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    MEDICAL FACULTY TRISAKTI

    UNIVERSITYJAKARTA, 10 JANUARY 2012

    By : Aditya Ilham Noer

    030.08.086

    CORRELATION BETWEEN CHRONIC OBSTRUCTIVE

    PULMONARY DISEASE AND VITAMIN D

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    INTRODUCTION

    Chronic Obstructive Pulmonary Disease (COPD)makes it hard for you to breathe. Coughing up mucus

    is often the first sign of COPD. Chronic bronchitis and

    emphysema are common COPDs. Cigarette smoking

    is the most common cause of COPD. Breathing inother kinds of irritants, like pollution, dust or

    chemicals, may also cause or contribute to COPD.

    Quitting smoking is the best way to avoid developing

    COPD.

    Vitamin D-binding protein (DBP) genetic

    polymorphisms have been associated with chronic

    obstructive pulmonary disease (COPD). DBP has an

    indirect role in macrophage activation; thus it was

    http://www.nlm.nih.gov/medlineplus/chronicbronchitis.htmlhttp://www.nlm.nih.gov/medlineplus/emphysema.htmlhttp://www.nlm.nih.gov/medlineplus/quittingsmoking.htmlhttp://www.nlm.nih.gov/medlineplus/quittingsmoking.htmlhttp://www.nlm.nih.gov/medlineplus/quittingsmoking.htmlhttp://www.nlm.nih.gov/medlineplus/quittingsmoking.htmlhttp://www.nlm.nih.gov/medlineplus/emphysema.htmlhttp://www.nlm.nih.gov/medlineplus/chronicbronchitis.html
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    COPD

    is the co-occurrence of chronic bronchitis andemphysema, a pair of commonly co-existing diseases

    of the lungs in which the airways become narrowed.[1]

    This leads to a limitation of the flow of air to and from

    the lungs, causing shortness of breath (dyspnea). Inclinical practice, COPD is defined by its

    characteristically low airflow on lung function tests.

    Classification

    1. Chronic bronchitis

    2. Emphysema

    http://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Airwayshttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Lung_function_testhttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Shortness_of_breathhttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Airwayshttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Chronic_bronchitishttp://en.wikipedia.org/wiki/Chronic_bronchitis
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    Chronic Bronchitis

    Lung damage and inflammation in the large airways

    results in chronic bronchitis. Chronic bronchitis isdefined in clinical terms as a cough with sputum

    production on most days for 3 months of a year, for 2

    consecutive years.

    Emphysema

    Lung damage and inflammation of the air sacs

    (alveoli) results in emphysema. Emphysema is

    defined as enlargement of the air spaces distal to the

    terminal bronchioles, with destruction of their walls.

    http://en.wikipedia.org/wiki/Sputumhttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Distalhttp://en.wikipedia.org/wiki/Terminal_bronchioleshttp://en.wikipedia.org/wiki/Terminal_bronchioleshttp://en.wikipedia.org/wiki/Terminal_bronchioleshttp://en.wikipedia.org/wiki/Terminal_bronchioleshttp://en.wikipedia.org/wiki/Distalhttp://en.wikipedia.org/wiki/Emphysemahttp://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Sputum
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    Sign and Symptom

    History of cigarette smoking.

    Chronic cough and sputum production (in chronic

    bronchitis)

    Dyspnea Rhonchi, decreased intensity of breath sounds, and

    prolonged expiration on physical examination

    Airflow limitation on pulmonary function testing that is

    not fully reversible and most often progressive.

    http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Rhonchihttp://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Rhonchihttp://en.wikipedia.org/wiki/Dyspnea
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    Etilogy

    Occupational exposures

    Intense and prolonged exposure to workplace dusts

    found in coal mining, gold mining, and the cotton

    textile industry and chemicals such as cadmium,

    isocyanates, and fumes from welding have been

    implicated in the development of airflow obstruction,

    even in nonsmokers. Workers who smoke and are

    exposed to these particles and gases are even more

    likely to develop COPD.

