Medical Nutrition Therapy for Rheumatic Disease

• Rheumatic disease and related conditions include more than 100 different manifestations of inflammation and loss of function of connective tissue and supporting body structures, including joints, tendons, ligaments, bones, muscles, and sometimes internal organs.

• According to the National Arthritis Data Workgroup, osteoarthritis (OA) affects 27 million Americans; gout, 3 million; fibromyalgia, 5 million; rheumatoid arthritis (RA), 1.5 million; Sjogren's syndrome (SS), 1 to 4 million; and systemic lupus erythematosus (SLE), 161,000 to 322,000.

• Arthritis is a generic term that comes from the Greek word Arthro, which means "joint," and the suffix -itis, which means "inflammation."

• There are two distinct categories of disease: systemic, autoimmune rheumatic disease and nonsystemic OA.

• The more debilitating and autoimmune arthritis group includes RA, juvenile rheumatoid arthritis gout, SS, fibromyalgia, SLE, and scleroderma.

• The OA group includes OA, bursitis, and tendonitis. • Other rheumatic diseases include spondyloarthropathies,

polymyalgia rheumatica, and polymyositis.

• Body changes associated with aging-including decreased somatic protein, body fluids, and bone density, and an increase in total body fat-may contribute to the onset and progression of arthritis.

• Unfortunately, the cause of most rheumatic conditions remains unknown.

PATHOPHYSIOLOGY ANDINFLAMMATION

• Inflammation plays an important role in health and disease.

• The inflammatory process normally occurs to protect and repair tissue damaged by infections, injuries, toxicity, or wounds via accumulation of fluid and cells.

• Once the cause is resolved, the inflammation usually subsides. Whether inflammation is due to stress on the joints (OA) or to an autoimmune response (RA), an uncontrolled inflammatoryreaction causes more damage than repair.

• Polyunsaturated fatty acids (PUFAs) play an important role in inflammation as precursors of a potent group of modulators of inflammation termed eicosanoids.

• Eicosanoids include the prostaglandins (PGs), thromboxanes (Txs) and leukotrienes (LTs) among others.

• PG and Tx are the product of the enzyme cyclooxy genase (COX) and are termed prostanoids, whereas LTs are the product of the enzyme lipoxygenase.

• For the synthesis of prostanoids, the COX reaction consumes two double bonds from the original PUFA, whereas lipoxygenase reaction consumes none.

• Depending on the PUF A used as substrate, different eicosanoids are produced: arachidonic acid (ARA) is the precursor of the series 2 of PG and Tx, and the series 4 ofL T.

• If eicosapentaenoic acid is the substrate, series 3 of PG and Tx and series 5 of LT are produced.

• Finally, dihomo-y-linoleic acid (DGLA) is the precursor of series 1 of PG and Tx, and of series 3 0f LT.

• The series 2 compounds (PG2 and TX2) are the most abundant because ARA is abundant in plasma membranes of cells involved in inflammation (macro phages , neutrophils, fibroblasts), and are the most potent inflammatory eicosanoids.

• On the other hand, PGI and TXb derived from DGLA, have antiinflammatory activities.

• Thus diets enriched with PUFAs that enhance the synthesis of antiinflammatory prostanoids are, at least theoretically, desirable for the long-term management of rheumatic disease, but usually do not replace the use of medications.

MEDICAL DIAGNOSISAND TREATMENT

• Laboratory testing can help to further refine the diagnosis and identify appropriate treatment.

• Biochemical Assessment:• Acute-phase proteins are plasma proteins whose concentration

increases of more than 25% during inflammatory states.• Two acute-phase proteins traditionally used to screen for and

monitor rheumatic disease are rheumatoid factor (RF) and C-reactive protein (CRP).

• The term RF is used to refer to a group of selfreacting antibodies (an abnormal IgM against normal IgG), found in the sera of rheumatic patients.

• The American College of Rheumatology (ACR) recommends periodic measurements of RF and CRP in addition to a detailed assessment of symptoms and functional status, and radiographic examination to determine the current level of disease activity in these patients.

