TRANSFER FACTOR is very effective adjuvant as Supportive Therapy for Leprosy Patients who are WHO, World Health Organization, Drug Resistant Case with Lepra Reaction and those suffering from Severe Skin Asthma according Dr. Ma. Luisa Abad-Venida, M.D., FPDS,- Consultant Dermatologist, Former Chair of the Department of Dermatology, JOSE REYES MEMORIAL MEDICAL CTR &; PRESIDENT of the SKIN RESEARCH FOUNDATION OF THE PHIIPPINES. [You may contact her at her Clinic- Telephone:(632)7116703, 9205041 or 9217252, Mobile: (63)9178173065]
Dr. Venida has tested Transfer Factor in combination with prescribed medication on several leprosy and severe skin asthma patients and she can attest to its effectiveness in improving the effects of standard therapeutic regimen. So Transfer Factor must be used in combination with approved regimen.
CASE STUDIES USING TRANSFER FACTOR ON LEPROSY WITH LEPRA REACTION
BY DR. MA. LUISA ABAD-VENIDA, M.D.
Dx. Lepromatous Leprosy,
WHO Drug Resistant Case
C.,21 yr old male
Tx.
Lymecycline 30 mg bid
Transfer Factor Plus 9 capsules a day
The Use of Transfer Factor in Lepra Reaction by Dr. Ma. Luisa Abad-Venida, M.D.
Introduction:
The decline in registered prevalence of leprosy worldwide stimulated the recent policy changes within the World Health Organization. The emphasis was shifted from tackling leprosy as a public health issue to sustaining quality services for people affected by the disease; to prevent deformities and thus remove the stigma attached to it. Deformities in leprosy are due to lepra reaction that damages the peripheral nerves leading to paralysis of the affected muscle or loss of function of skin appendages. Lepra reaction may occur before treatment, but more so during treatment and continuing intermittently or continuously until the body has totally eliminated the mycobacterium debris from the body. Prompt and proper treatment of lepra reaction is critical in preventing deformities. The most common treatment option available is corticosteroid that acts as T-cell suppressor(1,2,3,4,5) Although steroid is very effective in treating lepra reaction, its chronic use in cases of severe lepra reaction poses the problem of further compromising the cell mediated immunity status of patients in the lepromatous spectrum, encouraging emergence of resistant strains and/or the accompanying problem of steroid toxicity.
In the Philippines, absenteeism and default still continue to be a problem. Multidrug therapy (MDT) for leprosy containing rifampicin, dapsone and clofazimine should be taken continuously for 12 blister packs to ensure near adequate treatment. Drug resistance could emerge rapidly among patients whose treatment regimens were inappropriate. To date, all the official multi-drug therapy contain rifampicin (RMP), which is significantly more bactericidal than any other anti-leprosy drugs or any combination of ofloxacin, clarithromycin and minocycline.(6) Emergence therefore of RMP- resistance would create tremendous difficulty for the treatment of individual patient, and its dissemination would pose a serious threat to the achievement of leprosy control. Multiple resistance to Dapsone (DDS), RMP, and Ofloxacin (OFLO) have also been reported. (7) Problems of logistics, compliance, drugs resistance and drugs toxicity point to an urgent need for alternative approaches like immunotherapy to shorten current treatments. A potential immunotherapeutic agent is Transfer Factor. Discovered by Dr. H. Sherwood Lawrence in 1949(8), “An evaluation of Transfer Factor as immunotherapy for patients with lepromatous leprosy “was reported by Ward E. Bullock, M.D. in 1972 using human lymphocytes from sensitized donors. He concluded that delayed hypersensitivity reaction to M.leprae antigens can be produced, with lymphocytes or their extracts, in patients with anergic leprosy.(9) In mid 1980’s, two researchers discovered the presence of Transfer Factor in colostrums and later in egg yolk, that led to its availability in oral form. “Combination of drugs and Transfer Factor in the treatment of leprosy” has been shown to enhance bacterial killing and clearance, reported by Katoch K in 1986.(10)
The use of Transfer Factor led to the successful recovery of the three cases of severe lepra reaction that have already completed MDT treatment.
