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Jan29
Ulcerative Colitis and New Possible Treatments
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


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Jan26
Female sexual Dysfunctions
A sexual problem is anything that interferes with a woman’s satisfaction with sexual activity. When this happens, it is often referred by health professionals as female sexual dysfunction (FSD).
To understand why sexual problems occur, it is important to understand the sexual response cycle. This cycle is the same in both men and women, although at different rates and, obviously, with different physical changes.
Sexual response cycle: The cycle has 4 steps.
1. Desire (excitement phase) – Desire is a sexual “charge” that increases interest in and responsiveness to sexual activity. You feel “in the mood.” Your heartbeat and breathing quicken, and your skin becomes reddened (flushes).
2. Arousal (plateau phase) – Sexual stimulation–touch, vision, hearing, taste, smell, or imagination–brings about further physical changes. Fluids are secreted within the vagina, moistening the vagina, labia, and vulva. These fluids provide lubrication for intercourse. The vagina expands, and the clitoris enlarges. The nipples become hardened or erect.
3. Orgasm (climax) – At the peak of arousal, the muscles surrounding the vagina contract rhythmically, causing a pleasurable sensation. This is often referred to as the sexual climax.
4. Resolution – The vagina, clitoris, and surrounding areas return to their unaroused states. You feel content, relaxed, and possibly sleepy.
Every woman progresses through the cycle at her own rate, which is normal for her. A sexual problem may occur if any of these stages does not occur.
A. Sexual problems
The types of sexual problems in women correspond to the stages of the sexual response cycle. Inability to achieve any of the stages can interfere with sexual satisfaction and thus create a problem. Any of these can be very distressing for a woman, because everyone deserves a satisfying sex life. They can be distressing for her partner, too, and can lead to problems in the relationship.
Lack of sexual desire: – Lack of interest in sex, or desire for sex, is a common problem in both men and women, but especially in women. Lack of desire stops the sexual response cycle before it starts. Lack of desire is temporary in some people and an ongoing problem in others.
Difficulties becoming sexually aroused or achieving orgasm: – Inability to become sexually aroused is sometimes related to lack of desire. In other cases, the woman feels sexual desire but cannot become aroused. Orgasm may be delayed or does not occur at all (anorgasmia). This can be very distressing for a woman who feels desire and becomes aroused. It can create a vicious cycle in which the woman loses interest in sex because she does not have an orgasm.
Pain during intercourse: – Pain during intercourse (dyspareunia) is not uncommon. Like other sexual problems, it can cause a woman to lose interest in sex. A number of conditions may cause pain and / or discomfort during sexual intercourse. These conditions include:
1. Vaginal Infection: Certain vaginal infections such as vaginal yeast infections and trichomoniasis are often present without noticeable symptoms. However during sexual intercourse, the rubbing motion of the penis against the vagina and genitalia sometimes causes the symptoms of these vaginal infections to intensify causing stinging and burning. Genital herpes sores are another frequent cause of pain during sex.
2. Vaginal Irritation: Many products contain irritants which can cause vaginal irritation leading to discomfort or pain during vaginal sexual intercourse. These include: Any contraceptive foams, creams, or jellies, Allergic reactions to condoms, diaphragms, or latex gloves, Vaginal deodorant sprays, Scented tampons, Deodorant soaps, Laundry detergents in sensitive individuals, Excessive vaginal douching
3. Vaginal Dryness: Vaginal dryness often causes painful sexual intercourse. Normal vaginal lubrication is present for most women; however, during certain times the vagina may be dry and make vaginal penetration painful.
4. Vaginal Tightness: Occasionally this happens when you feel tense, or are not fully relaxed when penetration occurs. Difficulty in penetrating a tight vagina can happen even when vaginal lubrication is not a problem. Often, the first few times you engage in sexual intercourse, the vagina may be tight due to an unstretched hymen and cause pain at the time of penetration.