• Antinuclear antibodies (ANA)• Present in many autoimmune diseases and can assist with

proper diagnosis when used correctly; antineutrophil cytoplasmic antibodies and myositis-specific antibodies can provide information about the presence of rheumatic disease as well.

• Measurements of RF and anticyclic citrullinated peptide antibodies may provide unique data in the management of RA.

• Routine blood testing can include complement, a complete blood count, creatinine, hematocrit, and a white blood cell count, in addition to analysis of urine or synovial fluid secreted by the synovial membrane in the joints.

Pharmacotherapy

• Acetaminophen (Tylenol) are effective pain relievers.• Drugs commonly used to reduce inflammation affect

the synthesis of PGs by inhibiting COX activity, thus diminishing PG production.

• Glucocorticoid therapy decreases the release of ARA from cell membrane phospholipids by binding to the receptor in the cell cytoplasm.

• This forms a complex that moves into the nucleus as a transcription factor and interferes with expression for the enzyme phospholipase.

• Nonsteroidal antiinflammatory drugs (NSAIDs), which include ibuprofen (Advil or Motrin) and naproxen (Aleve), slow down the body's production of PGs by inhibiting COX-l enzyme activity.

• They are considered useful tools in the management of most rheumatic disorders; however, long-term use of NSAIDs may cause gastrointestinal problems such as gastritis, ulcers, abdominal burning, pain, cramping, nausea, gastrointestinal bleeding, or even renal failure.

• Celecoxib (Celebrex) have been shown to provide relief comparable to other NSAIDs with potentially less gastrointestinal and cardiovascular toxicity. Naproxen and celecoxib appear to be safer than other NSAIDs.

• Biologic response modifiers are a class of drugs that selectively target different elements of the disease, and include those directed against interleukin (IL)-l such as anakinra (Kineret), or against tumor necrosis factor (TNF)-a, like adalimumab (Humira), etanercept (Enbrel), and infliximab.

• Corticosteroids (cortisone [Cortone], prednisone [Deltasone],methylprednisolone [Medrol], and hydrocortisone [Cortef]) suppress the immune system and decrease inflammation, making them desirable treatments for many of the rheumatic diseases.

• As the most potent of the antiinflammatory drugs used to treat RA, steroids have extensive catabolic effects that can result in negative nitrogen balance.

• Hypercalciuria and reduced calcium absorption can increase the risk of osteoporosis

• Concomitant calcium (1 g/day) and vitamin D (at least 1000 IU/day) and monitoring of bone status may be suggested to minimize osteopenia.

• Care must be taken to avoid serum calcium levels greater than 11 mg/dL and 25-0H vitamin D levels less than 35 ng/mL.

• Edema often occurs and may require diet modification, including a sodium- and fluid-restricted diet.

• Other side effects of steroid use include cushingoid syndrome and gastrointestinal bleeding.

UNCONFIRMED THERAPIES

• Willow bark and ginger may relieve pain because their chemical composition is similar to NSAIDs, but excessive blood thinning is a concern

• It is best to avoid copper or copper salts, shark• cartilage, devil's claw, echinacea, guaifenesin, alfalfa,

wild yam, and methylsulfonylmethane (MSM). • Both comfrey and alfalfa are herbs that have been

promoted as potential cures for arthritis, yet both have been deemed toxic by the scientific community.

• Meditation, tai chi, relaxation techniques, thermotherapy and spiritual practice may offer pain reduction.

OSTOARTHRITlS

• formally known as degenerative arthritis or degenerative joint disease, is the most prevalent form of arthritis.

• Obesity, aging, female gender, white ethnicity, greater bone density, and repetitive-use injury associated with athletics have been identified as risk factors.

• It is caused by joint overuse, whereas RA is a systemic autoimmune disorder that results in symmetric joint inflammation.

Pathophysiology• OA is a chronic joint disease that involves the loss of

habitually weight-bearing articular (joint) cartilage.• The loss can result in stiffuess, pain, swelling, loss of

motion, and changes in joint shape, in addition to abnormal bone growth, which can result in osteophytes.

