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Send your queries and suggestions to:

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CONTACT


Dr.G.Madhu (patron)

Ph:+919447787255, email: dr_madhuin@yahoo.com

Dr.Abhilash.M (chief advisor)

Ph:+919446072887, email: abhildr@yahoo.co.in

Dr.Nithin Dev.S (Editor in charge)

Ph:+919446541238, email: devnithin@rediffmail.com

Dr.Sankaranarayanan.J (Editor in charge)

Ph:+919446052366, email drsankaranarayanan@gmail.com

What Homoeopathy can offer to AIDS ?

Homoeopathy uses an individualistic and holistic approach towards the sick individuals treats them at the physical, mental,and emotional levels by balancing their constitution. Same medicine may not be indicated in two patients with the same diagnosis as homoeopathy is based on individualization. 

HIV patients are more likely to get viral infection than usual.Even though there are no homoeopathic anti-viral agents, even correctly prescribed homoeopathic medicine has the potential of strengthening person’s own immune and defense system in a way that helps to fight the viral infection.So by using the homoeopathic medicine the patient can be made comparatively less susceptible to the day –to-day infections. since it is free from side effects it can be used as an adjunct with the allopathic treatment. Medical community must give more attention and research toward ways to enhance immune response, rather than ways to inhibit viral replication.
 
Homoeopathy medicine can provide positive results for people who are HIV positive, for those with early onset of AIDS, and for those with nonextreme cases of AIDS.It is also seen that a specific homoeopathic medicine can delay the onset of AIDS in HIV positive persons, delay the process of depletion of CD4 cells in such patients, increase in the T4 helper cells and a marked weight gain among AIDS patients.

Contribution of Central council for research in Homoeopathy(CCRH)New Delhi, India

A pilot study undertaken at its regional research institute Mumbai(1989-1991) showed homoeopathic medicines were effective in managing intercurrent illness and other clinical events related to HIV

Later, study on the same center (1995-1197) showed that an increase in CD4 cell count in the medicine group. These favourable results made the council to carry out a multicentric clinical trial in HIV infection at its institutes. It was observed that Homoeopathy can be safely used for delaying or slowing down the progression of infection in people who are not covered by anti retroviral therapy.

Council also undertook collaborative study with the university of California and Los angels entitled ‘AIDS prevention with traditional system of medicine’

A follow up study in 2005 by the council collaboration with UCLA (University of California, Los Angeles) entitled ‘Delivery of model HIV prevention and health promotion programmes in India by homoeopathivc physician’ in India and abroad.

Further reading

Cyclosporin homoeopathically

Alternative therapies for HIV treatment

Homeopathy in HIV infection: a trial report of double-blind placebo controlled study

OUR FAVOURITE POSTS

- Our Master and The Hahnemmanian Oath

-Excerpts from the scientific seminar of cure 2008 ( part 1)

-New way assesment of long term Glucose control.

-Vitiligo.... Is it an autoimmune disease?

-Summer ailments

-Blood groups You Can Receive

- Cancer UPDATES.....

-Over view of Road traffic accidents and its first aid

-Anti-cold pills recipe for stroke

-How to minimize cellphone radiation exposure

-What Homoeopathy can offer to AIDS ?

-Why waist to hip ratio is a better indicator than body mass index?

-Essentials of Endocrinology -part 1 and part2

Emerging risk factors of cardiovascular diseases

Most important indicators for cardiac risks are your personal health history. Age, hereditary factors, weight, cigarette smoking, blood pressure, and diabetes. Certain other factors like High-sensitivity C-reactive protein (hs-CRP) Homocysteine, Lipoprotein A Lp(a) and Fibrinogen also have some role  in predicting your cardiac risks.

High-sensitivity C-reactive protein (hs-CRP)   ( This test is different from the regular CRP test, which detects elevated levels of CRP in people with infections and inflammatory diseases. High levels of hs-CRP consistently predict recurrent coronary events in patients with unstable angina and acute myocardial infarction. High normal levels of hs-CRP in otherwise healthy individuals have been found to be predictive of the future risk of heart attack, stroke, sudden cardiac death, and peripheral arterial disease, even when lipid levels are within acceptable ranges. Several groups have recommended that this test be used in people with moderate risk of heart attack over the next 10 years. If hs-CRP is between 1.0 and 3.0 mg/L, a person has an average risk. If hs-CRP is higher than 3.0 mg/L, a person is at high risk.

Homocysteine:It is an amino acid that is produced in the human body. Homocysteine is normally changed into other amino acids for the use by the body. Dietery deficiency of ,folic acid,vitamin B6 and B12 associated with high levels of Haemocystein.To reduce haemocystein level ,you  require foods  rich in folic acid,vitaminB6 &B12.Other possible causes of a high homocysteine levels include low levels of thyroid hormone, kidney disease, psoriasis,some medicines or the condition runs in your family.Homocysteine may be requested as part of a cardiac risk assessment, depending on your age and other risk factors. It may also be used following a heart attack or stroke to determine treatment. Evidence suggests that measurement of homocysteine may be an even better indicator of  having a heart attack or stroke than other tests, such as cholesterol and the lipid profile.