CASE REPORTS
Case 1
A 15 year old male child from Malabon City, in type II lepra reaction, was diagnosed with lepromatous leprosy in 2003 at the age of 12 years old, with an average bacteriologic index (BI) of 4.6+, was given MDT on 1Jan03-31May03 and 17Jun05-30April06. Lepra reaction developed on his 2nd month of MDT, corticosteroid was started following the WHO recommendation. His intake of steroid beyond 12 weeks was either prescribed or as self medication. He was also prescribed NSAIDs, Colchicines and Squalene.(fig 1.1) Between May 2004 BI 2.8+ and May05 BI 2.6 with slackened drop in average BI and chronic use of steroid, coupled with high WBC 32.38 and high alkaline phosphatase 270 (44-155) it was deemed necessary to reinstitute another course of MDT under close monitoring. In March 06, there was worsening of the symptoms manifested as high grade fever 39C, joint pains, body malaise, increased erythema, swelling of digits of both hands and elevation and tenderness of plaques. There was also muscle weakness as he was incapable of feeding himself and writing his assignment.(fig.1.2 and 1.3)
With a BI 1.4+, an impression of steroid toxicity and or dapsone syndrome with lepra reaction required hospitalization, discontinue all medications and initiate supportive therapy. Transfer Factor 600mg TID was started initially, on his 3rd hospital day, joint pains disappeared together with body malaise and fever. Plaques and hand swelling gradually diminished and he was discharged after 5 days confinement. Home medications were Transfer Factor in supervised doses, Vitamin B complex, colchicines and petroleum jelly. Patient condition continued to improve after consuming 108,000 mg pure Transfer Factor and 54,000 mg plus cordyvant Transfer factors.(fig 1.4) AFS turned negative in 2007.
Case 2 (See Treatment Graph Above)
A 21 year old male from Bulacan, was diagnosed with lepromatous leprosy in 2004. His condition started as numbness on the R elbow 15 years prior to consult (PTC) but did not sought treatment. He was 13 years old when he was given MDT-MB but took only 3 blister packs and stopped because of improvement. For about 3 years PTC, he was suffering from increasing number of patches in his body and appearance of nodules on the face and earlobes before finally coming to our institution, and, with his younger brother who has the same problem.
His average BI 4.5+, highest on R earlobe 6+ solid, on admission, persisted from 4Nov04-25Sept05 until the end of his regular MDT-MB treatment. At this time, he complained of myalgia, dizziness and easy fatigability. CBC revealed severe anemia Hgb 77. Drug resistance to MDT and/or Dapsone syndrome was considered and so Ofloxacin 400mg OD 5Sept05-3Feb06 (fig 2.1) was added to his regimen with clofazimine 200mg daily in tapering dose with Dapsone was removed from the regimen.
He developed lepra reaction during his 2nd blister pack and was prescribed corticosteroid following the WHO recommendation, NSAIDs and colchicine plus supportive medications of aluminum MgSO4, Vit D, Calcium and B complex. (fig 2.2) His signs and symptoms were generalized erythematous plaques, nodules, vesicles, ulcers, crusting, joint pains, nerve tenderness and fever.
In Feb 2006, with a persistently high average BI 4.5+ (fig 2.1) despite the 5 months treatment of Modified MDT-MB, and worsening skin lesions, accompanied by chills and fever, joint pains and deteriorating liver function SGPT 68.5(0-38) and SGOT 222.9(10-40) it was recommended by Internal Medicine to totally discontinue present Modified MDT medications. Multiple drug resistance was considered with lepra reaction. Alternative drugs were given in Mar 06 namely Transfer Factor 300mg with cordyvants TID and Lymecycline 600mg OD for 4 months. Solid M. leprae bacillis on smears became granulated after 1 month dose and thereafter. (fig 2.3) Prednisone was tapered till 5mg every other day but self- medicated as necessary, when new ENL lesions and joint pains were noted occasionally. There was also irregular intake of Transfer Factor because of financial constraints. In Nov 07, noting the presence of one solid bacilli on smear, and an average BI 4+, he was given another 3 months course of Lymecycline 600mg OD together with more regular intake of full doses of Transfer Factor Plus cordyvant. AFS as of Feb 08 was average BI 1+. ( fig 2.4). The patient will be maintained on Transfer Factor 300mg TID plus cordyvant till AFS negative. As of this writing, he still suffers of few ENL lesions. (fig 2.5)
Case 3
A 22 year old male from Bulacan was diagnosed with Borderline leprosy in type II lepra reaction in 1Mar06. He was given MDT-MB treatment from 4April06-8March07 and Prednisone 40mg following the WHO recommendation with Clofazimine, Colchicine, Extra virgin coconut oil (EVCO), and Ranitidine. He was never totally off prednisone when in Oct. 30, 2007, he was brought to JRRMMC, wheelchair borne, unable to walk because of severe pain and swelling of both feet with deep necrotic ulcers. (fig 3.1) There was also ulceration on his knee. There was associated nausea and L abdominal pain. His baseline AFS was average BI 3+ and Ave. BI 2+ at the end of MDT-MB treatment.
