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बुधवार, 5 अक्तूबर 2011

Rheumatoid Arthritis/ Rakthavatha of Charaka


FREQUENCY
Approximately 12 to 15 million people in India are suffering from RA
70 to 90 million suffering world wide
Female to male ratio is 4:1
Age of onset is usually 25 to 50 years, peak during 4th and 5th decade
Juvenile arthritis, named when occurs below the age of 16, 3 phases- polyarticular, pauciarticular, and systemic.

CAUSES
Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology involving primarily the synovial membrane and articular structures of multiple joint.
Associated factors may include
  1. Genetic predisposition
  2. Female sex
  3. Psychological stress
  4. Immune response
  5. Hormone interaction
  6. Viral infection

PATHOPHYSIOLOGY
In short
Patho physiology of RA is not well understood
Factors associated with RA include possibility of
  1. Infectious triggers
  2. Genetic predisposition
  3. Autoimmune response
The disease course may be short and limited or progressive and severe

SIGHNS AND SYMPTOMS
Pain & morning stiffness in the smaller joints of the hands & feet.
Joints of wrist, elbows, shoulders, knees & ankles are also affected.
Symmetrical involvement of the joints.        
Patient feels tired & unwell.
Pain & stiffness are worse in morning & patient gets little relief with gentle activity.
Disturbed sleep.
Joints will be warm & tender with swelling.
Deformities & rheumatic nodules develop as the disease progresses.
Other extra articular symptoms may develop.

DIAGNOSTIC CRITERIAS
Morning stiffness for more than 1 hour.
Arthritis of 3 or more joints with tenderness & symmetric involvement.
Arthritis of hand joints & wrists
Above symptoms for 6 weeks or more.
Subcutaneous nodules & deformities.
Positive serum RA factor.
Radiographic evidence of RA.
Presence of four or more above criterias – confirms the diagnosis of RA.

INVESTIGATIONS
HB, TOTAL COUNT, DIFFERENTIAL COUNT, ESR.
CCP ANTIBODIES
RHEUMATOID FACTOR
C REACTIVE PROTIEN
X RAY OF AFFECTED JOINTS
IMMUNOGLOBULINS
PLATELET COUNT

DIFFERENTIAL DIAGNOSIS
Systemic Lupus Erythematosus
Rheumatic fever
Gout and Pseudogout
Inflammatory Bowel Disease
Polymyositis
Psoriasis
Carpal Tunnel Syndrome
Sarcoidosis
Sjogren Syndrome
Amyloidosis
Osteoarthritis (erosive)
Tendonitis
Tenosynovitis
Polyarteritis nodosa
Viral arthritis (eg, rubella, hepatitis B, parvovirus)
Scleroderma
Paraneoplastic syndromes
Multicentric reticulohistiocytosis
Cauda Equina Syndrome
Costochondritis
Polymyalgia Rheumatica

These are the main there are still more

TREATMENT IN MODERN MEDICINE
NSAID’S
Ibuprofen
Indomethacin etc
Disadvantage: Risk of gastritis, internal bleeding, nephrotic syndrome, glmerulo nephritis by short term or long term use.
Cox-2 inhibitors
Celecoxib: action similer to NSAID’s but with less adverse affects.
GOLD COMPOUNDS
Auranofin.
Disadvantage: Dermatitis, stomatitis, protenuria, cytopenia. Exacerbation after due course.
ANTI MALARIAL AGENTS
Comparitively safe but action seen is not the same in all, very slow, majority of the patients not benefited.
DISEASE MODIFYING AGENTS
Methotrexate: A well known, said to be the most effective immune modifying agent , widely used in present practice.
Disadvantage: MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems. So should be used with caution. May become fatal if co administered with NSAID’s
Sulfasalazine: Another immune modifying agent usually co administered with methotrexate.
Disadvantage: weak action, but toxic.
IMMUNOSUPPRESSANT AGENTS
TNF alfa inhibitors:
Eg: Infliximab, Etanercept
T-cell inhibitor
Abatacept
Disadvantage: Although these medicines improves the clinical symptoms, and stops the progression, the major disadvantage is serious infection and malignancies.
CORTICO STEROIDS
Prednisolone
Disadvantage: Reduces the symptoms, but not the damage and progression.Risk of serious side affects makes it very difficult to administer for long term and also this will not check the progression.

OVERALL DISADVANTAGE WITH MODERN MEDICINES
All the medicines mentioned do not give definite improvement. Exacerbation of the symptoms during the course of treatment is very common, and the same medicine may not work further.
Adverse affects of DMRD drugs like Methotrexate which is hepatotoxic, neurotoxic and nephrotoxic many times forced to stop medication du to adverse reactioins.
Immuno modulators like TNF alfa inhibitors, T cell inhibitors etc almost always ends with severe infection, and sometimes malignancy.

