Posts Tagged ‘Seronegative’

postheadericon AORTIC REGURGITATION AETIOLOGY AND CLINICAL FEATURES

Aetiology

The aortic valve cusps normally overlap on closure to the extent of about 25% of the cusp area. Aortic regurgitationcan arise from:

• Dilatation of the valve ring so that the cusps no longer meet adequately to prevent leakage

• Damage to the cusps themselves

• In some diseases, a combination of these factors.Dilatation of the valve ring occurs classically in syphiliticaortic regurgitation, but can also occur with hypertensionand aortic dissection; less common causes include cysticmedial necrosis in Marfan’s syndrome, and osteogenesis imperfecta.Damage to the valve cusps is a feature of rheumaticaortic regurgitation, infective endocarditis, and less common conditions such as Libman-Sacks endocarditis, mucopolysaccharidoses and pseudoxanthoma elasticum. The seronegative arthritides, ankylosing spondylitis,Reiter’s disease and psoriatic arthritis can be associatedwith an aortitis and cusp damage, leading to aortic regurgitation.Rarely, rheumatoid arthritis is associated with a nodular cusp damage leading to aortic regurgitation.Bicuspid aortic valve (found in 1% of the population)can lead to predominant aortic regurgitation. There are other congenital forms of aortic regurgitation, e.g. that associated with a supracristal ventricular septal defect.

Clinical features

Symptoms and pathophysiology Aortic regurgitation can be well tolerated for years if it develops slowly. Up to 80% regurgitation can be found in severe chronic aortic regurgitation, but acute regurgitation(such as follows aortic dissection or acute infective endocarditis) is poorly tolerated.The severity of the regurgitation is normally indicated by a low diastolic blood pressure and wide pulse pressure.These may appear more ‘normal’ in heart failure as the stroke volume falls and the end-diastolic pressure of theleft ventricle rises. As aortic regurgitation progresses,the increasing leakage requires a larger and larger forwardflow. This is usually achieved not by a tachycardia but by the left ventricular end-diastolic size increasing with anincreased stroke volume. Initially, the ejection fraction of the left ventricle is well maintained and exercise tolerance is excellent. However, after an unpredictable time there is a steady or sudden deterioration in left ventricular function, usually with a great increase in heart size and thedevelopment of symptoms of left ventricular failure. Eventually,right heart failure follows, with the development of pulmonary hypertension. The development of heart failure indicates serious dilatation of the left ventricleand the need for urgent consideration of valve surgery.Heart failure in aortic regurgitation is associated withrapidly worsening left ventricular function, which may never recover even with valve replacement. Angina can develop because the dilated left ventriclehas increased oxygen requirements (as in congestive cardiomyopathy),but is usually associated with coronary artery disease. AF occurs in about 15% of cases, usually those with long-standing failure.

Physical signs

The physical signs of aortic regurgitation are related to the large stroke volume, the peripheral vasodilatation and the compensatory increase in size of the left ventricle. The pulse may be collapsing or bisferiens, or feel normal if there is heart failure. The blood pressure indicates the large pulse pressure and low diastolic pressure. If the diastolic pressure is well maintained in the presence of severe aortic regurgitation,coincident hypertension should be suspected. The left ventricle is very active, and in severe cases the apex beatis displaced.The increased forward flow is often accompanied bya systolic flow murmur, which, of itself, does not indicate coincident stenosis. The early diastolic murmur is notoriously difficult to hear. The murmur is best heard with the diaphragm of the stethoscope, with the patient sitting forward having breathed out. It may be best heard at the left sternal edge, nearer the apex or in the aortic area,depending on the direction of the jet. Typically, valve ring dilatation regurgitation is better heard in the third right interspace rather than the third left.An Austin Flint murmur may be associated with aortic regurgitation. This is an apical diastolic murmur, similar tothat of mitral stenosis, arising from the anterior cusp of the mitral valve, which vibrates in the jet of aortic regurgitation.Because aortic regurgitation may be both difficult tohear and is a frequent lesion in infective endocarditis, a patient with a fever and steadily widening pulse pressureis regarded as having aortic regurgitation and endocarditisuntil proved otherwise.

Investigation

ECG shows left ventricular hypertrophy of the diastolicoverload type, in that, initially at least, voltage changes withprominent Q waves over the lateral leads predominateover T-wave changes. Later, the T waves invert.Chest X-ray shows increasing size of the left ventricleand often some dilatation of the proximal aorta.Generalized cardiac enlargement may follow and, eventually,changes of raised pulmonary venous pressure.Echocardiography. M mode shows the dilated left ventricleand its wall thickness. Calculation can be made of thestroke volume and ejection fraction, which are useful forfollowing progress. In many cases vibration of the anteriorcusp of the mitral valve or the septum can be seen, confirmingthe diagnosis. Doppler ultrasound will confirm thediagnosis but cannot quantify the lesion.Cardiac catheterization is necessary to examine left ventricularfunction, the severity of the aortic regurgitationand its anatomy, as well as looking for other pathology,such as mitral regurgitation and coronary artery disease.

Management

Surgery Those in heart failure have been left too late to obtain themaximum benefit from surgery, as a dilated ‘myopathic’heart never returns to normal and is associated with ahigh risk of sudden death. The currently used criteria forsurgery are based on echocardiographic dimensions; othersare now being developed based on the use of isotope leftventricular angiography. A fall in the ejection fraction ofthe left ventricle on exercise has been suggested as a criterionfor surgery, as the ejection fraction is normally wellmaintained or even increases. Acute aortic regurgitationrequires very close attention and urgent valve replacementat the first sign of heart failure. Delay can result in catastrophicheart failure and death, as the degree of regurgitation and size of the heart rapidly increase.

