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					                                UNIVERSITY OF THE WESTERN CAPE



                             Therapeutic Nutrition 311 & Nutritional Medicine 315


                                          Lecturer: Dr. A. van Graan
                                   Acknowledgements: Mrs Hilary Woodley




                               RHEUMATIC DISEASES

Learning objectives:


The student must be able to:


Discuss the etiology, symptoms & nutritional care of the following rheumatic disorders:


           Osteoarthritis
           Rheumatoid arthritis
           Sjogrens syndrome
           Gout
           Scleroderma
           Systemic lupus erythematosus
           Chronic fatigue syndrome
           Fibromyalgia




                                                                                          1
Medical Nutrition Therapy for Rheumatic Disorders

Introduction:
    Rheumatic diseases and related conditions includes more than 100 different
      manifestations of connective tissues and systematic, arthritic disease
    Marked by denegation, inflammation, pain and swelling of joints
    No identifiable cause or known cure
    Pharmacotherapy, physical and occupational treatment
    Medical nutritional therapy plays important roles
    Body changes associated with aging may contribute to onset and progression of
      arthritis
    Causes changes in neuroendocrine and immune regulators
    And metabolism that affect the inflammation process
    2 distinct categories: systemic, autoimmune rheumatic disease
    And non-systemic osteoarthritis
    Autoimmune arthritis group: rheumatoid arthritis (RA), gout, Sjogren's syndrome,
      fibromyalgia, lupus and scleroderma
    Osteoarthritis: osteoarthritis, bursitis, tendonitis


Etiology
    Remains unknown
    Some forms of rheumatic conditions can affect other organs like skin and blood
      vessels
    No known cure, usually chronic
    May present as acute episodes with short or intermittent duration
    Associated with alternating periods of remission, absence of symptoms, often
      occurring without any identifiable aetiology
    Various alternative diet theories and supplements have been proposed, scientific
      data limited


Pathophysiology
    Inflammation, predominant cause of pain, is the most debilitating component




                                                                                        2
    Pain reflects a neuro-endocrine process associated with levels of corticotrophin-
      releasing hormone, methyl-D-aspartate, inflammatory mediators, unmyelinated
      fibres sensitized to norepinephrine
    The inflammatory process normally occurs to protect and repair tissue damaged by
      infections, injuries, toxicity, or wound via accumulation of fluid and cells
    when the cause is resolved the inflammation usually subsides
    In most forms of arthritis the inflammatory reaction continues out of control
    Causing more damage than repair
    The inflammatory process is initiated by the production of histamine, prostaglandins
      (PG's), plasma protease and plasma-activating factors
    Many specific prostaglandins and other mediators potentiate the effects of
      inflammatory mediators such as histamine.
    Arachidonic acid, when released, from cell membranes, is oxygenated t
    To several classes of eicosanoids, incl PGe tromboxanes, le ukotrienes and
      prostacyclines – which are pro-inflammatory
    Glucocortoid therapy decreases release of AA from cell membrane phospholipids
    Tromboxane activates platelet aggregation to initiate clotting and release growth
      factors and proteases
    Leukotrienes stimulate the attraction of neutrophil, macrophages and fibroblasts
    PG'e are produced by neutrophils, macrophages and synovial fibroblasts in large
      quantities as a response to specific cytokines such as TNF, interferons and
      interleukins
    PG'e play a major role in the depletion of bone in RA


Medication commonly used to reduce inflammation
    Lowers the production of PG'e
    Nonsteroidal anti-inflammatory meds
    Long term use – many GIT problems – but still are more popular meds used in RA




Osteoarthritis


Pathophysiology
    Most prevalent
    Obesity, aging, gender and congenital abnormalities – major risk factors
    Other factors – bone density and genetics
                                                                                         3
    Chronic process, characterized by softening of the articular (joint) cartilage, vascular
       congestion and osteoblast activity in underlying bone, new growth of cartilage and
       bone at the joint margins and capsular fibrosis
    Is not systemic or autoimmune in origin but
    Involves cartilage destruction with asymmetrical inflammation
    It is caused by joint overuse
    Joints often affected – distal interphalangeal joints, thumb and knees, hips, ankles
       and spine, which bear bulk of the body's weight
    Elbow, wrist and ankle less often affected
    Early stage of the disease is marked by stiffness, and then progresses to soreness
    Inflammation occurs at times – but is not a primary symptom