Sometimes a more severe condition called vaginismus is responsible for vaginal tightness; women with vaginismus experience strong, involuntary muscle spasms of the vaginal muscles during sexual intercourse or vaginal penetration by any object including fingers and tampons.
5. Pain of the Clitoris: The clitoris is the most sensitive part of the female genitalia. Gentle touching or rubbing of the clitoris is extremely pleasurable for some women, while for others it is unbearably painful. Clitoral pain may also occur due to poor hygiene; vaginal secretions may collect under the clitoral hood and if not carefully washed away may lead to pain.
6. Pelvic Pain: Occasionally a women will experience pelvic pain upon deep, thrusting penetration. Many conditions may cause this pain including:
• Tears in the ligaments that support the uterus (causes include problems during childbirth, inappropriately performed abortion, previous violent sexual intercourse or rape)
• Cervical, uterine, or tubal infections such as pelvic inflammatory disease (PID)
• Pelvic adhesions (often the result of previous pelvic surgery or PID)
• Endometriosis
• Ovarian cysts
• Uterine Fibroid Tumors
B. Psychological Factors
Impact of events during childhood and adolescence
Most studies that have assessed the impact of childhood experiences on female sexual dysfunction are methodologically flawed. They rely on retrospective recall, which is particularly problematic when emotional responses to the event as well as the actual occurrence of the event are being reported. However, there have been some probative links between childhood sexual abuse and having a later sexual dysfunction.
Relationship factors
A substantial body of research has explored the role of interpersonal factors in sexual dysfunction among women, particularly in relation to orgasmic response. These studies have largely focused on the impact of the quality of the relationship on the sexual functioning of the partners. Some studies have evaluated the role of specific relationship variables, whereas others have examined overall relationship satisfaction. Some studies have explored events; others have focused on attitudes as an empirical measure of relationship functioning. Subject populations have varied from distressed couples to sexually dysfunctional clients to those in satisfied relationships. Some major areas are relationship conflicts; extra-marital affairs; current physical, verbal or sexual abuse; sexual libido, desire or practices different from partner and poor sexual communication.
Individual factors
There has been little investigation of the impact of individual factors on sexual dysfunction in women. Such factors include stress, levels of fatigue, gender identity, health, extra marital relationship, financial, family or job problems, family illness or death, depression and other individual attributes and experiences that may alter sexual desire or response.
Physical factors
The female sexual dysfunction may occur due to physical factors have ranged from 30% to 40%. The disorders most likely to result in sexual dysfunction are those that lead to problems in circulatory or neurological function. These factors have been more extensively explored in men than in women. Physical etiologies such as neurological and cardiovascular illnesses have been directly implicated in both premature and retarded ejaculation as well as in erectile disorder, but the contribution of physiological factors to female sexual dysfunction is not so clear. However, recent literature does suggest that there may be an impairment in the arousal phase among diabetic women. Given that diabetic women show a significant variability in their response to this medical disorder, it is not surprising that the disease’s influence on arousal is also highly variable. In fact, the lack of a clear association between medical disorders and sexual functioning suggests that psychological factors play a significant part in the impact of these disorders on sexual functioning.
Other factors
• Changes related to menopause
• Communication problems with partner
• Damage to nerves due to surgery or trauma
• Fear of pain, infection, or being pregnant
• Feelings of guilt and shame about sex
• Lack of appropriate stimulation
• Lack of lubrication
• Medication
Medications
A. Medications that cause disorders of desire

Psychoactive medications
Antipsychotics
Barbiturates
Benzodiazepines
Selective serotonin reuptake inhibitors
Lithium
Tricyclic antidepressants

Cardiovascular and antihypertensive medications
Antilipid medications
Beta blockers
Clonidine (Catapres)
Digoxin
Spironolactone (Aldactone)

Hormonal preparations
Danazol (Danocrine)
GnRh agonists (e.g., Lupron, Synarel)
Oral contraceptives
Others
Histamine H2-receptor blockers and promotility agents
Indomethacin (Indocin)
Ketoconazole (Nizoral)
Phenytoin sodium (Dilantin)