IgM, IgG, IgA, IgE RF ISOTYPES

n      Role of genetic factors in the regulation of RF isotype level production
n      HLA-DR3 & DR4 antigen was associated with low IgA RF
n      HLA-DR1 & DR2 antigen was associated with high IgA RF, IgM RF, AND IgE RF
n      IgM RF was positive in almost all sero positive patients and most of seronegative.
n      IgA RF was negative in sero negative patients but was mostly positive in other groups .
n      Patients with negative IgM and IgA RF had incactive or recent RA.
n      Anti nucleic antibodies with the highest values were significantly associated with high levels of IgM and IgA RF.
n      Almost all patents with extra articular features had higher level positive IgA, IgM, IgE RF when compared with RA without extra articular symptoms
n      Most of the researchers believe that IgA RF is associated with RA with poor prognosis and systemic symptoms.
n      IgE RF is associated with poor prognosis but without extra articular involvement.

POSSIBLE VARIETIES OF RA WHICH MAY HELP IN AYURVEDIC TREATMENT
n      IgG RF
n      IgM RF
n      IgA RF
n      IgE RF
n      COMBINED ISOTOPES (IgA & IgG etc.)
n      SERO POSITIVE
n      SERO NEGATIVE
n      RA WITH HIGH ESR WITH SEVERE SYMTPOMS
n      RA WITH CONSTANT LOW ESR WITH SEVERE SYMPTOMS
n      RA WITH EXTRA ARTICULAR SYMPTOMS
n      RA WITHOUT EXTRA ARTICULAR SYMPTOMS
n      RA WITH ORGAN INVOLVEMENT (ENDOCARDITIS,NEPHRITIS,VASCULITIS etc)
n      IgG, M, A, OR E DOMINANT IMMUNOGLOBULINS
n      OR RELATION BETWEEN ANY OF THE ABOVE GROUPS.
n      ANA POSITIVE(LOW TITRE) RA GROUP
n      HLA DR 1
n      HLA DR 2
n      HLA DR 3
n      HLA DR 4
We have filtered these to 16 varieties to consider the treatment. Right now, no facility to do Ig RF tests in near by place.

RA IN AYURVEDA- RAKTHAVATHA AND AMAVATHA
n      VATHARAKTHA & AMAVATHA are the two diseases where we see many similarities with the symptomatology.
n      Amavatha is a disease mentioned only in laghu thrayees that is after the 7th century, not mentioned in the previous texts.
n      Vatha raktha is the only disease mentioned in Brihath thrayees that can be co related with RA.

VATHARAKTHA- DIFFERENCE OF OPENION AMONG SCHOLARS
n      It seems that explanation regarding vatharaktha in Charaka and Sushrutha school of thought is different.
n      Lot of difference is there in the symptomatology.
n      Charaka mentions a joint condition whereas Sushrutha explains Vatharaktha briefly, but he has not given importance to the involvement of multiple joints nowhere mentioned the involvement of joint, but explains symptoms related with skin lesion, which is painful, reddish, with swelling and burning sensation or whitish with itching. But the main site of lesion is mainly feet, but sometimes hands, and symptom may spread to whole body as poisonous rat bite.
n      While explaining the symptoms he says that there may be severe tenderness at the site of lesion or sometimes numbness.
n      Sushrutha while explaining incurable vathashonitha, says that, if the lesion spreads up to knee (from foot), and ulcerates with secretion of serum, blood and pus & in case of muscle wasting & in a debilitated person,it is incurable. So here he clearly mentions ulceration in the leg, from foot up to knee as a complication and also incurable.
  
GAMBHIRA and UTHANA Vatharaktha are not two types according to Sushrutha
n      Sushrutha says that gambhira and Uthana are not two types of vatharaktha, but two stages of disease. This may be because Sushrutha was explaining skin condition with regards to ulcer and its stage as superficial and deep. Charakas two types depending upon the severity of illness as seen in RA.
n      So Sushruthas explanation may not be related with RA, or he may not have given much importance to vathashonitha as his main subject was surgery.
n      Hence explanation of Sushrutha holds good for Gout, Pseudogout, Peripheral vascular obstruction,ischemic ulcers,  venous ulcers etc.
n      Hence here we consider Vatharaktha of charaka as a co relative study to RA and also AMAVATHA.

WHY VATHARAKTHA IS RA?