Medical management
      Pt's medical history and level of pain – determine most appropriate treatment
      Non-pharmacological therapies should be included and in the treatment regime
      Should be followed by acetaminophen or NSAIDS for mild to moderate pain
      Adjunctive Rx, corticosteroid injections and surgery also viable options


Surgery
      Surgical reconstruction (total joint replacement) may be considered in pt's who are
       not responding to other therapy and are good candidates for surgery


Exercise
    Disease limits the ability to increase exercise
    critical that exercise is done in correct form as to not cause damage or exacerbate
       the problem
    Sport or strenuous activities that subject the joints to repetitive high impact and load
       increase risk of joint cartilage degeneration
    Increased muscle tone and strength, correct form, general flexibility and conditioning
       will help protect joints in habitual exercise.




Medical nutrition therapy
    Excess weight puts added burden on weight-bearing joints
    Obesity and injury two greatest risk factors
                                                                                                4
    Risk for knee OA increases as BMI increases Weight reduction medication have
       sometimes been used in problematic cases, close monitoring of potential side-
       effects, essential
    well-balanced diet that is consistent with dietary guidelines and that promotes
       maintenance of desirable body weight is important


Vitamins and Minerals
      Experimental data have shown - Vit B6 deficiency may be responsible for the
       development of osteoarthritis-type lesions
      Comprehensive nutrition interviewing and counselling should include
      Determination of acceptable sources of all nutrients and
      Sufficient amounts in the diet
      Folate and Cobalamin (B12) supplement has been tested as Rx for OA– with fairly
       good results, minimal costs and no side effects
      Supplements with 6400 mcg folate and 20 mcg of B12 in RCT – found to improve
       grip values – but was not duplicated in larger groups
      Cumulative damage to tissues mediated by reactive oxygen species (ROS) has
       been implicated as a pathway that leads to many degenerative changes
      Large doses of dietary antioxidants (AO) – Vit C, E. beta-carotene and selenium
       have had a beneficial effect on OA
      Further studies had mixed results which warrants further studies before routine
       dietary supplementation can be recommended
      Many pt's with OA have been shown to be deficient in consumption of dairy products
       and calcium and Vit D
      Low serum Vit D levels of Vit D have been associated with progression of OA




Herbs and Complementary Therapy
      Some alternative therapies includes glucosamine, chondroitin sulphate, oils, herbs
      Reports of progressive and gradual decline of joint pain and tenderness, improved
       mobility, sustained improvement and lack of toxicity
      Chondroitin sulphate and glucosamine are produce by cartilage but the mechanism
       for pain elimination has not been identified
      Analysis of several studies suggest that glucosamine sulphate may produce a
       gradual and progressive reduction in joint pain and tenderness as well as improved
       range of motion and walking speed
                                                                                            5
      Trails of glucosamine also showed consistent benefits, including >50% improvement
       in symptoms scores
      No reliable scientific evidence show structure-modifying action with respect to
       prohibiting, healing or restoring cartilage
      Although not effective for all afflicted individuals, the Arthritis Foundation suggests a
       safe dose of
      500mg glucosamine 3 x /d and
      400 chondroitin sulphate 3x/d
      People with shellfish allergies should avoid glucosamine sulphate
      A variety complementary therapies proposed: topical aids, acupuncture
      Capsaicinoids derived from chilli peppers have a fatty-acid receptors that stimulates
       then blocks small-diameter pain fibres
      1 RCT showed capsaicin reduced pain
      herbs and botanicals: willow bark contains salaicin Arthritis Foundation suggest that
       is it safer to use aspirin – willow bark supplements are not regulated




Rheumatoid arthritis (RA)
      Debilitating and crippling, has personal, social and economic effects
      Most frequently affected interstitial tissues, blood vessels , cartilage , bones,
       tendons, ligaments and synovial membranes
      More frequently in women
      Peak onset between 20 -45 years
      Postulated to be caused by a virus or constant stress that initiates the inflammatory
       process
      Epidemiological studies document- onset in Northern hemisphere more common in
       winter than summer
      Decaffeinated coffee intake has been independently and positively associated with
       RA onset in a prospective study




