User:JenOttawa/Notes/re-word

Queen's University Student Editing Initiative 2021

Hello, we are a group of medical student’s from 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:

• Chemotherapy and steroids, with melphalan plus dexamethasone, is mainstay treatment in AL people not eligible for transplant.[19]
• Suggested change: Chemotherapy treatment including cyclophosphamide-bortezomib-dexamethasone is currently the mainstay treatment for people with AL Amyloidosis not eligible for transplant MohamedGemae (talk) 20:27, 15 November 2021 (UTC)
• Feedback: This edit looks great. When you make your edit be sure to add the citation immediately after the punctuation like this.JenOttawa (talk) 13:12, 19 November 2021 (UTC)

Suggested Change #2:

• Original: There are about 30 different types of amyloidosis, each due to a specific protein misfolding.[5] Some are genetic while others are acquired.[3] They are grouped into localized forms, and systemic ones.[2]
• Suggested Change: To date, there are about 36 different types of amyloidosis, each due to a specific protein misfolding. Within these 36 proteins, 19 are grouped into localized forms, 14 are grouped as systemic forms, and 3 proteins can identify as either.^[2] These proteins can become irregular due to genetic effects, as well as through acquired environmental factors.^[2] MattKuchtaruk (talk) 23:01, 15 November 2021 (UTC)
• Feedback: This suggestion looks good. I would remove the use of "To date". People can read the citation to see the time frame but do not know when you added this information. "There are about 36 different types of amyloidosis, each due to a specific protein misfolding." is sufficient.JenOttawa (talk) 13:12, 19 November 2021 (UTC)

Suggested Change #3:

• Original: Diagnosis is confirmed by tissue biopsy.
• Suggested Change: Amyloidosis is typically diagnosed through tissue biopsy, with the exception of cardiac transthyretin amyloidosis, which can be diagnosed using scintigraphic imaging if stringent criteria are met.
• Rationale: The current version of the Wikipedia article suggests that tissue biopsy is required to confirm the diagnosis of all amyloidosis subtypes. The proposed change will include the noninvasive diagnosis of cardiac transthyretin amyloidosis using scintigraphic imaging, an exception that is an important consideration for patients and healthcare providers.KShearer17 (talk) 22:02, 17 November 2021 (UTC)
• Feedback: This edit looks excellent and great to correct this error of omission in the article. When you are making the actual edit, please include the citation after the punctuation like this: "Amyloidosis is typically diagnosed through tissue biopsy,".JenOttawa (talk) 13:12, 19 November 2021 (UTC)

Suggested Change #4: proposed addition to Pathogenesis section

• Proposed addition: For example, in ATTR amyloidosis the fibrils originate from TTR. In AL amyloidosis, the misfolded protein originates from an immunoglobulin heavy or light chain fragment that can aggregate in any organ except the central nervous system.
• Rationale: The pathogenesis section does not currently refer to the most common types of amyloidosis or which systems are most commonly affected. With the additional lines, the two most common types are introduced, giving a general description of affected systems. Tiffany.dickinson (talk) 00:18, 18 November 2021 (UTC)
• Feedback: I am assuming AL and ATTR are defined earlier in the article? When you are making the actual edit, please include the citation after the punctuation like this: and in ATTR amyloidosis, the heart is most commonly involved.JenOttawa (talk) 13:29, 19 November 2021 (UTC

Suggested Change #5: "Diagnosis" section, "Classification" heading.

• Original:

The names of amyloids usually start with the letter "A". Here is a brief description of the more common types of amyloid:^{[medical citation needed]}

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.

• Suggested change:

All amyloid fibril proteins start with the letter "A" followed by the protein suffix (and any applicable specification). See below for a list of amyloid fibril proteins which have been found in humans:

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 Transthyretin, variants	Heart mainly in males, lung, ligaments, tenosynovium PNS, ANS, heart, eye, leptomeninges	S S	A H
Aβ2M	β2-microglobulin, wild type β2-microglobulin, variants	Musculoskeletal system ANS	S S	A H
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 Aβ protein precursor, variant	CNS CNS	L L	A H
AαSyn	α-Synuclein	CNS	L	A
ATau	Tau	CNS	L	A
APrP	Prion protein, wild type Prion protein variants Prion protein variant	CJD, fatal insomnia CJD, GSS syndrome, fatal insomnia PNS	L L S	A H H
ACal	(Pro)calcitonin	C-cell thyroid tumours Kidney	L S	A 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

20ogk1 (talk) 03:33, 18 November 2021 (UTC)

Feedback: Looks great! Please reach out it you need help editing the table in the article. Great improvement suggestion!JenOttawa (talk) 13:29, 19 November 2021 (UTC)

Suggested Change #6:

Original: Senile amyloidosis resulting from deposition of normal transthyretin, mainly in the heart, is found in 10–36% of people over 80.[8]

Suggested Change: Wild-type transthyretin (ATTR) amyloidosis is being increasingly identified in the elderly, and is found in a quarter of elderly at postmortem. ATTR is found in 13-19% of people experiencing heart failure with preserved ejection fraction, making it a very common form of systemic amyloidosis.

