"I began relentlessly researching the “what the hell went wrong?
"It appears the “what the hell went wrong” question was largely ignored, unrecognized, and minimized in the medical community and buried by manufacturers of synthetic medical mesh whom I feel definitely patted themselves on the back, for their part in improving quality of life for people having issues with prolapses, hernias and incontinence.
"Research revealed a lack of long term studies regarding the safety and reliability of medical mesh implants, the lack of follow up with patients receiving the aforementioned mesh products, lack of understanding by the medical community that they had regarding the rates of failure, the cause of failure, and the consequences of prolonged and chronic exposure.
"I wish to challenge all my readers to question the use of synthetic medical mesh and ask for accountability from those who profited from the sale of these products at the expense of a significant number of patients living in the aftermath of synthetic medical mesh degradation and implant failure. With knowledge and truth we can join together to advocate for safety before profit. I hope to empower people to demand honest answers and demand change."
by Nonie Wideman, April 2013
When researching mesh complications, if one were to listen to the most knowledgeable experienced people on the subject, one would not be listening to doctors or mesh manufacturers. To know exactly what is going on it would seem prudent to first talk to, and listen carefully to, the women implanted with polypropylene meshes for prolapse (POP), stress urinary incontinence (SUI) and listening to men and women with mesh hernia repairs. In defense of their own health, to advocate for skilled medical intervention to reduce pain and gain back quality of life, they have had to research to find answers as to why they hurt, why doctors think their pain is anything but mesh related, why they are sick, why their complications are hard to diagnose, and why doctors are reluctant to diagnose what is obvious to women and men with computers, internet and Google skills.
It is sad when patients have done more research than doctors.
Listening to the women with first-hand knowledge of transvaginal mesh complications, one thing is being made very clear by women; not enough attention is being paid to the systemic injury of mesh complications. When listening to hernia patients, men and women are saying mesh complications affect your whole body, not just your abdomen. According to Jonathan Blac (1984):
“Evaluation of the host response to implanted biomaterials usually focuses on the implant site tissue response. This may lead to erroneous conclusions in the same way that examination of battles outside of their historic context does. A broader view discloses a variety of possible and actual systemic effects of carcinogenic, metabolic, immunological and bacteriological nature. Recognition of these effects in patients is hampered by a lack of epidemiological studies (19).”
Researching patients found they were not alone with their questions or symptoms. Patients like me discovered they could be considered by the medical community as high responders to medical mesh. In other words, we are all the population of patients experiencing chronic foreign body reaction to synthetic mesh implants. These synthetic meshes mentioned are predominately constructed of polypropylene or similar polymeric constructs. To break it down in simpler terms we all found that hypersensitivity to foreign body implants was, and is, the common denominator among us. You might say for simplicity‘s sake we high responders are all “allergic” to the materials doctors implanted in us.
With the recent trials over the injuries caused by the controversial transvaginal implants, it becomes very evident that research into the long-term effects of polypropylene in human bodies is, as I have discovered, is almost non –existent. I say “almost “, because there may be some study somewhere I have missed or others have missed that would enlighten us all. Alas, I have not found long-term studies that show what to expect with controversial synthetic meshes 3, 5, or 10 years into the future. Personal experience and research however indicates that complications may present with mesh implants as long as the implant remains in a live body.
With the new emerging information from the FDA that indicates complications rates to be higher than predicted or thought acceptable, for benefit to risk ratios, it appears more scrutiny is needed, and was needed. Scrutiny comes late, and comes at the expense of patients’ health (5).
When synthetic mesh is surgically placed in your body, if your body is over sensitive, it matters not how skilled the surgeon is or unskilled he is at placing mesh, when it is the properties of the mesh and the body’s ensuing expected foreign body response gone awry that causes oxidative processes in the body to try degrade the foreign body enough so that cells can “eat” or dispose of the foreign matter that it can’t push out like a puss surrounded splinter. That oxidative process of chronic foreign body response has been proven to degrade polypropylene (7).