Pathophysiology
      Chronic autoimmune, systemic disorder
      Unclear aetiology
      Inflammatory process seems to play a role
                                                                                                   6
     RA involve chronic inflammation that
     Begins in synovial membrane and progresses to damage in joint cartilage
     Can affect any joint – but most common
     small joints of extremities of hands and feet
     Pain, stiffness and swelling – frequent complaints
     Swelling is caused by accumulation of synovial fluid in membrane lining of joints
     And inflammation of surrounding tissues
     the appearance of rheumatoid factor (PF) – an abnormal circulating protein
     It is an immunoglobulin-classified antibody
     Anaemia may also be present




Medical management
     Pharmacological therapy - control pain and inflammation
     Primary drugs – salicylates, NSAIDS, immunosuppressive meds, remittive meds and
      steroids
     choice – based on pt response to meds, severity of adverse reactions and
      compliance
     Side-effects can occur and can influence
     Ingestion, digestion and absorption
     Salicylates - 1st line
     Chronic aspirin ingestion – associated with gastric mucosal injury and bleeding,
      increased bleeding time and increased excretion on Vit C
     Taking it with milk, food or antacid alleviates the GIT symptoms
     Vit C supplement – prescribed when serum and platelet levels are low
     NSAIDS - 2nd line -effectiveness lies in the inhibition of PG’e synthesis and immune
      modulation
     Immunosuppressive agents: methotrexate (MTX)
     Adverse effects: folate antagonist
     MTX induces rise in p-homocysteine – neutralized by folic acid
     Most pt diet adequate to avoid deficiency
     Folate supplementation needed to offset toxicity of drug and for
     protection against GIT disturbances and
     maintenance of RBC production
     Folate supplementation does not decrease the efficacy of MTX therapy
     Long term supplementation important to prevent neutropenia
                                                                                             7
      And to avoid discontinuation of Rx due to mouth ulcers, nausea and vomiting
      Low doses of steroids like Prednisone control most of inflammatory features
      Steroids have extensive catabolic impact and
      Can result in negative N-balance
      Hypercalciuria and reduced Ca absorption can increase risk of osteoporosis
      Concomitant calcium (1g) and Vit D ( 500IU) and
      Monitoring of bone status can minimize osteopenia
      Avoid s-ca levels>11 mg/dl
      Oedema often occurs – may require diet modification
      Na and fluid restriction
      Other side effects of steroids: Cushingoid changes in body, intestinal bleeding and
       DM
      Remittive agents: gold salt therapy, antimalarials, penicillamie may lead to remission
       of RA
      Proteinuria may occur
      Therefore toxicity must be monitored




Medical Nutrition Therapy
      Comprehensive assessment essential
      Includes physical and occupational therapy to determine range of motion and
       activities pt cam do independently
      Increase in metabolic rate secondary to inflammatory process leads to increased
       needs
      Taste alteration, dysphasia, anorexia, fatigue and pain may reduce intake
      Changes in GIT mucosa affect digestion and absorption
      Current weight and weight history reliable assessment
      weight change important
      Increased cytokine production may lead to reduced body cell mass and altered
       energy intake and metabolism
      Diet history should review usual diet, impact of handicap, types of food consumed,
       changes in food tolerance and GIT disorders
      Effect on food shopping and preparation, self-feeding ability, appetite also needs to
       be assessed
      Associated of foods with disease flares should be discusses due to possible
       undetected allergies
                                                                                               8
Energy requirements:
        Actual needs not been determined
        Totally sedentary REE adjust for weight fluctuations
             1.14-1.35 stress factor - active disease
             1.2 stress factor - limited mobility – physio
             1.3 stress factor - intensive physio
             Totally sedentary pt's REE and adjusted for weight changes
             Poor intake – enteral / parenteral supplementation




Protein
        Well-nourished individuals – normal RDA for age and gender
        Some study – suggest that that whole-body protein breakdown is increased which
         correlates with growth factor hormone, glucagon, TNF production
        Poorly nourished pt's or inflammatory phase increase to
        1.5 – 2g/kg


Lipids
        ROS important
        Low=fat diets lead to low serum Vit A and E
        And stimulates lipid peroxidation and eicosanoid production
        low fat diet could be counter productive
        Changing fat type more useful
        Omega 3- FA
        Marine oils and vegetable oils have indirect anti-inflammatory actions
        Fa have anti-inflammatory effect but does noy appear to correct the basic
         immunological process