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postheadericon A new treatment method for pain and inflammatory diseases

The present article is relaed to the observation made by the author in his two and half decades of clinical practice on the cure of the divergent inflammatory diseases such as Asthma, Arthritis, Tuberculosis, etc. by administering a single molecule/ medicine. Extensive literature and patent search could not present any scientific explanation for the phenomenon observed and reported. Preliminary research at the author’s clinic and lab has enabled the postulation and confirmation of a novel theory and immune pathway involving Histamine haemostasis referred to as the Rao’s Vicious Cycle.  In this study the medicine used belongs to the category of allergies, a new mechanism is proposed for the action of mediators during the inflammation. It has been postulated that the histamine liberated from the mast cells is the key link among the divergent diseases. During inflammation, histamine is released at the inflammatory sites as predicted by Rao’s vicious cycle. The later refers to the proliferation of TH2 type of reaction and its dominance over TH1 reaction.  In this method of cure known as Appa Hista, antihistamine antibodies, combat the histamine at the inflammatory sites and also block TH2 type of reaction, thus indirectly helping the TH1 type of reaction. The dual effect of Appa hista antibodies has been visualized in 1) Killing the intracellular organisms through TH1 type of reaction and; 2) Neutralizing the histamine at inflammation site at the same time blocking the excess TH2 type of reaction. Since Appa Hista directly attacks histamine where ever it is present, it may cure all inflammatory diseases.

INTRODUCTION

            The present investigation deals with the cure of some of the most stubborn problems such as paralytic stroke, arthritis, tuberculosis etc., by using histamine conjugated normal human immunoglobulin.  Histamine is a chemical mediator and also the prime mediator of inflammation.  It is a vasoactive amine, found long back and established as a chemical mediator of inflammation.  This compound is essential for vascular permeability and allows the vessels to leak the protein rich exudate and cells to the site of inflammation. The latter is divided into two groups: 1) Acute inflammation and 2) Chronic inflammation. While chronic inflammation may originate as chronic itself, an acute inflammation, may, over a period of time become chronic.  The inflammatory response is closely coupled with the process of healing or repair.  A foreign body (agent) always wants to destroy the host tissue for its settlement, while, the host always tries to get rid of the agent as it is foreign.  Thus, inflammation can be considered as a protective response of the host and serves to destroy, dilute or wall off the injurious agents, and, also as far as possible heal and reconstitute the tissues.

            Normally, inflammation is an immunological (protective) phenomenon and, pain is a protective signal to get rid of the stimuli (causes).  At times they become pathological and produce disease.1 Repair begins during the early phases of inflammation but reaches completion usually after the injurious influence has been neutralized. During repair the injured tissue is replaced by parenchymal (functional) cells or by filling of the defect with fibroblastic tissue (scarring) or most commonly by a combination of these two processes.  The defense mechanism is such that the system tries itself best to give protection by innate immunity. Alternately, if the agent is a stronger one, then only the acquired immunity is triggered either by humoral immunity (present in body fluids) or by cell mediated immunity or by both.  The humoral/cell mediated immunity is offered by several preformed or existing proteins like compliment and antibodies, or, by cells like macrophages, lymphocytes and neutrophils.  When an agent initiates an injury, the defense mechanism is triggered by release of mediators.  Rather than too few, there are a large number of mediators in the defense system.

 

Cells of the immune system:

            The cells that are developed in the bone narrow mature and liberate into the blood stream.  A few cells settle in the tissues and lympho reticular system to perform their immunological function.  The cells in the blood are red blood cells (RBC) white blood cells (WBC) and platelets.  Red cells supply oxygen to all the systems.  White blood cells defend body from foreign stimuli and platelets help in clotting.

            The WBC is further divided into Granulocytes, lymphocytes and monocytes.  It is well known that granulocytes are further divided into polymorpho nuclear leucocytes, Eosinophils and Basophiles. Lymphocytes are divided into T cells, B cells and NK cells.  Monocytes are referred to as monocytes in the blood and as macrophages and mast cells in the tissues.

Mediators:     

Mediators are found in cells as well as in plasma. Mediators are classified into preformed mediators and newly synthesized mediators. Preformed mediators always exist even in the absence of the inflammatory stimuli.  These are histamine, serotonin, lysosomal enzymes which are generated by the cellular sources mast cells, platelets, neutrophils, macrophages etc. The newly synthesized mediators, on the other hand, are formed in the presence of an inflammatory stimulus.  These are prostaglandins, leucoterines, and platelet activating factors, cytokines, and nitric oxide etc., generated from cellular sources such as leucocytes, platelets endothelium and macrophages.

            Under the influence of an inflammatory stimulus certain proteins in the plasma like complement under go chain reactions releasing intermediary substances like C3a, C5a and C5b – 9.  C3a is an anaphylotoxin attracting histamine to the site, while C5a attracts neutrophils to the site.  C5b – 9b, on the other hand, are believed to create MACs (membrane activating complexes) and cause target cells lysis (destruction). A plasma protein known as Hegeman factor, on the other hand, activates, clotting/ kinin cascades resulting in blood clotting and pain.

 

Immune response (IR):  

            The response initiated by an antigenic stimulus in the cells and mediators in a host is known as immune response.  As is well documented IR can be divided in to two types such as the humoral (antibody mediated immunity (AMI)) and the cellular (cell mediated immunity (CMI)). AMI refers to interaction of antigens with antibodies present in the plasma and in the interstitial fluids (extracellular), resulting in neutralization.  CMI refers to the direct killing (lysis) of intracellular bacteria through various cytokines secreted by T lymphocytes.

            The current state of understanding regarding immunological reactions can be summarized as follows.  Briefly the I Anaphylactic, II Cytolytic and III Immune complex reactions eventually generate TH2 (T Helper cell sub set 2). The latter generate the IL4 IL5 and IL10 (interleukin cytokines) which take part in allergic reactions, basic healing and also provide opposition to the TH1 subset. TH1 subset forms in delayed type of hypersensitivity reaction (type IV) and includes the cytokines IL2, TNF and IFN contributing to intracellular killing.

 

RESULTS

            Two decades of clinical practice in curing various inflammatory diseases and the possible common link between these is summarized in Table 1. The latter clearly points out the administering of the medicine for a primary disease such as Asthma which was found to have a beneficial affect on Arthritis, and so on.  Thus, a single medicine normally used in treatment of allergies had resulted in cure of several inflammatory diseases which are hitherto being treated separately.  Animal experimentation at All India Institute of Medical Sciences (AIIMS) confirmed the anti inflammatory properties of the medicine.2 This necessitated a re-look in to the fundamentals of cells, mediators and immunological response.  Literature and patent search revealed that in 1994 a US patent was granted to Yoshi et al from Japan.