B. Medications that cause disorders of arousal
Anticholinergics
Antihistamines
Antihypertensives
Psychoactive medications
Benzodiazepines
Selective serotonin reuptake inhibitors
Monoamine oxidase inhibitors
Tricyclic antidepressants
C. Medications that cause orgasmic dysfunction
Methyldopa (Aldomet)
Amphetamines and related anorexic drugs
Antipsychotics
Benzodiazepines
Selective serotonin reuptake inhibitors
Narcotics
Trazadone (Desyrel)
Tricyclic antidepressants

Diagnostic features
The DSM-IV (American Psychiatric Association) diagnostic criteria for female sexual arousal disorders are outlined here:
A. Persistent or recurrent inability to attain, or to maintain until completion of the sexual activity, an adequate lubrication-swelling response of sexual excitement.
B. The disturbance causes marked distress or interpersonal difficulty.
C. The sexual dysfunction is not better accounted for by another Axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Treatment
A. Provide education
Provide information and education (e.g., about normal anatomy, sexual function, normal changes of aging, pregnancy, and menopause). Provide booklets, encourage reading; discuss sexual issues when a medical condition is diagnosed, a new medication is started, and during pre- and postoperative periods; give permission for sexual experimentation.
B. Enhance stimulation and eliminate routine
Encourage use of erotic materials (videos, books); suggest masturbation to maximize familiarity with pleasurable sensations; encourage communication during sexual activity; recommend use of vibrators, discuss varying positions, times of day or placesetc.
C. Provide distraction techniques
Encourage erotic or nonerotic fantasy; recommend pelvic muscle contraction and relaxation (similar to Kegel’s exercise) exercise with intercourse; recommend use of background music, videos or television.
D. Encourage noncoital behaviors
Recommend sensual massage, sensate-focus exercises (sensual massage with no involvement of sexual areas, where one partner provides the massage and the receiving partner provides feedback as to what feels good; aimed to promote comfort and communication between partners, oral or noncoital stimulation, with or without orgasm.
E. Minimize dyspareunia
Treat the causes of dyspareunia. Ask the patient to use jelly in case of vaginal dryness.

Homeopathic Medication
Dyspareunia : Arg. Nit, Sepia, Nat. mur, Lyss, Platina, Calc phos, Thuja, Acid nit.
Vaginismus : Cact, Plb, Bell, Canth, Puls, Silicia, Lyco, Nat mur, Ignatia, Ferrum.
Aversion to sex: Asar, Caust, Nat mur, Sepia
Anorgasmia : Berberis, Caust, Phos, Ferrum, Sepia
Diminished sexual desire : Caust, Nat mur, Ferrum, Sepia, Acid phos, Graph, Lyco
Dryness of vagina : Nat mur, sepia, Graph, Lycop, Ferrum

Dr. SUNEETH MATHEW BHMS, M.Sc(Psy), M.Phil(Clinical Psy), PG Dip in Criminology & Forensic Science.
Reader, Dept of Practice of Medicine, Hahnemann Homeopathic Medical College, Rasipuram, Salem.
Consultant, Dept of Psychosexual medicine, V-Care Multispecialty Homeopathy, Coimbatore, Baluserry, Mananthavadi and Ideal Speciality Institute, Perambra.
Cell: 09486382600 URL: www.holykings.info


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Jan23
Spirometry for obstructive & restrictive lung disease
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


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Jan18
Ozonucleolysis
Ozonucleolysis for slipped/prolapsed Disc

Dr (Maj) Pankaj N Surange
MBBS, MD, FIP
Interventional pain and spine specialist
09871985514

Ozone may be a wonder molecule to the clinicians though its potentials yet to be fully explored. It has role in controlling bacterial, fungal & viral infections including AIDS, treating non-healing ulcers, Rheumatoid and other kinds of arthritis, different kind of skin diseases and many others.

What is ozone?

