
AApoCIII | Apolipoprotein C III, variants | Kidney | S | H |
AGel | Gelsolin, variants | Kidney, PNS, cornea | S | H |
ALys | Lysozyme, variants | Kidney | S | H |
ALECT2 | Leukocyte chemotactic factor-2 | Kidney, primarily | S | A |
AFib | Fibrinogen a, variants | Kidney, primarily | S | H |
ACys | Cystatin C, variants | CNS, PNS, skin | S | H |
ABri | ABriPP, variants | CNS | S | H |
ADanb | ADanPP, variants | CNS | L | H |
Aβ | Aβ protein precursor, wild type
|
CNS | L
|
A
|
AαSyn | α-Synuclein | CNS | L | A |
ATau | Tau | CNS | L | A |
APrP | Prion protein, wild type
|
CJD, fatal insomnia
|
L
|
A
|
ACal | (Pro)calcitonin | C-cell thyroid tumours
|
L
|
A
|
AIAPP | Islet amyloid polypeptidec | Islets of Langerhans, insulinomas | L | A |
AANF | Atrial natriuretic factor | Cardiac atria | L | A |
APro | Prolactin | Pituitary prolactinomas, aging pituitary | L | A |
AIns | Insulin | Iatrogenic, local injection | L | A |
ASPCd | Lung surfactant protein | Lung | L | A |
ACor | Corneodesmosin | Cornified epithelia, hair follicles | L | A |
AMed | Lactadherin | Senile aortic, media | L | A |
AKer | Kerato-epithelin | Cornea, hereditary | L | A |
ALac | Lactoferrin | Cornea | L | A |
AOAAP | Odontogenic ameloblast-associated protein | Odontogenic tumours | L | A |
ASem1 | Semenogelin 1 | Vesicula seminalis | L | A |
AEnf | Enfurvitide | Iatrogenic | L | A |
ACatKe | Cathepsin K | Tumour associated | L | A |
AEFEMP1e | EGF-containing fibulin-like extracellular
matrix protein 1 (EFEMP1) |
Portal veins, Aging associated | L | A |
References
20ogk1 ( talk) 03:33, 18 November 2021 (UTC)
Suggested Change #6:
References
Suggested Change #7:
Diflunisal binds to misfolded mutant TTR protein to prevent its buildup, like how tafamidis works. Low-certainty evidence indicates that it reduces worsening of peripheral neuropathy and disability from disease progression.ref name=":5">Magrinelli, Francesca; Fabrizi, Gian Maria; Santoro, Lucio; Manganelli, Fiore; Zanette, Giampietro; Cavallaro, Tiziana; Tamburin, Stefano (2020-04-20). Cochrane Neuromuscular Group (ed.).
"Pharmacological treatment for familial amyloid polyneuropathy". Cochrane Database of Systematic Reviews.
doi:
10.1002/14651858.CD012395.pub2.
PMC
7170468.
PMID
32311072.{{
cite journal}}
: CS1 maint: PMC format (
link)</ref>
Inotersen blocks gene expression of both wild-type and mutant TTR, reducing amyloid precursor. Moderate-certainty evidence suggests that it reduces worsening of peripheral neuropathy. Long-term efficacy and safety of inotersen use in people with mutant TTR-related amyloidosis is still being evaluated in a phase-3 clinical trial as of 2021. Both diflunisal and inotersen may also reduce decreases in quality-of-life, though the evidence for this effect is yet unclear. [2] For people with cardiac ATTR the effect of inotersen use is inconclusive and requires further investigation. [3]
Patisiran functions similarly to inotersen. Moderate-certainty evidence suggests that patisiran reduces worsening of peripheral neuropathy and disability from disease progression. Additionally, low-certainty evidence suggests that patisiran reduces decreases in quality-of-life and slightly reduces the rate of adverse events versus placebo. There is no evidence of an effect on mortality rate. [2] A review of early data from use of patisiran in people with variant cardiac ATTR suggests that it may reduce mortality and hospitalization, however this is still being investigated and requires . [3] Jmo7865 ( talk) 18:27, 18 November 2021 (UTC)
References
:4
was invoked but never defined (see the
help page).:5
was invoked but never defined (see the
help page).Suggested Change #8: Amyloidosis Treatment section
Original: In 2018, inotersen was approved by the European Medicines Agency to treat polyneuropathy in adults with hereditary transthyretin amyloidosis [1].