Subsequently relief by the treatment has been observed in the following inflammatory diseases;

(a) Rheumatic diseases: Rheumatoid arthritis, SLE, Seronegative arthropathies, including reactive arthritis, ankylosing spondylitis, psoriatic arthritis, and various vasculitides.

(b) Nervous system: Paralysis (Cerebro vascular accident due to vasculitis), Encephalitis, Tuberculomas, multiple sclerosis, Epilepsy, peripheral neuritis, migraine, Guillian-Barr’e syndrome.

(c) Respiratory system: Bronchial asthma, TB, Drug resistant tuberculosis, and pulmonary mycotic conditions.

(d) Renal: Glomerulo nephritis, chronic renal failure, nephrotic syndrome.

(e) Genitourinary system: Chronic UTI, Stress incontinence, chronic leucorrhoea, and infertility.

(f) Heart: Hypertension, Rheumatic heart diseases, (also with CCF, Choria) Congestive cardiac failure, Atherosclerosis. Global hypokinesia.

(g) Skin: Chronic venous (Sephanous) ulcers, psoriasis, Lepraneuritis, and Vitiligo (Early Stage).

(h) Eye/ ENT: Iridocyclitis, Uveitis, Retinal detachment, Glucoma, Vasomotorrhnitis, Epistaxis, Allergy, Miners disease.

(i) Gastrointestinal diseases: Peptic ulcer, IBS, Ulcerative colitis.

(j) Psychiatric: Stress related syndromes. Dementias.

(k) Infectious diseases: Cerebral Malaria, Filariasis, Fungal infections and DIC.

(l) Pains: Cancer pains, chronic pains, few cancers arrested.

(m) Endocrine disorders: Thyroid, Diabetes.

 

 

DISCUSSION

COMMON LINK AMONG INFLAMMATORY DISEASES

Reorganization of cells

In the present methodology, the cells are reorganised into cells presenting antigens, cells required in processing antigens and intermediary cells, and, cells found at the site of inflammation. Of particular importance is the role played by intermediaries such as mast cells and basophiles. As will be seen later these are essential for release of histamine, and therefore, key agents for initiating and maintaining the inflammation.  It is thus imperative that any control on mast cells should control the inflammatory diseases.

Mast cells

mast cells4,5are bone marrow derived tissue resident cells, relatively large in diameter (10-15 mm) and heterogeneous in shape.  Under optical microscope the mast cells reveal 50 to 200 densely packed granules in each cell, each granule in turn is bound to membrane. A typical granule of 0.1 to 0.4 mm contains relatively large amounts of histamine, heparin, TNF and other preformed inflammatory mediators.  The surface of the each of the cells is coated with high affinity receptors ecoR1, which attracts IgE molecules on the surface of mast cells. Following the attachment of the IgE molecules on the mast cell surfaces, the granules start degranulating.  Although mast cells are found in connective tissues through out the body, these are present in large numbers beneath the surface tissues such as skin, lung alveoli, gastrointestinal mucosa and nasal mucus membranes. Thus, mast cells are strategically positioned to interact with inhaled or ingested antigens.

Mechanism of Mediators:6

            Histamine at the inflammatory site has a long life (30-60 mts), and, is stable as compared to most mediators derived from phospholipids and nitric oxide.  As is well known histamine triggers all the mediators and vice versa. Therefore, in any physical injury such as trauma, cold or heat, the activation of already stored histamine from the mast cells is expected to play a dominant role.

 

Histamine receptors on lymphocytes:7,8,9 

            In the proposed protocol it has been postulated that histamine can trigger lymphocytes in releasing other mediators.  This is possible only if there is histamine receptors present on the lymphocytes.  This assumption has received a recent support from several researchers. Similarly, the action of T cells in the histamine homeostasis10 (self-regulating information feedback) is proposed to take place as illustrated in Fig. 1. An important point to note is that IL6, IL8 and TNF etc., present at the inflammatory site due to tissue injury are also capable of liberating histamine.

 

IgE B Cells:

            The IL4 cytokine is expected to play a dominant role in sensitizing CD4 cells and through it the effector cells i.e. B cells and CD8 cells.  Further, in a double pronged manner IL4 can directly sensitize an IgE B cell which in turn releases IgE and acts on mast cells to liberate histamine.  The latter in turn goes to the inflammatory site and causes healing through TH2 type of reaction.  In case the inflammation is larger, it may turn in to chronic due to liberation of cytokines IL4 IL6 TNF etc.11  These in turn, in a positive feed back cycle, trigger histamine release and aid in maintaining chronic inflammation.  This vicious cycle of generation of histamine at the site of injury and its subsequent triggering of IgE B cells ( Histamine pathway II) and CD4 cells ( Histamine pathway I) is termed as Rao’s Vicious cycle.  That is strong inflammation can turn into chronic inflammation by the continuous generation of excess histamine in repeated positive feed back cycles.  Micro organisms may be exploiting this phenomenon in producing chronic inflammation and autoimmune diseases.

 

Rao’s Vicious Cycle and it’s interaction with three immunological pathways

            As is well known, any immunological reaction operates through three different path ways as shown in Fig.2.  The path way 1 is known as IgE / mast cell / mediator path way can be sub divided to reflect physiological and pathological conditions as path 1a and path 1b respectively.  It can be noticed that in all the physiological conditions histamine is liberated and together with TH2 affect the cure.  The pathological conditions of inflammation on the other hand may turn in to chronic inflammation due to the excessive generation of histamine in a cyclic manner as explained earlier by Rao’s vicious cycle.

            Fig. 2 depicts the details of physiological and pathological path ways.  The difference between the 3 path ways is in the sources of histamine and also in the intermediaries.

Evidently, the histamine at the inflammatory site together with TH2 cures the inflammation.  Thus, histamine physiologically plays a role as type of switch for TH1 or TH2.          