Ozone is a tri-atomic Oxygen molecule, O3, with a different molecular structure than Oxygen. Its name is derived from the Greek word ozein meaning “to smell”. At room temperature, Ozone is a colorless gas with a characteristic odor (similar smell after thunderstorms, at high altitudes or near the sea etc). At ground level its concentration 0.03 - 0.04 ppm. Ozone in the atmosphere is produced by action of UV rays and thunderstorm on the atmospheric Oxygen; but Medical Ozone is produced from pure medical grade oxygen with the help of high voltage electrical discharge. Medical ozone is a mixture of oxygen and ozone of different concentration. Medical ozone is always freshly prepared on site (in a special generator) for immediate administration. A trained physician according to the medical indication and the patient’s condition determines the exact dose of ozone.

Safety and efficacy of Ozone therapy

Treating patients with ozone is not a new procedure. The first ozone generators were developed by Werner von Siemens in Germany in 1857, and 1870 saw the first report on ozone being used therapeutically to purify blood, by C. Lender in Germany.
During World War 1, ozone was used to treat wounds, trench foot, gangrene and the effects of poison gas. Dr. Albert Wolff of Berlin also used ozone for colon cancer, cervical cancer and decubitus ulcers in 1915. Today, after 125 years of usage, ozone therapy is a recognized modality in many nations: Germany, France, Italy, Russia, Romania, Czech Republic, Poland, Hungary, Bulgaria, Israel, Cuba, Japan, Mexico, and in five US states. It was also used extensively to treat war wounds during World War-II.
It was not popularized before, as ozone resistant materials were not used to produce ozone generators. Also the exact concentration of ozone was unknown. Former Ozone generators are either UV light Ozone generators or plasma type Ozone generators. Here, it was very difficult to know the precise concentration of ozone. Now with the present Corona-discharge Ozone generators, it is possible to know the exact concentration of Ozone. Also, by changing the current or the oxygen flow, Ozone concentration can be precisely modified.
Ozone has been found to be an extremely safe medical therapy, free from side effects. In a 1980 study done by the German Medical Society for Ozone Therapy, 644 therapists were polled regarding their 384,775 patients, comprising a total of 5,579,238 ozone treatments administered. There were only 40 cases of side effects noted out of this number that represents the incredibly low rate of .000007%. Ozone Therapy has been described as the safest known medical therapy.

Indications of Ozone therapy

Among the various diseases presented with pain the following has been treated with very good results; e.g. rheumatoid arthritis, systemic lupus erythemoatosis, scleroderma, polymyositis/fibromyositis, ankylosing spondylitis, osteo-arthritis, Reiter syndrome, psoriasis, synovitis, gout, chrondrocalcinosis, pyrophosphate arthropathy, calcific peri-arthritis, calcific tendinitis, calcinosis and inter-vertebral disc prolapse. In my Pain Clinic I have been treating osteo-arthritis of knee, trigger point injections for fibromyalgia/ Myofascial pain, and inter-vertebral disc prolapse or slipped disc successfully.

How Ozone should be administered?

There are different methods like injections of ozone/oxygen mixture; insufflations through rectum; treating with ozonated water (drinking, dressing wound/ulcers etc.); auto-transfusion of ozonated blood, application of ozonated oil and so on depending on type and site of disease. But for treatment of different pain we use injection of different concentrations of ozone gas only. Ozone molecule is not stable. It has a half-life of 20 minutes only. So, within 20 minutes only half of the original ozone remains, the rest becomes oxygen. Increase in temperature decreases its half-life. For injection it is always freshly prepared on site for immediate administration. Only Ozone resistant syringes can be used for injecting it. The contraindications for treatment with ozone are only a few. They are active bleeding from any site, pregnancy, and active hyperthyroidism.