His diagnosis was Lucio Phenomenon, released from treatment (RFT). Transfer factor 300mg TID plus cordyvants was prescribed as well as gradual tapering of steroid. Debridement with sandwich dressing was done on 2 weekly follow-ups and he was able to walk and go up the stairs on his 3rd week. His latest ave.BI is .5+ as of Feb08. He will continue to take transfer factor plus until he is AFS negative and aim at removing prednisone 5mg q2d as security blanket treatment.
DISCUSSION
Advances in civilization, scientific and technical progress, achievements in medicine, have not helped reduce infectious diseases; rather there are newer groups of infections that are attacking people. Leprosy, a disease known to men, existing even before Christ have long been recognized to be due to poor cellular defense against Mycobacterium leprae among advanced stages. 90% of Filipino patients with leprosy suffers from the multibacillary form of the 2,517 new cases detected in 2006, which brings to fore the high possibility of leprae reaction to 50%.
Multi-drug therapy (MDT), a regimen recommended by WHO was introduced in the Philippines in 1982. Despite very encouraging reports on MDT, nerve damage and disability in leprosy still occurs and this is induced by lepra reaction. It has been estimated that at a global level, there may be 3 million people with leprosy related impairments and disabilities.
The problem of logistics, compliance, drug intolerance and side effects to MDT-MB treatment, points to an urgent need for a supportive approach like immunotherapy. Immunotherapy has been found to shorten the course of treatment and clearance ensuring early relief from lepra reaction.
Lepra reactions are episodes of sudden increase in the immune activity of the disease versus the host. There are 2 forms of lepra reaction, type I being less severe compared to type II lepra reaction that occurs in multibacillary forms. The treatment of reactions is based on suppression of inflammation and WHO recommends the use of prednisone to do this.A high dose of prednisone 40-60mg daily taken for 12 weeks may result in several undesirable effects. These are Cushing’s syndrome, steroid induced diabetes, osteoporosis, hypertension, psychosis, depression, striae and increased susceptibility to infection especially tuberculosis. It has been reported that in borderline (BB) treatment of lepra reaction takes weeks, borderline-lepromatous (BL) wks and lepromatous leprosy (LL) wks. In these patients, there is high antibody response and the dominant cytokine circulating in their body are IL4 which promotes B cell growth and differentiation and IL10 which inhibits ThI cytokine production. Leprosy is one of infectious diseases that manifest the Th1-Th2 paradigm shift with progressive evolution of the disease from tuberculoid (TT) form exhibiting the Th1 status to lepromatous (LL) form exhibiting the Th2 status. With this basic information in mind, an important enhancement against M.leprae in our general immune system should be one of our therapeutic goals.
Transfer Factor as was used to supplement the treatment in these 3 cases has been used to effectively treat a wide range of diseases. Transfer Factor is an immune modulator. The main function of these peptides in the body is to provide immune protection against microbes (bacteria, viruses, fungi, protozoa), cancerous cells and other antigens capable of disturbing vital processes in the body. It stimulates the cellular arm of the immune system (killer lymphocytes), activates immune cytokine synthesis and regulates immune function. An evaluation of Transfer Factor as immunotherapy for patients with lepromatous leprosy was first used by Bullock, using whole lymphocytes from donors with delayed hypersensitivity to antigens of mycobacterium leprae were employed to reconstitute delayed hypersensitivity in nine patients with anergic leprosy. Six of seven converted from anergy to delayed hypersensitivity response to m. leprae antigens. Two of 3 patients showed an increase in perivascular lymphocytic infiltration in the post-transfer skin test biopsy site. Delayed hypersensitivity reactions to M. leprae antigens can be produced, with lymphocytes or their extracts, in patients with anergic leprosy. In a study by Fabre of Mexico, in his study of Transfer Factor as immunotherapy and supplement of chemotherapy in experimental pulmonary tuberculosis. When BALB/c mice are infected via trachea with M. tuberculosis, H37Rv, there is an initial phase of partial resistance dominated by Th-1 type cytokines plus tumor necrosis factor-alpha (TNFa) and the inducible isoform of nitric oxide synthetase (iNOS) followed by a phase of progressive disease characterized by increasing expression of IL-4, diminished expression of TNFa and iNOS and low DTH. Animals in this late progressive phase of the disease were treated with different doses of transfer factor ( one injection per week) obtained from spleen. The peak of immune protection in this animal model is reached on day 21(11)
Since its discovery by Sherwood Lawrence, more than 50 years ago, the therapeutic and prophylactic applications have been most important and interesting aspects of Transfer Factor. It has been found to be very effective in those diseases in which CMI plays a relevant role in protection and control of the disease , such as viral infections (herpes simplex, varicella zoster), intracellular bacterial diseases (tuberculosis, leprosy) and parasitic infections (leishmaniasis, toxoplasmosis), as well as in immunodeficiencies (chronic granulomatosis, Wiscott Aldrich syndrome and some types of cancer. Transfer Factor (TF) are protein that transfer the ability to express cell mediated immunity from immune donors to non-immune recipients. TF treatment were found to selectively affects cytokine production in response to antigenic stimulation.(12)
Transfer factors are tiny molecules also found in colostrum which provides immune knowledge from mother’s immune system to her baby used in fighting outside threats. By transferring information from cell to cell, transfer factors serve as “teacher” to the new cells, ensuring a strong immune system capable of surviving, and thriving in its new environment. Transfer factor are not species-specific and can therefore be extracted from any mammal and then be given to another mammal with the same efficacy. Transfer factor naturally supports the body’s immune system, communicating immune information more efficiently among the cells in the body, and ultimately enhancing the body’s ability to withstand attacks on its health.