Suggested Change: In 2018, inotersen was approved by the European Medicines Agency to treat polyneuropathy in adult patients with hereditary transthyretin amyloidosis. It has since been approved for use in Canada, the European Union and in the USA [2] [3].
Rationale for proposed change: The current status of geographical approval of inotersen use for amyloidosis has been expanded beyond Europe and is now approved in Canada and the U.S. Thus, the current sentence requires an updated source reflecting the most recent information available about where inotersen is approved for use. Additionally, a link to details on inotersen was added for readers interested in learning about the drug. 14sks13 ( talk) 23:14, 18 November 2021 (UTC)
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Suggested Change #9: Treatment of Secondary Amyloidosis
18lar2 ( talk) 00:03, 19 November 2021 (UTC)
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Suggested Change #10: Pathogenesis Section
It is suggested to add the following two lines to the Pathogenesis section, after the first sentence of the last paragraph: The beta-sheet form of amyloid is proteolysis-resistant, meaning it can not be degraded or broken down. [1] As a result, amyloid deposits into the body’s extracellular space. [1] RResearcher ( talk) 03:06, 19 November 2021 (UTC)
References
Suggested Change #11: Signs and Symptoms Section
Suggested change is to add these sentences to the liver subsection of Signs and Symptoms: Accumulation of amyloid proteins in the gastrointestinal system may be caused by a wide range of amyloid disorders and have different presentations depending on the degree of organ involvement. [1] Potential symptoms include weight loss, diarrhea, abdominal pain, heartburn (gastrointestinal reflux), and GI bleeding. Amyloidosis may also affect accessory digestive organs including the liver, and may present with jaundice, fatty stool, anorexia, fluid buildup in the abdomen, and spleen enlargement. [2] Helenlin315 ( talk) 04:10, 19 November 2021 (UTC)
Suggested Change #12:
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Suggested change #13 : Signs & Symptoms - Brain
Rationale for proposed change: The suggested additions will provide a more comprehensive understanding of the signs and symptoms of amyloidosis in the nervous system, specifically emphasizing the widespread, systemic impacts of amyloidosis neuropathy. The current “Brain” section does not do well in expanding upon the potential signs of symptoms of brain amyloidosis or acknowledge the peripheral impacts of neuropathy.
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(see the
help page). This can lead to high levels of protein in the urine (proteinuria) and nephrotic syndrome.[2] Several types of amyloidosis, including the AL and AA types, are associated with nephrotic syndrome. 20% and 40-60% of people with AL and AA respectively progress to dialysis.
[1][1] Lewis J.B., & Neilson E.G. (2018). Glomerular diseases. Jameson J, & Fauci A.S., & Kasper D.L., & Hauser S.L., & Longo D.L., & Loscalzo J(Eds.), Harrison's Principles of Internal Medicine, 20e. McGraw Hill. https://accessmedicine-mhmedical-com.proxy.queensu.ca/content.aspx?bookid=2129§ionid=192281295 [2] U.S. Department of Health and Human Services. (n.d.). Amyloidosis & Kidney Disease. National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved November 19, 2021, from https://www.niddk.nih.gov/health-information/kidney-disease/amyloidosis. Ameliaboughn ( talk) 22:19, 19 November 2021 (UTC)
References
Suggested Change #15
Original: Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein. [1]
Suggested Change: Outcomes in a person with AA amyloidosis depend on the underlying disease, organ(s) affected, and correlate with the concentration of serum amyloid A protein. [2]
Rationale: The updated reference helps to provide prognosis context in a more broad sense, as the original reference was focused on GI amyloidosis. This updated reference allows for the most recent prognosis summary for amyloidosis from a reputable source. It also emphasizes how prognosis can be greatly influenced by which organ(s) is affected.
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Gajsiv ( talk) 00:03, 20 November 2021 (UTC)
Suggested Change #16
Original: People with ATTR have a better prognosis and may survive for over a decade. [1]
Suggested Change: People with ATTR, mATTR and wATTR have a better prognosis when compared to people with AL and may survive for over a decade. [2] [3] Survival time is not associated with gender or age, however, some measures of reduced heart function are associated with a shorter survival time. [4]
Rationale: The current sentence is incomplete as it is missing the context of a comparison group. Simply stating that people with ATTR have a better prognosis does not provide useful information unless it is compared to a different subtype of amyloidosis. To correct this we have added more information on subtypes and a comparison group to provide the needed context. Gpauliqmed ( talk) 00:19, 20 November 2021 (UTC)
References
Hello,
I am curious why, in the table of amyloidosis classifications, the central nervous system (CNS) is linked at every mention? This is surely superfluous, as other organs or their systems in the table are not linked.