Polypropylene mesh does not remain inert when constantly attacked by the oxidative processes of Foreign Body Response (12).( Should mesh actually ever have been considered inert in the first place as it is recognized by the human body as a foreign body as soon as it is implanted? )
Degradation products of polypropylene are Alkyl radical, Alkoxy radical ,Peroxy radical and Hydroperoxide (1). Note that these degradation products are free radicals, and they are considered toxic. If polypropylene has been treated with other surfactants to help dye fixation, as in blue dyed medical mesh, or treated with chemicals for sterilization because heat sterilization damages the mesh, then there are other degradation products to worry about.
Polymeric materials have long been identified as leaching estrogenic mimicking chemicals that are known to make cancer cells multiply; for example blue polypropylene piperettes used in lab experiments were found to be the source of experiment contamination in lab research. Women are wondering about nonylphenol leaching out of meshes and its estrogenic role in enabling cancer.
Scientists know polypropylene degrades under oxidative stress. Did no one think to test what chemicals could leach out and cause toxic chaos inside of peoples’ bodies? You would think because the implants were designed to be permanent, substantial testing would have occurred before marketing such medical devices. Substantial testing was not done (16).
Where am I going with this?
I am listing the ingredients of a recipe for autoimmune disease to develop. It is a recipe for a systemic storm. It is a storm that also can predisposes one to cancer. Predisposition for higher rates of cancer after mesh complications, is a subject deserving of an article all of its own. This article’s purpose is to draw attention the fact that there appears to be a high rate of autoimmune disorders in the population of women with chronic FBR that has caused implant failure and degradation.
I took a survey of patients with medical mesh complications that validated my suspicions and the suspicions of other patients. Many thanks go out to those who took the survey in order to get a real snapshot of what the unrecognized systemic diseases are that mesh complication patients are dealing with, seeking validation for, and seeking skilled medical intervention for. I will share survey information at the conclusion of this article.
I draw your attention back to the recipe for a devastating storm. The number one ingredient in this systemic storm is ignorance. Doctors appear to have no tests to predict hypersensitivity to polypropylene in candidates for synthetic mesh implants. Hypersensitivity (which may be a genetic predisposition or an acquired condition) should be a contraindication for a patient to be implanted with a synthetic material known to cause an inflammatory response, just as having an underlying autoimmune disease is a contraindication for mesh implantation according to some mesh manufacturer’s instructions for physicians (13). That contraindication warning for surgeons makes me wonder what manufacturers really knew about the connection between FBR and autoimmunity and implant failure or success and failed to share with physicians and surgeons.
The second ingredient for a harmful systemic storm is a combination of the short term acute inflammation of FBR that usually decreases after thirty days from when the mesh is implanted, preceded by decreasing low grade chronic inflammation thereafter. (2) However decreasing FBR is not always the outcome. Women with synthetic mesh implant complications have learned the hard way, that for women with mesh complications and implant failure, FBR does not decrease but increases, causing distressing cycles of burning sensation and pelvic cramping pain that many women say exceeds the pain of child birth and never ends. According to an article by a cancer treatment centre (3) “inflammation can become chronic if the cause of the inflammation persists, or because of deregulation in the control mechanisms responsible for shutting down the inflammation process.” Cancer researchers know there are links between chronic inflammation and cancer development (17, 18 ). Autoimmune researchers know there are links between autoimmune disease development and chronic inflammation (23 ). Some surgeons know there is a link between implants and autoimmune disease development (14).
Now the 3rd ingredient is a hit and miss in this recipe . It is like an optional ingredient you would never want .That ingredient is chronic infection. Many patients with mesh complications have chronic infections, infections safely hidden in mesh structures too small for “good guy” cells to go in and attack bacterial infection.
Prof. Garth L. Nicolson states in his article Autoimmune Illnesses and Degenerative Diseases, “chronic infections play an important role in autoimmune and degenerative disease, along with genetic predisposition and immune dysfunction (22).” Nicolson also states infection could be the cause of autoimmune disease or a cofactor.