IgE/mast cell/mediator path way12 (Fig. 3a) depicts the physiological path way which sets TH2 type of reaction after an allergic inflammation, there by affecting cure. Fig. 3b depicts pathological path way where in the presence of local cytokines IL4, IL6, INF etc., at the inflammatory site trigger the release of excess histamine over and above that required for maintaining histamine homeostasis.  This in turn triggers IgE B cells and in a cyclic manner contributes to release of more histamine making the inflammation chronic.  This in brief is the Rao’s vicious cycle proposed to be applicable for chronic inflammatory conditions.

            The IgG, IgM/Complement/neutrophil pathway as shown in Fig. 4, includes the pathological path 2b.  Typically IgG / IgM immune complex interacts with complement, which releases C3a and C5a and bring histamine and neutrophilis into the site. The presence of IL4, IL6, IL8 etc. at the inflammatory site trigger histamine and in turn the Rao’s Vicious Cycle.  The TH2 type of reaction, although, helps in healing process in physiological (2a) inflammation through the parenchymal cells, the excess of TH2 found in pathological inflammations can cause over healing, resulting in scaring and stiffening.

In the physiological path way 3a as shown in Fig. 5, theCD8 cells kill the intracellular organisms by TH1 type of reaction, and, the TH2 type of reaction set by histamine heals

through parenchymal cells. Pathological path 3b (T lymphocyte / lymphokine pathway) directly kills the intracellular organisms by TH1 reaction through the cytokines liberated by CD8 cells. However, the TH2 cytokines liberated from IgE B cells and the associated excess histamine through Rao’s Vicious cycle contribute to the chronic nature of inflammation.  Thus, in spite of the killing of intracellular organism (TH1 action) the inflammation continues (by TH2 action which opposes TH1).  The pain13, stress, and cancer cytokines are also the same as those that cause inflammation and, so can trigger Rao’s Vicious cycle.

 

Appa Hista:

            Appa Hista refers to the proposed method of curing inflammation using anti- histamine antibodies while exploiting the fundamental phenomena of Rao’s Vicious cycle.  It is by now clear that the histamine homeostasis in the body is disturbed during inflammation.  Antigen administered in the physiological condition of inflammation reacts with IgE B cells generating the IgE and in turn through TH2 type of reactions affecting the cure.  More serious is the pathological condition leading to chronic inflammation. Rao’s vicious cycle plays a major role in generating and maintaining histamine levels above those required for histamine homeostasis.  It is interesting to note that the generation of excess histamine is found in acute and chronic inflammation.  The cure therefore is to see that antibodies are generated to combat against histamine.  In Appa Hista method, histamine conjugated normal human immunoglobulin is intramuscularly injected. It works like a vaccine. This most likely reaches all the lymph nodes and stimulates B cells to produce IgG antihistamine antibodies (also referred to as Appa Hista).  The antibodies in turn reach the inflammatory site and neutralize the histamine i.e. it breaks the Rao’s vicious cycle, either directly or enhance the histamine binding ability of the plasma.  The histamine binding/ diluting ability is as high as 30 times in normal individuals as compared to that of suffering from allergic inflammation in normal individuals.14

            Appa Hista’s main advantage is that it neither interferes in primary histamine release nor causes any immuno suppression.  During the past two decades of clinical practice, the author had cured couple of hundreds of patients of both sexes with age groups ranging from 10 to 60 years. The relief from inflammatory diseases found in most cases range from good to excellent (patent application status). The intensity of the disease is found to be reduced on the administration of the medicine along with the gradual increase in the time periods at which the medicine has to be re-administered.  This may takes 3 weeks to 3 months depending up on the intensity of symptom.  An interesting feature is that the patients felt totally comfortable during in between drug administration periods along with a general feeling of well being, which was not the case with steroids or any other drugs.

 

Side effects:

            There are no side effects observed in the Appa Hista method of cure and applications.  It is however found that the method is not very effective in the case of smokers, and alcoholics. From an economic view point the treatment is inexpensive as compared to current day methods used.  Also, the drug, which is already bio-assayed and available in the market for last 30 years can be easily procured and administered.

 

CONCLUSIONS:

            A link is observed among the inflammatory diseases and it is identified as Rao’s vicious cycle. Histamine is present in human body in levels corresponding to that required to maintain histamine homeostasis.  During inflammation, histamine is released at the- inflammatory sites as predicted by Rao’s vicious cycle. The later refers to the proliferation of TH2 type of reaction and its dominance over TH1 reaction.  In the Appa Hista method of cure, antihistamine antibodies combat the histamine at the inflammatory sites and also block TH2 type of reaction, thus indirectly helping the TH1 type of reaction. The dual effect of Appa hista antibodies can be visualized in:

1) killing the intracellular organisms through TH1 type of reaction, and,

2) neutralizing the histamine at inflammation site at the same time blocking the excess TH2 type of reaction.

Since Appa Hista directly attacks histamine where ever it is present, can cure all inflammatory diseases.

 

REFERENCES

 

1)      Espinoza, L. R. & Cuellar, M. L. Molecular Pathogenic Mechanisms of Spondyloarthropathies: (Medical Intelligence Unit). Publisher: (Springer,  Berlin, Germany), 125 pp (1995).

2)      Dr. Appa Rao Peddapalli. Use of Histamine Conjugated Normal Human Immunoglobulin for treatment of all types of pain and inflammation, Indian Patent Application: 3165/DEL/98, (1998).

3)      3) Dr. Appa Rao Peddapalli. Use of Histamine Conjugated Normal Human Immunoglobulin for treatment of all types of pain and inflammation, Indian Patent Application: 1301/DEL/2002, Dec 26th, (2002).

4)      3) Yoshii Haruo,  Fukata &  Yuriko. Immunomodulating and antiinflammatory agent. United States Patent 5,780,026  July 14, (1998).

5)      Valent, P.; et al. Variable expression of activation-linked surface antigens on human mast cells in health and disease.   Immunological Reviews, 179, 74-81 (2001).