THASYA STHANAM KARAU PADAVANGULYAHA SARVASANDHAYAHA.
HASTHAPADE THU MOOLAM- DEHE VIDHAVATHI. Charaka samhitha chi. Sthana.
n      Leading symptoms seen in sandhis, mainly phalangeal joints and toes, and then multiple joints.
VATHARAKTHA- CLINICAL FEATURES
n      Multiple joint pain
n      Pricking pain
n      Tenderness
n      Reccurent exacerbation and remission
n      Malaise
n      Formation of nodules
n      Skin rashes, excessive or no sweating, tingling and itching sensation over joints.
n      Joint deformities, stiffness, rigidity
n      In gambhira vatharaktha, pain is severe and paka usually occurs.
n      Almost all the features of RA is explained except morning stiffness and symmetrical involvement, which is also a diagnostic criteria to consider RA.
n      Extra articular symptoms like necrotic ulcers(paka) as seen in vasculitis, mandalothpatti (butterfly rash in sle), visarpa (skin lesions with bullous ulcers, necrotic or gangrenous ulcers with systemic symptoms)
n      So considering all the criterias, RA comes under vatharaktha of Charaka and all differential diagnosis of RA should also be considered under vatharaktha.

AMAVATHA FEATURES
n      Bodyache, anorexia, malaise, heavyness, fever, lightness of the body are the common features.
n      Paka is not the symptom of amavatha (apakaha)
n      Multiple joint pain
n      Excessive urination
n      Abd distension etc are the other features.

Amavatha is mild and mild to moderate RA (and also fibromyalgia)
n      In amavatha extra articular symptoms with systemic involvemnt is not explained as in vatharaktha
n      But grahani (?enteric arthritis), abdominal pain, vomitting is said as upadrava
n      Amavatha with involvement of almost all the joints, swelling, and tridosha are considered as difficult to cure. With single dosha as sadhya, and two dosha as yapya.
n      So there is no asadhya amavatha explained in the text as in vatharaktha, vatharaktha with tridosha involvement and upadravas are asadhya.


RA AND Ukkinadkas Ayurveda
n      In our hospital we have treated more than 2800 cases of RA since last 13 years, and started keen observation since 8 years. But detailed documentation was not done. 90% of the observation is in OP level, and few of the patients might have belonged to Ankylosing spondylitis and such other collagen disorders.
For the better management we have classified RA under 3 catagories.
n      MILD (laghu) RA
n      MODERATE (madhyama) RA
n      SEVERE (theevra)RA

WHAT IS MILD RA?
n      The symptoms are similar as explained before, but the deformity of joints will not be seen even after a very lengthy course of the disease. And response to the Ayurvedic treatment is very fast, like 1 to 3 weeks. The symptoms will be reduced to ¾ th with in 1 or 3 weeks.  (? NEGATIVE IgA & IgM RF TYPE OF RA)

WHAT IS MODERATE RA?
n      In this condition also the symptoms are similar as explained earlier, but the severity of pain & other symptoms will be severe. In this case also there will not be any deformities even after a very lengthy course, but the response to the Ayurvedic treatment is slow when compared with mild RA. (? Ig E RF TYPE OF RA)
WHAT IS SEVERE RA?
n      In this condition the signs & symptoms are very severe & most of the times deformity is seen within 6 months of onset of symptoms & the sufferings (pain & systemic manifestations) are more in this variety of RA. The response to Ayurvedic treatment is poor & slow. (? IgA RF TYPE OF RA)

HOW WE TREAT THE PATIENTS?
n      In our Hospital, mild & moderate RA cases are treated as out patients.
    In mild & moderate cases we prescribe-Kashaya powder or Liquid kashayas, Herbal & Herbo-mineral tablets internally, and in moderate cases we add lehyas and herbal powder according to the need. For external application we use Lepa powders or oils  according to the need.         
IN SEVERE & CHRONIC CASES
n      In these types of patients we hospitalise the patient for three weeks in our hospital for the panchakarma treatments, which gives very good result particular group of the severe and severe to moderate cases of RA.
n      Internally we prescribe-Kashaya powder or concentrated Liquid kashayas, Herbal & Herbo-mineral tablets, lehyas and herbal powder according to the need. For external application we use Lepa powders or oils according to the need.
RESULTS OF TREATMENT
MILD RA-
n      60% of RA patients visiting our hospital comes under this group
n      Shamanoushadhis & patient education
n      Short course, multi drug combination is preferred, low dosage is usually sufficient.
n      Result is seen within 3 weeks in almost all cases (90-100%).
n      Course of the treatment usually varies from 3 months up to 1 year.