    Air pollution

    Studies in many countries have found people who live

    in large cities have a higher rate of COPD comparedto eo le who live in rural areas. Urban air ollution

    http://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Cadmiumhttp://en.wikipedia.org/wiki/Isocyanateshttp://en.wikipedia.org/wiki/Weldinghttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Air_pollutionhttp://en.wikipedia.org/wiki/Weldinghttp://en.wikipedia.org/wiki/Isocyanateshttp://en.wikipedia.org/wiki/Cadmiumhttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Gold_mininghttp://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Coal_mininghttp://en.wikipedia.org/wiki/Coal_mining
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    Genetics

    Alpha 1-antitrypsin deficiency is a genetic conditionthat is responsible for about 2% of cases of COPD. In

    this condition, the body does not make enough of aprotein, alpha 1-antitrypsin. Alpha 1-antitrypsinprotects the lungs from damage caused by proteaseenzymes, such as elastase and trypsin, that can be

    released as a result of an inflammatory response totobacco smoke.[7]

    Autoimmune disease

    There is mounting evidence that there may be an

    autoimmune component to COPD, triggered bylifelong smoking. Many individuals with COPD whohave stopped smoking have active inflammation inthe lungs. The disease may continue to get worse formany years after stopping smoking due to this

    ongoing inflammation. This sustained inflammation is

    http://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Enzymeshttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Trypsinhttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Autoantibodieshttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Trypsinhttp://en.wikipedia.org/wiki/Elastasehttp://en.wikipedia.org/wiki/Enzymeshttp://en.wikipedia.org/wiki/Proteasehttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsinhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiency
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    PHATOPHYSIOLOGY Narrowing of the airways reduces the rate at which air can flow to

    and from the air sacs (alveoli) and limits the effectiveness of thelungs. In COPD, the greatest reduction in air flow occurs whenbreathing out (during expiration) because the pressure in thechest tends to compress rather than expand the airways. In

    theory, air flow could be increased by breathing more forcefully,increasing the pressure in the chest during expiration. In COPD,there is often a limit to how much this can actually increase airflow, a situation known as expiratory flow limitation.[5]

    If the rate of airflow is too low, a person with COPD may not be

    able to completely finish breathing out (expiration) before he orshe needs to take another breath. This is particularly commonduring exercise, when breathing has to be faster. A little of the airof the previous breath remains within the lungs when the nextbreath is started, resulting in an increase in the volume of air inthe lungs, a process called dynamic hyperinflation.[5]

    Dynamic hyperinflation is closely linked to dyspnea in COPD. It is

    http://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Hyperaerationhttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Alveoli
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    DIAGNOSISChest X-ray

    Spirometry The diagnosis of COPD is confirmed by spirometry, a

    test that measures the forced expiratory volume inone second (FEV1), which is the greatest volume of

    air that can be breathed out in the first second of alarge breath

    More specifically, the diagnosis of COPD is madewhen the FEV1/FVC ratio is

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    Spirometry can help to determine the severity of COPD.[4]

    The FEV1 (measured after bronchodilator medication) is

    expressed as a percentage of a predicted "normal" valuebased on a person's age, gender, height and weight:

    1. Severity of COPD (GOLD scale) = FEV1 % predicted

    2. Mild (GOLD 1) = 80

    3. Moderate (GOLD 2) = 5079

    4. Severe (GOLD 3)3 = 049

    5. Very severe (GOLD 4) =

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    TREATMENT

    The goals of COPD treatment are: to prevent further deterioration in lung function;

    to alleviate symptoms;

    to improve performance of daily activities and quality oflife.

    The treatment strategies include:

    quitting cigarette smoking;

    taking medications to dilate airways (bronchodilators) and

    decrease airway inflammation; vaccination against flu influenza and pneumonia;

    regular oxygen supplementation; and

    pulmonary rehabilitation.

    http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=9098http://www.medicinenet.com/script/main/art.asp?articlekey=9097http://www.medicinenet.com/script/main/art.asp?articlekey=9097http://www.medicinenet.com/script/main/art.asp?articlekey=9098http://www.medicinenet.com/script/main/art.asp?articlekey=9098http://www.medicinenet.com/script/main/art.asp?articlekey=9098http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=11815http://www.medicinenet.com/script/main/art.asp?articlekey=11815
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    Bronchodilators

    Bronchodilators are medicines that relax smoothmuscle around the airways, increasing the calibre of

    the airways and improving air flow. They can reducethe symptoms of shortness of breath, wheeze andexercise limitation, resulting in an improved quality oflife for people with COPD.