Reading the study, Localized Immunosuppressive Environment in the Foreign Body Response to Implanted Biomaterials by David M. Higgins,* Randall J. Basaraba,* April C. Hohnbaum,* Eric J. Lee,* David W. Grainger,† and Mercedes Gonzalez-Juarrero , you become more aware of the serious harm of chronic infection and implant failure. According to these researchers “It is estimated that at least 20 million people in the United States have a biomaterial device implant. Implant device failure or implant-associated infections can have disastrous consequences for the implant device function and the host. Although the risk of implant-associated infections is small (1 to 7%), these infections are associated with considerable morbidity, expensive health care, and prolonged antibiotic therapy.2 The medical and surgical cost of treating certain device failures or implant-associated infections can average up to $50,000 per patient.3,4 These significant burdens and the increasing use of biomaterial implants in a myriad of medical applications warrants a clear understanding of the immune response to these materials (15 ) .”
So now we have recognized the following ingredients for a health disaster.
#1) hypersensitivity undiagnosed
#2) chronic inflammation causing degradation of mesh
#3) chronic infection.
Now let’s add the 4th ingredient to the systemic storm recipe. Let’s add chemical irritation and insult. One product of the body’s attempt to break down polypropylene via peroxide (hydrogen peroxide produced by the body) is the dangerous Hydroxyl radical. Life Extension Magazine published a report in 1995 on the Hydroxyl radical. It was stated “the uncontrolled action of hydroxyl radicals the most damaging free radical by far can have devastating effects with the body.”
Consequences of hydroxyl can be seen in many diseases such as atherosclerosis, cancer and neurological disorders (4). To add to the evidence that degradation of polypropylene releases damaging hydroxyls note the quote from S. A. M. Ali, P. J. Doherty, D. F. Williams*Article first published online: 10 MAR 2003.
“Degradation is an essential factor in polymer biocompatibility. The physiological environment of the human body can be aggressive to polymers. Most implanted polymers suffer degradation and the kinetics and mechanisms of the processes can be significantly affected by various biologically active species, especially enzymes, lipids, peroxides, free radicals, and phagocytic cells. Iron enhances the toxicity of oxygen free radicals. Superoxide and hydrogen peroxide can interact to form the very toxic hydroxyl radical in the presence of iron. The data have shown that the hydroxyl radical is likely to be one of the main causes of polymer degradation in implantable devices. “
I could go on and on about the damage of free radicals but the point again is once again about inflammation; inflammation increased by chemical irritation. Inflammation is heightened by the reaction of damaged tissues surrounding the implant, tissues subjected to the peroxide attack against the implant material. Inflammation, chronic inflammation, has long been recognized as being a cause of diabetes, a cause of heart disease and a symptom of autoimmune disease. Perhaps more research should be done to address the fact that inflammation may not only be a symptom of autoimmune diseases but in fact be the cause of an autoimmune disease.
Lupus is one of the very scary autoimmune diseases some women are being diagnosed with after mesh implantation, after suffering months if not years of chronic pelvic inflammation from FBR to synthetic mesh. Many other autoimmune diseases are being diagnosed and suspected in this cohort of women, and in the population of hernia patents experiencing chronic FBR. Read the following abstract regarding Lupus by Zafar Rasheed, , Rizwan Ahmad, Naila Rasheed and Rashid Ali (2007)
“Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with autoantibodies as a near universal feature of the disease. Earlier investigations from our laboratory revealed increased oxidative damage in SLE patients. Therefore, we hypothesized that oxidative by-products, such as hydroxyl radical (√OH), could lead to neoantigens like √OH damaged human serum albumin (HSA), which could in turn initiate autoimmunity in SLE (21).”
So back to the recipe,
So now we have,
#1) hypersensitivity undiagnosed
#2) chronic inflammation causing degradation of mesh
#3) chronic infections from mesh porosity size allowing bacteria a safe haven
#4) chemical insults, the degradation products of the oxidative process caused by FBR which are free radicals, the most worrisome being hydroxyl
The recipe for a systemic storm is not complete yet.
Consider a statement by Kurien BT, Hensley K, Bachmann M, Scofield RH. 2006 May 23.
“Free radical-mediated oxidative damage and consequent protein modification by the end products of oxidative damage are important mediators of cell toxicity and disease pathogenesis”.
(Free Radic Biol Med. 2006 Aug 15;41(4):549-56. Epub 2006 May 23. Oxidatively modified autoantigens in autoimmune diseases.)