Mechanism of action

The mechanisms of action of ozone are many. Most of its actions are due to the active oxygen atom liberated from breaking down of ozone molecule. Besides its action as bactericidal, fungicidal, viricidal agent, it activates cellular metabolism, modulates the immune system & increases and activates body's own antioxidants and radical scavengers. In the treatment of pain different other mechanism acts. There is enhancement of circulation. Ozone reduces or eliminates clumping and red cell. Its flexibility is restored, along with oxygen carrying ability (due to the stimulation of 2,3-diphosphoglycerate). Oxygenation of the tissues increases as the arterial partial pressure increases and viscosity decreases. Ozone also oxidizes the plaque in arteries, allowing the removal of the breakdown products, unclogging the blood vessels. All these leads to an increase in the amount of oxygen released to the diseased tissues. There is also reduced formation of inflammatory mediators like different prostaglandins and so there is an anti-inflammatory action.

Ozone in PIVD/Slipped disc

In case of prolapsed inter-vertebral disc (or, slipped disc) different other mechanism acts. Inter-vertebral disc is filled with nucleus pulposus which is a jelly like material which holds water (90% of disc material is water). When ozone is injected into the disc the proteo-glycan bridges in the jelly-like material are broken down and they no longer capable of holding water. As a result disc shrinks and mummified which is equivalent to surgical discectomy and so the procedure is called ozone discectomy or ozonucleolysis. It has been published in ANESTHESIA AND PAIN journals that up to 85% of disc operation can be avoided with these non-surgical interventions. Success rate is about 88% which is comparable to surgical discectomy (50% to 90%). Complications are remarkably low and much less than surgery.

Future

Ozone is gradually gaining popularity in various medical fields especially in pain management. Newer modification in techniques and administration of ozone, more and more publication of scientific materials in the medical journals and animal studies have made it more acceptable to the medical community and gradually it is becoming more popular.


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Jan15
Properties of Chloroquine
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


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Jan14
website on stricture urethra
I have started a special website on Stricture Urethra – www.stricturecure.com . Almost all my patients X-rays (RGU’s & MCU’s) both pre-op, post-op, & follow up results have been uploaded. Once it is fully constructed it will be a unique one with the following attributes :

1. Patients will be able to see their own data, X-rays, & follow up Investigations etc after they log in with a unique ID.
2. A person suffering from stricture urethra will be able to identify himself with all such patients who have the same type of stricture as himself & see their surgical outcome(anonymity being maintained).
3. Any patient/doctor can post/upload the RGU & MCU Images and get expert opinion as to the type of management/surgery required.
4. This is a first of its kind site dedicated to stricture urethra disease.

With Warm regards,
This is my small effort towards Copenhagen, Nopenhagen, Hopanhegen …….. . Our processing is technology driven. We have lowered the use of paper & X-ray films by over 75% thus reducing our carbon footprints.


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Jan06
Adverse effect of Rosuvastatin
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.


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Jan01
Risk Free Treament For Chronic Psoriatic Patients Found
Risk Free Treament For Chronic Psoriatic Patients Found
Psorcure Treatment Plan for Psoriasis can help patients avoid the side effects of using conventional treatments such as Steroids, Calcipotriol and Methotrexate and Biologics, a study concludes.

(PRWEB) September 8, 2005 -- A recently concluded study puts Psorcure Treatment Plan as a better option in psoriasis management. During the study period it managed the flare-ups effectively after clearing the skin from psoriasis and none of patient under study developed any major side effect symptoms which are generally associated with the use of conventional psoriasis treatments.

It is well known that there are major side effects associated with conventional treatment methods for psoriasis, yet patients are not properly educated about them.

Objective of Study

Conventional Treatments for Psoriasis include use of Steroids, Calcipotriol and methotrexate. Biologics are recently developed treatments. All the four treatment methods are associated with risks of major side effects.

Hyperglycemia (high blood sugar) and glucosuria (high sugar in the urine), Cushing's Syndrome (muscular weakness), High Blood Pressure, Depression, Skin inability to fight infection, Thinning of skin, HPA Axis Suppression are some of the known major risks associated with the long term use or excessive use of tropical steroids.

Dry skin, high blood calcium levels, peeling, rash, red or inflamed skin or hair follicles, skin discoloration, skin wasting, worsening of psoriasis on rebound are the known major risks associated with Calcipotriol.

