Scleroderma

Neprinol Targets the Underlying Causes of Scleroderma

Scleroderma, also known as systemic sclerosis, is a deadly autoimmune disease that affects the connective tissue, the fibrous network that provides the framework for and supports body tissues and organs. Scleroderma causes inflammation, blood vessel damage and eventually substantial scarring of the skin, muscles, blood vessels and internal organs. The word scleroderma literally means “hard skin.”

There are two main types of scleroderma: diffuse and limited. Diffuse scleroderma affects the skin and a number of internal organs. It often progresses very rapidly and can be fatal. Limited scleroderma, on the other hand, progresses more slowly. It generally follows a pattern of symptoms known as the CREST syndrome:

  • Calcinosis Cutis – tiny calcium deposits that form under the skin
  • Raynaud’s Phenomenon – discoloration of the fingers and toes when exposed to changes in temperature or stress
  • Esophageal Involvement – difficulty swallowing and gastric reflux
  • Sclerodactyly – tightened, hardened skin, especially on the fingers and toes
  • Telangiectasia – red spots or lines on the hands and/or face

While scleroderma is the deadliest autoimmune disease [1], current medications and therapies only target symptoms. They are unable to prevent, slow down or stop scar tissue formation, which is the mechanism behind the disease [2]. However, Neprinol, a proprietary combination of serratiopeptidase (serrapeptase), nattokinase, lipase, protease, amla, papain, bromelain, rutin, coenzyme Q10 and magnesium, is specially formulated to assist your body in defending against the damaging effects of fibrin, a major component of scar tissue. Neprinol’s combination of protein-digesting, fibrin-dissolving enzymes and other nutrients not only improve CREST symptoms, but also counteract the processes that underlie scleroderma development and progression.

Combating Causes of the Disease

Researchers are still investigating what causes the excessive production and buildup of collagen, fibronectin and other proteins that accumulate in the skin and organs and lead to scleroderma [3]. Currently researchers believe that a combination of genetic and environmental factors interact to cause damage to the blood vessels [4,5]. This damage puts the body into repair mode, which increases inflammation. The damage also increases the amount of free radicals in the blood, which encourages the formation of antibodies and leads to fibrin overproduction.  This is a complicated process that doesn’t always occur in a step-by-step fashion. However, the enzymes and other natural ingredients in Neprinol are able to interfere and be of assistance at almost every stage of the disease progression.

Blood Vessel Injury

Blood vessel injury is the first step in the development of scleroderma. It encompasses a wide range of changes, from damage to the inner lining of the vessel to thickening of the vessel wall and partial or complete blockage of the vessel [5]. These blood vessel changes limit the amount of blood, oxygen and nutrients that tissues receive—which can lead to tissue damage and cause scarring. Therefore, preventing or treating blood vessel damage is vital for controlling the progression of scleroderma and preventing organ damage.

In studies using animals nattokinase, a fibrin-degrading enzyme extracted from a popular Japanese fermented soybean food [6], stopped arterial thickening following vessel damage [7-9]. This was attributed to the ability of nattokinase to breakdown blood clots that form at the vessel wall.

Inflammation

There are two different types of inflammation that affect people with scleroderma. The first occurs early in the disease as a response to vascular damage. The second is inflammation that later occurs anywhere in the body and can cause a variety of symptoms depending on where it is localized:

  • arthritis – inflammation of the joints
  • myositis – inflammation of the muscles
  • serositis – inflammation of the lining of the heart
  • pleuritis – inflammation of the lungs

Neprinol contains a number of potent, clinically proven anti-inflammatory enzymes. Fibrin-degrading enzymes have been shown to have anti-inflammatory properties [10,11], and serrapeptase in particular is especially good at reducing inflammation in the lungs [12]. Alma, also known as Indian Gooseberry, has been used in traditional Asian medicine to treat tissue inflammation for centuries [13,14]. Papain, an enzyme extracted from papayas, has also shown anti-inflammatory activity in scientific studies of rheumatic disorders [15]. When taken in combination with other ingredients papain also relieves inflammation and swelling of the throat [16-18]. Bromelain, an extract from pineapples, and rutin, a plant bioflavonoid, also have anti-inflammatory activity [19-21].

Reducing inflammation is especially important in conditions like scleroderma, not only because it helps reduce pain and other symptoms, but also because it helps limit tissue damage and promotes the growth of new, healthy tissue [22].

Free Radical Damage

Free radicals are highly destructive molecules in the body that are naturally occurring and also produced due to toxins. In people with scleroderma, researchers have found that free radicals play a major role in damaging healthy tissue and causing scar tissue formation [2]. They also reduce the amount of naturally-occurring enzymes that break down clots and scar tissue, contributing to scleroderma lung fibrosis [23]. Continuous damage by free radicals is likely the driving force behind the progressive tissue damage associated with scleroderma [2].

