The many faces of scleroderma sine scleroderma: a literature review focusing on cardiopulmonary complications

Scleroderma sine scleroderma (ssSSc) is an occult form of systemic sclerosis that may cause diagnostic difficulties due to the absence of skin involvement. Delays in the diagnosis of ssSSc means lost opportunites to address and treat the often lethal involvement of internal organs such as the lungs and heart. In this systemic review we collected all published cases of ssSSc using EMBASE, MEDLINE, PubMed, and Web of Science from 1950 to present.

Our purpose was to describe the range and frequency of the clinical manifestations of ssSSc. A total of 108 published cases of ssSSc were analyzed. Lung involvement was present in 66% of cases. Peripheral vascular system involvement was present in all patients whereas gastrointestinal manifestations were present in 82% of the cases. Overall the clinical presentation is subtle and heightened clinical awareness is required to facilitate prompt recognition and treatment.

Non-Hodgkin's lymphoma in systemic sclerosis: case and literature review.

Clin Rheumatol. 2010 Jan;29(1):1-6. Epub 2009 Oct 7.

The occurrence of non-Hodgkin's lymphoma in systemic sclerosis is an uncommon event. In our scleroderma cohort, a case of primary gastric B-cell lymphoma was diagnosed in 2007. The patient was a 45-year-old woman suffering from late systemic sclerosis sine scleroderma in whom non-Hodgkin's lymphoma presented with progressive weight loss, later with gastrointestinal symptoms.

Subsequently, we retrospectively analyzed the charts of 251 systemic sclerosis patients consecutively admitted to our Unit from 2000 to 2008 to search for other non-Hodgkin's lymphoma cases (prevalence, 0.49%). Then we performed a Pubmed search for "systemic sclerosis & non-Hodgkin's lymphoma," limited to the English language.

Twenty detailed cases of such an association were found, pointing out the following: non-Hodgkin's lymphoma seems to be associated to old age, female sex, diffuse cutaneous subset and early disease; B-cell lymphoma subtypes are the majority; the interval between systemic sclerosis and lymphoma onset is usually short; systemic sclerosis could present as a paraneoplastic syndrome in some cases.

We concluded that, although rare, the association of systemic sclerosis and non-Hodgkin's lymphoma may not be coincidental and the clinician should be aware of the risk for lymphoproliferative disorders in scleroderma patients.

This is the first description of non-Hodgkin's lymphoma in systemic sclerosis sine scleroderma. The insidious onset of gastric lymphomas, mimicking the most common features of gastrointestinal involvement in systemic sclerosis is underlined.

Why the Conventional Treatment of Scleroderma is Flawed

Scleroderma is a relatively common and often debilitating condition. In light of that, one might reasonably assume that scientists and medical professionals would be able to devise a successful method for the treatment of the disorder. Unfortunately, that's not the case. The conventional means by which the medical profession addresses Scleroderma merely masks symptoms while ignoring its underlying causes. Ironically, the most frequently prescribed treatments may actually contribute to a worsening of the condition.

The Conventional Treatment of Scleroderma

The most common response to Scleroderma involves the use of medications. These include immunosuppressants like Mehotrexate and Cytoxan, no steroidal anti-inflammatory drugs (NSAIDs) and cortiosteroids. Doctors may recommend the use of antacids, medications to aid in breathing and blood pressure medications to aid in the treatment of some of Scleroderma's symptoms, as well.

A Symptom-Only Approach

Unforunately, the usual treatment of Scleroderma is focused exclusively on mitigating its symptoms. That is a perfectly reasonable way to provide patients with some degree of relief, but it does absolutely nothing to eliminate the root causes of the malady. Medicating symptoms away is akin to regularly changing bandages on an otherwise untreated open wound. It may make things seem a little better, but it isn't encouraging real healing.