• The joints most often affected in OA are the distal interphalangeal joints, the thumb joint, and, in particular, the joints of the knees, hips, ankles, and spine, which bear the bulk of the body's weight.

• The elbows, wrists, and ankles are less often affected.

• OA generally presents as pain that worsens with weight bearing and activity and improves with rest, and patients often report morning stiffness or "gelling" of the affected joint after periods of inactivity.

Medical and Surgical Management• The patient's medical history and level of pain should

determine the most appropriate treatment.• Should include nonpharmacologic modalities (patient

education, physical and occupational therapy), pharmacologic agents, and surgical procedures with the goals of pain control, improved function and health-related quality of life, and avoidance of toxic effects from treatment.

• Weight loss and/or achievement of ideal body weight (body mass index [BM!] of 18.5-24.9) should be part of the medical treatment as it improves OA dramatically

• Patients with severe symptomatic OA pain who have not responded adequately to medical treatment and who have been progressively limited in their activities of daily living (ADLs), such as walking, bathing, dressing, and toileting, should be evaluated by an orthopedic surgeon.

• Surgical options include arthroscopic debridement (with or without arthroplasty), total joint arthroplasty, and osteotomy.

• Surgical reconstruction has been quite successful but should not be viewed as a replacement for overall good nutrition, maintenance of healthy body weight, and exercise.

Exercise

• OA limits the ability to increase energy expenditure through exercise.

• It is critical that the exercise be done with correct form so as not to cause damage or exacerbate an existing problem.

• Nonloading aerobic (swimming), range-of-motion, and weightbearing exercises have all been shown to reduce symptoms, increase mobility, and lessen continuing damage from OA.

Medical Nutrition Therapy• Weight and Adiposity Management• Excess weight puts an added burden on the weight-bearing

joints. • Epidemiologic studies have shown that obesity and injury are

the two greatest risk factors for OA.• The risk for knee OA increases as the BMI increases.• Controlling obesity can reduce the burden of OA through both

disease prevention and improvement in symptoms• A well-balanced diet that is consistent with established

dietary guidelines and promotes attainment and maintenance of a desirable body weight is an important part of MNT for OA

• Anti-Inflammatory Diet• Recently, the anti-inflammatory diet, a diet resembling

the Mediterranean diet, has been useful.• The diet aims for variety, the inclusion of as much fresh

food as possible, the least amount of processed foods and fast food, and an abundance of fruits and vegetables.

• When combined with moderate exercise, diet-induced weight loss has been shown to be an effective intervention for knee OA.

• There is also an anti-inflammatory effect from weight loss in OA management because the reduced fat mass results in the presence of less inflammatory mediators from adipose tissue.

• Vitamins and Minerals• Cumulative damage to tissues mediated by reactive

oxygen species has been implicated as a pathway that leads to many of the degenerative changes seen with aging.

• However, large doses of dietary antioxidants, including vitamin C, the tocopherols (vitamin E), b-carotene, and selenium have shown no benefit for the management of symptomatic OA.

• Many patients with OA consume deficient levels of calcium, and vitamin D. Low serum levels of vitamin D are being studied for their role in OA progression.

• special attention given to vitamin B6, vitamin D, vitamin K, folate, and magnesium.

• Alternative Therapies• Topical aids, manipulative therapies, and acupuncture. • Capsaicinoids, derived from chili peppers, have a fatty acid

receptor that stimulates, then blocks, small-diameter pain fibers by depleting them of the neurotransmitter substance P, thought to be the principal chemomediator of pain impulses from the periphery.

• Capsaicin, applied with glyceryl trinitrate to reduce onsite burning, can reduce pain in OA patients

• Certain pulsed electromagnetic fields can also affect the growth of bone and cartilage with potential use in OA.

• S-adenosyl- L-methionine (SAM-e) has also shown promise for reducing pain and improving mobility in people with OA at doses of 600 to 1200 mg/day.

