Ulcerative Colitis and New Possible Treatments

Ulcerative colitis is a disease that causes inflammation and sores, called ulcers, in the lining of the rectum and colon. Ulcers form where inflammation has killed the cells that usually line the colon, then bleed and produce pus. Inflammation in the colon also causes the colon to empty frequently, causing diarrhea.
When the inflammation occurs in the rectum and lower part of the colon it is called ulcerative proctitis. If the entire colon is affected it is called pancolitis. If only the left side of the colon is affected it is called limited or distal colitis.
Ulcerative colitis is an inflammatory bowel disease (IBD), the general name for diseases that cause inflammation in the small intestine and colon. It can be difficult to diagnose because its symptoms are similar to other intestinal disorders and to another type of IBD called Crohn’s disease. Crohn’s disease differs because it causes inflammation deeper within the intestinal wall and can occur in other parts of the digestive system including the small intestine, mouth, esophagus, and stomach.
Ulcerative colitis can occur in people of any age, but it usually starts between the ages of 15 and 30, and less frequently between 50 and 70 years of age. It affects men and women equally and appears to run in families, with reports of up to 20 percent of people with ulcerative colitis having a family member or relative with ulcerative colitis or Crohn’s disease. A higher incidence of ulcerative colitis is seen in Whites and people of Jewish



Symptoms of Ulcerative Colitis ?



The most common symptoms of ulcerative colitis are abdominal pain and bloody diarrhea. Patients also may experience
• anemia
• fatigue
• weight loss
• loss of appetite
• rectal bleeding
• loss of body fluids and nutrients
• skin lesions
• joint pain
• growth failure (specifically in children)
About half of the people diagnosed with ulcerative colitis have mild symptoms. Others suffer frequent fevers, bloody diarrhea, nausea, and severe abdominal cramps. Ulcerative colitis may also cause problems such as arthritis, inflammation of the eye, liver disease, and osteoporosis. It is not known why these problems occur outside the colon. Scientists think these complications may be the result of inflammation triggered by the immune system. Some of these problems go away when the colitis is treated.
Causes ulcerative colitis?
Many theories exist about what causes ulcerative colitis. People with ulcerative colitis have abnormalities of the immune system, but doctors do not know whether these abnormalities are a cause or a result of the disease. The body’s immune system is believed to react abnormally to the bacteria in the digestive tract.
Ulcerative colitis is not caused by emotional distress or sensitivity to certain foods or food products, but these factors may trigger symptoms in some people. The stress of living with ulcerative colitis may also contribute to a worsening of symptoms.
Diagnosis
Many tests are used to diagnose ulcerative colitis. A physical exam and medical history are usually the first step.
Blood tests may be done to check for anemia, which could indicate bleeding in the colon or rectum, or they may uncover a high white blood cell count, which is a sign of inflammation somewhere in the body.
A stool sample can also reveal white blood cells, whose presence indicates ulcerative colitis or inflammatory disease. In addition, a stool sample allows the doctor to detect bleeding or infection in the colon or rectum caused by bacteria, a virus, or parasites.
A colonoscopy or sigmoidoscopy are the most accurate methods for making a diagnosis of ulcerative colitis and ruling-out other possible conditions, such as Crohn’s disease, diverticular disease, or cancer. For both tests, the doctor inserts an endoscope—a long, flexible, lighted tube connected to a computer and TV monitor—into the anus to see the inside of the colon and rectum. The doctor will be able to see any inflammation, bleeding, or ulcers on the colon wall. During the exam, the doctor may do a biopsy, which involves taking a sample of tissue from the lining of the colon to view with a microscope.
Sometimes x rays such as a barium enema or CT scans are also used to diagnose ulcerative colitis or its complications.
A major genetic link to the development of Crohn's disease and ulcerative colitis, as well as other inflammatory diseases, has been revealed in a recent study. "This genetic discovery is special because it may have a rapid impact on diagnosis and treatment of these chronic digestive diseases," says Jonathan Braun, M.D., Ph.D., Chair of the National Scientific Advisory Committee of the Crohn's & Colitis Foundation of America (CCFA)