The status quo subscribes to this method of treatment because the medical community maintains there is a lack of certainty regarding the core cause of Scleroderma. They note a potential genetic tendency toward the condition, but don't make claims regarding its triggers. However, there is growing evidence indicating that pathogenic nano bacteria are a major factor in the development of Scleroderma. The multiplication of the bacteria hardens and destroys skin cells while creating visible superficial Calcinosis, according to some researchers.

How the Treatment of Scleroderma Backfires

The ability of the body to respond to pathogenic nano bacteria is carefully tied to the way the body reacts to toxins in general. Those with overreactive systems find themselves at war with foreign toxins, encouraging more pathogenic bacteria growth while being unable to effectively combat the development.

Ironically, the very medications used to combat Scleroderma leads to the accumulation of toxins within the body. Defeating the symptoms also serves as a trigger for the disorder, according to this school of thought. This means that the normal treatment of Scleroderma is worse than ineffective--it's actually destructive. The "cure" actually encourages the disorder.

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The 2 Types of Scleroderma

What is Scleroderma?

Scleroderma refers to a widespread disease afflicting connective tissues. It can produce deleterious changes in internal organs, muscles, blood vessels and the skin. The symptoms of the two types of Scleroderma are quite diverse. They range from hair loss and skin hardening to breathing problems, heartburn and difficulties with swallowing in severe cases of diffuse Scleroderma, the internal organs can be fatally damaged.

The Two Types of Scleroderma

Scleroderma takes two primary forms. The first is known as limited Scleroderma. It's also referred to as morphea Scleroderma. CREST is another descriptor for this condition.

While limited Scleroderma can be quite serious, especially when it contributes to pulmonary hypertension, symptoms are generally limited to the face and extremities. Join pain, skin hardening, red marks, and other symptoms are quite common.

Diffuse Scleroderma is the more serious of the two types of this disease. Also known as system-wide, the condition tends to progress much more quickly than limited Scleroderma and with greater negative impact.

Those who suffer from diffuse Scleroderma will often suffer from the same symptoms as those who have morphea Scleroderma diagnoses. However, they may often encounter problems with critical internal organs, including the heart, lungs and kidneys. Often those with diffuse conditions will suffer the same kind of skin-related symptoms over a larger area than those with a limited case of the disorder.

Obviously, any case of Scleroderma must be taken seriously. Both types are progressive, have serious symptoms and can be fatal. That being said, the prognosis for those with limited Scleroderma is better than it is for those with a system-wide manifestation

Causes and Cures for Scleroderma

Considering the seriousness of the condition and its relatively high frequency, it would be reasonable to assume that the cause of the malady was well-known and that effective treatment regimens were available. That's not really the case, however.

The medical community isn't prepared to offer a clear position regarding the causes of Scleroderma and treatments currently focus on the management of symptoms, not the elimination of the conditions themselves. However, there is a growing body of evidence suggesting that both types may be related to the body's ability to handle toxicity and the resultant multiplication of microscopic pathogenic bacteria. This opens the door for natural treatment regimens that may be capable of producing real results for those diagnosed with Scleroderma.

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Does Cherry Juice Really Help Gout and Arthritis Pain?

I Keep On Baking Because I Think It'll make You Love Me by littlebluepenguin featuring Alexander McQueen tops

The question many joint pain suffers are asking is does tart cherry juice reduces joint pain caused by gout and arthritis? Will this natural product help to reduce pain with less side effects than prescription drugs. Let's look at the published research dating back to the 1950's to begin our examination of the tart cherry.

In the 1950's the results of study reported that Ludwig Blau indicated that Mr. Blau was able to get up out of his wheelchair and walk again due to eating cherries. According to the published results, Ludwig Blau's pain was due to gout and he was unable to leave his wheelchair, however after eating tart cherries he was able to walk again.