6)      Orth,  Reid N.; Wu, Min; Holowka, David, A.; Craighead, Harold, G. & Baird, Barbara A.  mast Cell Activation on Patterned Lipid Bilayers of Subcellular Dimensions. Langmuir, 19(5),  1599-1605 (2003).

7)      Falus, Andras; Laszlo, Valeria; Darvas, Zsuzsa & Bencsath, Martha. Histamine – an early messenger in the immune system and inflammation. Central-European Journal of Immunology, 21(1), 52-54 (1996).

8)      Schneider, Elke; Rolli-Derkinderen, Malvyne; Arock, Michel & Dy, Michel.  Trends in histamine research: new functions during immune responses and hematopoiesis. Trends in Immunology, 23(5),  255-263 (2002)

9)      Coge, Francis; et al. Genomic organization and characterization of splice variants of the human histamine H3 receptor. Biochemical Journal, 355(2), 279-288 (2001).

10)  Mannaioni, P. F.; Fantozzi, R.; Giannella, E.; Masini, E. & Dep., Preclin. Pathophysiological significance of the distribution of histamine receptor sub-types:  a proposed dual role for histamine in inflammation and type I hypersensitivity reactions. Univ. Florence, Florence, Italy.  24(1-2),  26-34 (1988).

11)  Lichtenstein, L. M. & Osler, A. G. Studies on the mechanisms of hypersensitivity phenomena. ix histamine release from human leukocytes by ragweed pollen antigen. Journal of Experimental Medicine. 120, 507-30 (1964).

12)  De Rossi, Marco; Bernasconi, Pia; Baggi, Fulvio; De Waal Malefyt, Rene & Mantegazza, Renato.  Cytokines and chemokines are both expressed by human myoblasts: possible relevance for the immune pathogenesis of muscle inflammation. International Immunology, 12(9), 1329-1335 (2000).

13)  Schwarz, M.; Sunder-Plassmann R.; Cerwenka A.; Pickl, W. F. & Holter, W.Regulation of cytokine production by human T-lymphocytes in allergic immune response. Wiener Klinische Wochenschrift, General Review, 105(23), 672-6 (1993).

14)  Dickenson, A. & Besson, J.M. The Pharmacology of Pain. Handbook, Exp. Pharmacol., Publisher: (Springer,  Berlin, Germany.) 130, 479pp (1997). 

15)  Kokai Tokkyo Koho. Nippon Zoki Pharmaceutical Co. Ltd. Japan, Allergy treatment. Japanese Patent, Application: JP 78-162375  19781223,6 pp (1980).

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postheadericon Knee Arthritis

Rheumatoid arthritis of the knee

Further information: Rheumatoid arthritis

Rheumatoid arthritis is a chronic inflammatory disorder that most typically affects the small joints in your hands and feet. This form of arthritis is the most common and is found in the same areas as RA. It worsens over time and as with RA, there is no cure. RA tampers with the lining of the joints and causes swelling that is painful and can lead to joint deformity in the body. It begins by attacking the smaller joints of the body and progresses into the shoulders, elbows, hips, and knees. Most cases will see the condition affect both knees. Symptoms include joint pain, swelling, red and puffy hands, and fatigue.

Osteoarthritis of the knee

Further information: Osteoarthritis

Osteoarthritis is a joint disease that causes the cushion layer between your bones, or cartilage to wear away. It is also called degenerative joint disease. Symptoms are similar to RA and develop in the same slow manner. They include pain, tenderness in the knee, stiffness when standing or walking, loss of flexibility, and grating sensations that can be heard when the knee joint is used.

Osteoarthritis in the knee begins with the gradual deterioration of cartilage. Without the protective cartilage, the bones begin to rub together, causing pain, loss of mobility, and deformity. It affects approximately 16 million people. The majority of arthritis cases involving the knee are osteoarthritic cases.

Causes

It is not always sure why arthritis of the knee develops. Most physicians believe that it is a combination of factors that can include muscle weakness, obesity, heredity, joint injury or stress, and aging. Cartilage in the knee begins to break down and leaves the bones of the knee rubbing against each other as you walk. Persons who work in a place that applies repetitive stress on the knees are at a high risk of developing this condition. Bone deformities increase the risk for RA of the knee since the joints are already malformed and contain defective cartilage. Having gout, rheumatoid arthritis, Paget’s disease of bone or septic arthritis can increase your risk of developing osteoarthritis.

Treatment

Depending on the level of pain and damage suffered by a patient, a physician will recommend a treatment regimen that will relieve symptoms. Some of the most common recommendations include avoiding activities that make the pain worse, ice the knee for 20 to 30 minutes throughout the day to reduce inflammation, use over the counter anti-inflammatory medications, and physical therapy.

Exercises can help increase range of motion and flexibility as well as help strengthen the muscles in the leg. Physical therapy and exercise are often effective in reducing pain and improving function. Working with a physical therapist to find exercises that promote function without risking further injury is effective for most patients. Many of the exercises used can be performed while sitting in a chair or standing in place. They are performed so that additional stress or weight is not placed on the knee joint. Water exercises are highly recommended along with the use of elastic bands.

Supportive devices like knee braces can be used. In most cases, the arthritis is centered on a single side of the knee, so braces are effective in providing stability to one side. Two different forms of braces are available. A support brace provides the aid the entire knee requires, where an up-loader brace shifts the pressure away from the specific part of the knee that is experiencing the pain. Shoes or inserts that are considered to be energy absorbing are found useful for some patients as well as walking devices like a cane.

The use of oral steroids and anti-inflammatory medicines help to reduce the amount of inflammation and pain felt in the knee. If over the counter medicines like ibuprofen or naproxen are not strong enough, prescription strength medicines are used. If oral medicine and physical therapy don’t help your knee enough, your doctor may consider giving you an injection with pain medicine. Hyaluronic acid is present in the knee, but injections of it can be used to protect the joint when the acid becomes thinner and can’t do it alone. These injections can provide more pain relief than oral medications lasting from six months to a year.

Surgery is the final option but may be required to relieve symptoms. Arthroscopy is performed through tiny cuts where damaged parts of the knee can be removed. Osteotomy is performed to reshape the bones in the knee and is only performed if one side of the knee is damaged. Arthroplasty is a replacement surgery where an artificial joint is used.