Methotrexate increases the risk of Liver Disease, Kidney Disease, Diabetes, Asthma, Infection, A stomach Ulcer.

Recently Food and Drug Administration warned doctors about more potential side effects that could be caused by the psoriasis drug Raptiva (Biologic Treatment). The risk includes immune-mediated hemolytic anemia, causing a loss of red blood cells, and serious infections and reduced platelet count, a condition known as thrombocytopenia.

The objective of this study was to see the effectiveness of Psorcure Treatment Plan in managing rebounds and aggravated flare ups and to observe development of major side effects generally associated with conventional treatments for psoriasis.

Study Methodology

30 willing patients were included in this study and were observed for 3 years.

They were monitored during the treatment for effectiveness and after the treatment period for side effects.

Following tests were taken before and after the treatment period to evaluate the effectiveness of treatment.

1..PASSI Score.
2..Skin Biopsy

Following tests and examinations were made at regular intervals during the entire period of study to evaluate the safety of treatment.

Thyroid Profile Test (T3, T4, TSH)
Blood Sugar Test
HDL/LDL ratio
Red Blood Cells and Platelet counts
SGOT and SGPT for Liver
Blood Urea and Serum Creatinine for Kidney

Clinical observations were made and recorded during the study period for following

Nausea/Vomiting, Diarrhea, Alopecia, Blood Pressure, Change in weight, Hair Loss, Dizziness, Depression

Effectiveness of Treatment

The main treatment period was 3-6 months (average 4 months) and it was followed by maintenance treatment for 3 months.

3 patients left the treatment or did not allow us to take biopsy and other tests after the treatment.

In all 27 patients were tested and examined and their results are taken into our study.

Every patient responded to this treatment.

Following changes in skin were observed through skin biopsy.

1.Marked reduction in parakeratosis
2.Marked reduction in Acanthosis
3.Diminished height of rete ridges

Average reduction of 98% in PASSI score was observed.

Rebound or Flare ups

During the entire study period, no patient got any rebound or significant flare up. We recorded 3 years long remission period which indicates the strength of Psorcure Treatment Plan in managing the flare ups and also confirms that this treatment plan does not suppress the immunity level of patients. These results were further confirmed by counting T cells of patients which were found in the normal range during the treatment and even 6 months after the treatment.

It is to be noted here that to get quick results all the conventional treatment methods function with suppressing immunity levels which results in major flare up or rebound as and when patient terminates the conventional treatment method. There is a major difference in the functioning of Psorcure Treatment Plan which restore the immunity levels. The fact that no patient reported any infection during study period is also significant in this regard.

Side Effects

No major side effect was noticed during the study period.

All the results of pathological tests were within normal range through out the study period.The fluctuation range of various tests was +/- 2% during the study period.

The following were significant changes observed during the study period.

Patients were energetic and cheerful in general in contrast to depressed conditions observed at the start of this treatment.

Mean serum creatinine at the start of treatment was 1.0 which was reduced to 0.8 at the end of treatment period. The reduction indicates improved functioning of kidney. The result requires further study taking a group of patients with >1.2 mean serum creatinine. If results are confirmed again, this might lead to a treatment for kidney patients.

There was marked improvement in hair loss and hair thinness for scalp psoriasis patients .Many patients reported re growth of hair on bald patches.

Improvements were noticed in HDL/LDL ratio.

Some obese patients saw reduction in their weights.

Conclusion

Psorcure Treatment Plan is faster in clearing the skin from psoriasis and restoration of immunity levels with better management of flare ups and rebounds and no significant side effect are some of the major benefits which one can draw from this treatment plan.

Psorcure Treatment Plan

The treatment plan developed by Dr. S Dhawan is a combination of

External Applications

Internal Medications

Dietary Management

Specially designed Yoga Exercises.