A more recent study from Michigan State University published in 1999 points to the naturally occurring Anthocyanins of the tart cherry. This tiny fruit is one of the leading sources of Anthocyanins and the study indicated the Anthocyanins in the cherry are natural Cox inhibitors. In addition, these Anthocyanins help to protect the lining of the stomach to reduce stomach related issues unlike some prescription arthritis drugs. So the cherry is a natural inhibitor and protects the stomach, this a win-win for pain suffers.

Also, according to the Arthritis Foundation, drinking three glasses of tart cherry juice per day may help some people with arthritis. This is a very influential and research based organization so this information bodes well for the cherry and arthritis pain. So if you are looking a way to reduce joint pain naturally consider cherry juice. However, according to some people I talked with while researching this article indicated that drinking cherry juice everyday may be difficult for many. This reason is cherry juice needs to be refrigerated and it is difficult to take while traveling.

I discovered that tart cherry capsules are also available. In fact, according the Ralph Oakes, a manager of a local health store in Indianapolis, Indiana, the tart cherry capsules deliver more antioxidant then the cherry juice. According to Mr. Oakes, "The tart cherry capsules provide not only the pulp of the cherry, but the skin as well. Most of antioxidants of fruit is found in the skin, so I recommend my customers to take the capsules over the juice for both convenient and getting the skin." One company he recommends for cherry-based products is Traverse Bay Farms. They offer a complete line of cherry products including cherry juice, cherry capsules and dried cherries.

So the next time you are looking a natural way to fight joint pain, consider drinking a glass of cherry juice or taking some cherry capsules, your joints will thank you.

Download a free copy of the Tart Cherry Health Report at http://www.traversebayfarms.com Traverse Bay Farms. Ms. Cushman writes about the healing power of foods.

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The Health Benefits of Zinc

Zinc is a mineral found in almost every cell and is an essential nutrient for the body. Zinc is available in various food sources and is also made available as supplements (as single-ingredient or multi-vitamins).

1. Benefits of zinc

Zinc promotes biochemical reactions in the body by stimulating activity in about 100 enzymes. Zinc is essential for a healthy immune system, aids in wound healing, helps maintain the sense of smell and taste, supports normal growth and development, and is essential for DNA synthesis. In the form of zinc salts, it helps fight against pathogens when directly applied.

The ingestion of zinc salts also help in gastrointestinal infections, providing antimicrobial action in the GI tract. Zinc salts are also used as lozenges, to help kill bacteria and viruses. It should be noted however, that the administration of zinc to fight against pathogens without damaging tissues, is still being studied.

2. Food sources of zinc

Oysters are found to be rich in zinc. Other food sources that contain zinc, albeit a lesser degree, include sunflower seeds, pumpkin seeds, nuts, whole grains, beans, and most animal proteins. Phytates, a compound found in legumes, cereals, and grain breads, may decrease the absorption of zinc.

3. Recommended dosage

According to the Recommended Dietary Allowance (RDA), the recommended dosage of zinc for healthy individuals varies across age groups. For infants from 0 through 6 months, 2.0 mg of zinc per day is recommended. The recommended dosage for zinc is 3 mg per day for those 7 months to 3 years, 5mg for those 4 to 8 years, and 8 mg for those 9 to 13 years.

Those 14 and above are advised to take 11 mg of zinc for males, and 9 mg for females. Higher dosages may be needed for pregnant and lactating women. The RDA suggests 13 mg of zinc for women who are pregnant at age 14 to 18 years, and 11 mg for those pregnant at age 19 years and up. About 14 mg is the dosage recommended for lactating women at age 14 to 18, and 12 mg for lactating women at age 19 and up.

3. Zinc deficiency

Zinc deficiency may result to skin lesions, hair loss, diarrhea, poor taste, smell, and eyesight, malfunction of said organs, wasting of body tissues, and, even death. Congenital abnormalities may also lead to Acrodermatitis enteropathica.

TIP: Zinc and other nutritional supplements are unregulated by the Food and Drug Administration Board. It is best to choose a manufacturer that rigorously complies with GMP standards to avoid product contamination and misrepresentation of dosage and contents.