Previous genetic studies uncovered a link between Crohn's and variants of the gene CARD15 (also known as NOD2), but this gene plays a role in only some Crohn's patients, and does not affect the risk for colitis. The new discovery, which involves a gene called the interleukin-23 (IL-23) receptor, has a much larger effect on these inflammatory diseases.
Interleukin (IL)-23 is a heterodimeric cytokine closely related to IL-12. Yet, despite a strong structural relationship that includes a shared p40 subunit, this does not translate into functional similarity. In fact, the opposite is true, in that these two cytokines appear to have profoundly different roles in regulating host immune responses. It is now clear that IL-23 has key roles in autoimmune destruction in experimental allergic encephalomyelitis, collagen-induced arthritis and inflammatory bowel disease. IL-23 drives the development of autoreactive IL-17-producing T cells and promotes chronic inflammation dominated by IL-17, IL-6, IL-8 and tumor necrosis factor as well as neutrophils and monocytes. It is unlikely that IL-23 and its downstream effects evolved just to cause autoimmunity, but its real benefit to the host and the lineage relationship between IL-17-producing cells and T helper 1 cells remain unclear. By comparing the pathophysiological function of IL-12 and IL-23 in the context of host defense and autoimmune inflammation, we are beginning to understand the novel IL-23-IL-17 immune pathway.



Colon Cancer:
About 5 percent of people with ulcerative colitis develop colon cancer. The risk of cancer increases with the duration of the disease and how much the colon has been damaged. For example, if only the lower colon and rectum are involved, the risk of cancer is no higher than normal. However, if the entire colon is involved, the risk of cancer may be as much as 32 times the normal rate.
Sometimes precancerous changes occur in the cells lining the colon. These changes are called "dysplasia." People who have dysplasia are more likely to develop cancer than those who do not. Doctors look for signs of dysplasia when doing a colonoscopy or sigmoidoscopy and when examining tissue removed during these tests.
According to the 2002 updated guidelines for colon cancer screening, people who have had IBD throughout their colon for at least 8 years and those who have had IBD in only the left colon for 12 to 15 years should have a colonoscopy with biopsies every 1 to 2 years to check for dysplasia.

