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1. Lower temperatures in more distal joints (may affect crystalisation of uric acid)
2. pH is lower in more distal joints --> closer to the pH that uric acid crystalises at
3. Distal joints (esp MPJ) are subject to more trauma ->crystal deposition is more common in traumatised joints.
fair enough craig, but as i can vouch for (the last few days) gout occurs in the distal jts as there is a much greater chance of same jts accidentally contacting unforgiving objects( by g.. it hurts), the creator plays games with us mortals
I have a pt who has gout and is an industrial chemist and he assured me that the change in solubility of urea decreases by about a factor of 10 with a drop of only a few degrees....I believed him
Regards Phill
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gout; accumulation of monosodium urate crystals occurs inthe avuacular tissues (tendons and ligaments). the peripheral joint invlement concept is not completely true. in the upper quadrant the elbow ahs high incidence. inthe foot and ankle region the first MTPJ is common site. the PIPJs are not affected.
Low temperature: the dorsalis pedis artery is a big vessel which suples the distal foot. temp is dependent on vasular supply. hoever the low temp theory may be true in pts with PVD and vascular insufficiency compromising blood supply to the distal foot. (toes are normal;ly cold in these pts not the MTPJ- open to interpretation). literature identifies a direct correlation betweeen gout incidence and PVD and HTN. considering the tendon as the target site, there is no major difference inthe temp from the muscle spindle. the solubilityof the uric cid decreases by 2.25 mg/dL with every degree fall of temp from 36 degree. a temp of 30 degree is required to bring uric acid solubility to 4 mg/dL enoug to cause a flare.
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ph: ph of the tissue is directly proportional to temp. and that brings us to the pevious post on temp. influence of uriic acid solubility on ph is not documented.
possible expanation for firsst MTPJ being affected: the medial aspect of the first MTPJ - two tendons cross the medial aspect of the joint (abductor halucis and flexor digitorum brevis). increased load on the medial aspect of the first MTPJ (forgot the article) (during propulsion) increass the thickness of the articular cartuilage on that side. hence the risk factors are more on the meidal side of the FMTPJ (tendon and articular cartilage) could be the reason.
explanation for as to why uric acid leaves the circulation - will post if ur interested.
Davsur 08
Could you forward your references, and PIP jts not being affected.
Sally
Hi Sally,
the involvement of DPIPJs of the hand is emphasised in gout (Dalbeth et al. 2007, Journal of Rheumatology) title - gout hand study. during my search of literature ive found 2 cohorts (Roodys et al. 2007 and Grahame and Smith, 2006) where incdence of gout in different joints has been investigated. PIPJ invoovement of the foot is not reported. there are 15 case studies of gout and none on PIPJ of foot. there no article which specifically state gout does not affect PIPj of the foot. it was my conclusion from the previous studies. (could be one of the difference between rheumatoid and gout foot).
regarding the especially re not finding uric acid crystals in the joint space
i dont see ive made that comment.
uric acid crystals in the form of monosodium urate crystals are found in the joint spaces of the affected joints.
david
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I asked 2 learned Rheumatologists who said nobody knows why this is. And as we all know Rheumatologists know everything. They pointed out that no one knows why rheumatoid affects the MTPJs not the IPJs either. The list goes on. Temeperature as an expalanation does not fully make sense to me as it is so tightly regulated by the body. Also you get tophi in the ears (amongst other places) and I can't believe ear muffs are the answer!
"explanation for as to why uric acid leaves the circulation -"
we need to look closely at the lyphantic draining system and its involvement at molecular level as there is no such thing as no one knows,,,,,,,,Davsur08, i like your line of thinking!!
Last edited by MR NAKE : 21st October 2010 at 09:43 AM.