We can now add oxidative damage or stress to the growing list of recipe ingredients for a damaging systemic storm. According to many research articles oxidative stress is implicated in autoimmunity onset, progression and exacerbation. (8, 9, 10,11 ).
For example, in the paper by MR Namazi, (http://www.jautoimdis.com/content/6/1/4 Cytochrome-P450 enzymes and autoimmunity: expansion of the relationship and introduction of free radicals as the link …..) we can read about the link between chronic oxidative stress and the evolution or trigger of autoimmune disease.
“ Hydroxyl radicals are also very highly reactive and could attack a wide range of targets. The presence of rheumatoid factors in some autoimmune diseases, such as vitiligo [9,11] and rheumatoid arthritis, can be explained by this mechanism. Over time, chronic oxidative stress could generate several adducted and/or non-adducted molecules that would essentially act as a "neo-antigens". This is consistent with the slow maturation of auto-antibodies in the evolution of autoimmune diseases. During chronic oxidative stress, neo-antigens potentially cause tissue damage and release a plethora of sequestered auto-antigens. This process is referred to as the "bystander effect". Such an outburst of auto-antigens from the target tissue would potentially amplify the effect of the neo-antigens, leading to the breakdown of self-tolerance .”
Furthermore , according to Dr. Ray D. Strand, MD,
“There has been great interest among researchers for the past 20 years involving the role of oxidative stress in the development of arthritis. Most studies have not separated rheumatoid arthritis and osteoarthritis (degenerative arthritis) when looking at free radical reactions and these diseases. Information provided here is consistent with a comprehensive review article written by Dr. Henrotin in 1992 regarding oxidative stress and how it is involved in inflammatory joint disease. Several recent studies have further established oxidative stress as being the plausible cause of these diseases."
"The immune system is intended to be our reliable protector. It is always checking for self (one's own body) while it is looking for non-self (any foreign substance or abnormal cell). When the immune system finds a virus, bacteria, or foreign body it destroys and eliminates it from the body. However, in autoimmune diseases the immune system actually attacks itself rather than a foreign substance. If it attacks the joint space, a person is diagnosed as having rheumatoid arthritis. If it attacks the bowels, it manifests as Crohn's disease or ulcerative colitis. When the connective tissue is attacked, a person might end up with scleraderma or lupus. If the myelin sheath around the nerve is the target, multiple sclerosis (MS) ensues. (www.raystrand.com/recommendations )”
Note the statement that recent studies established oxidative stress as being the plausible cause of autoimmune diseases. Now who in their right mind would argue that mesh complication patients don’t have oxidative stress when enduring chronic painful FBR? So I will add oxidative stress to the recipe.
So now we have,
#1) hypersensitivity undiagnosed
#2) chronic inflammation causing degradation of mesh
#3) chronic infections from mesh porosity size allowing bacteria a safe haven
#4) chemical insults, degradation products of the oxidative process caused by FBR which are free radicals, the most worrisome being hydroxyl
#5) oxidative stress
When you look at that recipe and realize that chronic FBR goes undetected for long periods of time (sometimes years) in mesh complication patients, you may wonder why is it going undetected for so long? It appears that doctors are not looking for FBR symptoms! They don’t see what they do not recognize! Chronic FBR causes mesh degradation, causes systemic chain reactions, and causes autoimmune vulnerability. When delays in diagnosing mesh complications initiated by FBR happen, when misdiagnosing mesh complications as irritable bladder happen, it is like planting an autoimmune disease seed in a hot bed and then wondering why it grew so quickly and strong! The recipe ingredients outlined are all in mesh complication patients! Why are so many doctors seemingly oblivious to the obvious? My answer would be liability and accountability. The links are all there if one chooses to seek them…, one reaction sets off a chain reaction. So no surprise is among mesh victims sharing info about autoimmune issues after FBR to synthetic mesh. There is sadness, anger, and grief as many mesh complication victims not only learn to live with chronic pain but irreversible autoimmune diseases as well.
I believe future studies will prove that autoimmune diseases, are being diagnosed at higher rates in the population of women who have experienced extreme chronic FBR to synthetic mesh than those of the population with no synthetic implants or no known FBR to implants that have not degraded or caused adverse events. I believe this statement would hold true for our male counterparts with hernia mesh complications. Research needs to be focused on the systemic effects of FBR induced mesh complications.