• Glucosamine and Chondroitin• Sodium chondroitin sulfate (chondroitin sulfate) and

glucosamine hydrochloride (glucosamine) are both involved in cartilage production, but their mechanism for eliminating pain has not been identified.

• In some cases glucosamine may be equal or superior to ibuprofen.

• Although it is not effective for all afflicted individuals, a safe dose of glucosamine and chondroitin sulfate is 1500 mg/day and 1200 mg/day in divided doses, respectively.

• chondroitin is chemically similar to commonly used blood thinners and could cause excessive bleeding if used in combination with blood thinners.

• Chondroitin may also elicit a reaction in those with shellfish allergies.

Rheumatoid arthritis (RA)

• RA affects the interstitial tissues, blood vessels, cartilage, bone, tendons, and ligaments, as well as the synovial membranes that line joint surfaces.

• RA occurs more frequently in women than in men peak onset commonly occurs between 20 and 45 years of age.

Pathophysiology• RA is a chronic, autoimmune, systemic disorder in which cytoklnes

and the inflammatory process playa role.• RA has articular manifestations that involve chronic inflammation

that begins in the synovial membrane and progresses to subsequent damage in the joint cartilage.

• Although the exact cause of RA is still unknown, certain genes have been discovered that play a role.

• The likely trigger is a viral or bacterial infection.• Drinking large amounts of tea may increase the risk of developing

RA (Walitt et al, 2010); however, other studies have suggested that teas are protective.

• More research is clearly needed.

• Medical Management• The appearance of rheumatoid factor (RF), may

precede symptoms of RA. Pain, stiffness, swelling, loss of function and anemia are common.

• RA patients are at increased risk for cardiovascular disease, explained by the systemic inflammatory response.

• Many of the drugs used to treat RA can result in hyperhornocysteinemia, hypertension, and hyperglycemia, all risk factors for cardiovascular disease.

• Pharmacologic Therapy• Medications to control pain and inflammation are the

mainstay of treatment for RA.• Salicylates and NSAIDs are oftenthe first line of

treatment, and methotrexate (MTX) is commonly prescribed as well, but these drugs may cause significant side effects.

• Disease-modifying antirheumatic drugs (DMARDs) may be prescribed because of their unique ability to slow or prevent further joint damage caused by arthritis.

• These include MTX, sulfasalazine (Azulfidine), hydroxychloroquine (Plaquenil), azathioprine (Imuran), and leflunomide (Arava).

• Surgery• Surgical treatment for RA may be considered if

pharmacologic and nonpharmacologic treatment cannot adequately control the pain or maintain acceptable levels of functioning.

• Common surgical options include ynovectomy, joint replacement, and tendon reconstruction.

• Exercise• To maintain joint function, recommendations may

be given for energy conservation, along with range-of-motion and strengthening exercises.

• A loss of body cell mass that accompanies RA, called rheumatoid cachexia, involves the skeletal muscle, viscera, and immune system.

• This can lead to muscle weakness and loss of function, which may hasten morbidity and mortality in RA.

• Physical activity, including both aerobic exercise and strength training, seems to help.

• Medical Nutrition Therapy• The association of foods with disease flares should be

discussed. Whether food intake can modify the course of RA is an issue of continued scientific debate and interest.

• Dietary manipulation by either modifying food composition or reducing body weight may give some clinical benefit in improving RA symptoms.

• Some literature has suggested that fasting may be beneficial in reducing pain at the inflammation site; nevertheless fasting has never been shown as an effective treatment for RA symptoms.

• A vegan, gluten-free diet causes improvement in some patients, possibly because of the reduction of immunoreactivity to food antigens.

• Energy• Although traditional measures to assess energy

requirements can be used, weight should be monitored and energy intake modified as needed to achieve desirable or usual body weight.

• For patients who are totally sedentary, calculations should be estimated at the resting energy expenditure and adjusted for weight changes that occur over time.