Rationale: The previous information on ATTR is from 2008, thus the statistics needed to reflect current findings (proposed information is from 2021). In this article ATTR amyloidosis is referred to many times, but Senile amyloidosis is not. ATTR is often referred to as Senile amyloidosis, but it can be misleading for the reader, thus I updated this section to use the terminology (ATTR) that is referenced throughout the wikipedia article. 13mjs21 (talk) 13:45, 18 November 2021 (UTC)

Feedback:This looks like a good edit. Can you shorten your sentence a little? For example, it may not be necessary to write "is being increasingly identified in the elderly," if you are then adding that it is found in 1/4 of elderly people at postmortem. Either way is fine though if you feel that it is important to include. Very minor edit: Please do not leave a space between your punctuation (in this case the period) and the citation. "Your citation should look like this: making it a very common form of systemic amyloidosis."JenOttawa (talk) 13:29, 19 November 2021 (UTC)

Suggested Change #7: Original: 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.[29] The latter two drugs have shown their benefit in neurological impairment scores and quality of life measures.[29] However, their role in cardiac ATTR amyloidosis is still being investigated.[29]

Suggested Change: New drug therapies include diflunisal, inotersen, and patisiran.

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.

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. For people with cardiac ATTR the effect of inotersen use is inconclusive and requires further investigation.

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. 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 .Jmo7865 (talk) 18:27, 18 November 2021 (UTC)

Feedback: This looks like a good edit. Be sure that you add the citations properly in the actual article. I addd them for you. Did the last sentence get cut off? I just noticed it ends with "and requires...". I like how you used the secondary sources to add background information and also evidence supporting efficacy. JenOttawa (talk) 13:29, 19 November 2021 (UTC)

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 .

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 .

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)

Feedback: This looks good. I like the use of Wikilinks for inotersen. Very minor edit: Please do not leave a space between your punctuation (in this case the period) and the citation. Your citation should look like this: Canada, the European Union and in the USA. For some reason, the citation tool did not auto-generate all the information into the citation template when you pasted the website. I have added it in. Please use this version of your references: JenOttawa (talk) 13:29, 19 November 2021 (UTC)

Suggested Change #9: Treatment of Secondary Amyloidosis

Original: Eprodisate theoretically slowed renal impairment by inhibiting polymerization of amyloid fibrils, however after a negative phase three trial, it seems unlikely to be effective .

Suggested Change: In people who have inflammation caused by AA amyloidosis, tumour necrosis factor (TNF)-alpha inhibitors such as infliximab and etanercept are used for an average duration of 20 months. If TNF-alpha inhibitors are not effective, Interleukin-1 inhibitors (e.g. anakinra, canakinumab, rilonacept) and interleukin-6 inhibitors (e.g. tocilizumab) may be considered.

Reason for change: Original source was a randomized control trial, new source is a clinical guideline with more recent recommendations from experts in the field. 18lar2 (talk) 00:03, 19 November 2021 (UTC)

Feedback: Great edit to replace a non Wikipedia:Identifying reliable sources (medicine) source with a stronger secondary source. I realize the editing talk pages is a little different as they do not have the visual editor option. I re-added your citation using the proper formatting. The only other (very) minor edit was to move the location of the citation to be immediately after the punctuation. JenOttawa (talk) 13:29, 19 November 2021 (UTC)

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. As a result, amyloid deposits into the body’s extracellular space. RResearcher (talk) 03:06, 19 November 2021 (UTC)

Feedback: This looks great. For some reason your second reference is not coming up. @RResearcher:Do you want to re-use your first reference or are you using two? I can help adjust if you are re-using it. JenOttawa (talk) 13:29, 19 November 2021 (UTC)

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. 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. Helenlin315 (talk) 04:10, 19 November 2021 (UTC)

Feedback: Your edit looks great. If all this info came from the same source it would be best to re-use the source after each sentence. This is how Wikipedia is a little different compared to academia. I added a citation needed tag as an example. You can click "cite" then rather than adding a new citation, look for the "re-use" tab. It is also more difficult to be editing on talk pages as they do not have the 'visual' editor tool. If you want to practice re-adding your citation in your sandbox that is fine! JenOttawa (talk) 13:29, 19 November 2021 (UTC)

References