Doctors, especially primary care givers need to be educated to know the signs of FBR in their mesh implanted patients, and understand the progression from FBR to implant failure to autoimmune disease. Mesh complications are complicated!
It is not just about pain, erosion, extrusion, infection, organ perforation, the inability to sit, to have sexual relationships. It really is about quality of life issues that are not reversible, that are a whole body injury from a less than perfect implant material. Systemic effects from mesh can kill slowly or quickly.
Make no mistake, mesh can kill. Call it slow death by mesh if no doctor can remove your mesh implant or is willing to try when you are one of the not so rare patients experiencing chronic FBR, and in the eye of the perfect storm for a disaster. Am I being dramatic? Some doctors might think so. Patients with mesh complications would say no, no drama; it just is the way it is.
12% developed diabetes, or been diagnosed as pre-diabetic.
51% experienced Weight loss
3% developed asthma
20% reported exacerbation of pre-existing asthma
3% diagnosed with Lupus
12% developed rheumatoid arthritis
10% reported exacerbation of pre-existing arthritis
100% noticed a marked lack of energy post implantation, chronic fatigue
14% diagnosed with chronic fatigue syndrome
71 % have undiagnosed chronic fatigue symptoms
24% diagnosed with fibromyalgia
41% reported symptoms of fibromyalgia to be addressed or being addressed
63% reported blurred vision post mesh implant
44% reported having elevated fever, higher body temperature
39% reported lower body temperature
44% reported Hair loss, loss of facial and scalp hair
17% reported Hyperpigmentation, or dark tanning in skin
29% reported Painful skin rash,
25% reported Fragile thin skin
36% reported Skin that bruises easily
24% reported acne
24% reported Skin rashes, especially "butterfly rash" on the nose and cheeks
41% reported Sun sensitivity
46% reported dry eyes
44% reported dry mouth
51% reported extreme sensitivity to cold in the hands and feet
76% reported Recurring abdominal bloating and pain
39% High blood pressure
90% Irritability, anxiety and depression
92% reported "Brain Fog," difficulty concentrating,
53% reported Lack of coordination or unsteady gait
61% reported Dizziness, vertigo
58% reported Numbness, weakness, tingling or paralysis in one or more limbs
25% Cysts on Ovaries
41% Increase in snoring
63% Shortness of breath and tightness in the chest
22% Unexplained anemia (low count of red blood cells
8% diagnosed with a connective tissue disorder post mesh
2% have you been diagnosed with cancer post mesh implantation
32% reported chemical sensitivities started post mesh implantation
41 % reported food sensitivities started post mesh
What could these symptoms indicate ?
What are these symptoms associated with? You guessed it ….autoimmune diseases! Clearly we need research and scrutiny into the progression from foreign body response from synthetic mesh to autoimmune diseases development. Clearly if one researches one can see the dots connect! I suspect those who have the most to lose will not look, research or admit to causing autoimmune problems by using non-inert mesh in highly susceptible patients. And here is a big question … if mesh becomes non-inert in 33% of the people it is implanted into, is the mesh defective?
Clearly, mesh degrades. Is that not a defect? It is designed to be permanently implanted so one would not find it a stable product if 33% of the meshes implanted degrade and the implants fail. This is a Pandora’s box. Who is brave enough to take on the manufacturers ? Is the ultimate liability so scary the judicial system will avoid finding the product defective but give higher punitive awards for failure to warn?
Well, that question is food for more thought, to add to what I have already tried to piece together for a clearer picture of why implant rejection and failure is more than just a localized wound, but the starting point for a host of autoimmune systemic problems going unrecognized, unresearched, and untreated.