Reason: spelling error
Dear Mr. Nake,
Uric acid is released by damaged cells as a "danger signal" to alert immune responses. In individuals with no renal pathology or insufficiency this excess uric acid gets flushed out of the system, maintaining normal levels. In individuals with renal insufficiency, renal clearance of uric acid is reduced leading to elevated serum uric acid levels, which is precipitated to accumulate in the tissues (joints, tendons, subcutaneous, lungs, heart, liver). predominently the peripheral joints are afffected (feet more than hands). There are other exceptions like in post menopausal women the incidence of gout escalates same as to that of males. Reduction in Progesterone is thought to be the cause as this harmone can increase GRF and urate clearance (Atallah et al. 1988 : Progesterone increases glomular filtration rate; Braz J med Biol Res 1988.21:71-74)
The reason for the target sites for accumulation is not certain. some research suggest monosodium urate crystalises when in contact with synovial fluid. others OPINION is that reduced temp at the peripheral joints, Sodium-urate nucleation influence to the sites been frequently affected. research has looked at "why and how MSU crystalises within the joints" and not at "why these joints"? the reason because gout flares donot occur unless MSU crystalises in the event if it doesn't crystalise it would be flushed out throught the lymph i assume. Gentle. 1997 study showed that uric acid is released from a joint which undergoes abnoxious movement (a movement which is not the primary movement of the joint). extending this result a bit further the first MTP joint undergoes greater stress during gait and in the presence of Functional Hallux limitus the possibility of abnoxious movement within this joint would increase. In a healthy individual the uric acid would get flushed out by the lymphatic system (a Study found uric acid in lymph nodes of babies. the study looked at affects of dehydration in new born babies). HOwever in renal insufficiency the accumulated uric acid would crystalise causing a flare. This could be true if the temperature at the MTP joint is lower. but we all know that during joint movement temperature would increase. Either the rise in temperature in not high enough to reduce urate saturation or the reason could not be temperature at all. I am yet to investigate the sodium-urate nucleation concept. I have only come across this recently.
I would imagine that once the MSU has crystalised, it would not be absorbed in to the lymphathics due to their macro size.
This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference. Gout is the most prevalent inflammatory arthropathy. It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle. A number of factors are known to reduce urate solubility and enhance nucleation of monosodium urate crystals including decreased temperature, lower pH and physical shock, all of which may be particularly relevant to crystal deposition in the foot. An association has also been proposed between monosodium urate crystal deposition and osteoarthritis, which also targets the first metatarsophalangeal joint. Cadaveric, clinical and radiographic studies indicate that monosodium urate crystals more readily deposit in osteoarthritic cartilage. Transient intra-articular hyperuricaemia and precipitation of monosodium urate crystals is thought to follow overnight resolution of synovial effusion within the osteoarthritic first metatarsophalangeal joint. The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.
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According to the way I see, Gout occurs more in peripheral joints because they are more susceptible to micro-trauma during gait. There is more resistance in the first MTP joint during gait, so in cases of functional hallux limitus, the monosodium urate crystal are more likely to occur.
There is usually an increase of uric acid levels in the blood serum of patients who are on anti-hypertensive medications (especially the -thiazides), these patients usually become aware of the condition once they encounter a trauma to their foot or sometimes the knee (usually a knock-knee or osteoarthritic knee joint) This can justify that trauma might be the leading cause of gout in more distal joints.....
A biochemist told me that the solubility of the urates drops a great deal with fairly small drop in temp that occurs as blood goes to peripherals......this would be a big reason.
regards Phill
Sicknote,
The web page your were referring to, highlights foods that might cause a gout flare. there is nothing suggests a change in Ph. do you mean to say the whole body would become acidic or a particular joint turing acidic?
Beer has a tendency to accumulate lactic acid in the kidneys, hence can delay uric acid elimination. In patient with renal insufficiency this delay can be determental as such the circulating uric acid can potentially accumulate within the joints. I dont have the reference for this in my memory. am not sure of the high purine part of it???
The website doesnot say anything about the body becoming "Acidic". Please note the web page has no references and is written by a computer management person who is training to be a freelanc journalist.
An article written on buzzle.com by someone with a mathematics degree with no references could not be further from being an authoritative source of info than you can get.
Sicknote ... what you say does not explain why it affects the peripheral joints more than the axial joints. Care to explain that?
Bearing in mind that arthritis gets everywhere in a body at the same time an assumption could be that Gout a part of inflammation of the joints could well be part of the overall condition!
I have one at the moment with arthritis in most if not all joints with the latest definitely gouty but without the swelling!
Deformed bone material at the joint with contraction of tendons a secondary effect!
Bodies accidic state I assume and wait to see what the doctor is going to do next apart from himself, the doctor, taking the tablets, himself for the patient???....?
My major problem is trying to prevent the patient limping on both feet at the same time!
Yours,
Colin.
Last edited by C Bain : 9th May 2012 at 01:57 AM.
Reason: My computer can't spell!
This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference. Gout is the most prevalent inflammatory arthropathy. It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle. A number of factors are known to reduce urate solubility and enhance nucleation of monosodium urate crystals including decreased temperature, lower pH and physical shock, all of which may be particularly relevant to crystal deposition in the foot. An association has also been proposed between monosodium urate crystal deposition and osteoarthritis, which also targets the first metatarsophalangeal joint. Cadaveric, clinical and radiographic studies indicate that monosodium urate crystals more readily deposit in osteoarthritic cartilage. Transient intra-articular hyperuricaemia and precipitation of monosodium urate crystals is thought to follow overnight resolution of synovial effusion within the osteoarthritic first metatarsophalangeal joint. The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.
