Natural Scleroderma Relief

Natural Scleroderma Relief

Here's a quick look at what this new report covers: Calcium deposits (Calcinosis) noticible on the top layre of skin. How to permanently kill all the pathogenic nano bacteria using an easy to find supermarket product. A simple procedure which will stop the pathogenic bugs from ever returning. The easiest way to rid your body of all its harmful toxins & pollutants. Treating bacterial and fungal problems associated with the gastro-Intestinal tract naturally. A simple detoxification and cleansing agent for the kidneys. Re-build and strengthen your Immune-system. Restore your digestive system to its normal healthy state. Expelling excess free radicals from your body. Removing heavy metals deposits trapped in your body. Dealing with your depression. Re-charging your energy levels. Ease joints. Break down & remove excess calcium from your body without any medical intervention. Stop Acid Reflux problems in days without drugs

Natural Scleroderma Relief Summary


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Author: Sally Deacon

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Histopathological Assessment Of Acute And Chronic Gvhd

Histopathology can be an important element in the analysis of GVHD. In irradiated AGVHD models, the main tissues affected are the liver, intestinal tract, and skin in unirradiated P F1 AGVHD models, the skin is comparatively unaffected. Changes in the liver include lymphocytic infiltrates in the peribiliary areas, intraepithelial infiltrates in the bile ducts and ductules, and degeneration of hepatocytes (acidophilic bodies) and biliary epithelial cells. In the intestine, lesions consist of shortening and loss of crypts and degeneration of crypt epithelial cells, infiltraton of lymphocytes into the lamina propria, and erosion of the mucosal epithelia. Skin lesions affect primarily the epidermis, including vacuolar degeneration of basal epithelial cells, dyskeratotic squamous epithelial cells, and epidermal clefts. In CGVHD, the skin is again a major target organ, but the changes differ from those of AGVHD CGHVD skin lesions are characterized by dermal fibrosis and immunoglobulin...

Background Information

Whereas AGVHD models emphasize cellmediated immune processes, chronic GVHD (CGVHD) models focus upon the development of chronic, B cell-stimulatory autoimmune disorders (Goldman et al., 1991) AGVHD appears to be an inflammatory process mediated by TH1 cytokines, whereas CGVHD is mediated by Th2 cytokines. CGVHD is characterized by prolonged splenomegaly and lym-phadenopathy. Mice develop symptoms of systemic autoimmune disorders, including immune complex glomerulonephritis (Ito et al., 1992), primary biliary cirrhosis (Saitoh et al., 1991), and Sj0gren-syndrome- or scleroderma-like lesions (Fujiwara et al., 1991). Elevated levels of immunoglobulins, particularly IgG1 and IgE, and a variety of autoantibodies (including anti-DNA) are present in the serum. In general, the autoimmune syndrome of CGVHD is lethal within 6 months, due to development of immune complex-mediated glomerular nephritis. Murine CGVHD models share many of the pathologic features of the clinical disorder of chronic...

Metabolic derangements that accompany liver failure

Scleroderma may cause aperistalsis due to fibrosis and atrophy of smooth .muscle. Lower LES becomes incompetent, and patients may develop GERD. Look for positive antinuclear antibody and mask-like fades, other autoimmune symptoms (CREST calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias).

CAMs in Cutaneous Lupus Erythematosus

Figurate Erythema Dermatology

Endothelial VCAM-1 staining was increased in biopsy samples from LE lesions compared with scleroderma and morphea (Jones et al. 1996), and increased expression of VCAM-1 has been found in nonlesional skin in patients with SLE and correlated to disease activity (Belmont et al. 1994). Activated endothelium, perhaps associated with increased endothelial expression of nitric oxide synthase, has been proposed as a unifying hypothesis for the diverse nature of SLE vascular lesions (Bel-mont and Abramson 1997). Patients with LE display aberrant kinetics and a prolonged time course of the epidermal expression of inducible nitric oxide synthase after UV provocation (Kuhn et al. 1998).

Elevated Eosinophil and Basophil Counts

Reactive Bronchial Cells

Bacterial and viral infections are both unlikely ever to lead to eosinophilia except in a few patients with scarlet fever, mononucleosis, or infectious lymphocytosis. The second most common group of causes of eosinophilia are allergic conditions these include asthma, hay fever, and various dermatoses (urticaria, psoriasis). This second group also includes drug-induced hypersensitivity with its almost infinitely multifarious triggers, among which various antibiotics, gold preparations, hydantoin derivatives, phenothiazines, and dextrans appear to be the most prevalent. Eosinophilia is also seen in autoimmune diseases, especially in scleroderma and panarteritis. All neoplasias can lead to paraneoplastic eosinophilia, and in Hodgkin's disease it appears to play a special role in the pathology, although it is nevertheless not always present.