Neprinol is able to combat free radicals with the potent antioxidants alma and rutin. In laboratory studies, alma extracts demonstrated long-lasting and broad-spectrum antioxidant activity, protecting tissue from the oxidative stress caused by free radicals and other agents [24]. Rutin inhibits the production of free radicals via inflammatory processes [25].

Magnesium supplementation also has potential for preventing blood vessel damage caused by free radicals. It has been reported that magnesium deficiencies in rodents increase free radical production that may be linked to blood vessel injury and aorta thickening similar to what is seem in human patients with scleroderma [26].

Autoimmunity

Seventy to ninety-five percent of people with scleroderma have antibodies that are programmed to attack healthy body tissues [27]. When Neprinol is taken on an empty stomach, its enzymes circulate through the blood [28-30], breaking down things such as undigested food particles, toxic particles, dead cells and antibodies bound to foreign particles, like bacteria and viruses. These things can cause infection and autoimmune reactions. Removing waste material from the bloodstream calms down the immune system and helps reestablish the body’s natural balance. Using enzymes to balance the immune system also allows the body to properly repair damaged tissue [31,32].

Fibrosis

The buildup of scar tissue in scleroderma is thought to be caused by the body’s failure to stop the wound healing process, thereby allowing an overproduction of scar tissue. The healing process is normally balanced by enzymes that breakdown fibrin. However, inflammation, free radicals and other things can allow for excess fibrin and scar tissue formation [2].

Nattokinase, serrapeptase and bromelain are enzymes that dissolve fibrin and increase fibrin removal [33,34]. For more detailed information about the mode of action of these enzymes, see the article Neprinol and Fibrin < http://www.neprinol.org/?page_id=6>.

Treatments that break down fibrin have beneficial effects in scleroderma patients, making their skin softer and thinner, increasing range of motion, and slowing down the decline in lung function [35,36]. Treatment with fibrin-dissolving agents has also been demonstrated to improve Raynaud’s phenomenon in people with advanced scleroderma [37,38] and could prevent the most common scleroderma complication, interstitial lung disease. See the article on Pulmonary Fibrosis <http://www.neprinol.org/?page_id=639> for more information.

Choosing Neprinol Enzyme Therapy for Scleroderma

No two cases of scleroderma are alike; therefore, identifying your disease subtype, stage and involved organs is very important when considering your treatment options. However, since the unique combination of enzymes and other nutrients in Neprinol affects nearly every process involved in scleroderma development and progression, reduces common symptoms and prevents complications, Neprinol provides another choice outside of traditional prescription treatments.

References:

  1. Rao A, Khanna D. Scleroderma and Fibrosing Disorders: Advances in Management. Adv Rheumatol. 2010;8(2):53-62.
  2. Gabrielli A, Svegliati S, Moroncini G, Pomponio G, Santillo M, Avvedimento EV. Oxidative stress and the pathogenesis of scleroderma: the Murrell’s hypothesis revisited. Semin Immunopathol. 2008;30:329-337.
  3. Black CM, Stephens CO. Scleroderma-systemic sclerosis. In: Maddison PJ, Isenberg DA, Woo P, Glass DN, eds. Oxford textbook of rheumatology. Vol. 2. New York, NY: Oxford University Press; 1993:771-789.
  4. Charles C, Clements P, Furst DE. Systemic sclerosis: hypothesis-driven treatment strategies. Lancet. 2006;367:1683-1691.
  5. Prescott RJ, Freemont AJ, Jones CJ, et al. Sequential dermal microvascular and perivascular changes in the development of scleroderma. J Pathol. 1992;166:255-263.
  6. Sumi H, Hamada H, Tsushima H, Mihara H, Muraki H. A novel fibrinolytic enzyme (nattokinase) in the vegetable cheese Natto; a typical and popular soybean food in the Japanese diet. Experientia. 1987;43:1110-1111.
  7. Gong M, Lin HB, Wang Q, Xu JP. Effect of nattokinase on restenosis after percutaneous transluminal angioplasty of the abdominal artery in rabbits. Nan Fang Yi Ke Da Xue Xue Bao. 2008;28(9):1538-1541.
  8. Suzuki Y, Kondo K, Matsumoto Y, et al. Dietary supplementation of fermented soybean, natto, suppresses intimal thickening and modulates the lysis of mural thrombi after endothelial injury in rat femoral artery. Life Sci. 2003;73:1289-1298.
  9. Suzuki Y, Kondo K, Ichise, H, et al. Dietary supplementation with fermented soybeans suppresses intimal thickening. Nutrition. 2003;19:261-264.
  10. Selezneva AA, Bolshakova MD. Proteolytic complex from Aspergillus terricola. Prikl Biokhim Mikrobiol. 1986;22(1):3-11.
  11. Selezneva AA, Babenko GA, Bolshakova MD, Rozhanskaia TI, Margolina NA. Preparative isolation of terrilytin components and study of their enzymatic properties. Prikl Biokhim Mikrobiol. 1976;12(3):416-420.
  12. Mazzone A, Catalani M, Costanzo M, et al. Evaluation of Serratia peptidase in acute or chronic inflammation of otorhinolaryngology pathology: a multicentre, double-blind, randomized trial versus placebo. J Int Med Res. 1990;18:379-388.
  13. Asmawi MZ, Kankaanranta H, Moilanen E, Vapaatalo H. Anti-inflammatory activities of Emblica officinalis Gaertn leaf extracts. J Pharm Pharmacol. 1993;45:581-584.
  14. Ihantola-Vormisto A, Summanen J, Kankaanranta H, et al. Anti-inflammatory activity of extracts from leaves of Phyllanthus emblica. Planta Med. 1997;63:518-524.
  15. Leipner J, Iten F, Saller R. Therapy with proteolytic enzymes in rheumatic disorders. BioDrugs. 2001;15(12):779-789.
  16. Raus I. Clinical studies on Frubienzyme in a controlled double-blind trial. Fortschr Med. 1976;94:1579-1582.
  17. Bienen H, Raus I. Therapeutic comparison of throat lozenges. MMW Munch Med Wochenschr. 1981;123:745-747.
  18. Reinecke M. Treatment of inflammatory diseases of the mouth and throat with Larypront in ENT practice. MMW Munch Med Wochenschr. 1976;118:1253-1254.
  19. Hale LP, Greer PK, Sempowski GD. Bromelain treatment alters leukocyte expression of cell surface molecules involved in cellular adhesion and activation. Clin Immunol. 2002;104:183-190.
  20. Cruz T, Galvez J, Ocete MA, et al. Oral administration of rutoside can ameliorate inflammatory bowel disease in rats. Life Sci. 1998;62:687-95.
  21. Galvez J, Cruz T, Crespo E, et al. Rutoside as mucosal protective in acetic acid-induced rat colitis. Planta Med. 1997;63:409-414.
  22. Pizzorno JE, Murray MT. Textbook of Natural Medicine. 3rd ed. New York, NY: Churchill Livingstone; 2005:1138.
  23. Kinnula VL, Fattman CL, Tan RJ, et al. Oxidative stress in pulmonary fibrosis. A possible role for redox modulatory therapy. Am J Respir Crit Care Med. 2005;172:417-422.
  24. Chaudhuri RK. Emblica cascading antioxidant: a novel natural skin care ingredient. Skin Pharmacol Appl Skin Physiol. 2002;15(5):374-380.
  25. Ronzio B. Polyphenols as Anti-Inflammatory Agents. J Naturopath Med. 2000;9(1):44-50.
  26. Shivakumar K, Kumar BP. Magnesium deficiency enhances oxidative stress and collagen synthesis in the aorta of rats. Int J Biochem Cell Biol. 1997;29(11):1273-1278.
  27. Harris ML, Rosen A. Autoimmunity in scleroderma: the origin, pathogenetic role and clinical significance of autoantibodies. Curr Opin Rheumatol. 2003;15:778-784.
  28. Moriya N, Nakata M, Nakamura M, et al. Intestinal absorption of serrapeptase (TSP) in rats. Biotechnol Appl Biochem. 1994;20(Pt 1):101-108.
  29. Erlund I, Kosonen T, Alfthan G, et al. Pharmacokinetics of quercetin from quercetin aglycone and rutin in healthy volunteers. Eur J Clin Pharmacol. 2000;56:545-553.
  30. Fujita M, Hong K, Ito Y, Misawa S, Takeuchi N, Kariya K, Nishimuro S. Transport of nattokinase across the rat intestinal tract. Biol Pharm Bull. 1995;18(9):1194-1196.
  31. Vokálová I. Systémová enzýmoterapia v liečbe detí s recidivujúcemi respiračními infekcemi. Vox Pediatriae. 2002;2(9):29-30.
  32. Onken JE, Greer PK, Calingaert B, et al. Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro. Clin Immunol. 2008;126(3):345-352.
  33. Fujita M, Hong K, Ito Y, et al. Thrombolytic effect of nattokinase on a chemically induced thrombosis model in rat. Biol Pharm Bull. 1995;18:1387-1391.
  34. Maurer HR. Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001;58:1234-1245.
  35. Zarafonetis CJ. Para-aminobenzoic acid therapy in scleroderma and lymphoblastoma cutis. J Lab Clin Med. 1948;33:1462-1463.
  36. Zarafonetis CJ, Dabich L, Devol EB, et al. Retrospective studies in scleroderma: pulmonary findings and effect of potassium p-aminobenzoate on vital capacity. Respiration. 1989;56:22-33.
  37. Jarrett PE, Morland M. Treatment of Raynaud’s phenomenon by fibrinolytic enhancement. Br Med J. 1978;2:523.
  38. Ayres ML, Jarrett PEM, Browse NL. Blood viscosity, Raynaud’s phenomenon and the effect of fibrinolytic enhancement. Br J Surg. 1981;68(1):51-54.

Leave a Reply

You must be logged in to post a comment.