• When intakes are poor, enteral or parenteral supplementation may be required, and home nutrition support is beneficial for chronic cases

• Protein• Well-nourished individuals require protein at

levels comparable to the DRIs for age and sex. • Patients with RA tend to have increased

whole-body protein breakdown (regardless of age) from growth hormone factor, glucagon, and TNF-a production.

• Protein may be needed at levels of 1.5 to 2 g/kg/day.

• Lipids• Low-fat diets (including use of low-fat substitutes) lead to low

serum levels of vitamins A and E and actually stimulate lipid peroxidation and eicosanoid production, thus aggravating RA.

• Therefore low-fat or fat-free dieting may actually be counterproductive for patients susceptible to or afflicted by RA.

• Changing the type of fat in the diet is useful and likely offers advantages for both the arthritis and cardiovascular systems.

• Omega-3 fatty acids have increased in popularity in the management of RA because of their role in inflammatory pathways.

• Fish oil alleviates RA symptoms and reduces the use of NSAIDS in RA patients The beneficial effects are generally delayed for up to 12 weeks after they are started but last up to 6 weeks after discontinuing therapy .

• Minerals, Vitamins, and Antioxidants• Several vitamins and minerals function as antioxidants and

therefore affect inflammation. • Vitamin E is just such a vitamin, and along with O-3 and O-6

fatty acids, may affect cytokine and eicosanoid production by decreasing proinflammatory cytokines and lipid mediators.

• RA patients often have nutritional intakes below the DRIs for folic acid, calcium, vitamin D, vitamin E, zinc, vitamin B, and selenium.

• Adequate intakes of folate and vitamins B6 and Bl2 should be encouraged. Calcium and vitamin D malabsorption and bone demineralization are characteristic of advanced stages of the disease, leading to osteoporosis or fractures.

• Supplementation with calcium and vitamin D should be considered.

• Alternative Therapies• Gamma-linolenic acid (GLA) is an (0-6 fatty

acid found in the oils of black currant, borage, and evening primrose that can be converted into the antiinflammatory PG E, or into ARA, a precursor of the inflammatory PG E2.

• This antiinflammatory PGEI may relieve pain, morning stiffness, and joint tenderness with no serious side effects.

• Thunder god vine (Tripterygium wilfordit) has been used in China to treat patients with a number of autoimmune diseases.

SJOGREN'S SYNDROME

• Sjogren's syndrome (55) is a chronic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands, particularly the salivary and lacrimal glands, leading to dryness of the mouth (xerostomia) and of the eyes (xerophthalmia).

• Pathophysiology• Common signs include thirst, burning sensation in the oral

mucosa, inflammation of the tongue (glossitis), and lips (cheilitis), cracking of the corners of the lips (cheilosis), difficulties in chewing and swallowing (dysphagia), severe dental caries, progressive dental decay, and nocturnal oral discomfort.

• SS can be present alone (primary SS) or as secondary SS, as a result of another rheumatic disorder (RA, lupus).

• Nutrient insufficiency may playa role in the development or progression of SS.

• Altered consumption of several nutrients has been noted in SS patients including higher intake of supplemental calcium and lower intake of nonsupplemental vitamin C, PUFAs, linoleic acid, and (0-3 fatty acids.

• Biochemical deficiency of vitamin B6 (pyridoxine) has also been observed

• Medical Management• Medications for SS address the issues of dry eyes

and dry mouth. These include artificial tears and immunosuppressant drops such as cevimeline (Evoxac) and pilocarpine (Salagen), respectively.

• Medical Nutrition Therapy• The goal of dietary management in patients with

SS is to relieve symptoms and reduce eating discomfort, which can result in lack of appetite, weight loss, fatigue, difficulty chewing and swallowing, mouth infections, and anemia.

• Sugary foods should be reduced or eliminated from the diet to minimize cavities.

• Ready-to-eat foods may be useful. • Foods should all be moist, and extremes in temperature

should be avoided. • The most common modifications include soaking or

overcooking certain foods to make them softer; chopping and cutting meats and fruits to make them smaller; and limiting consumption of citrus fruits, irritant foods, and spices.