Humoral Autoimmune Responses Against Nuclear Proteins

Patients with systemic rheumatic diseases such as systemic lupus erythematosus (SLE), scleroderma, and Sjogren's syndrome characteristically produce antinuclear antibodies (ANAs) that recognize intracellular nucleoprotein complexes. Systemic rheumatic diseases constitute chronic, life-threatening, multiorgan autoimmune disorders (Reichlin 1998). Their etiology is unknown, but genetic, hormonal, and environmental factors are involved. SLE is best characterized as a systemic immune complex vasculitis due to continued production of autoantibodies directed against nucleoplasmic antigens (e.g., DNA, histones, spliceosomal components, ribonucleo-proteins), whereas scleroderma-associated autoantibodies primarily detect nucleo-lus-associated proteins such as DNA topoisomerase I (Scl-70) and centromeres. Autoantibodies target evolutionary, conserved epitopes of nucleoprotein complexes, which often constitute the functional regions (Tan 1989). Thus, the immunofluores-cence staining patterns...

Erythropoietic protoporphyria

Perioral furrowing, and aged-appearing, thickened, or hyperkeratotic skin of the dorsal hands with sustained, more intense, or frequent exposures, waxy scleroderma-like induration and or weather-beaten or cobblestone textures of the face and dorsal aspects of hands progressive liver failure in rare instances, with hepatosplenomegaly and jaundice

Hydroxamate Inhibitors for Blocking Tumors

Some hydroxamate-based inhibitors have also been developed for other clinical applications. Galardin or GM6001, another hydroxamate inhibitor, is one of the most potent peptide inhibitors of human skin fibroblast collagenase with a K of 0.4 nM.110 While it is effective in inhibiting MMP-1, it is not specific since similar Ki values have been measured for neutrophil collagenase, and gelatinases A and B.111 GM6001 has been shown to inhibit angiogenesis in rats and chick chorioallantoic membranes,112,113 corneal ulceration due to chemical and infectious insults in rabbits113 and phorbol ester-induced skin inflammation and thickening when applied topically to the ears of hairless mice.111 Interestingly, GM1489, in which a carboxylic acid group replaces the hydroxamate and a phenylmethyl group replaces methyl at the P3' position, was as effective as GM6001 in reducing skin thickening, although GM1489 is specific for MMP-1 over MMP-2, MMP-3, MMP-8 and MMP-9 by at least several orders of...

Clinical manifestation

Type III very similar to type I, but onset within the first 2 years of life Type IV occurs in prepubertal children sharply demarcated areas of follicular hyperkeratosis and erythema of the knees and elbows, without progression Type V most cases of familial disease belong to this group early onset and chronic course prominent follicular hyper-keratosis scleroderma-like changes on the palms and soles infrequent erythema Type VI HIV-associated nodulocystic and pustular acneiform lesions resistant to standard treatments but sometimes responds to antiretroviral therapies

Miscellaneous fibrotic conditions

Progressive systemic sclerosis (scleroderma) Microscopy Similar to scleroderma but more intense and lacking perivascular infiltrate (Fig. 259). Sometimes there is epithelial dysplasia, which is possibly prcmalignant. fig. 258 Scleroderma submucosal fibrosis with muscle destruction in the tongue and perivascular lymphocytic infiltrate. fig. 259 Oral submucous fibrosis deeper extension of fibrosis and muscle destruction than in scleroderma. fig. 259 Oral submucous fibrosis deeper extension of fibrosis and muscle destruction than in scleroderma.

Intravenous Immunoglobulin

The exact mechanisms of action of intravenous immunoglobulin (IVIg) are unknown, but there is evidence for the solubilization of immune complexes or anti-idio-typic down-regulation of autoantibody production as well as induction of immuno-modulating cytokines such as transforming growth factor p and IL-10 (Ballow 1997, McMurray 2001, Rutter and Luger 2002). Considering the role of autoantibodies such as anti-ds-DNA antibodies in the pathogenesis of SLE, treatments such as IVIg designed to remove or neutralize these antibodies seemed to be promising. IVIg is currently approved for the treatment of Kawasaki disease, immune thrombocy-topenic purpura, and Guillain-Barre syndrome. In addition, skin diseases such as autoimmune blistering diseases, scleroderma, and dermatomyositis have been successfully treated with IVIg. Some studies using IVIg for the management of LE indicate improvement in nephritis, SLAM scores, myocardial dysfunction, cerebritis, and autoantibodies titers (Levy et al....