Notes

^ Arthritis Causes, Symptoms, Diagnosis and Treatment Information on MedicineNet.com, Retrieved on 2010-01-22.

^ Rheumatoid Arthritis – Mayoclinic.com, Retrieved on 2010-01-22.

^ Osteoarthritis of the knee – familydoctor.org, Retrieved on 2010-01-22.

^ What is Osteoarthritis Retrieved on 2010-02-08

^ How Osteoarthritis Affects Your Knee – WebMD.com, Retrieved on 2010-01-22.

^ Osteoarthritis: Risk Factors – MayoClinic.com, Retrieved on 2010-01-22.

^ Arthritis of the Knee – American Academy of Orthopaetic Surgeons, Retrieved on 2010-01-22.

^ Osteoarthritis of the Knee: Treatment – Familydoctor.org, Retrieved on 2010-01-22.

v  d  e

Musculoskeletal disorders: Arthropathies (M00-M19, 711-719)

Arthritis

(monoarthritis/

polyarthritis)

Inflammation

(Neutrophilia)

Infectious

Septic arthritis  Tuberculosis arthritis  Reactive arthritis (indirectly)

Noninfectious

Seronegative spondyloarthropathy: Reactive arthritis  Psoriatic arthritis  Ankylosing spondylitis

Rheumatoid arthritis: Juvenile idiopathic arthritis  Adult-onset Still’s disease  Felty’s syndrome

Crystal arthropathy: Gout  Chondrocalcinosis

Noninflammatory

Osteoarthritis: Heberden’s node  Bouchard’s nodes

Other

hemorrhage (Hemarthrosis)  pain (Arthralgia)  Osteophyte  Hypermobility  villonodular synovitis (Pigmented villonodular synovitis)  Joint stiffness

joint navs: anat, non-congenital arthropathies/deformities/dorsopathies/soft tissue arthropathy/congenital, eponymous signs, proc

v  d  e

Inflammation

Acute

Plasma derived mediators

Bradykinin  complement (C3, C5a, MAC)  coagulation (Factor XII, Plasmin, Thrombin)

Cell derived mediators

preformed: Lysosome granules  vasoactive amines (Histamine, Serotonin)

synthesized on demand: cytokines (IFN-, IL-8, TNF-, IL-1)  eicosanoids (Leukotriene B4, Prostaglandins)  Nitric oxide  Kinins

Chronic

Macrophage  Epithelioid cell  Giant cell  Granuloma

Processes

Traditional: Rubor  Calor  Tumor  Dolor (pain)  Functio laesa

Modern: Acute-phase reaction/Fever  Vasodilation  Increased vascular permeability  Exudate  Leukocyte extravasation  Chemotaxis

Specific types

Nervous

CNS (Encephalitis, Myelitis)  Meningitis (Arachnoiditis)  PNS (Neuritis)  eye (Dacryoadenitis, Scleritis, Keratitis, Choroiditis, Retinitis, Chorioretinitis, Blepharitis, Conjunctivitis, Iritis, Uveitis)  ear (Otitis, Labyrinthitis, Mastoiditis)

Cardiovascular

Carditis (Endocarditis, Myocarditis, Pericarditis)  Vasculitis (Arteritis, Phlebitis, Capillaritis)

Respiratory

upper (Sinusitis, Rhinitis, Pharyngitis, Laryngitis)  lower (Tracheitis, Bronchitis, Bronchiolitis, Pneumonitis, Pleuritis)  Mediastinitis

Digestive

mouth (Stomatitis, Gingivitis, Gingivostomatitis, Glossitis, Tonsillitis, Sialadenitis/Parotitis, Cheilitis, Pulpitis, Gnathitis)  tract (Esophagitis, Gastritis, Gastroenteritis, Enteritis, Colitis, Enterocolitis, Duodenitis, Ileitis, Caecitis, Appendicitis, Proctitis)  accessory (Hepatitis, Cholangitis, Cholecystitis, Pancreatitis)  Peritonitis

Integumentary

Dermatitis (Folliculitis)  Cellulitis  Hidradenitis

Musculoskeletal

Arthritis  Dermatomyositis  soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis)

Osteochondritis: Osteitis (Spondylitis, Periostitis)  Chondritis

Urinary

Nephritis (Glomerulonephritis, Pyelonephritis)  Ureteritis  Cystitis  Urethritis

Reproductive

female: Oophoritis  Salpingitis  Endometritis  Parametritis  Cervicitis  Vaginitis  Vulvitis  Mastitis

male: Orchitis  Epididymitis  Prostatitis  Balanitis  Balanoposthitis

pregnancy/newborn: Chorioamnionitis  Omphalitis

Endocrine

Insulitis  Hypophysitis  Thyroiditis  Parathyroiditis  Adrenalitis

Lymphatic

Lymphangitis  Lymphadenitis

Categories: Aging-associated diseases | Arthritis | Inflammations | Rheumatology | Skeletal disorders

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postheadericon Reactive Arthritis

Reactive arthritis, referred to also as Reiter’s syndrome although this name is lapsing, is an arthritic condition related to infections such as Salmonella in the gastro-intestinal system and Chlamydia in the genito-urinary system. Reactive arthritis has a strong link with a human leucocyte antigen known as HLAB27 which is well known to be related to another arthritic condition called ankylosing spondylitis. This link puts both these conditions into a group classified as seronegative spondyloarthropathies. The arthritis usually occurs with infections such as urethritis or conjunctivitis but can occur also without them.

Once a person has an infection of the genitourinary system or the gastrointestinal system then the arthritis can come on around two to four weeks later, with a respiratory infection with Chlamydia also a possible causative factor. There may be no apparent preceding infection in around ten percent of patients. Many anatomical structures can be affected by the inflammation, including the mucous membrane, the eyes, the joints, the spine, the ligament-bone and tendon-bone junctions and the gastro-intestinal system. Patients with HLAB27 are fifty times more likely to develop reactive arthritis than those without it.