Differential Diagnosis:
The entire length of the colon, starting at the rectosigmoid junction and ending at the cecum, can be visualized by transabdominal sonography after retrograde water instillation into the colon. By this method, termed hydrocolonic sonography, it is possible to evaluate in detail the lumen, the colon wall, and the surrounding tissue. Five layers of different echogenicity can be differentiated within the colon wall.
METHODS: In a prospective study of 440 patients, it had been compared the value of conventional abdominal sonography and hydrocolonic sonography with that of colonoscopy, in the diagnosis and differential diagnosis of ulcerative colitis and colonic Crohn's disease.
RESULTS: In 93% of patients with Crohn's disease, the normal five-layer structure of the colonic wall was no longer in evidence, and the wall appeared hypoechogenic and clearly thickened.
In patients with ulcerative colitis, the five-layer structure could clearly be discerned, and although the colon wall remained hypoechogenic, it was only moderately thickened.
Colonic Crohn's disease and ulcerative colitis were detectable by hydrocolonic sonography, with a sensitivity of 96% and 91%, respectively.
The sensitivity achieved by conventional abdominal sonography is only 71% and 62% respectively. Furthermore, hydrocolonic sonography made possible the differentiation of Crohn's disease from Ulcerative colitis in 93% of the cases.
Pathological Diagnosis:
Crohn's disease and ulcerative colitis are distinct entities, but in 5 to 10% of patients and resected specimens, a clear separation may not be possible. The pathological diagnosis and differential diagnosis of Crohn's disease, including ulcerative colitis, indeterminate colitis and other diseases may mimic Crohn's disease. It is often difficult or impossible to distinguish diversion colitis and pouchitis from recurrence of Crohn's disease.
Increased expression of CD44v6 and CD44v3 in Ulcerative Colitis but not colonic Crohn's Disease:
Immune mechanisms, possibly involving cell-surface molecules such as CD44, have been invoked to explain the pathogenesis of inflammatory bowel disease. Monoclonal antibodies were used against epitopes encoded within the variable region of CD44 to investigate CD44 isoform expression in colon, small intestine, and liver in patients with various intestinal disorders and in controls. Biopsy samples from patients with ulcerative colitis showed significantly increased epithelial expression of CD44 isoforms containing the v6 and v3 epitopes, detected with antibodies 2F10 and 3G5, respectively. CD44v6 was detected on colonic crypt epithelial cells in 23 of 25 ulcerative colitis samples compared with 3 of 18 colonic Crohn's disease samples (p = 3.0 x 10(-6); odds ratio 57.5 [95% CI 6.83-702]) and 3 of 52 controls (22 normal colon, 10 infective colitis, 2 radiation colitis, and 18 colonic Crohn's disease; p < 1 x 10(-8); odds ratio 199 [25.5-2294]). No significant expression of CD44v6, CD44v3, or CD44v8/9 was found in samples of normal proximal colon from 4 patients with distal ulcerative colitis, whereas samples from the affected area showed staining for CD44v6 and CD44v3. No expression of CD44 variants was found in 15 samples of normal small intestine, 11 small-bowel pouchitis, 8 coeliac disease, 3 small-bowel Crohn's disease, 6 normal liver, 6 primary biliary cirrhosis, or 9 primary sclerosing cholangitis. The high intensity of CD44v6 and v3 epitope expression on crypt epithelial cells in ulcerative colitis suggests that CD44 isoforms may have an important role in ulcerative colitis. Their detection could have diagnostic potential in differentiating ulcerative colitis from other forms of colonic inflammation including Crohn's disease.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed
&cmd=Retrieve&dopt=abstractplus&list_uids=7537840
Poor diagnostic value of colonic CD44v6 expression and serum concentrations of its soluble form in the differentiation of Ulcerative Colitis from Crohn's disease:
Increased expression of CD44v6 on colonic crypt epithelial cells in ulcerative colitis has been suggested as a diagnostic tool to distinguish ulcerative colitis from colonic Crohn's disease. AIMS: To investigate colonic CD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6) in patients with ulcerative colitis and Crohn's disease.
METHODS: Colonic biopsy samples were obtained from 16 patients with ulcerative colitis, 13 with ileocolonic Crohn's disease, and 10 undergoing polypectomy. Serum samples were obtained from 15 patients with active ulcerative colitis, 20 with active Crohn's disease, and 20 healthy donors. Colonic CD44v6 expression was evaluated immunohistochemically by monoclonal antibody 2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6 concentrations were measured by ELISA.
RESULTS: 2F10 stained colonic epithelium of inflamed ulcerative colitis and Crohn's disease samples in 80% and 40% of cases, respectively, and VFF18 in 95% and 87%, respectively. Both monoclonal antibodies displayed a sensitivity and specificity of 60% and 87% to differentiate ulcerative colitis from colonic Crohn's disease. Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis (median 153 ng/ml; interquartile range (IQR) 122-211) compared with Crohn's disease (219; IQR 180-243) and healthy donors (221; IQR 197-241 (p = 0.002)). Its sensitivity and specificity to discriminate ulcerative colitis from Crohn's disease was 75% and 71%, respectively.
CONCLUSION: Colonic CD44v6 and serum sCD44v6 concentrations do not facilitate reliable differential diagnosis between ulcerative colitis and Crohn's disease.
Evaluation of serological markers to differentiate between ulcerative colitis and Crohn's disease: pANCA, ASCA and agglutinating antibodies to anaerobic coccoid rods
The value of these serological tests in differentiating ulcerative colitis from Crohn's disease is limited when used separately but, by combining two or more tests, the positive predictive value and specificity can be improved substantially. These tests might be of help in studying disease heterogeneity, and may contribute to defining various subgroups of patients with different pathogeneses.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed
&cmd=Retrieve&dopt=abstractplus&list_uids=12352222
Genetic association between ulcerative colitis and the anti-inflammatory cytokine interleukin-1 receptor antagonist:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed
&list_uids=8119534&dopt=Abstract
Cytokine profile in colonic mucosa of ulcerative colitis correlates with disease activity and response to granulocytapheresis
http://www.blackwell-synergy.com/links/doi/10.1111/j.1572-0241.2002.07029.x/abs/
Use of CT findings in differential diagnosis:
The mean colon wall thickness in Crohn colitis (11.0 mm +/- 5.1) is significantly greater than in ulcerative colitis (7.8 mm +/- 1.9) (P < .002). Submucosal fat deposition, not observed in the acute colitis, is significantly present more oftenly in ulcerative (61%) than in Crohn colitis (8%) (P = .0001). Exclusive involvement of the right colon and small bowel was most frequent with Crohn and infectious colitis. Abscess was associated almost exclusively with Crohn colitis (35%) but was seen in one patient with radiation colitis.
CONCLUSION: Although many CT findings in patients with colitis are nonspecific, some features are helpful in suggesting a specific diagnosis.