Transfer Factor TM was tested for its ability to increase Natural Killer Cell (NK) activity. Peripheral blood mononuclear cells (PBMC) isolated from human volunteers showed boosting of NK cell activity by 103% above normal immune response. NK cells are important in strengthening and supporting the immune system . In advanced stage leprosy (LL)where there is poor to absent CMI activity, it was found by Bullock, etal the positive effect of Transfer factor in anergic leprosy, it was also found by Katoch etal the early clearance of bacilli in LL patients given MDT and Transfer Factor.
Conclusion:
The positive effect of Transfer Factor TM in treating Lepra reaction (case 1), combination with Lymecycline , a second generation cycline that is as effective as minocycline in treating RMP and OFLO resistance (case2) and in treating Lucio phenomenon, a very severe form of lepra reaction makes this food supplement a good material for clinical research. Transfer Factor TM, was found to be safe in oral form , has no adverse reactions and is effective in both children and adults in treating lepra reactions It was also found to enhance bacterial clearance.
References:
1). WHO Expert Committee on Leprosy. Seventh Report. WHO Technical Report Series No. 874. World Health Organization, Geneva, 1998
2). Briton, WJ. The management of leprosy reversal reactions (Editorial). Lepr Rev, 1998: 69: 225-234.
3). Rose P, Waters MF, Reversal reactions in leprosy and their management (Editorial). Kepr Rev, 1991; 62: 121-131.
4). Naafs B. Treatment of reactions and nerve damage. Int J Lepr, 1996: 64:S21-28.
5). Becx-Bleumink M, Berhe D. Occurrence of reactions, their diagnosis and management in leprosy patients treated with multidrug therapy: experience in the Leprosy Control Program of the All Africa Leprosy and rehabilitation Training Center (ALERT) in Ethiopia. Int J Lepr, 1992; 60: 173-184
6). Ji, B., E. G. Perani, C. Petinom and J. H. Grosset. 1996 Bactericidal activities of combinations of new drugs against Mycobacterium leprae in nude mice. Antimicrob Agents Chemother, 42(1998)1115-1120. 2. JI, B., etal Bactericidal activities of combination of new drugs against mycobacterium leprae in nude mice. Antimicrof.Ag Chemother, 40:393-399.
7). Ji, B., P. Jamet, S. Sow, E.G. Perani, I. Traore, and J.H. Grosset. 1997 High relapse rate among lepromatous leprosy patients treated with Rifampicin plus Ofloxacin daily for 4 weeks. Antimicrob Agents Chemother, 41: 1953-1956.
8). Lawrence H.S. The transfer in humans of delayed skin sensitivity to streptococcal M substances and to tuberculin with disrupted leucocytes.1955 J Clin Invest. 34:219-30.
9). Bullock, W.E., Fields, J.P. amd Bandvias M.W.1972 Am evaluation of transfer factor as immunotherapy for patients with lepromatous leprosy. New Eng J Med. 287:10-53.
10). Katoch 1986 Combination drug therapy
11). Fabre R A, Perez T M, Aguilar, L D, Rangel M J, Estrada-Garcia I, Hernandez-Pando R, and Estrada Parra S. Transfer factors as immunotherapy and supplement of chemotherapy in experimental pulmonary tuberculosis 2004 Clin Exp Immunol 136(2): 215-223.
12). Alvarez-Thull L, Kirkpatrick C H. Profiles of cytokine production in recipients of transfer factors. 1996 Biotherapy 9(1-3) 55-9
13). Fitzpatrick etc
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