Lipoprotein A (Lp(a): Lp(a) is a lipoprotein consisting of an LDL molecule with another protein (Apolipoprotein (a)) attached to it. Since the level of Lp(a) appears to be genetically determined and not easily altered,Lp(a) does not respond to typical strategies to lower LDL such as diet, exercise, or most lipid-lowering drugs. Studies have shown that Lipoprotein(a)act as a risk predictor for cardiac mortality in patients with acute coronary syndrome

Fibrinogen: It is circulating glycoprotein involved in final steps of coagulation,other actions include vasoconstriction at sites of vascular injury,stimulation of platelet aggregation,Influence on blood viscosity It is an acute phase reactant, increasing up to 4-fold after infectious or inflammatory stimuli,levels also increased by cigarette smoking diabetes, hypertension, obesity,sedentary lifestyle.Levels lowered with fibrates and niacin

Besides this, Certain studies reveled that an increased serum uric acid levels were independently and significantly associated with the risk of cardiovascular mortality.Elevated levels of serum uric acid level increases the risk of heart attack.Support has been given to the concept of a bacterial infection component of heart disease. The organisms chlamidia pneumonia and cytomegalovirus  both increase CRP and are associated with increased heart disease risk. 

ANNUAL CONFERENCE AND INAUGURATION OF BLOG OF IHMA KARUNAGAPPALLY

The annual conference of Indian homoeopathic medical association , karunagappally chapter was held on march 15th at town club hall. A continuing medical education class was also conducted as part of it. The class was on Repertory of mind rubrics by Dr.Narayana Prasad, pg scholar of ghmct.the class was very infotaining. The election of new office bearers for the years 2009 - 2011 was also held. The name and contact details of the newly elected office bearers are posted separately on the blog. The blog of karunagappally chapter was officially inaugurated by Dr.G.Madhu of our chapter.

IHMA KARUNAGAPALLY CHAPTER OFFICE BEARERS 2009-2011

PRESIDENT

Dr.Nithin dev.S

krishna vihar

pada south 

karunagappally

ph:04762621238,9446541238

SECRETARY

Dr.Abhilash.M

abhilash sadanam

chavara bridge po

kollam-691583

ph:04762680737,9446072887

VICE PRESIDENT

Dr.Rosaline Ninan

karunya homoeo clinic

victory building 

karunagappally po

kollam-690518

JOINT SECRETARY

Dr.Indumol

tharayil

putenthura po

kollam

TREASURER

Dr.Jyothylekshmy.M.G

jyothy nivas

south mynagappally

mynagappally po

kollam-690519

S.W.C MEMBER

Dr.Sankaranarayanan.J

kasuthubham

thazhava po

kollam-690523

ph:04762662366,9446052366

EXECUTIVE MEMBERS

Dr.Biju

anaswara

kakkakunnu po

kumaranchira 

kollam-690522

ph:04762830401,9447025648

Dr.G.Madhu

vellengattu soubhagya

adinadu north pokarunagappally 

kollam-690542

ph:07462897255,9447787255

Dr.Sreedevi bose.S.K

mullapallil

amrithapuri po

karunagappally

kollam

Dr.Dhanya Raj

sankar vilasam

koivila po

kollam

Excerpts from the scientific seminar of cure 2008 ( part 1)

Rheumatic Fever

Definition

•Diffuse non suppurative  inflammatory disease of connective tissue as a sequalae to Group A beta hemolytic streptococcal infection of the throat by rheumatogenic strains, primarily involving heart, blood vessels, joints, subcut. tissue and CNS

Magnitude of Pattern

•Common cause of CV morbidity and mortality in underdeveloped and developing countries

•Less in developed world

Prevalence of RHD in school children

•USA                          :           0.6 / 1000

•JAPAN                      :           0.7 / 1000

•ALGERIA                :           15 / 1000 ( WHO 1970)

•INDIA                      :           6 – 11 / 1000 (WHO 1970)

                                                6 / 1000 (5 CITIES – 1 Cm²)

 

Aetiopathogenesis

Incompletely understood

•Non suppurative sequelea to  ‘GAS’

•Repeated infection important

•Genetic predisposition ?

•Autoimmunity – Antigenic mimicry between st.cell wall component and human myocardium, valvular glycoprotein etc.

•Delayed immune response to infection with group.A beta hemolytic streptococci.