Can this be removed? A surfeit of links can be distracting while trying to read. Zyploc ( talk) 19:50, 24 October 2023 (UTC)
Amyloidosis is listed on the intracerebral hemorrhage page as a big risk factor for that condition, yet the amyloidosis page makes no mention of this. There is a "Organ-limited amyloidosis" subsection of the "Amyloidosis" infobox at the bottom of the page, but I wonder if there is somewhere within the main article to note the risk factor connection to intracerebral hemorrhage?
I propose to add a "Brain" section under the "Signs and symptoms" section of the amyloidosis page that could indicate the brain hemorrhage connection as well as noting cerebral amyloid angiopathy (CAA) which appears in the brain subsection of the amyloidosis infobox. The following statement appears on the CAA page: "The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis." That disclaimer, I believe, also applies to the other conditions noted in the infobox: Alzheimer's disease and Familial amyloid neuropathy. SteveChervitzTrutane ( talk) 09:08, 7 May 2024 (UTC)
The purpura image on the landing page is not indicative of the presenting symptom disease state for 99.99% of amyloidosis victims. There is a constellation of symptoms which include bruising. The extreme nature of this image diminishes the plethora of other critically important early symptoms such as carpal tunnel. I believe the landing page imagery should be changed to an updated slide of early warning symptoms which may include purpura. Seattle Amyloidosis Group ( talk) 17:12, 13 May 2024 (UTC)
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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.
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. 71.93.201.164 ( talk) 16:40, 1 February 2014 (UTC)Carolyn Smith
"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."
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)
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)
Is it fatal? what percentage of people die from it. Robert Jordan is one of my favorite authors, so I am really quite concerned.
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)
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)
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)
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)
Hi, Is Amyloidosis a prion disease? Could it be diet-related? Thanks, Bennie —Preceding unsigned comment added by 66.57.189.224 ( talk) 18:18, 17 May 2008 (UTC)
Who is John Smith? 128.208.1.225 ( talk) —Preceding comment was added at 21:33, 11 July 2008 (UTC)
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.
http://sites.google.com/site/curedofamy/ —Preceding unsigned comment added by Jrhelwig ( talk • contribs) 23:44, 22 November 2008 (UTC)
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)
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)
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:
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)
"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."
http://www.amyloidosis.org/whatisit.asp
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)
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)
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)
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
B) Subsection classification:
C) other
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.
5.80.198.100 ( 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)
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)
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)
Given that this ( amyloid purpura) is very far from common (15% according to the ref on that WL) it's perhaps not appropriate to have this image so prominent. Perhaps it should be under signs and symptoms? Thoughts? - Snori ( talk) 03:19, 15 April 2019 (UTC)
Hello, we are a group of medical students from Queen’s University. We are working to improve this article over the next month and will posting our planned changes on this talk page. We look forward to working with the existing Wikipedia medical editing community to improve this article and share evidence. We welcome feedback and suggestions as we learn to edit. Thank you. Jan2020-med2024 ( talk) 20:17, 23 November 2020 (UTC)
Croissanttabletennis ( talk) 17:24, 4 December 2020 (UTC)
Thank you for the feedback! Croissanttabletennis ( talk) 17:39, 4 December 2020 (UTC)
References
Targeted sentence: “In ATTR, liver transplant is a curative therapy because mutated transthyretin which forms amyloids is produced in the liver.[7] ”
Proposed Changed: Management of ATTR amyloidosis will depend on its classification as wild type or variant. [1] Both may be treated with tafamidis, a low toxicity oral agent that prevents destabilization of correctly folded protein. [1] Studies showed tafamidis reduced mortality and hospitalization due to heart failure. [1] Previously, for variant ATTR amyloidosis, liver transplant was the only effective treatment. [1] However, newer therapies including diflunisal, an anti-inflammatory drug, and inotersen and patisiran, drugs which prevent misfolded protein formation, have shown early promises in slowing disease progression. [1] The latter two drugs have shown their benefit in neurological impairment scores and quality of life measures. [1] However, their role in cardiac ATTR amyloidosis is still being investigated. [1]
Rationale for proposed change: This sentence was outdated: The supporting reference is from 1997 and management has evolved since then. Newer agents have emerged that have demonstrated effects on slowing disease progression.