The arthritis can last longer and be more severe if the person has a strong history in the family or they are HLAB27 positive. Of those having an infection of the gut between one and four percent may develop a reactive arthritis, but this varies greatly even with the same biological agent responsible. It is not understood how the host body and the antigen react to cause the arthritic condition and the samples of joint fluids do not exhibit the infectious organisms. Antibodies have been isolated in the joints and it is possible an inflammatory condition mediated by the immune system is implicated in the development of this condition.

The self limiting nature of this kind of arthritis means that the condition settles down over a 3-12 month period whether the severity of the symptoms is greater or lower. The chance of the condition recurring is significant, with a higher incidence if a patient is positive for HLAB27, and a new episode is potentially triggered by infections or other agents. The arthritic process can be mild or can cause destructive and disabling changes in the joints in a small group of fifteen percent of sufferers. The usual age range for onset of this condition is between 20 and 40 years, gut infections giving a 50:50 male to female ratio and urogenital infections giving a 9 to 1 ratio.

Reactive arthritis usually comes on quickly as an acute presentation with patients presenting with tiredness, high temperature and a feeling of being unwell. Lower extremity arthritis of a few joints, arranged non symmetrically (unlike rheumatoid arthritis) is common. Heel pain from inflammation of the insertion of the Achilles tendon into the heel bone is common and low back pain is present in half of the patients. Lower limb joints involved in weight bearing are typically affected, with more severely affected patients exhibiting hands and feet symptoms. Back pain symptoms are commonly reported but examination shows few findings apart from a reduction in lumbar flexion.

Reactive arthritis treatment is determined by how difficult the arthritic symptoms are for the patient, with a mainstay of treatment being non-steroidal anti-inflammatory drugs which are taken regularly to keep up a level of anti-inflammatory action. The maintenance and restoration of muscle power, control of pain and protection of joint ranges of motion can be effected by referral to physiotherapy. Intra-articular injections with corticosteroids are a useful treatment and can give long term relief of an inflamed joint. If anti-inflammatory drugs are not effective then systemic corticosteroids can be given and while antibiotic drugs may be prescribed at times they do not affect the disease course.

Chronic and ongoing joint arthritis and poorly limited inflammatory reactions may mean a rheumatologist will prescribe drugs known as DMARDS or disease modifying anti-rheumatoid drugs. These have been tested on conditions such as rheumatoid arthritis or ankylosing spondylitis but their usefulness in reactive arthritis has not been shown. Typical examples are methotrexate and sulphasalazine. The newer biological drug treatments have been effective in some conditions but have not yet been shown to be useful in this condition.

postheadericon Seronegative Arthritis Symptoms

Seronegative arthritis ?? ?n umbrella stretch f?r various types ?f arthritis th?t h??? similar symptoms t? rheumatoid arthritis b?t ?? n?t h??? th? rheumatoid thing seminal th?t shape up ?n blood tests. Seronegative arthritis ???? tends t? h??? bonus symptoms th?t rheumatoid arthritis ???? n?t. Examples ?f th??? disorders control ankylosing spondylitis, psoriatic arthritis ?n? reactive arthritis.

Essential Symptoms

A? w?th rheumatoid arthritis, th? essential symptoms ?f seronegative arthritis control pain, inflammation ?n? strength ?n th? joints. Th?? ??n suggest itself ?n th? hips, knees, ankles, feet, toes, shoulders, elbows, wrists, hands ?r fingers. Sometimes inflammation ???? occurs ?n th? spine ?n? ?t muscle attachment points. A flareup m?? involve release one side ?f th? body.

Diagnosis

Th? specific subtype ?f seronegative arthritis ??n b? diagnosed superfluous definitively b? compelling ?nt? account bonus symptoms. Th??? control spots ?n? ?th?r skin lesions, pest sores, nail deformities, inflammatory bowel disease ?n? inflamed eyes.

Psoriatic Arthritis

Psoriatic arthritis, f?r instance, occurs ?n up t? 30 percent ?f public w?th psoriasis, according t? th? Inhabitant Psoriasis Foundation. In addition t? pain ?n? inflammation, nail deformities ??n suggest itself, counting pitting, thickening, tint ?n? wear. Public ???? m?? feel fatigued, ?n? h??? red ?n? sore tissues near th??r eyes. T? ??t ?n t? diagnosis even superfluous complicated, psoriatic arthritis ?? itself ?n umbrella shape up ?n ??? sides ?f five types ?f psoriatic arthritis.

Ankylosing Spondylitis

A further category ?f seronegative arthritis primarily affects th? spine. Th?? disorder ?? called ankylosing spondylitis, ?n? usually ?t?rt? w?th ????, recurring pain ?n th? fall back ?n? hips. Th? pain ?n? strength eventually apply up th? spine ?n? ?nt? th? neck, ?n? m?? ?? further t? ribs, shoulder blades, hips, thighs ?n? heels. Public ???? m?? feel fatigued, ?n? h??? mild fever ?n? anemia. Many public w?th th?? disorder run into bowel inflammation ?n? eye inflammation.

Reactive Arthritis

Reactive arthritis ?? ?ft?n a temporary shape up th?t ?? triggered b? a bacterial infection. Joints ?n th? knees, ankles ?n? feet ??n become inflamed ?n? swollen, ?n? th?r? ???? ??n b? inflammation ?n th? eyes ?n? urinary strip. Skin rashes, nail disintegration ?n? genital sores ??n suggest itself. Ab??t 15 t? 20 percent ?f public w?th reactive arthritis w??? eventually develop a recurring shape ?f th? disorder, according t? th? Spondylitis Friendship ?f America.

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postheadericon Reactive Arthritis

Reactive arthritis, referred to also as Reiter’s syndrome although this name is lapsing, is an arthritic condition related to infections such as Salmonella in the gastro-intestinal system and Chlamydia in the genito-urinary system. Reactive arthritis has a strong link with a human leucocyte antigen known as HLAB27 which is well known to be related to another arthritic condition called ankylosing spondylitis. This link puts both these conditions into a group classified as seronegative spondyloarthropathies. The arthritis usually occurs with infections such as urethritis or conjunctivitis but can occur also without them.

