Find information on thousands of medical conditions and prescription drugs.

Scleroderma

Scleroderma is a rare, chronic disease characterized by excessive deposits of collagen. Progressive systemic scleroderma or systemic sclerosis, the generalised type of the disease, can be fatal. The localised type of the disease tends not to be fatal. more...

Home
Diseases
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
Sabinas brittle hair...
Saccharopinuria
Sacral agenesis
Saethre-Chotzen syndrome
Salla disease
Salmonellosis
Sandhoff disease
Sanfilippo syndrome
Sarcoidosis
Say Meyer syndrome
Scabies
Scabiophobia
Scarlet fever
Schamberg disease...
Schistosomiasis
Schizencephaly
Schizophrenia
Schmitt Gillenwater Kelly...
Sciatica
Scimitar syndrome
Sciophobia
Scleroderma
Scrapie
Scurvy
Selachophobia
Selective mutism
Seminoma
Sensorineural hearing loss
Seplophobia
Sepsis
Septo-optic dysplasia
Serum sickness
Severe acute respiratory...
Severe combined...
Sezary syndrome
Sheehan syndrome
Shigellosis
Shingles
Shock
Short bowel syndrome
Short QT syndrome
Shprintzen syndrome
Shulman-Upshaw syndrome
Shwachman syndrome
Shwachman-Diamond syndrome
Shy-Drager syndrome
Sialidosis
Sickle-cell disease
Sickle-cell disease
Sickle-cell disease
Siderosis
Silicosis
Silver-Russell dwarfism
Sipple syndrome
Sirenomelia
Sjogren's syndrome
Sly syndrome
Smallpox
Smith-Magenis Syndrome
Sociophobia
Soft tissue sarcoma
Somniphobia
Sotos syndrome
Spasmodic dysphonia
Spasmodic torticollis
Spherocytosis
Sphingolipidosis
Spinal cord injury
Spinal muscular atrophy
Spinal shock
Spinal stenosis
Spinocerebellar ataxia
Splenic-flexure syndrome
Splenomegaly
Spondylitis
Spondyloepiphyseal...
Spondylometaphyseal...
Sporotrichosis
Squamous cell carcinoma
St. Anthony's fire
Stein-Leventhal syndrome
Stevens-Johnson syndrome
Stickler syndrome
Stiff man syndrome
Still's disease
Stomach cancer
Stomatitis
Strabismus
Strep throat
Strongyloidiasis
Strumpell-lorrain disease
Sturge-Weber syndrome
Subacute sclerosing...
Sudden infant death syndrome
Sugarman syndrome
Sweet syndrome
Swimmer's ear
Swyer syndrome
Sydenham's chorea
Syncope
Syndactyly
Syndrome X
Synovial osteochondromatosis
Synovial sarcoma
Synovitis
Syphilis
Syringomas
Syringomyelia
Systemic carnitine...
Systemic lupus erythematosus
Systemic mastocytosis
Systemic sclerosis
T
U
V
W
X
Y
Z
Medicines

The term 'localised, generalised sclerderma' can be used to describe cases where the disease covers a large area of the body - typically more than 40%.

Signs and symptoms

Scleroderma affects the skin, and in more serious cases, it can affect the blood vessels and internal organs. The most evident symptom is the hardening of the skin and associated scarring. Typically the skin appears reddish or scaly in appearance. Blood vessels may also be more visible. Where large areas are affected, fat and muscle wastage will weaken limbs and affect appearance.

The seriousness of the disease varies hugely between cases. The two most important factors to consider are, the level of internal involvement (beneath the skin), and the total area covered by the disease. For example there are cases where the patient has no more than one or two lesions (affected areas), perhaps covering a few inches. These are less serious cases and tend not to involve the internal bodily functions.

Cases with larger coverage are far more likely to affect the internal tissues and organs. Where an entire limb is affected, symptoms will almost certainly have serious consequences on the use of that limb. The heart and lungs will be affected when the disease covers this area of the torso. Some patients also experience gastrointestinal problems, including heartburn and acid reflux. Internal scarring may sometimes spread beyond what can be seen by the naked eye.

There is discoloration of the hands and feet in response to cold. Most patients (>80%) have Raynaud's phenomenon, a vascular symptom that can affect the fingers, and toes.

Systemic scleroderma and Raynaud's can cause painful ulcers on the fingers or toes, which are known as digital ulcers.

Types

There are three major forms of scleroderma: diffuse, limited (CREST syndrome) and morphea/linear. Diffuse and limited scleroderma are both a systemic disease, whereas the linear/morphea form is localized to the skin. (Some physicians consider CREST and limited scleroderma one and the same, others treat them as two separate forms of scleroderma.)

Diffuse scleroderma

Diffuse scleroderma is the most severe form - it has a rapid onset, involves more widespread skin hardening, will generally cause much internal organ damage (specifically the lungs and gastrointestinal tract), and is generally more life threatening.

Limited scleroderma/CREST syndrome

The limited form is much milder: it has a slow onset and progression, skin hardening is usually confined to the hands and face, internal organ involvement is less severe, and a much better prognosis is expected.