Area of controversy: There is some ambiguity on this topic as some of the information regarding management with medication is still being uncovered. When proposing changes, I tried to make it clear that these are early promises.
This sentence is incomplete: The sentence does not differentiate between wild type and variant type ATTR amyloidosis which have some differences in management. Also, it did not specifically describe the benefits of treatment including the mortality and quality of life. KarnPuri22 ( talk) 18:39, 4 December 2020 (UTC)
References
I propose the following addition to the Amyloidosis#pathology section: Proposed addition: The vast majority of proteins that have been found to form amyloid deposits are secreted proteins, so the misfolding and formation of the amyloid occurs outside cells, in the extracellular space. [1] There is currently no evidence of any structural or functional similarities between the different types of proteins vulnerable to misfold into amyloid. [1] Thirty-seven proteins have been identified as being vulnerable to amyloid formation, and only four are cytosolic. [1] One third of amyloid disease is hereditary, in which case there is normally an early age of onset. [1] Half of amyloid-related diseases are sporadic and have a late age of onset – in these cases, the protein aggregation is due to a progressive loss of the body’s ability to regulate protein formation, with aging. A small number of amyloid disorders occur as a result of medical treatment. [1]
Rationale for proposed change: I propose adding the above text to give readers more context about the origin of amyloidosis in terms of risk factors – I think it could be helpful to someone who’s just been diagnosed with amyloidosis to know that there is often little rhyme or reason to who gets the disease, in case they’re having feelings of guilt or fears around risk factors they could have been exposed to. Also, I talked a little bit about where things happen spatially, which I hope could be helpful for people trying to visualize these processes, as histological processes are often hard to picture or conceptualize.
Thank you! I appreciate your time and look forward to your feedback. REIJONES ( talk) 18:52, 4 December 2020 (UTC)
References
Original text: “Tissue can come from any involved organ, but in systemic disease the first-line site of the biopsy is subcutaneous abdominal fat, known as a "fat pad biopsy", due to its ease of acquisition versus biopsy of the rectum, salivary gland or internal organs. An abdominal fat biopsy is not completely sensitive, and sometimes, biopsy of an involved organ (such as the kidney) is required to achieve a diagnosis. For example, in AL amyloidosis only 85% of people will have a positive fatpad biopsy using Congo red stain. By comparison, rectal biopsy has sensitivity of 74–94%.”
Proposed change to text: A sample of tissue can be biopsied or obtained directly from the affected internal organ, but the first-line site of biopsy is subcutaneous abdominal fat, known as a “fat pad biopsy”, due to its ease of acquisition. An abdominal fat biopsy is not completely sensitive and may result in false negatives, which means a negative result does not exclude amyloidosis diagnosis. [1] [2] However, direct biopsy of the affected organ may still be unnecessary as other less invasive methods of biopsy can also be used, including rectal salivary gland biopsy, lip, or bone marrow biopsy which can achieve a diagnosis in up to 85% of people. [1]
Rationale for proposed change:
The article previously did not explain what was meant by “involved” organ, and lists the “rectum, salivary gland, or internal organs” as examples. I wanted to be more clear and specify that there is a difference between sampling the internal organ and sampling other tissue. I also provided an explanation for what it means when a test is not “completely sensitive” by explaining that false negatives may occur, which means that a diagnosis cannot be excluded yet. The article then states that the biopsy of the “involved” organ is required to achieve diagnosis, but then proceeds to give “rectal biopsy” as an example, yet the rectum is not related to the usual “involved” internal organs (i.e. rectal biopsy is not biopsy of the “involved organ”; it is another alternative to direct organ biopsy). I wanted to make it clear that direct organ biopsy (e.g. if you suspect the kidney has amyloid tissue, then you would sample the kidney) is often unnecessary as many less invasive diagnostic techniques exist. I also wanted to update the provided statistic using a more recent source. -- Jwoodly ( talk) 19:21, 4 December 2020 (UTC)
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Jan2020-med2024 ( talk) 19:42, 4 December 2020 (UTC)
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Original: “The three most common forms of amyloidosis are AL, AA, and ATTR amyloidoses. The median age at diagnosis is 64.[8]
In the western hemisphere, AL is the most prevalent, comprising 90% of cases.[14] In the United States it is estimated that there are 1,275 to 3,200 new cases of AL amyloidoses a year."