Subsets of Systemic Lupus Erythematosus

High titer in syndromes with features of polymyositis, lupus, scleroderma, and mixed connective tissue disease if present in SLE without anti-DNA, risk of nephritis is low In 1972, Sharp et al. (Sharp et al. 1972) described a mixed connective tissue disease subset with clinical features of SLE, scleroderma, and polymyositis. Serologically, this group is defined by the occurrence of ANAs, with a coarse speckled pattern revealing anti-UlRNP specificity (without anti-Sm antibodies). Rheumatoid factors and hypergammaglobulinemia are often present. Nearly all patients demonstrate Raynaud's phenomenon, acrocyanosis, edematous sclerodactyly, telangiectasias, and other ery-thematous skin lesions (Schneider and Fischer 2000). Dysphagia due to disturbance of esophageal motility is a frequent symptom, and microstomia and pulmonary basal fibrosis are also indicative of overlapping scleroderma as inflammatory myopathy for polymyositis. Renal or cerebral involvement is very rare, but transition...

Lupus Erythematosus and Sjgrens Syndrome

Anti-La SSB occurs in approximately 15 of patients, and most have SS and may be diagnosed as having SS-SLE overlap syndromes. Anti-Ro SSA (without anti-La SSB) occurs in approximately 30 of patients with SLE without dry eyes or mouth. SS can precede LE by years, but LE can precede the appearance of SS also. Anti-Ro SSA antibodies etc found in polymyositis, scleroderma, and primary biliary cirrhosis, and association with SS is invariably (Venables 1988). The skin changes associated with SS include dry eyes, dry mouth, and dry genitals as major clinical symptoms. Other clinical symptoms include annular erythema, Sweet's syndrome-like lesions, vitiligo-like changes, sarcoidosis, and LP-like and amyloidosis nodularis-like symptoms (Ueki 1994, personal communication). Annular erythema is one of the prominent clinical features of both SS and SLE. Katayama et al. (Katayama et al. 1991) subdivided annular erythema into three types. Type I is an isolated annular erythema with an elevated and...

Menetrier Disease

Annular Pancreas Ugi

Dilatation in hollow peristaltic organs occurs either because of distal obstruction or because of intrinsic neural, or muscular, abnormality. Excluding a mechanical obstruction, the most common cause of dilatation is adynamic ileus. The precise mechanism is often unclear. It can result from local irritation, apparently involving the autonomic nerve plexi in the bowel wall. Dilatation caused by intrinsic structural changes in the bowel is relatively uncommon. Achalasia is a classic prototype in which deficiency of ganglion cells in Auerbach's plexus of the esophagus results in hypotonia and progressive dilatation. Gastroparesis from diabetic neuropathy and smooth muscle atony and atrophy in scleroderma (progressive systemic sclerosis) due to collagen vascular disease are other examples.


Photopheresis is another variation of apheresis in which the white cell component is exposed to ultraviolet radiation ex vivo. In this technique, a photoactive dye such as psoralen (8-methoxypsoralen or 8 MOP) is taken by mouth. Several hours later, the apheresis procedure is performed. Ex vivo, the white cell component is separated and exposed to ultraviolet radiation causing drug activation. Although the precise mechanism of action is not understood, it is considered that the photochemical reaction causes both a cell membrane and a nucleic acid effect. The only clearly accepted indication for photopheresis is in the treatment of cutaneous T-cell lymphoma (CTCL) where dramatic remissions in skin lesions are often observed. There have been enthusiastic claims for the benefits of photopheresis in scleroderma, although a clear indication is uncertain at this time. Photopheresis has also been used in the prophylactic management of acute graft rejection in patients with cardiac...

Mouse Phenotype

Although embryonic development of the r r mice appeared to be normal, as early as approximately 4 weeks of age they began to develop thick skin and patchy hair loss accounted for by dermal fibrosis. In older mice ( 5-6 months) skin abnormalities consisting of thickening and roughening, associated with patchy hair loss and small ulcerations were regularly observed.33 Indeed, in our initial report, we had not yet systematically examined the younger mice. Examination of skin sections revealed that the dermis from the r r mutant mice was significantly thicker than that from control (r r) mice and was filled with dense collagen fibers (Fig.10.4). The collagen fibers were irregular in form and penetrated deeply into the hypodermis. The overall increased thickness of the skin in the homozygous r r mice, extending from the epidermis to the muscular layer, was accounted for by the increase in thickness in the dermis. The hair follicles appeared to be buried within the dense collagenous...