• Iron and vitamin deficiencies such as vitamin C, vitamin B12, vitamin B6 and folate are possible, but these can be easily avoided with a well-balanced diet or appropriate vitamin supplementation.

TEMPOROMANDIBULARDISORDERS

• Temporomandibular disorders (TMDs) affect the temporomandibular joint, which connects the lower jaw (mandible) to the temporal bone.

• TMDs can be classified as myofascial pain, internal derangement of the joint, or degenerative joint disease.

• Pathophysiology• Besides experiencing a severe jaw injury, there is little

scientific evidence to suggest a cause for TMD. It is generally agreed that physical or mental stress may aggravate this condition.

• Medical Nutrition Therapy• The goal of dietary management is to alter food

consistency to reduce pain while chewing.• Diet should be mechanically soft in consistency; all

foods should be cut into bite-size pieces to minimize the need to chew or open the jaw widely; and chewing gum, sticky foods, and biting hard foods such as raw vegetables, candy, and nuts should be avoided.

• Intake of fiber is often reduced.

CHRONIC FATIGUE SYNDROMEAND FIBROMYALGIA

• Chronic fatigue syndrome (CFS) and fibromyalgia have rheumatic symptoms.

• The etiology and pathogenic mechanisms of fibromyalgia and CFS are to date not fully understood.

• In fibromyalgia, central nervous system dysfunction, mitochondrial dysfunction, nutrient deficiencies, and other systemic abnormalities have been suggested.

• Mitochondrial dysfunction can result in lack of energy (ATP) for muscular work.

• Some symptoms include poor growth, loss of muscle coordination and muscle weakness

• Pathophysiology• In fibromyalgia, nonarticular aches at specific

pressure points and fatigue cause disabling symptoms including muscle tenderness, sleep disturbances, fatigue, morning stiffness, numbness and tingling, symptoms of anxiety and depression, chronic headaches, irritable bowel, and irritable bladder.

• In CFS, chronic fatigue is the major symptom. It lasts 6 months or longer and is accompanied by hypotension, sore throat, multiple joint pains, headaches, postexertion lethargy, muscle pain, and impaired concentration.

• Medical Management• Treatment program for CFS should be

multidisciplinary and include exercise, MNT, appropriate sleep hygiene, low dose tricyclic antidepressants or selective serotonin reuptake inhibitors (SSRIs), and cognitive behavior therapy.

• Serotonin norepinephrine reuptake inhibitors (SNRIs) such as duloxetine (Cymbalta) and milnacipran (Savella) and the anticonvulsant pregabalin (Lyrica) have been suggested for fibromyalgia patients and are FDA approved for this purpose.

• Exercise is helpful; supervised moderate-intensity graded aerobic exercise, or water aerobics (minimum 12 weeks, 3x/ week) is suggested.

• Medical Nutrition Therapy• Data regarding MNT for CFS are extremely limited. • When hypotension is identified medically in CFS

patients, increases in sodium and fluid intakes have been suggested.

• Vegetarian diets could have some beneficial effects probably due to the increase in antioxidant intake.

• Weight control seems to be an effective tool to improve the symptoms in these patients.

• Vitamin therapies such as riboflavin, coenzyme Q, and carnitine (a specialized amino acid) may provide subjective improvement in fatigue and energy levels in some patients.

GOUT

• A disorder of purine metabolism in which abnormally high levels of uric acid accumulate in the blood (hyperuricemia).

• Renal disease is common, and uric acid nephrolithiasis can occur.

• As the disease advances, symptoms occur more frequently and are more prolonged.

• The disease usually occurs after the age of 35 years and predominantly affects men.

• Pathophysiology• Gout is characterized by the sudden and acute onset

of localized arthritic pain that usually begins in the big toe and continues up the leg.

• The urate deposits can destroy joint tissues, leading to chronic symptoms of arthritis.

• As a consequence, sodium urates are formed and deposited as tophi in the small joints and surrounding tissues.