Available treatment for ulcerative colitis:
1. Aminosalicylates: drugs that contain 5-aminosalicyclic acid (5-ASA), help control inflammation. Sulfasalazine is a combination of sulfapyridine and 5-ASA.
2. Corticosteroids such as prednisone, methylprednisone, and hydrocortisone also reduce inflammation. They may be used by people who have moderate to severe ulcerative colitis or who do not respond to 5-ASA drugs.
3. Immunomodulators such as azathioprine and 6-mercapto-purine (6-MP) reduce inflammation by affecting the immune system. These drugs are used for patients who have not responded to 5-ASAs or corticosteroids or who are dependent on corticosteroids. Immunomodulators are administered orally, however, they are slow-acting and it may take up to 6 months before the full benefit.
4. Surgery (a) Ileostomy, (b) Ileoanal anastomosis.

New Possible Treatments:
1. Dr. Braun notes that while the disease state of all Crohn's and colitis patients is not likely to be driven by IL-23, the drugs necessary to affect change in the behavior of this protein receptor already exist. In fact, one such therapy was recently reported by a team at the National Institutes of Health (NIH). The investigators were able to show that therapy targeting p40 a subunit of IL-23 can inhibit the activity of IL-23 in Crohn's disease (Mannon P, N Engl J Med 351:2069, 2004). This genetic discovery is likely to accelerate tests of this and other drugs, and to better identify which patients will benefit from such diseases, and affects risk for both Crohn's and Colitis.

"The genetic variants in the IL-23 receptor gene have been identified that confer increased risk for IBD, but we are most excited about our discovery of a genetic factor in the same gene that confers protection against developing IBD," said Dr. Duerr. "There is hope that ongoing research will tease out the specific downstream effects of these genetic variants so that this knowledge can be used to develop better, more targeted therapies for patients with IBD.”.
2. LCAP (Leucocytapheresis)
Leukocyctapheresis (LCAP) is a blood purification treatment for ulcerative colitis (UC) [1]. LCAP is known to have a low incidence of side effects. LCAP is carried out using a column (Cellsorba E) filled with a non-woven fabric made up of polyester fibers. The fabric had a dual structure; an inner layer composed of superfine fibers 0.8-2.8 in diameter, and an outer layer composed of fibers 10-40 in diameter. The blood is filtrated from the outside into the inside of the non-woven fabric wound into a cylindrical shape in the column, and leukocyte components are removed. The blood, with leukocyte removed, is guided out from the column and heated, and the returned to the corresponding vein of the patient’s other arm or leg of the patient. The blood flow rate is set at 30-50 , and 2-3 L of blood is treated in each session of LCAP. The treatment is carried out for one hour per session once in a week, for 10 wks.

3. Non-pathogenic Escherichia coli versus Mesalazine for the treatment of ulcerative colitis:
Ulcerative colitis has been suggested to be caused by infection and there is circumstantial evidence linking Escherichia coli with the condition. I had been tried to find out whether the administration of a non-pathogenic strain of E. coli (Nissle 1917) is as effective as mesalazine in preventing relapse of ulcerative colitis. It has also been examined whether the addition of E. coli to standard medical therapy increased the chance of remission of active ulcerative colitis.
Trial study: This was a single-centre, randomised, double-dummy study in which 120 patients with active ulcerative colitis were invited to take part. 116 patients accepted; 59 were randomised to mesalazine and 57 to E. coli. All patients also received standard medical therapy together with a 1-week course of oral gentamicin. After remission, patients were maintained on either mesalazine or E. coli and followed up for a maximum of 12 months. A two-stage, conditional, intention-to-treat analysis was done.
FINDINGS: 44 (75%) patients in the mesalazine group attained remission compared with 39 (68%) in the E. coli group. Mean time to remission was 44 days (median 42) in the mesalazine group and 42 days (median 37) for those treated with E. coli. In the mesalazine group, 32 (73%) patients relapsed compared with 26 (67%) in the E. coli group. Mean duration of remission was 206 days in the mesalazine group (median 175) and 221 days (median 185) in the E. coli group.
INTERPRETATION: The results suggest that treatment with a non-pathogenic E. coli has an equivalent effect to mesalazine in maintaining remission of ulcerative colitis. The beneficial effect of live E. coli may provide clues to the cause of Ulcerative Colitis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed
&list_uids=10466665&dopt=Citation