Changes:
Amyloidosis has a combined estimated prevalence of 30 per 100,000 persons with the three most common forms being AL, ATTR, and AA. The median age at diagnosis is 64.
[1]
[2]
AL has the highest incidence at approximately 12 cases per million persons per year and an estimated prevalence of 30,000 to 45,000 cases in the US and European Union. [2]
Rationale for proposed change: I changed the first sentence to include the combined prevalence of all types of amyloidosis. This is a good statistic to provide as it gives the reader an idea of how rare amyloidosis is. Also, I rearranged the order of the last two types of amyloidosis and placed ATTR before AA. This is important because it organizes the types of amyloidosis from most to least common and reflects the current understanding that AA has become rarer than the first two types due to advancements in treating chronic infectious diseases. The information for both changes come from two review articles published within the past 3 years from JAMA and Current Medical Research and Opinion, two highly reputable journals.
Next, I changed the two sentences about AL amyloidosis. The first sentence’s statistic regarding “90% of cases” was unfounded in the cited source. Furthermore, they provided an outdated statistic/source from 1997 for the incidence in the second sentence. I replaced these two sentences with a sentence that provided the prevalence and incidence from reputable sources updated within the past 3 years. The information for this sentence change comes from JAMA and Current Medical Research and Opinion. Jlowe24 ( talk) 22:35, 4 December 2020 (UTC)
References
Suggested Change #15
Original: Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein. [1]
Suggested Change: Outcomes in a person with AA amyloidosis depend on the underlying disease, organ(s) affected, and correlate with the concentration of serum amyloid A protein. [2]
Rationale: The updated reference helps to provide prognosis context in a more broad sense, as the original reference was focused on GI amyloidosis. This updated reference allows for the most recent prognosis summary for amyloidosis from a reputable source. It also emphasizes how prognosis can be greatly influenced by which organ(s) is affected.
Gajsiv ( talk) 23:55, 19 November 2021 (UTC)
Suggested Change #16
Original: People with ATTR have a better prognosis and may survive for over a decade. [3]
Suggested Change: People with ATTR, mATTR and wATTR have a better prognosis when compared to people with AL and may survive for over a decade. [4] [5] Survival time is not associated with gender or age, however, some measures of reduced heart function are associated with a shorter survival time. [6]
Rationale: The current sentence is incomplete as it is missing the context of a comparison group. Simply stating that people with ATTR have a better prognosis does not provide useful information unless it is compared to a different subtype of amyloidosis. To correct this we have added more information on subtypes and a comparison group to provide the needed context.
References
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"rectal salivary gland biopsy"
Looks like a missing or. S C Cheese ( talk) 15:59, 22 May 2021 (UTC)
Hello, we are a group of medical student’s from Queen’s University. We are working to improve this article over the next month and will posting our planned changes on this talk page. We look forward to working with the existing Wikipedia medical editing community to improve this article and share evidence. We welcome feedback and suggestions as we learn to edit. Thank you. MohamedGemae ( talk) 20:27, 15 November 2021 (UTC)
Suggested Change #1:
References
Suggested Change #2:
References
Suggested Change #3:
References
Suggested Change #4: proposed addition to Pathogenesis section
References
Suggested Change #5: "Diagnosis" section, "Classification" heading.