•After a latent period of 1-3 weeks, antibody induced immunological damage  occur to heart valves, joints, subcutaneous tissue & basal ganglia of brain 

Determinants

•Severity of throat infection

–Severe exudative infection - upto 3%

–Mild sporadic – 0.5 to 1%

•Immune response (ASO) – 1 to 5%

•GAS persisting in throat

•Previous RF : many times

•Established RHD – very high

–Recurrence rate –  50% - 1^st year

                                    10% after 5 years 

Pathologic Lesions

•Fibrinoid degeneration of connective tissue,inflammatory edema, inflammatory cell infiltration &  proliferation of specific cells resulting in formation of  Aschoff nodules, resulting in

                        -Pancarditis in the heart

                        -Arthritis in the joints

                        -Aschoff nodules in the subcutaneous tissue

                        -Basal gangliar lesions resulting in chorea 

•Rheumatic fever licks the joint & bites the heart 

Incubation period

•1 to 5 weeks

•Shortest for Arthritis

•Longest for Chorea 

Clinical features

Commonest age – 5- 15 years

Arthritis

•Migratory polyarthritis

•Mainly - major joints, no residual deformity

•Usually mild in young children esp. <>

•Prominent in older children and adolescents

•Occur upto 30%, more in girls

•May appear even 6 m after the attack of RF

•Clumsiness, deterioration of handwriting, emotional lability or grimacing of face

•Clinical signs- pronator sign, jack in the box sign, milking sign of hands

•Occur in 2 %

•Painless, pea-sized, palpable nodules:- 0.5 - 2 cm, mainly over extensor surfaces of  

  joints, spine, scapulae & scalp

•Typically appear > 3 wk after the onset

•Always associated with severe carditis

•Rarely seen in our population -.5 to 2%

•Transient, serpiginous, non-itchy, pale center with red irregular margin, mainly trunks/ limbs

•Often associated with carditis

Carditis - Pancarditis

Endocarditis – Valvulitis, Mitral & /or aortic

•Significant murmur – MR, AR, Carey Coombs

Myocarditis

 Cardiomegaly–Clinical, X-Ray CCF, Prolonged PR, relative Tachycardia, Soft S₁, S₃

Pericarditis

•Pericardial rub  ± effusion 

Diagnosis of RF

•No single symptom

•No single sign

•No single lab test 

Revised Jones Criteria for Guidance in Diagnosis

•1994 – by Dr. T. Duckett Jones

•Modified by AHA in 1956, 1965, 1982, 1992

•1987 – WHO study group accepted 1982 AHA criteria

Revised Jones Criteria, AHA 1992

Major:

            Carditis

            Arthritis

            Chorea

            Erythema marginatum

            Subcutaneous nodules

Minor:

            Clinical:    Arthralgia

                                  Fever 

            Lab:   ­ level of acute phase reactants –ESR & C-reactive protein

                          Prolonged PR interval 

Essential criteria:

            Evidence of antecedent group A Streptococcal infection

 

Diagnosis of rheumatic fever highly probable

If

Two major criteria      

or

One major & two minor criteria

With

Essential criteria satisfied

Relaxation of Criteria

•Chorea as sole manifestation (other causes excluded)

•Insidious onset / Late onset carditis

•Established RHD

–One major criteria

–Fever with arthralgia + increased acute phase reactants

If evidence of recent GAS infection present

Acute Carditis in Chronic RHD often difficult

•New murmur

•Sudden increase in heart size

•Recent onset CHF

•Pericardial rub

•Erythema marginatum / Subcutaneous nodules

            Previous carditis – recurrence of RF ® Carditis almost always present

Supportive evidence of Streptococcal infection

•ASO + others

•Throat culture – positive

•Recent scarlet fever

•History of sore throat – commonest viral

 

Laboratory Findings

•High ESR, Elevated C-reactive protein

•Anemia, leucocytosis

•ECG - prolonged PR interval, non specific ST-T changes  rarely heart blocks

•2D Echo cardiography - valve edema, mitral regurgitation, LA & LV dilatation, decreased contractility, pericardial effusion,

Streptococcal antibody tests

ASO - most commonly used

•> 200 IU  suggestive, rising titre in 2 to 4 wks

•Peaks in 4to 6  wks , remain high for 4 to 6 wks and comes down

•Sensitivity- 80%

•Specificity low – skin infection, other strep. Inf.

Others

–Antistreptokinase, Antihyaluronidase

–Anti DNAse, Antistreptozyme(most sensitive)

Throat Culture

•Positive in minority (latency, antibiotic Use)

•About 20 % school children – carrier state

 

Differential Diagnosis

•Rheumatoid Arthritis

•SLE

•Infective Endocarditis

•Serum sickness

•Gonococcal Arthritis

•Tuberculosis

•Viral myopericarditis

•Leukaemias

Overdiagnosis - Problems

•Trauma + anxiety – parent + children

•Unnecessary prophylaxis – risk

•Missing another disease

 

Under Diagnosis

No prophylaxis

Risk of reactivation

Natural History of RF

•Period of activity 

                        75%          - 6 weeks

                        90%          - 12 weeks

                        < style="mso-spacerun:yes">     - upto 6 months (Chronic RF) 

•Arthritis

                        > 12 years – 80%

                        3 to 6 years – 50% 

•Carditis

                        <>

                        14 to 17 years – 30%

Natural History – RF with Carditis

•Initial attack, no carditis – excellent prognosis

•Initial attack, mild carditis – 70% normal heart after 10 years

•Initial attack, severe carditis – 40% normal heart at 10 years