References:
http://ccfa.i33.com/media/pdf/profchallenges.pdf
http://www3.interscience.wiley.com/cgi-bin/abstract/108061210/ABSTRACT?CRETRY=1&SRETRY=0
http://jimmunol.highwire.org/cgi/content/abstract/172/1/525
http://jimmunol.highwire.org/cgi/content/abstract/170/11/5438
http://jimmunol.highwire.org/cgi/content/abstract/173/3/1887
http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/425021
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed
&list_uids=16290228&dopt=Citation
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed
&list_uids=15158199&dopt=Abstract&holding=f1000,f1000m,isrctn
http://jimmunol.highwire.org/cgi/content/abstract/166/12/7563
Ubiquitous Transgenic Expression of the IL-23 Subunit p19 Induces Multi-organ inflammation, Runting, Infertility, and Premature Death
Dr Tejinder M Aggrwal
GAMS, MBBS &
RESEARCH ASSOCIATE
CSE & BIO-INFORMATICS
FAU BOCA RATON 33431 FL USA

Respiratory system performs functions of ventilation (V), perfusion (Q), and diffusion (DL). All respiratory function tests are based on the measurement of these functions. Spirometry measures the echanical function of the lung, chest wall, and respiratory muscles by assessing the total
volume of air exhaled from a full lung (total lung capacity [TLC]) to an empty lung (residual volume). This volume, the forced vital capacity (FVC) and the forced expiratory volume in the first second of the forceful exhalation (FEV1), should be reproducible to within 0.15 L upon
repeat efforts unless the largest value for either parameter is less than 1 L. Flow-volume loop recording is one of the dynamic ventilatory function tests. This is a safe, simple and reproducible. It is performed routinely in general practice. The shape of the flow-volume loop can differentiate between normal or abnormal lung function. Abnormalities like obstructive or restrictive lung conditions can be differentiated. Although these tests cannot give a pathological
diagnosis and assesses the mechanical functional impairment of various respiratory conditions, but they support other respiratory function tests. Moreover, they are important prognostic indicators of disease process and are commonly used to monitor drug therapy. This review explains the interpretation of flow volume curves in health and disease which will provide an
easy guide for both clinicians and physiologists.
Keywords: Spirometry, FEV1, FVC, Obstructive lung disease, Restrictive lung disease

Properties of Chloroquine
A few years back, I had written to the Departments of Medicine and Pharmacology, Post-Graduate Institute of Medical Education and Research, Chandigarh, that Chloroquine is anti-viral despite being anti-malaria. The anti-viral properties of Chloroquine, I had emphasized, needed further evaluation and thorough research. There is no doubt that the anti-malaria properties of Chloroquine are pronounced throughout the world, along with its disease modifying properties.
The anti-viral properties of Chloroquine need to be exploited for the benefit of people, especially during the outbreak of viral fever in Chandigarh. Chloroquine, in usual dosage, may be distributed among the residents. It should be swallowed in a single dose before the onset of fever or before the outbreak of viral fever. Moreover, Chloroquine in recommended prophylactic dose doesn’t have any side-effect. It is effective in controlling malaria also.
In my independent findings of Chloroquine during my studies and experience of clinical practice during the past 23 years, I found enthusiastic results of anti-viral properties of this wonderful medicine. This is very much encouraging.
Suffice it to mention that the use of Chloroquine helps prevent the spread of viral fever as a prophylactic drug but not as a therapeutic drug. This needs to be noted. Once there is fever, it takes its own time to subside.
Dr Tejinder M. Aggrwal, National Integrated Medical Association, Chandigarh

25th September, 2002 - The Tribune, Chandigarh

Dr Tejinder M. Aggrwal, MBBS, GAMS
Phoenix Hospital & Diagnostic Centre
SCO 8, Sector 16, Panchkula 134109
Ph: 0172-5054321, 5011333
Fax: 0172-5011334
M: 0-931-610-1112

REVERSE EFFECT OF ROSUVASTATIN

I have put more than 100 patients on Rosuvastatin (10mg) to treat mixed dyslipidemia and had good results after six months of treatment with diet control and exercise is as follows:
Cholesterol level fell up to 10-15%,
TG level decreased by 5-6%,
LDL Cholesterol decreased upto 10-12% and
HDL level elevated upto 6-8%
Except in 4 patients who had similar results, but their TG level elevated to 60-70% with similar diet control and exercise.
When these patients were put on Fenofibrates (160mg ) with Statin their TG level remarkably improved.

Theory by Lead Researcher
Theory by Lead Researcher Gives New Hope for Permanent Cure of Psoriatic Conditions

(PRWEB) July 25, 2005 -- Defective bone marrow is the critical link for the psoriatic conditions, claims the lead researcher Dr. S Dhawan in his latest article titled, "Chronic Psoriasis – causes and treatment A new hope for permanent cure.