Abbr. | Amyloid type/Gene | Description | OMIM |
---|---|---|---|
Aβ2M | β2 microglobulin | Not to be confused with Aβ, β2m is a normal serum protein, part of major histocompatibility complex (MHC) Class 1 molecules. Haemodialysis-associated amyloidosis | |
Aβ | β amyloid/ APP | Found in Alzheimer disease brain lesions. | 605714 |
ATTR | transthyretin | Transthyretin is a protein that is mainly formed in the liver that transports thyroxine and retinol binding protein. A mutant form of a normal serum protein that is deposited in the genetically determined familial amyloid polyneuropathies. TTR is also deposited in the heart in wild-type transthyretin amyloidosis, also known as senile systemic amyloidosis. Also found in leptomeningeal amyloidosis. | 105210 |
APrP | prion protein | In prion diseases, misfolded prion proteins deposit in tissues and resemble amyloid proteins. Some examples are Creutzfeldt–Jakob disease (humans), BSE or "mad cow disease" (cattle), and scrapie (sheep and goats). A recently described familial prion disease presents with peripheral amyloidosis causing autonomic neuropathy and diarrhea. | 123400 |
APro | prolactin | Prolactinoma | |
ALys | LYZ | Familial visceral amyloidosis | 105200 |
ALECT2 | LECT2 | In LECT2 amyloidosis, the LECT2 protein deposits in the kidneys and various other tissues but only kidneys show signs or symptoms; these are typical those of kidney failure. | |
AL | amyloid light chain | AL amyloidosis / multiple myeloma. Contains immunoglobulin light-chains (λ,κ) derived from plasma cells. | 254500 |
AKer | keratoepithelin | Familial corneal amyloidosis | |
AIAPP | amylin | Found in the pancreas of people with type 2 diabetes. | |
AGel | GSN | Finnish type amyloidosis | 105120 |
AFib | FGA | Familial visceral amyloidosis | 105200 |
ACys | CST3 | Cerebral amyloid angiopathy, Icelandic-type | 105150 |
ACal | calcitonin | Medullary carcinoma of the thyroid | |
ABri
ADan |
ITM2B |
Cerebral amyloid angiopathy, British-type
Danish-type |
176500
117300 |
AApoA1 | APOA1 | Familial visceral amyloidosis | 105200 |
AANF | atrial natriuretic factor | Senile amyloid of atria of heart | |
AA | SAA | Serum amyloid A protein (SAA) is an acute-phase reactant that is produced in times of inflammation. | |
? | OSMR | Primary cutaneous amyloidosis | 105250 |
As of 2010, 27 human and 9 animal fibril proteins were classified, along with 8 inclusion bodies.
Fibril protein | Precursor protein | Target Organs | Systemic and/or localized | Acquired or hereditary |
---|---|---|---|---|
AL | Immunoglobulin light chain | All organs, usually except CNS | S, L | A, H |
AH | Immunoglobulin heavy chain | All organs except CNS | S, L | A |
AA | (Apo) serum amyloid A | All organs except CNS | S | A |
ATTR |
Transthyretin, wild type
|
Heart mainly in males, lung, ligaments, tenosynovium
|
S
|
A
|
Aβ2M |
β2-microglobulin, wild type
|
Musculoskeletal system
|
S
|
A
|
AApoAI | Apolipoprotein A I, variants | Heart, liver, kidney, PNS, testis, larynx (C
terminal variants), skin (C terminal variants) |
S | H |
AApoAII | Apolipoprotein A II, variants | Kidney | S | H |
AApoAIV | Apolipoprotein A IV, wild type | Kidney medulla and systemic | S | A |
AApoCII | Apolipoprotein C II, variants | Kidney | S | H |
AApoCIII | Apolipoprotein C III, variants | Kidney | S | H |
AGel | Gelsolin, variants | Kidney, PNS, cornea | S | H |
ALys | Lysozyme, variants | Kidney | S | H |
ALECT2 | Leukocyte chemotactic factor-2 | Kidney, primarily | S | A |
AFib | Fibrinogen a, variants | Kidney, primarily | S | H |
ACys | Cystatin C, variants | CNS, PNS, skin | S | H |
ABri | ABriPP, variants | CNS | S | H |
ADanb | ADanPP, variants | CNS | L | H |
Aβ | Aβ protein precursor, wild type
|
CNS | L
|
A
|
AαSyn | α-Synuclein | CNS | L | A |
ATau | Tau | CNS | L | A |
APrP | Prion protein, wild type
|
CJD, fatal insomnia
|
L
|
A
|
ACal | (Pro)calcitonin | C-cell thyroid tumours
|
L
|
A
|
AIAPP | Islet amyloid polypeptidec | Islets of Langerhans, insulinomas | L | A |
AANF | Atrial natriuretic factor | Cardiac atria | L | A |
APro | Prolactin | Pituitary prolactinomas, aging pituitary | L | A |
AIns | Insulin | Iatrogenic, local injection | L | A |
ASPCd | Lung surfactant protein | Lung | L | A |
ACor | Corneodesmosin | Cornified epithelia, hair follicles | L | A |
AMed | Lactadherin | Senile aortic, media | L | A |
AKer | Kerato-epithelin | Cornea, hereditary | L | A |
ALac | Lactoferrin | Cornea | L | A |
AOAAP | Odontogenic ameloblast-associated protein | Odontogenic tumours | L | A |
ASem1 | Semenogelin 1 | Vesicula seminalis | L | A |
AEnf | Enfurvitide | Iatrogenic | L | A |
ACatKe | Cathepsin K | Tumour associated | L | A |
AEFEMP1e | EGF-containing fibulin-like extracellular
matrix protein 1 (EFEMP1) |
Portal veins, Aging associated | L | A |
References
20ogk1 ( talk) 03:33, 18 November 2021 (UTC)
Suggested Change #6:
References
Suggested Change #7:
Diflunisal binds to misfolded mutant TTR protein to prevent its buildup, like how tafamidis works. Low-certainty evidence indicates that it reduces worsening of peripheral neuropathy and disability from disease progression.ref name=":5">Magrinelli, Francesca; Fabrizi, Gian Maria; Santoro, Lucio; Manganelli, Fiore; Zanette, Giampietro; Cavallaro, Tiziana; Tamburin, Stefano (2020-04-20). Cochrane Neuromuscular Group (ed.).