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Localized scleroderma and zinc: a pilot study.

Eur J Dermatol. 2010 Feb 2

Esthetic or functional repercussions in localized scleroderma may be considerable. Numerous treatments have been proposed with limited effectiveness. The purpose of this study was to evaluate the efficacy of high-dose zinc gluconate in the treatment of morphea. We are reporting a retrospective study of 17 patients with histologically confirmed localized scleroderma active for more than one year and whose treatment with a high potency dermocorticosteroid was a failure.

The patients received 60 to 90 mg of zinc metal daily. The clinical evaluation was performed by the physician and the patient. An efficacy of 53% was obtained (5 partial remissions and 4 complete remissions) with a mean dose of 83.3 mg/day of zinc metal. Two patients (11.8%) had epigastralgia; no discontinuation of zinc gluconate for poor tolerability was noted.

We conclude that high-dose zinc gluconate can therefore be a valuable alternative treatment for localized scleroderma, with good tolerability, although placebo-controlled studies are necessary to confirm our results.

Autoantibodies as predictive tools in systemic sclerosis.

Nat Rev Rheumatol. 2010 Feb;6(2):112-6.

The pathogenetic role of autoantibodies in systemic sclerosis (SSc) remains unclear, but these autoantibodies have been established as strong predictors of disease outcome and the pattern of organ complications in patients with this condition.

The three most frequently observed types of SSc-specific autoantibody-anti-centromere antibodies, anti-topoisomerase antibodies and anti-RNA polymerase III antibodies-are found in over 50% of patients; the presence of each is generally exclusive of the others.

Although a lot less frequently observed, antibodies directed against U3RNP and Th/To are also specific for scleroderma, whereas anti-Pm/Scl, anti-Ku and anti-U1RNP antibodies are seen mainly in patients with overlap syndromes. Up to 11% of patients with SSc can test negative for antinuclear antibodies.

Strong links exist between autoantibody specificities and disease presentation and outcome, which make autoantibodies essential assessment tools in patients with SSc.

Mechanisms in the loss of capillaries in systemic sclerosis: angiogenesis versus vasculogenesis.

J Cell Mol Med. 2010 Jan 30

Abstract

Systemic sclerosis (SSc, scleroderma) is a chronic, multisystem connective tissue disorder affecting the skin and various internal organs. Although the disease is characterized by a triad of widespread microangiopathy, fibrosis, and autoimmunity, increasing evidence indicates that vascular damage is a primary event in the pathogenesis of SSc.

The progressive vascular injury includes persistent endothelial cell activation/damage and apoptosis, intimal thickening, delamination, vessel narrowing and obliteration. These profound vascular changes lead to vascular tone dysfunction and reduced capillary blood flow, with consequent tissue ischemia and severe clinical manifestations, such as digital ulceration or amputation, pulmonary arterial hypertension, and scleroderma renal crisis.

The resulting tissue hypoxia induces complex cellular and molecular mechanisms in the attempt to recover endothelial cell function and tissue perfusion. Nevertheless, in SSc patients there is no evidence of significant angiogenesis and the disease evolves towards chronic tissue ischemia, with progressive and irreversible structural changes in multiple vascular beds culminating in the loss of capillaries.

A severe imbalance between pro-angiogenic and angiostatic factors may also lead to impaired angiogenic response during SSc. Besides insufficient angiogenesis, defective vasculogenesis with altered numbers and functional defects of bone marrow-derived endothelial progenitor cells may contribute to the vascular pathogenesis of SSc.

The purpose of this article is to review the contribution of recent studies to the understanding of the complex mechanisms of impaired vascular repair in SSc. Indeed, understanding the pathophysiology of SSc-associated vascular disease may be the key in dissecting the disease pathogenesis and developing novel therapies.

Either angiogenic or vasculogenic mechanisms may potentially become in the future the target of therapeutic strategies to promote capillary regeneration in SSc.