2) Long-term foreign-body reaction to preperitoneal polypropylene mesh in the pig, G. L. Beets, H. van Mameren, P. M. N. Y. H. Go
4) Oxidative Medicine and Cellular Longevity Volume 2011 (2011), Article ID 809696, 9 pages doi:10.1155/2011/809696 Review Article Hydroxyl Radical and Its Scavengers in Health and Disease,Boguslaw Lipinski, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA Received 30 March 2011; Accepted 7 June 2011 Academic Editor: Kennet Maiese http://www.hindawi.com/journals/oximed/2011/809696/
5) Systemic effects of biomaterials Biomaterials ,Volume 5, Issue 1, January 1984,Pages http://www.sciencedirect.com/science/article/pii/0142961284900619
University of Pennsylvania, Philadelphia, Pennsylvania, USA
http://dx.doi.org/10.1016/0142-9612(84)90061-9, How to Cite or Link Using
Abstract: Evaluation of the host response to implanted biomaterials usually focuses on the implant site tissue response. This may lead to erroneous conclusions in the same way that examination of battles outside of their historic context does. A broader view discloses a variety of possible and actual systemic effects of carcinogenic, metabolic, immunological and bacteriological nature. Recognition of these effects in patients is hampered by a lack of epidemiological studies.
6) Autoimmunity. 2007 Nov;40(7):512-20.
Enhanced recognition of reactive oxygen species damaged human serum albumin by circulating systemic lupus erythematosus autoantibodies.
Sheikh Z, Ahmad R, Sheikh N, Ali R.,Source Department of Biochemistry, Faculty of Medicine, AMU, Aligarh, India. firstname.lastname@example.org http://www.ncbi.nlm.nih.gov/pubmed/17966041
7) The mechanisms of oxidative degradation of biomedical polymers by free radicals
S. A. M. Ali, P. J. Doherty, D. F. Williams*
Article first published online: 10 MAR 2003
Degradation is an essential factor in polymer biocompatibility. The physiological environment of the human body can be aggressive to polymers. Most implanted polymers suffer degradation and the kinetics and mechanisms of the processes can be significantly affected by various biologically active species, especially enzymes, lipids, peroxides, free radicals, and phagocytic cells. Iron enhances the toxicity of oxygen free radicals. Superoxide and hydrogen peroxide can interact to form the very toxic hydroxyl radical in the presence of iron. The data have shown that the hydroxyl radical is likely to be one of the main causes of polymer degradation in implantable devices. © 1994 John Wiley & Sons, Inc.
“Increasing evidence shows that oxidative stress plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).”
Oxidative stress promotes hypertension and albuminuria during the autoimmune disease systemic lupus erythematosus.
10) Source http://www.ncbi.nlm.nih.gov/pubmed/22291449
Mathis KW, Venegas-Pont M, Masterson CW, Stewart NJ, Wasson KL, Ryan MJ.Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
Abstract: Several lines of evidence suggest that essential hypertension originates from an autoimmune-mediated mechanism. One consequence of chronic immune activation is the generation of oxygen-derived free radicals, resulting in oxidative stress.
Kurien BT, Hensley K, Bachmann M, Scofield RH.
Source :Free Radic Biol Med. 2006 Aug 15;41(4):549-56. Epub 2006 May 23.
Oxidatively modified autoantigens in autoimmune diseases. Arthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, OK 73104, USA.
AbstractFree radical-mediated oxidative damage and consequent protein modification by the end products of oxidative damage are important mediators of cell toxicity and disease pathogenesis. Aldehydic products, mainly the 4-hydroxy-2-alkenals, form adducts with proteins and make them highly immunogenic. Oxidative modification of proteins has been shown to elicit antibodies in a variety of diseases including systemic lupus erythematosus (SLE), alcoholic liver disease, diabetes mellitus (DM), and rheumatoid arthritis (RA). Oxidatively modified DNA (8-oxodeoxyguanine) and low-density lipoproteins (LDL) occur in SLE, a disease in which premature atherosclerosis is a serious problem
12)http://journals.lww.com/greenjournal/Abstract/2010/10000/Polypropylene_Vaginal_Mesh_Grafts_in_Gynecology.24.aspx Polypropylene Vaginal Mesh Grafts in Gynecology,Ostergard, Donald R. MD,Obstetrics & Gynecology:
October 2010 - Volume 116 - Issue 4 - pp 962-966
“ Noninert polypropylene degrades into potentially toxic compounds that would be expected to stimulate a greater inflammatory reaction leading to erosion……….Manufacturers need encouragement to develop meshes that are inert and incorporate without contraction along with routine clinical tests to detect “high responders” to avoid complications. Polypropylene is not inert within the human body.”