MODERATE RA           
n      25% of the patients visiting our hospital comes under this group
n      Shamanoushadhi, preferably combinations with potent medicines like rasna panchaka , in higher dose, but not multi drug combinations like maharasnadi.
n      In moderate to severe cases panchakarma is preferred.
n      Good result was seen within 1.5 to 4 months in 60-80% of the patients.
n      Course of the treatment usually varies from 6 months up to 2 years or more.

SEVERE RA
15% of total RA cases visiting our hospital come under this group.
n      Very difficult to treat.
n      As deformities occur very fast, risk of systemic involvement, organ damage, and delayed action makes the treatment much difficult.
n      But still with the shamanoushadhis we get very good result in about 15 to 20 % of severe RA and moderate result in other 20% of cases. But rest of the severe RA patients develop joint deformities very fast and in such patients we have tried with the combination of shamanoushadhis and panchakarma, the response was very good and many patients who had no response earlier started improving, so now a days in severe RA we start with panchakarma treatment and the overall result raised up to 40%.
n      In rest of the severe RA patients prognosis was poor with Ayurvedic medicines alone. But integrated approach was beneficial in about another 30% of the patient
n      Course of the treatment is 2 to 5 years, may extend up to life time also in this group.

SEVERE RA & INTEGRATED APPROACH WITH DMRD
n      Since last 2 years in severe RA trying with integrated approach with DMRD(under rheumatologists prescription), presently we have such many patients under treatment, symptomatic improvement is excellent, but complete withdrawal of modern medicine is not possible in most of the cases because of fear of aggravation. But we noted remarkable improvement with the symptoms, HB and ESR in all cases after starting Ayurvedic medicines.
n      In a female patient aged 28 years, we have successfully reduced the dose of DMRD drugs to 100% with very good result. She was taking TNF alfa inhibitor and suffered from TB. So switched over to other mild DMRD, her symptoms aggravated, then she approached us, treated initially with panchakarma followed by shamanaushadhis for next two years. Now she is working in London without any symptoms and medicines. Another important thing is she had deformity in left elbow, the progression could be stopped and she is devoid of any symptoms of RA now except for the damage which already happened

OTHER INTEGRATED APPROACH
n      In many cases of severe RA with unsatisfactory result, we have tried our medicines along with NSAID’s (Indomethacin 25 mg, 1 OD or BD),.
n      We have observed positive result in many cases after a very long course of treatment, in few cases we could stop the NSAID after long time.
n      Some patients had intermittent exacerbation and required NSAID’s in between.

WHY AYURVEDA IS A SUPERIOR TREATMETN IN MILD AND MODERATE RA?
As per our observation over all –by Ayurvedic management we can control 60% of RA cases very easily with simple treatments, other 25% of patients with some long duration. But another 15% of the patients are the most unfortunate patients with greater difficulties & still we can control the disease in 40% of the severe RA cases.
NEED OF A DEFINITE CURATIVE REMEDY
None of the system gives or claims cure or standardised treatment for RA.
Ayurvedic treatment many times proved to be a superior treatment. But evidence based study in terms of both Ayurveda and modern parameters in a vast group of patient are necessary to assess the effectiveness and safety of the treatment.    

CONCLUSION
n      In modern medicine there is no remedy for mild, mild to moderate and moderate types of RA. Other than NSAID’s, no other medicines are advisable in this stage, none of the medicines reverse the process of auto immunity, but just blocks the chain of auto immunity as well as normal immunity, so it’s systemic adverse affect restricts the use at this stage.(Now a days Rheumatologists suggest use of immunosuppressive from beginning!!)
n      If not treated some mild to moderate & moderate RA may turn in to moderate or moderate to severe RA in due course.
n      So Ayurveda is a treatment of choice for those with mild and mild to moderate and moderate RA.
n      In moderate to severe and severe cases, the main disadvantage of ayurveda.treatment is lack of effective pain killer, controlling  the pain is very important to improve the patients work efficiency.
n      In severe RA- controlling the fast progressive nature and early deformity as early as possible is a challenge in getting good result.
n      Getting result in 30 to 40% of severe RA is really not bad.
n      But in many patients the trial & error method of drug selection & delayed action makes it difficult to treat severe RA cases as the deformity is fast.
n       So by considering the various gene isotopes and other factors, we can try to make the 40% success rate of severe RA to even more. By administering the medicine in a vast group of RA patients, we can study the action of different groups of medicine in patients with different groups of gene isotopes and other factors.
n      Hopefully this may give us some guide to use specific group of medicine in particular type of RA to achieve fast and accurate result in large number of RA patients.


Jayagovinda Ukkinadka
http://www.facebook.com/profile.php?id=1812422041





3 टिप्‍पणियां:

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