• In chronic gout a classic site is the helix of the ear.• Genetic factors play an important role in the

pathogenesis of gout and regulation of serum uric acid levels.

• One comorbidity of gout is obesity.

• Medical Management• The goals of treatment are to reduce the pain associated

with acute attacks, to prevent future attacks, and to avoid the formation of tophi and nephrolithiasis.

• The primary treatment for gout involves pharmacologic therapy (colchicine, allopurinol, NSAIDs, and others depending on the acute or chronic condition and renal function).

• Maintaining a serum urate level of less than 6 mg/ dL may reduce the risk of recurrent gout attacks.

• Probenecid (Benemid) and sulfinpyrazone decrease the blood uric acid level by increasing elimination through the kidneys.

• Allopurinol inhibits uric acid production.

• Medical Nutrition Therapy• Although gout has traditionally been treated with a

low-purine diet, drugs have largely replaced the need for rigid restriction of the diet.

• However, the patient can takean active role by adhering to the nutrition guidelines for the management of gout as well.

• Higher levels of meat and seafood consumption were associated with increased serum uric acid.

• High intake of fluids (8 to 16 cups of fluid/day, at least half as water) should be encouraged to assist with the excretion of uric acid and to minimize the possibility of renal calculi formation

SCLERODERMA• Scleroderma is a chronic, systemic sclerosis or hardening

of the skin and visceral organs characterized by deposition of fibrous connective tissue.

• Scleroderma is considered an autoimmune rheumatic disease with a genetic component.

• Free-radical, oxidative damage from cytokines, in which fibroblast proteins are modified, is involved

• Gastrointestinal symptoms include gastroesophageal reflux, nausea and vomiting, dysphagia, diarrhea, constipation, fecal incontinence, and small intestine bacterial overgrowth.

• Joint stiffness and pain, renal dysfunction, hypertension, pulmonary fibrosis, and pulmonary arterial hypertension are also common.

• Treatment• Some studies have been undertaken with the

use of anti- TNF therapies with some promising results.

• Treatments for the pulmonary hypertension and renal crises have shown good results overall

• Medical Nutrition Therapy• Dysphagia requires nutrition intervention • Dry mouth with resultant tooth decay, loose teeth,

and tightening facial skin can make eating difficult.• Consuming adequate fluids, choosing moist foods,

chewing sugarless gum, and using saliva substitutes help moisten the mouth and may offer some relief.

• A high-energy, high-protein supplement or enteral feeding may prevent or correct weight loss.

• Home enteral or parenteral nutrition is often required when problems such as chronic diarrhea persist.

SYSTEMIC LUPUSERYTHEMATOSUS

• Systemic lupus erythematosus (SLE) is commonly known as lupus. Lupus is most prevalent in women of childbearing age and is more common in blacks and women of Hispanic, Asian, and Native American descent than in whites.

• Common symptoms include extreme fatigue, painful or swollen joints, unexplained fever, skin rashes, mouth ulcers, and kidney problems.

• Pathophysiology• SLE has a genetic predisposition and

overproduction of type 1 interferon and other cytotoxic cells

• SLE is considered to be an autoimmune disease that affects all organ systems.

• Renal function is deranged in lupus, thus causing excessive excretion of protein and often renal failure.

• Medical Management• Lupus itself and the medications used

(corticosteroids, NSAIDs, immunosuppressants, antimalarials) affect nutrient metabolism, needs, and excretion.

• Plaquenil, an antimalarial drug, appears to be effective in clearing up skin lesions for some individuals with lupus but has side effects that include nausea, abdominal cramping, and diarrhea.

• Immunosuppressives such as cyclophosphamide may be useful when there is renal involvement, but gastrointestinal and fertility problems may occur.

• Medical Nutrition Therapy• No specific dietary guidelines for managing SLE

exist.• Rather, the diet needs to be tailored to the

individual needs of the patient.• Protein, fluid, and sodium requirements are

altered as a result of disordered renal function and steroid-induced side effects.

• The goal should be to attain and maintain the usual body weight.

• Enteral nutrition support may be required in chronic cases

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