Yet nobody is talking about nutrition as the cause of so many foot injuries.
Yet nobody is talking about nutrition as the cause of so many foot injuries.
Incredible.
We all know gout is related to nutrition, but this whole thread is why does gout have a predilection for the foot joints and not other joints. Care to explain why you think it affects the foot more than other joints based on nutrition?
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The incidence of gout is increasing throughout the world and it is now the most common form of inflammatory arthritis affecting men. However, there are other factors to consider that include diet, age, socio-economic background, ethnicity, environmental and co-morbidities that all could contribute to the disease.
Why the foot and in particular the big toe…is still unknown. From a biomechanical perspective people with chronic gout have increasing peak plantar pressures on lateral side of the foot when walking and maybe indicative of different toe off strategies.
Why the foot and in particular the big toe…is still unknown. .
Hello Prof. Rome,
Gentle. (1997) study showed that uric acid accumulates in a joint which undergoes abnoxious movement (a movement which is not the primary movement of the joint). extending this result a bit further the first MTP joint is exposed to greater stress from ground reaction forces (Corbett et al., 1993. Foot and ankle international).
Let us take a case of Functional Hallux limitus (FHL), ground reaction forces were reported to be significantly increased (Menz and Moris, 2005. Gait and POsture) under the first MTPj. The frontal plane and transverse plane compensations of the hallux on the first metatarsal head (As seen in Hallux Abducto Valgus) can be defined as abnoxious movements. This could be a cause of the first MTPJ predominence to gout flares. In our study Keith, dorsiflexion of the first MTPJ was reduced in gout subjects.
When a joint or body structure is injured uric acid is released. This mechanism is thought to be means of alerting the immune system ( i dont remember the reference but i have it some where) of its state by flashing a "danger signal', here Uric acid. Here Roodys article fits in well. OA effected joints (Loss of articular cartilage, increased joint compression forces, abnoxious movements) are more effected by gout.
Not all individuals with OA have Gout. In individuals with renal insufficency uric acid accumulation is greatly reduced. The circulating Uric acid precipitates in to joints with higher stress. there were reports of Gout flares after cross country running. these indivuduals did not have any while running on flat surfaces (I recall reading this on Arena). An Healthy renal function should eliminate excess uric acid before it precipitates. Having said that not all renal insufficiency patients have gout.
There is no one single answer for why gout affects first MTPJ predominently. identifying risk factors helps to recognise these individuals and treat accordingly.we should consider a whole array of factors. Renal, Biomechanics, ethinicity, Genetics (Hx of gout of in family) Age, Nutrition, gender, Co-morbidities...
Keith, have you looked at significance of orthotic therapy in Gout. I would love to assist if this is in the near future.
Back in organic chemistry lab, I remember being told to scrape the side of the beaker to try and help form a crystal of a salt when it was being boiled to remove water (increase concentration of salt). Pressure is probably another factor along with temperature in the formation of salt crystals. I'll bet someone could spend a little internet time and look up what effects Ksp the soluabilty constant for various salts in solution. The windlass mechanism will create some very high pressures within the first MPJ.
Eric
Last edited by efuller : 10th May 2012 at 11:40 AM.
Reason: concentration added
Back in organic chemistry lab, I remember being told to scrape the side of the beaker to try and help form a crystal of a salt when it was being boiled to remove water (increase concentration of salt). Pressure is probably another factor along with temperature in the formation of salt crystals. I'll bet someone could spend a little internet time and look up what effects Ksp the soluabilty constant for various salts in solution. The windlass mechanism will create some very high pressures within the first MPJ.
Eric
how does scraping the side of the beaker allow to form a crystal? i know stirring the solution allows crystal formation.
Pressure is probably another factor along with temperature in the formation of salt crystals. The windlass mechanism will create some very high pressures within the first MPJ.
Eric
Le Chatelier's principle: If a chemical system at equilibrium experiences a change in concentration, temperature, volume, or partial pressure, then the equilibrium shifts to counteract the imposed change and a new equilibrium is established.
Effect of change in pressure
Changes in pressure are attributable to changes in volume. The equilibrium concentrations of the products and reactants do not directly depend on the pressure subjected to the system. However, a change in pressure due to a change in volume of the system will shift the equilibrium.
(http://en.wikipedia.org/wiki/Lenz%27s_law)
We all know gout is related to nutrition, but this whole thread is why does gout have a predilection for the foot joints and not other joints. Care to explain why you think it affects the foot more than other joints based on nutrition?
Because of gravity.
Water retention in the ankles works on the same principal.
Reason for gout in more peripheral joints
o you notice what TIME of year it occurs most often?Why?
Re: Reason for gout in more peripheral joints
Linear Mode