The limited form is often referred to as "CREST" syndrome. CREST is an acronym for:

Read more at Wikipedia.org


[List your site here Free!]


Scleroderma — a case study of autoimmunity - Autoimmune Disease in Women
From Townsend Letter for Doctors and Patients, 5/1/03

Scleroderma is a chronic, degenerative condition that leads to over-production of collagen, excessive soft tissue calcification leading to hardening and tightening of the skin, and blood vessel deterioration. Systemic scleroderma is life-threatening and affects articular structures and internal organs including the esophagus, intestinal tract, heart, and kidneys. It is estimated to affect 300,000 people in the US, 80% being women of childbearing age. The following case study describes a patient diagnosed with scleroderma and her response through guided nutritional therapy based upon her HTMA tests.

The patient was approximately 50 years of age when diagnosed in 1995 with scleroderma, Raynaud's disease as well as polymyositis and arthritis. The diagnosis was confirmed by third and fourth opinions of several experts in the field. Prognosis was guarded and therapy involved hospitalization for several months with high dose steroid treatment. The patient and family decided to look for other alternative therapy and requested to be discharged from the hospital. Steroids were discontinued and at that time the patient was given a life expectancy of two to two and one-half years.

After consulting other doctors the patient eventually was referred to Mrs. Virginia Lucia in Massachusetts. Mrs. Lucia is an experienced nutritional consultant with many other skills as well as having extensive knowledge and experience with HTMA. A hair sample was submitted to TEI for analysis on March 6, 1997. At that time the patient's condition had advanced, with further tightening of the skin, difficulty swallowing, muscle weakness and considerable weight loss. The patient's initial HTMA test results are shown in figure 3.

The initial HTMA pattern revealed a parasympathetic dominance (slow metabolic type), reflecting a cellular (thymus) immune dominance. The pattern revealed a very low zinc level as well as a low zinc/copper (Zn/Cu) ratio indicating an estrogen dominance. The marked elevation in the calcium! magnesium (Ca/mg) ratio indicated a parathyroid and insulin dominance. Dietary recommendations were based upon the patient's metabolic type. Nutritional supplementation included Para Pack, a synergistic metabolic formulation as well as specific vitamin and mineral supplements based upon the HTMA pattern. Minerals were full spectrum amino acid chelates.

The patient's follow-up HTMA patterns revealed a marked and continuous rise in calcium to over 300mg% and the copper level rose to over 4.8mg% (figure 4). The rise in these elements is not unusual and is expected. As excessive tissue calcium is mobilized from soft tissues HTMA levels frequently increase before returning to normal values. Excessive tissue accumulation of copper also often increase as it is being mobilized and excreted from tissue and organ storage sites. Nutritional recommendations and supplement recommendations were modified based upon changes in the patient's HTMA pattern.

The following graph (figure 5) shows the patient's current HTMA pattern as of October 2001.

Over the course of nutritional therapy and dietary modification based upon follow-up HTMA test, the patient's CPK levels showed improvement with each test and returned to within normal limits by March of 1998. Other blood parameters improved significantly as well.

Currently the patient is enjoying a normal and productive lifestyle. Her skin is almost totally back to normal except for some areas on the forearms. Dexterity in her hands has improved to the point that she has regained her ability to crochet.

Discussion

We cannot specifically recognize what triggered this patient's autoimmune response, however from the HTMA study we can recognize several factors that may have contributed. The nutritional mineral imbalances are obvious from the HTMA laboratory results and nutritional balance is well recognized as an important part of normal immunity. The patient is a mother and could have fetal cells present although this was undetermined. Stress is certainly part of the puzzle whether brought on by the disease itself, or preexisting. The low Zn/Cu ratio and eventual manifestation of excess tissue copper indicates that estrogen may have been dominant and therefore, a triggering factor. The marked elevation of calcium in a parasympathetic pattern suggests the presence of an underlying viral condition. Tissue calcium as well as copper is known to rise following a viral event. Excess tissue calcium is known to activate dormant viruses as well. Determination of an underlying virus was not ascertained.

The resulting decrease in tissue calcium and normalization of the Zn/Cu ratio indicates a reduction in the patient's hyperactive cellular immune response. The rise in sodium and potassium indicates an adrenal response, which has a number of effects. A normal adrenal response is necessary for recovery from most cellular autoimmune conditions in that adrenal hormones enhance the ability of the body to recognize and respond to the condition. The adrenals initiate an alarm response and aids in the progression to resistance and recovery. The adrenal hormones also suppress thymus over activity thereby reducing autoimmune activity. It should be obvious that further thymus support in patients with this HTMA pattern would be detrimental.

[FIGURE 3 OMITTED]

[FIGURE 4 OMITTED]

[FIGURE 5 OMITTED]

COPYRIGHT 2003 The Townsend Letter Group
COPYRIGHT 2003 Gale Group

Return to Scleroderma
Home Contact Resources Exchange Links ebay