"Pharmacological treatment for familial amyloid polyneuropathy". Cochrane Database of Systematic Reviews.
doi:
10.1002/14651858.CD012395.pub2.
PMC
7170468.
PMID
32311072.{{
cite journal}}
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Inotersen blocks gene expression of both wild-type and mutant TTR, reducing amyloid precursor. Moderate-certainty evidence suggests that it reduces worsening of peripheral neuropathy. Long-term efficacy and safety of inotersen use in people with mutant TTR-related amyloidosis is still being evaluated in a phase-3 clinical trial as of 2021. Both diflunisal and inotersen may also reduce decreases in quality-of-life, though the evidence for this effect is yet unclear. [2] For people with cardiac ATTR the effect of inotersen use is inconclusive and requires further investigation. [3]
Patisiran functions similarly to inotersen. Moderate-certainty evidence suggests that patisiran reduces worsening of peripheral neuropathy and disability from disease progression. Additionally, low-certainty evidence suggests that patisiran reduces decreases in quality-of-life and slightly reduces the rate of adverse events versus placebo. There is no evidence of an effect on mortality rate. [2] A review of early data from use of patisiran in people with variant cardiac ATTR suggests that it may reduce mortality and hospitalization, however this is still being investigated and requires . [3] Jmo7865 ( talk) 18:27, 18 November 2021 (UTC)
References
:4
was invoked but never defined (see the
help page).:5
was invoked but never defined (see the
help page).Suggested Change #8: Amyloidosis Treatment section
Original: In 2018, inotersen was approved by the European Medicines Agency to treat polyneuropathy in adults with hereditary transthyretin amyloidosis [1].
Suggested Change: In 2018, inotersen was approved by the European Medicines Agency to treat polyneuropathy in adult patients with hereditary transthyretin amyloidosis. It has since been approved for use in Canada, the European Union and in the USA [2] [3].
Rationale for proposed change: The current status of geographical approval of inotersen use for amyloidosis has been expanded beyond Europe and is now approved in Canada and the U.S. Thus, the current sentence requires an updated source reflecting the most recent information available about where inotersen is approved for use. Additionally, a link to details on inotersen was added for readers interested in learning about the drug. 14sks13 ( talk) 23:14, 18 November 2021 (UTC)
References
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Suggested Change #9: Treatment of Secondary Amyloidosis
18lar2 ( talk) 00:03, 19 November 2021 (UTC)
References
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help page).:8
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help page).{{
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Suggested Change #10: Pathogenesis Section
It is suggested to add the following two lines to the Pathogenesis section, after the first sentence of the last paragraph: The beta-sheet form of amyloid is proteolysis-resistant, meaning it can not be degraded or broken down. [1] As a result, amyloid deposits into the body’s extracellular space. [1] RResearcher ( talk) 03:06, 19 November 2021 (UTC)
References
Suggested Change #11: Signs and Symptoms Section
Suggested change is to add these sentences to the liver subsection of Signs and Symptoms: Accumulation of amyloid proteins in the gastrointestinal system may be caused by a wide range of amyloid disorders and have different presentations depending on the degree of organ involvement. [1] Potential symptoms include weight loss, diarrhea, abdominal pain, heartburn (gastrointestinal reflux), and GI bleeding. Amyloidosis may also affect accessory digestive organs including the liver, and may present with jaundice, fatty stool, anorexia, fluid buildup in the abdomen, and spleen enlargement. [2] Helenlin315 ( talk) 04:10, 19 November 2021 (UTC)
Suggested Change #12:
References
Suggested change #13 : Signs & Symptoms - Brain
Rationale for proposed change: The suggested additions will provide a more comprehensive understanding of the signs and symptoms of amyloidosis in the nervous system, specifically emphasizing the widespread, systemic impacts of amyloidosis neuropathy. The current “Brain” section does not do well in expanding upon the potential signs of symptoms of brain amyloidosis or acknowledge the peripheral impacts of neuropathy.