13) http://www.lifebeatonline.com/procedure/ProcedureLanding.bsci/,,/navRelId/1000.1002/method/Procedure/id/10001031/attributeTypeId/1/resourceTypeId/91/seo.serve CONTRAINDICATIONS….Autoimmune connective tissue disease……
IMPLANT SYNDROME ,William J. Rea, M.D., F.A.C.S., F.A.A.E.M.
“The surgical use of artificial implants can induce both autoimmune disease and chemical sensitivity.”
A standardized description of graft-containing meshes and recommended steps before the introduction of medical devices for prolapse surgery
Mark Slack, Donald Ostergard, Mauro Cervigni, Jan Deprest,International Urogynecology Journal,April 2012, Volume 23, Issue 1 Supplement, pp 15-26
Abstract: Over the past decade, a huge number of new implants and ancillary devices have been introduced to the market. Most of these have become clinically available with little or no clinical data or research. This is a less-than-ideal situation, and this subgroup of the ad hoc IUGA roundtable conference wants to open the discussion to change this, by proposing a pragmatic minimum clearance track for new products being introduced to the market. It consists of an accurate and more standardized product description, data on the biological properties gathered in animal experiments, anatomical cadaveric studies, and upfront clinical studies followed by a compulsory registry on the first 1,000 patients implanted. Ideally, manufacturers should support well-designed prospective (randomized) clinical trials that can support the claimed benefits of the new product. Data were presented at the 2nd IUGA Grafts Roundtable June 2010.
17) http://clinicaltrials.gov/ct2/show/NCT01428167?term=chronic+inflammation&rank=85 Hashimotos Thyroiditis and Thyroid Cancer
Sponsor:The University of Texas, Galveston Information provided by (Responsible Party):The University of Texas, Galveston ,ClinicalTrials.gov Identifier:NCT01428167,First received: August 10, 2011 Last updated: June 5,
Thyroid cancer (TC) is the most common endocrine malignancy. The association between inflammation and cancer is well established.
Inflammation can become chronic if the cause of the inflammation persists, or because of deregulation in the control mechanisms responsible for shutting down the inflammation process. When these inflammatory responses become chronic, cell mutation and proliferation can result and often create an environment that is conducive to the development of cancer.
Inflammation is the body’s response to tissue damage, caused by physical injury, ischemic injury (caused by an insufficient supply of blood to an organ), infection, exposure to toxins, or other types of trauma. The body’s inflammatory response causes cellular changes and immune responses that result in repair of the damaged tissue and cellular proliferation at the site of the injured tissue. Inflammation can become chronic if the cause of the inflammation persists, or because of deregulation in the control mechanisms responsible for shutting down the inflammation process. When these inflammatory responses become chronic, cell mutation and proliferation can result and often create an environment that is conducive to the development of cancer. This is often referred to as “the perfect storm.”
Jonathan Blac, Systemic effects of biomaterials, Biomaterials Volume 5, Issue 1, January 1984, Pages 11–18Biointeractions '84 Materials/Interactions-Conference Systemic effects of biomaterialsUniversity of Pennsylvania, Philadelphia, Pennsylvania, USA
The mechanisms of oxidative degradation of biomedical polymers by free radicals ,S. A. M. Ali, P. J. Doherty, D. F. Williams*,Article first published online: 10 MAR 2003 ,DOI: 10.1002/app.1994.070510805
2007, Vol. 40, No. 7 , Pages 512-520 (doi:10.1080/08916930701574331)
HTML PDF (213 KB) PDF Plus (217 KB) Department of Biochemistry, Faculty of Medicine, AMU, Aligarh, 202002, IndiaDepartment of Biochemistry, SBSPGI, Balawala, Dehradun, 248161, IndiaDivision of Pharmacology, Central Drug Research Institute, P.B. No. 173, Lucknow, Indi
H Ahsan, A Ali, R Ali - Clinical & Experimental Immunology, 2003 - Wiley Online
Summary: Reactive oxygen species generated during various metabolic and biochemical reactions have multifarious effects that include oxidative damage to DNA leading to various human degenerative and autoimmune diseases. #