All the applications and medications are totally herbal and are prepared as per WHO guidelines for herbal Medicines. Accordingly no synthetic or chemically defined active substance have been added in finished product like (steroids and methotrexate ) and all the herbal Medicines contain only active ingredients present in plants. All the medicines, its constituents, the formulation, and the herbs used in Psorcure Treatment Plan are approved by Director of Ayurveda and siddha, Ministry of Health and family Welfare ,Government of India


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Jan01
Theory by Lead Researcher Gives New Hope for Permanent Cure of Psoriatic Conditions
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.


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Jan01
New hope for chronic psoriasis patients
New Hope for Chronic Psoriatic Patients
Psorcure Oil can treat chronic psoriasis disease with no re-occurrence of lesions – a major breakthrough in Psoriasis Treatment.

Clinical trial showed that Psorcure Oil is much more effective than calcipotriol in stopping the lesions to reappear after the treatment.

Psorcure Oil is part of treatment plan developed by Dr S Dhawan to cure Psoriatic patients permanently. Psorcure Oil is a specially formulated extracts of herbs optimized to treat psoriatic patients.

To reduce scales in Psoriatic Patients, most of the Dermatologists recommend and prefer to use the Vitamin D3 analog (calcipotriol) as an external application. This application also helps inhibiting T cell proliferation.

A 6 week clinic trial was conducted to compare the effectiveness of Psorcure Oil and Calcipotriol. For this purpose 25 chronic plaque psoriatic patients were selected from the list of volunteers who offered themselves for this trial. The selection was made based on redness; scales level and PASI score to maintain the uniformity in severity of patients selected for trial. Average PASI score was determined separately for left side and right side of every patient’s body. The score was 20.1 and 20.3 respectively.

Patients mix was widely distributed. Out of 25 patients, 14 patients were male and 11 were females. All the patients were in the age group of 6years to 65 years.

Every patient was tested for Biochemical and Hematological investigations before and after trial period. The investigations include Whole blood count, Total calcium and phosphate, alkaline phosphate, Total proteins and creatanin levels.

Trial Methodology

During the trial period, every patient was given calcipotriol ointment to apply on the right side of the body and psorcure oil to apply on the left side of the body. After application of Oil, left part of body for every patient was exposed to sun light for 15 minutes as part of treatment.

During the trial period no patient was allowed to take any other treatment, application, calcium supplements or any other oral or topical psoriatic therapy. Further no internal medication was given to any of the patients during trial period.

Trial Results

Out of 25 patients 3 patients defaulted, 2 patients developed worsened with calcipotriol and one patient developed rashes with psorcure oil.

The PASI score after 6 weeks trial period

Calcipotriol group 3.8 (A reduction of 87% in PASI Score)

Psorcure Oil Group 2.8 (A reduction of 90% in PASI Score)

After the end of 3 months observation period

Calcipotriol group Lesions reappeared in 50% of cases

Psorcure Oil Group Lesions reappeared in only 5% of cases.

Conclusion

Psorcure Oil is more effective for longer remission periods and relief. In combination with other medicines it helps curing psoriasis permanently.

Dr. S Dhawan has dedicated his life for the research and treatment of psoriasis. During his long research he formed a theory on the causes of psoriasis and based on this theory he developed a herbal based specially formulated treatment plan to cure psoriatic conditions. Any one can read his theory at http://clinicpsoriasis.com/ayurvedic-science.asp

He has treated more than 1500 patients with his new treatment plan during the last 3 years. He monitors the conditions of all his patients even after completion of treatment period. Not even a single patient has reported any major reappearance of psoriatic conditions after getting cured. You can see complete analysis of his patient’s register at http://clinicpsoriasis.com/patient-analysis.asp

An observation period of 3 years is not enough to claim that my treatment provides total cure, says Dr. S Dhawan, but no major reappearance of psoriasis in any of my patients under my treatment is the longest remission period observed ever under any treatment plan available in the world. This in itself is a remarkable achievement in psoriasis treatment quest.

Dr. Dhawan is available for free consultation at www.vedawave.com


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