References
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(see the
help page). This can lead to high levels of protein in the urine (proteinuria) and nephrotic syndrome.[2] Several types of amyloidosis, including the AL and AA types, are associated with nephrotic syndrome. 20% and 40-60% of people with AL and AA respectively progress to dialysis.
[1][1] Lewis J.B., & Neilson E.G. (2018). Glomerular diseases. Jameson J, & Fauci A.S., & Kasper D.L., & Hauser S.L., & Longo D.L., & Loscalzo J(Eds.), Harrison's Principles of Internal Medicine, 20e. McGraw Hill. https://accessmedicine-mhmedical-com.proxy.queensu.ca/content.aspx?bookid=2129§ionid=192281295 [2] U.S. Department of Health and Human Services. (n.d.). Amyloidosis & Kidney Disease. National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved November 19, 2021, from https://www.niddk.nih.gov/health-information/kidney-disease/amyloidosis. Ameliaboughn ( talk) 22:19, 19 November 2021 (UTC)
References
Suggested Change #15
Original: Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein. [1]
Suggested Change: Outcomes in a person with AA amyloidosis depend on the underlying disease, organ(s) affected, and correlate with the concentration of serum amyloid A protein. [2]
Rationale: The updated reference helps to provide prognosis context in a more broad sense, as the original reference was focused on GI amyloidosis. This updated reference allows for the most recent prognosis summary for amyloidosis from a reputable source. It also emphasizes how prognosis can be greatly influenced by which organ(s) is affected.
References
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Gajsiv ( talk) 00:03, 20 November 2021 (UTC)
Suggested Change #16
Original: People with ATTR have a better prognosis and may survive for over a decade. [1]
Suggested Change: People with ATTR, mATTR and wATTR have a better prognosis when compared to people with AL and may survive for over a decade. [2] [3] Survival time is not associated with gender or age, however, some measures of reduced heart function are associated with a shorter survival time. [4]
Rationale: The current sentence is incomplete as it is missing the context of a comparison group. Simply stating that people with ATTR have a better prognosis does not provide useful information unless it is compared to a different subtype of amyloidosis. To correct this we have added more information on subtypes and a comparison group to provide the needed context. Gpauliqmed ( talk) 00:19, 20 November 2021 (UTC)
References
Hello,
I am curious why, in the table of amyloidosis classifications, the central nervous system (CNS) is linked at every mention? This is surely superfluous, as other organs or their systems in the table are not linked.
Can this be removed? A surfeit of links can be distracting while trying to read. Zyploc ( talk) 19:50, 24 October 2023 (UTC)
Amyloidosis is listed on the intracerebral hemorrhage page as a big risk factor for that condition, yet the amyloidosis page makes no mention of this. There is a "Organ-limited amyloidosis" subsection of the "Amyloidosis" infobox at the bottom of the page, but I wonder if there is somewhere within the main article to note the risk factor connection to intracerebral hemorrhage?
I propose to add a "Brain" section under the "Signs and symptoms" section of the amyloidosis page that could indicate the brain hemorrhage connection as well as noting cerebral amyloid angiopathy (CAA) which appears in the brain subsection of the amyloidosis infobox. The following statement appears on the CAA page: "The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis." That disclaimer, I believe, also applies to the other conditions noted in the infobox: Alzheimer's disease and Familial amyloid neuropathy. SteveChervitzTrutane ( talk) 09:08, 7 May 2024 (UTC)
The purpura image on the landing page is not indicative of the presenting symptom disease state for 99.99% of amyloidosis victims. There is a constellation of symptoms which include bruising. The extreme nature of this image diminishes the plethora of other critically important early symptoms such as carpal tunnel. I believe the landing page imagery should be changed to an updated slide of early warning symptoms which may include purpura. Seattle Amyloidosis Group ( talk) 17:12, 13 May 2024 (UTC)