Vitamins, minerals and AO :
             Omega-3 fatty acid supplement:
                      3-6g per day
                      effect only seen after 8 weeks (be careful with combining with vitamin
                       E due to bleeding)
                      evidence stronger than for vitamin E


                                                                                                9
         Vitamin E:
                 may also affect cytokine and eicosanoid production
                 on individual basis you could look at supplementing 100-400iu/day (be
                  careful with combining with omega-3 due to bleeding)
                 Selenium: no clinical benefits in RCT
         Selenium showed no clinical benefits
         Earlier studies showed juvenile pts have low serum AO and may benefit from
           dietary supplements when intake does not reach desired intakes
                 Trails shown significant pain reduction in RA when Rx with Vit E and
                  other AO
                 Pt's often have intakes < RDA for calcium, folate, Vit E, zinc, selenium
                 Mounting evidence supports supplementation beyond minimum levels
                  for some nutrients
                 Vitamin therapy may complement conventional therapy: Vit E, D &
                  folate
                 Intakes of supplemental AO have been linked with beneficial effects in
                  prevention and therapy
                 With metabolic bone disease such as osteoporosis, calcium and Vit D
                  is indicated
                 MTX leads to increased homocysteine – adequate intakes of B6 and
                  12


Herbs and complementary therapy
         GLA (gamma- linolenic acid):
                 Body uses to produce anti-inflammatory PG
                 may relieve pain and stiffness and joint tenderness
                 ? dose
         Thunder god vine:
                 China treat autoimmune disease – stimulates prostaglandin and inhibit
                  production of inflammatory cytokines
                 360mg/day positive benefits but further studies needed in RA
         Feverfew:
                 folklore use in arthritis concentration varies widely
         Curcumin:
Decreases inflammationSjogrens syndrome
                                                                                         10
          Chronic inflammatory condition
          Characterized by:
                  polyglandular tissue destruction
                  keratoconjunctivitis
                  xerostomia
                  reduced production of tears
                  xerophthalmia
          Half individuals with RA have this syndrome


Nutritional management:
          Goal:
          relief of symptoms and eating discomfort which include:
                  decreased appetite
                  weight loss
                  fatigue
                  chewing and swallowing problems
                  cavities
                  anaemia
          Xerostomia:
                  dental care
                  frequent rinsing with water
                  tooth-brushing
          Swallowing:
                  moist foods
                  avoid extremes of temperature
          Lack of saliva:
                  lemon drops to stimulate
                  fake saliva
          avoid deficiencies of:
                  iron
                  vitamin B12
                  folate
          by ensuring adequate dietary intake




Temporomandibular joint syndrome (TMS)
                                                                     11
          Painful eating- associated with RA
          Goal of nutritional management:
                     alter consistency of foods to reduce chewing
                     soft and bite size foods
          Work with OT to design diet minimizing:
                     pain and frustration with preparation and consumption
                     finger foods that don’t fall apart easily


Gout
          Disorder of purine metabolism – abnormal high levels of uric acid accumulate
            in the blood (hyperuricemia)
          Sodium urates are formed and deposit as tophi in small joints and
            surrounding tissues
                     helix of the ear
                     large toe
                     elbow
          Deposits destroy joint tissues and lead to chronic symptoms of arthritis
          Usually occurs in men >35 years
          Results in sudden and acute onset of pain eg in the big toe radiating up the
            leg
          Renal disease is also common


Possible causes
          Trivial injury
          Unaccustomed exercise may precipitate episodes
          Excessive eating, drinking and exercise
          Ketosis (after fasting or following a low CHO diet)
          Abdominal fat distribution aggravates risk of IR in gout patients, increases risk
            of atherosclerosis