    There are two major types of bronchodilator,1. 2 agonists and

    2. anticholinergics.

    Anticholinergics appear to be superior to 2 agonists

    in COPD. Anticholinergics reduce respiratory deathswhile 2 agonists have no effect on respiratorydeaths.

    http://en.wikipedia.org/wiki/Bronchodilatorshttp://en.wikipedia.org/wiki/Smooth_musclehttp://en.wikipedia.org/wiki/Smooth_musclehttp://en.wikipedia.org/wiki/Smooth_musclehttp://en.wikipedia.org/wiki/Smooth_musclehttp://en.wikipedia.org/wiki/Smooth_musclehttp://en.wikipedia.org/wiki/Bronchodilators
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    2 agonists

    2 agonists stimulate 2 receptors on airway smooth

    muscles, causing them to relax. There are several 2

    agonists available. Salbutamol (common brand name:

    Ventolin) and terbutaline are widely used short acting 2

    agonists and provide rapid relief of COPD symptoms.

    Long acting 2 agonists (LABAs) such as salmeterol and

    formoterol are used as maintenance therapy and lead toimproved airflow, exercise capacity, and quality of life.

    Anticholinergics

    Anticholinergic drugs cause airway smooth muscles torelax by blocking stimulation from cholinergic nerves.

    Ipratropium provides short-acting rapid relief of COPD

    symptoms. Tiotropium is a long-acting anticholinergic

    whose regular use is associated with improvements in

    http://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Salbutamolhttp://en.wikipedia.org/wiki/Terbutalinehttp://en.wikipedia.org/wiki/Salmeterolhttp://en.wikipedia.org/wiki/Formoterolhttp://en.wikipedia.org/wiki/Cholinergichttp://en.wikipedia.org/wiki/Ipratropiumhttp://en.wikipedia.org/wiki/Tiotropiumhttp://en.wikipedia.org/wiki/Tiotropiumhttp://en.wikipedia.org/wiki/Ipratropiumhttp://en.wikipedia.org/wiki/Cholinergichttp://en.wikipedia.org/wiki/Formoterolhttp://en.wikipedia.org/wiki/Salmeterolhttp://en.wikipedia.org/wiki/Terbutalinehttp://en.wikipedia.org/wiki/Salbutamolhttp://en.wikipedia.org/wiki/Receptor_(biochemistry)
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    Corticosteroids

    Corticosteroids are used in tablet or inhaled form

    to treat and prevent acute exacerbations ofCOPD. Well-inhaled corticosteroids (ICS) have

    not been shown to be of benefit for people with

    mild COPD, however, they have been shown to

    decrease acute exacerbations in those with eithermoderate or severe COPD.

    http://en.wikipedia.org/wiki/Corticosteroidhttp://en.wikipedia.org/wiki/Corticosteroid
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    PROGNOSIS

    COPD usually gradually gets worse over time andcan lead to death. The rate at which it gets worsevaries between individuals. The factors thatpredict a poorer prognosis are:[6]

    Severe airflow obstruction (low FEV1) Poor exercise capacity

    Shortness of breath

    Significantly underweight or overweight

    Complications like respiratory failure or corpulmonale

    Continued smoking

    Frequent acute exacerbations

    http://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_diseasehttp://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease
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    VITAMIN D

    Definition

    Vitamin D is a fat-soluble vitamin. Fat-soluble vitamins

    are stored in the body's fatty tissue.

    Function

    Vitamin D helps the body absorb calcium. Calcium

    and phosphate are two minerals that are essential for

    normal bone formation.

    Throughout childhood, your body uses these mineralsto produce bones. If you do not get enough calcium,

    or if your body does not absorb enough calcium from

    your diet, bone production and bone tissues may

    suffer.

    http://www.nlm.nih.gov/medlineplus/ency/article/002412.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002412.htm
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    FOOD SOURCES

    The body makes vitamin D when the skin is directlyexposed to the sun. That is why it is often called the"sunshine" vitamin. Most people meet at least some oftheir vitamin D needs this way.

    Very few foods naturally contain vitamin D. As a result,many foods are fortified with vitamin D. Fortified meansthat vitamins have been added to the food.