" Bone marrow is the production center of T Cells and in Psoriatic conditions these T Cells attack our own skin cells as if they are antigen presenting cells (APC) or alien toxins. This over burden leads to accelerated cell formation. The defective bone marrow changes the behavior of T Cells.

According to Ayurvedic texts, nature has given us a very efficient and powerful system of energy generation in our body. The process of this energy generation system (EGS) starts when we intake food, liquids etc. and it ends at formation of immunity (called Ojja in aurvedic text books).

The entire process got 8 stages.

1. In the digestion process, food gets converted into Rasa Dhatu.
2.From rasa dhatu develops RAKATA(Blood).
3. From rakta develops MASA(muscles).
4. From masa develops MEDA(fat).
5. From meda develops ASTHI(Bones).
6. From asthi develops MAJJA(Bone marrow).
7. From majja develops SHUKRA(semen).
8. From Semen develops the OJJA (Immunity)
Ayurvedic texts has mentioned that it takes 90 days for food to get converted into Shukra (Semen), and another 60 days from Shukra to Ojja (Immunity). Where any of the above stages are not functioning properly (for example leakage in intestine) or food as input is contaminated or contains opposite properties or is not digested properly in the first place, it produces all kind of problems in the body. For example instead of producing Rasa Dhatu during digestion process, the system will produces Ama Rasa (toxins or macro globules) . With this every other stage also gets contaminated. For example next stage produces Ama Rakta then Ama Masa, Ama Meda, Ama Asthi, Ama Majja, Ama Shukra and finally Ama Oaj. Improper digestion leads to ama majja (defective bone marrow ). Bone marrow is the production center for T cells. (Can you see the chain and main cause for psoriasis?). The validation study conducted in our clinic also confirms the results of this theory. A total of 968 patients were taken for this validation study. The distribution pattern was wide and dispersed with regard to age, gender and type of psoriatic conditions. All the patients were studied with regard to formation of psoriatic conditions, their food habits, working conditions and family conditions. Following conclusions were drawn from this study.

#1. A total of 80% of patients had problem of indigestion/constipation

In 25% of patients indigestion/constipation was the major trigger for flare-ups and severe psoriatic conditions. This is #2 trigger after stress (35% of patients).

18% of patients had the family history of Psoriasis but severity of psoriasis has no relation with family history.

Medical Research on the Intestine/Psoriasis Connection:

It is interesting to note here that scientists have long recognized that toxins leaking from the intestines are involved in psoriasis. The technical term for leaky intestines is called "intestinal permeability." Several researchers have written on this subject in the medical journals. Psoriasis is an autoimmune disorder and production of Ama Oaj is an indication of immunodeficiency. To cure any psoriatic patient permanently it is important to control all the stages of energy generation system of body so that all the 7 Dhatus from food (rakat,masa,meda,asthi,majja,shukra and oaj ) are produced in their purest form. By curing Ama majja (defective bone marrow) we are treating the patients at immunity levels. By producing pure Ojja, we are making patients immune to psoriasis triggers. "12 years back when I took psoriasis as my subject for research," says Dr. S Dhawan in his article, "I was also caught into the dilemma of following perception which most of the scientific community carries around the world."

"Psoriasis is a skin disease which appears in 2-4% of the population. The cause of this chronic skin disease is unknown. Research has proven that psoriasis is an auto-immune disease, and not long ago the psoriasis gene(s) were found. The disease, or the tendency to get it, is inherited. It is possible to have psoriasis without any visible symptoms. This makes research on it quite complicated."

Being the firm believer of Ayurveda and its treatments methods, I took Ayurveda and its text books as the basis of my research work. During the 10 years of my research I delicately correlated the information gathered by the scientific community on symptoms and triggers for various psoriasis ailments and symptoms and causes given in ayurvedic text books. Finally I was able to form a complete chain leading to psoriatic conditions. I developed treatment method based on this theory and treating my patients for the last three years.

Treatment Method

We can divide our treatment method primarily into 3 major segments

Working on Hyperkeratosis (fast cell division) – External Treatment
Working on APC(Antigen Presenting cells ) – Internal Treatment
Working on Major triggers – Stress, Indigestion/constipation

This treatment method is totally herbal based with no known side effects. Various studies have been conducted which confirmed the strength of medicinal formulations administered under this treatment method The effectiveness or efficacy of this treatment method is evident from the vary fact that there are more that 1500 patients treated with this method during the last 3 years and none has reported reappearance of psoriatic conditions after the completion of treatment period. This success story is growing every day with more patients getting cured permanently.