Nutritional Management
          Endogenous formation of uric acid – accounts for 85% of urate formed
          Little influence by dietary regulation but limiting foods high in purine – reduces
            metabolic stress and medication use
          Acute stage:
                     restrict purine use to 100-150mg/day
                                                                                           12
                   Sources of high purine foods
                          See box 44.2 pg 1136 Krause 11th Ed
                          Remember to show them in the context of other foods what they
                           need to avoid otherwise they feel there is nothing they can eat
         Between attacks:
         Healthy varied diet, to prevent ketosis
         Achieve and maintain an ideal weight
         Fluids:
                   3litres / day to dilute urine
         Moderate protein:
                   increase low fat dairy products
                   tofu alters plasma protein concentration and increases uric acid
                    clearance and excretion
         High CHO ( 50-55%):
                   CHO increase urate excretion
         Low fat (30%):
                   Fat reduce urate excretion
         Cholesterol:
                   < 300mg day
         Avoid/Limit Alcohol (increases urate production)


Drug Therapy
         Used to inhibit or eliminate uric acid synthesis
         Probenecid (Benemid)
                   increase elimination through kidneys
         Sulfinpyrazone
                   increase elimination through kidneys
         Allopurinol
                   inhibits uric acid production
         Colchicine
                   relieve joint pain
         Anti-inflammatory drug
                   indomethacin/phenylbutazone
                   use in acute stage


Scleroderma
                                                                                             13
          Progressive, systemic sclerosis characterised by deposit of fibrous connective
             tissue in the skin and visceral organs and GIT
          More common in women than men 4:1


Problems that present:
          Manifestation of Raynauds syndrome
                   ischemial coldness in the small extremities, such as fingers
                   difficulty with food preparation and consumption
          Sjogrens syndrome often present
          Weight loss
          Renal dysfunction
          Multiple organ system dysfunction (MOSD)
          GI symptoms:
                   Heart burn
                   Nausea
                   Vomiting
                   Dysphagia
                   Diarrhoea
                   Constipation
                   Faecal incontinence
          Malabsorption
                   Lactose
                   Vitamins
                   Fatty acids
                   Minerals


Nutritional Management
          High-energy, high protein- supplement/enteral feeding to correct or prevent
             weight loss
          Vitamin and mineral supplement




Systemic lupus erythematosus (SLE)
          Auto-immune disease - affects all organ systems
          Etiology?
                   Genetic predisposition
                                                                                         14
                  presence of anti-DNA antibodies
                  environmental factors - viral infection could play a role
          Affect women of childbearing age
          25% develop Sjogren’s syndrome
          Renal function reduced:
                  excessive protein excretion and often renal failure


Nutritional Management
          Individual needs
          Protein requirements altered due to renal function / steroids
          Sodium and fluid restricted
          Low saturated fat diet suggested - effectiveness ?
          Energy- to attain and maintain usual dry body weight
          Role of vitamins, minerals, omega 3 fatty acids – under investigation


Drug therapy
          Corticosteroids
                  effect protein, sodium, fluid and calcium requirements
          Immuno-suppressors eg azathioprine
                  GI side effects
          Antimalarial eg Plaquenil
                  Clears skin lesions
                  Nausea, abdominal cramps and diarrhoea


Chronic fatigue disease syndrome (CFDS)
          Rheumatic symptoms – but no proven cure
          CFDS – chronic fatigue for longer than 6 months, accompanied by:
                  hypotension (low blood pressure)
                  sore throat
                  multiple joint pains
                  headaches
                  post-exercise lethargy
                  muscle pain and
                  impaired concentration


Nutritional Management
                                                                                   15
          If hypotensive:
                    consider increasing sodium intake
                    increase fluid intake


Unproven therapies
          mega doses of vitamins
          graduated exercise programs
          antioxidant therapy
          low fat diets
          magnesium sulphate
          IV immunoglobin therapy




Fibromyalgia
          Rheumatic symptoms – but no proven cure
          Non-articular aches and fatigue causing disabling symptoms similar RA
          Symptoms include:
                    muscle tenderness
                    sleep disturbances
                    irritable bowel
                    chronic headaches
                    irritable bladder
                    fatigue
                    morning stiffness
                    numbness and tingling


Hypotheses
          central nervous system dysfunction
          central pain derangement
          nutrient deficiencies
                    magnesium
                    malic acid
                    manganese
                    thiamin
          other systemic abnormalities


                                                                                   16
Nutritional Management
          Short term vegan diet has shown to be beneficial


Complementary therapy
          30 minutes exercise x 3 / week
          Acupuncture


Therapies needing further study
          pain therapy
          physical reconditiong
          psychological counselling
          calcium channel blockers




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