    It can be very hard to get enough vitamin D from food

    sources alone. As a result, some people may need totake a vitamin D supplement. Vitamin D found insupplements and fortified foods comes in two differentforms:

    D2 (ergocalciferol)

    D3 (cholecalciferol)

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    FOOD SOURCESDairy products

    Cheese

    Butter Cream

    Fortified milk (allmilk in the U.S. isfortified withvitamin D)

    Fatty fish (suchas tuna,

    salmon, andmackerel)

    Fortifiedbreakfastcereals,

    margarine, andsoy milk (check

    the Nutrition

    Fact Panel onthe food label)

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    Too much vitamin D can make the intestines absorb too

    much calcium. This may cause high levels of calcium in the

    blood. High blood calcium can lead to:

    Confusionand

    disorientation

    Damage tothe kidneys

    Calciumdeposits insoft tissues

    such as theheart andlungs

    Kidney stones

    http://www.nlm.nih.gov/medlineplus/ency/article/000458.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000458.htm
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    RECOMMENDATIONS

    Ten to 15 minutes of sunshine three times weekly isenough to produce the body's requirement of vitamin

    D. The sun needs to shine on the skin of your face,

    arms, back, or legs (without sunscreen). Because

    exposure to sunlight is a risk for skin cancer, youshould use sunscreen after a few minutes in the sun.

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    Infants (adequate intake of vitamin D)

    0 - 6 months: 400 IU (10 micrograms (mcg) per day) 7 - 12 months: 400 IU (5 mcg/day)

    Children

    1 - 3 years: 600 IU (15 mcg/day) 4 - 8 years: 600 IU (15 mcg/day)

    Older children and adults

    9 - 70 years: 600 IU (15 mcg/day)

    Adults over 70 years: 800 IU (20 mcg/day)

    Pregnancy and breast-feeding: 600 IU (15 mcg/day)

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    CORRELATION BETWEEN VITAMIN D AND COPD

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    CONCLUSION Vitamin D deficiency occurs frequently in COPD and

    correlates with severity of COPD. The data warrantvitamin D supplementation in patients with severeCOPD, especially in those carrying at-risk rs7041

    variants. whether prevention of vitamin D deficiencyor its supplementation can reverse the course ofCOPD. Vitamin D and its deficiency are intricatelyinvolved in many of the pathogenic mechanisms ofCOPD and its severity increases proportionately with

    the severity of deficiency. The authors describedseveral of the chemical and biological pathways bywhich vitamin D supplementation may benefitpatients. They concluded there is urgent need for

    controlled trials to investigate the efficacy of vitamin Dfor reversing the disease's progression.

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    Rabe KF, Hurd S, Anzueto A, et al. (2007). "Global Strategy for the Diagnosis, Management, and Prevention ofChronic Obstructive Pulmonary Disease: GOLD Executive Summary". Am. J. Respir. Crit. Care Med.176 (6):53255.

    Mathers CD, Loncar D (November 2006). "Projections of Global Mortality and Burden of Disease from 2002 to

    2030". PLoS Med.3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC1664601. PMID17132052.

    Burrows B, Fletcher CM, Heard BE, et al(1966). "The emphysematous and bronchial types of chronic airwaysobstruction. A clinicopathological study of patients in London and Chicago". Lancet87: 8305.

    Kitaguchi Y, Fujimoto K, Kubo K, Honda T (October 2006). "Characteristics of COPD phenotypes classified

    according to the findings of HRCT". Respir Med100 (10): 174252. doi:10.1016/j.rmed.2006.02.003. PaolettiM, Camiciottoli G, Meoni E, et al. (December 2009). "Explorative data analysis techniques and unsupervisedclustering methods to support clinical assessment of Chronic Obstructive Pulmonary Disease (COPD)

    phenotypes". J Biomed Inform42 (6): 101321. doi:10.1016/j.jbi.2009.05.008.

    Petty TL (2002). "COPD: clinical phenotypes". Pulm Pharmacol Ther15 (4): 34151.

    Lacasse Y, Brosseau L, Milne S, et al. (2002). Lacasse, Yves. ed. "Pulmonary rehabilitation for chronicobstructive pulmonary disease". Cochrane database of systematic reviews (Online) (3): CD003793

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