Once a person has an infection of the genitourinary system or the gastrointestinal system then the arthritis can come on around two to four weeks later, with a respiratory infection with Chlamydia also a possible causative factor. There may be no apparent preceding infection in around ten percent of patients. Many anatomical structures can be affected by the inflammation, including the mucous membrane, the eyes, the joints, the spine, the ligament-bone and tendon-bone junctions and the gastro-intestinal system. Patients with HLAB27 are fifty times more likely to develop reactive arthritis than those without it.

The arthritis can last longer and be more severe if the person has a strong history in the family or they are HLAB27 positive. Of those having an infection of the gut between one and four percent may develop a reactive arthritis, but this varies greatly even with the same biological agent responsible. It is not understood how the host body and the antigen react to cause the arthritic condition and the samples of joint fluids do not exhibit the infectious organisms. Antibodies have been isolated in the joints and it is possible an inflammatory condition mediated by the immune system is implicated in the development of this condition.

The self limiting nature of this kind of arthritis means that the condition settles down over a 3-12 month period whether the severity of the symptoms is greater or lower. The chance of the condition recurring is significant, with a higher incidence if a patient is positive for HLAB27, and a new episode is potentially triggered by infections or other agents. The arthritic process can be mild or can cause destructive and disabling changes in the joints in a small group of fifteen percent of sufferers. The usual age range for onset of this condition is between 20 and 40 years, gut infections giving a 50:50 male to female ratio and urogenital infections giving a 9 to 1 ratio.

Reactive arthritis usually comes on quickly as an acute presentation with patients presenting with tiredness, high temperature and a feeling of being unwell. Lower extremity arthritis of a few joints, arranged non symmetrically (unlike rheumatoid arthritis) is common. Heel pain from inflammation of the insertion of the Achilles tendon into the heel bone is common and low back pain is present in half of the patients. Lower limb joints involved in weight bearing are typically affected, with more severely affected patients exhibiting hands and feet symptoms. Back pain symptoms are commonly reported but examination shows few findings apart from a reduction in lumbar flexion.

Reactive arthritis treatment is determined by how difficult the arthritic symptoms are for the patient, with a mainstay of treatment being non-steroidal anti-inflammatory drugs which are taken regularly to keep up a level of anti-inflammatory action. The maintenance and restoration of muscle power, control of pain and protection of joint ranges of motion can be effected by referral to physiotherapy. Intra-articular injections with corticosteroids are a useful treatment and can give long term relief of an inflamed joint. If anti-inflammatory drugs are not effective then systemic corticosteroids can be given and while antibiotic drugs may be prescribed at times they do not affect the disease course.

Chronic and ongoing joint arthritis and poorly limited inflammatory reactions may mean a rheumatologist will prescribe drugs known as DMARDS or disease modifying anti-rheumatoid drugs. These have been tested on conditions such as rheumatoid arthritis or ankylosing spondylitis but their usefulness in reactive arthritis has not been shown. Typical examples are methotrexate and sulphasalazine. The newer biological drug treatments have been effective in some conditions but have not yet been shown to be useful in this condition.

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postheadericon Seronegative Arthritis Symptoms

Seronegative arthritis ?? ?n umbrella stretch f?r various types ?f arthritis th?t h??? similar symptoms t? rheumatoid arthritis b?t ?? n?t h??? th? rheumatoid thing seminal th?t shape up ?n blood tests. Seronegative arthritis ???? tends t? h??? bonus symptoms th?t rheumatoid arthritis ???? n?t. Examples ?f th??? disorders control ankylosing spondylitis, psoriatic arthritis ?n? reactive arthritis.

Essential Symptoms

A? w?th rheumatoid arthritis, th? essential symptoms ?f seronegative arthritis control pain, inflammation ?n? strength ?n th? joints. Th?? ??n suggest itself ?n th? hips, knees, ankles, feet, toes, shoulders, elbows, wrists, hands ?r fingers. Sometimes inflammation ???? occurs ?n th? spine ?n? ?t muscle attachment points. A flareup m?? involve release one side ?f th? body.

Diagnosis

Th? specific subtype ?f seronegative arthritis ??n b? diagnosed superfluous definitively b? compelling ?nt? account bonus symptoms. Th??? control spots ?n? ?th?r skin lesions, pest sores, nail deformities, inflammatory bowel disease ?n? inflamed eyes.

Psoriatic Arthritis

Psoriatic arthritis, f?r instance, occurs ?n up t? 30 percent ?f public w?th psoriasis, according t? th? Inhabitant Psoriasis Foundation. In addition t? pain ?n? inflammation, nail deformities ??n suggest itself, counting pitting, thickening, tint ?n? wear. Public ???? m?? feel fatigued, ?n? h??? red ?n? sore tissues near th??r eyes. T? ??t ?n t? diagnosis even superfluous complicated, psoriatic arthritis ?? itself ?n umbrella shape up ?n ??? sides ?f five types ?f psoriatic arthritis.

Ankylosing Spondylitis

A further category ?f seronegative arthritis primarily affects th? spine. Th?? disorder ?? called ankylosing spondylitis, ?n? usually ?t?rt? w?th ????, recurring pain ?n th? fall back ?n? hips. Th? pain ?n? strength eventually apply up th? spine ?n? ?nt? th? neck, ?n? m?? ?? further t? ribs, shoulder blades, hips, thighs ?n? heels. Public ???? m?? feel fatigued, ?n? h??? mild fever ?n? anemia. Many public w?th th?? disorder run into bowel inflammation ?n? eye inflammation.

Reactive Arthritis

Reactive arthritis ?? ?ft?n a temporary shape up th?t ?? triggered b? a bacterial infection. Joints ?n th? knees, ankles ?n? feet ??n become inflamed ?n? swollen, ?n? th?r? ???? ??n b? inflammation ?n th? eyes ?n? urinary strip. Skin rashes, nail disintegration ?n? genital sores ??n suggest itself. Ab??t 15 t? 20 percent ?f public w?th reactive arthritis w??? eventually develop a recurring shape ?f th? disorder, according t? th? Spondylitis Friendship ?f America.

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