ASSESSMENT AND MANAGEMENT OF PATIENTS WITH RHEUMATIC DISORDERS I.

RHEUMATIC DISORDERS a chronic, progressive disease involving inflammation of synovial joints. Three times greater in women than in men. Onset is between 30 and 60 but can develop at any age.

ETIOLOGY – an autoimmune disorder; its cause is unknown. Exacerbations may be associated with increased physical or emotional stress. PATHOPHYSIOLOGY – begins as inflammation and progress to destruction of joints, producing deformity and loss of motion. The disease may affect only joints or may extend to body organs and blood vessels. ASSESSMENT FINDINGS 1. Clinical Manifestations a. b. c. d. e. f. Edematous, warm, tender joints Limited ROM in affected joints Generalized edema or nodules around affected joints Impaired mobility and ability to perform ADLs Fatigue, weakness and anorexia In later stages, weight loss, fever, anemia, muscle atrophy and Sjogren’s syndrome

2. Laboratory and diagnostic study findings. a. b. c. d. Radiographic studies reveal abnormalities like progressive joint damage. Rheumatoid factor is present in more than 80% of clients. ESR is significantly elevated. RBC and C4 complement component are decreased.

NURSING MANAGEMENT 1. Administer prescribed medications.- NSAIDs, aspirin, slow-acting antirheumatic medications and corticosteroids. 2. Provide pain relief. o provide comfort measures including massage and position changes. o Apply hot or cold therapy to affected joints according to the client’s needs. 3. Promote self-care. 4. Promote client and family coping. 5. Promote adequate rest and sleep to prevent fatigue; provide comfort measures including a foam mattress and supportive pillows; and discuss energy conservation techniques. 6. Encourage proper body alignment to prevent contractures. 7. Collaborate with the PT to design and provide the client with a physical therapy program, which begins after the acute phase resolves. o encourage a muscle activity program for self-care o water exercises are excellent because water promotes buoyancy, which eases joint movements. 8. Recommend a weight reduction program, if appropriate. 9. Collaborate with the OT and promote the use of braces, splints, and assistive mobility devices, if appropriate. 10. Discuss maintaining optimal nutritional status.

II. DIFFUSE CONNECTIVE TISSUE DISEASES A. SYSTEMIC LUPUS ERYTHEMATOSUS a chronic systemic inflammatory disease affecting multiple body systems.

with renal involvement.- Women are affected at least 8 times more often than men Women of childbearing age are more susceptible. SLE can lead to potentially serious complications. elbows. Other Systems . Integumentary systems . erythematous and purpuric lesions on fingertips. severe anemia. Respiratory System . the glomeruli of kidneys are usually affected. LABORATORY AND DIAGNOSTIC STUDY FINDINGS a.Pleural effusion . Red and White Blood Cell counts may be decreased. autoantibody production and decreased T-cell functions. Neurologic System . Pathophysiology 1. revealing thrombocytopenia. Involves markedly increased B-cell activity. c. . and neurologic problems and severe bacterial infections. Disease progression. however. 2. forearms and hands d. ETIOLOGY – an autoimmune disorder. autoantibody production. including CV.Subacute cutaneous lupus erythematosus results in a butterfly rash across the bridge of the nose and cheeks. Urine testing reveals proteinuria and cellular casts in urine. hypergammaglobulinemia. Prognosis is good with early detection and treatment.subtle changes in personality and cognitive ability . - Discoid lupus erythematosus results in skin involvement that may be provoked by sunlight or artificial UV light. leukocytosis. Administer prescribed medications which may include corticosteroids. a. ad leucopenia. ASSESSMENT FINDINGS Clinical manifestations may be insidious or acute. clinical manifestations involve multiple body systems. CV System .Pleuritis e.depression and psychosis f. which is characterized by recurring remissions and exacerbations.Arthralgias and arthritis (synovitis) . and salicylates to help control the joint pain and oral and topical corticosteroids to help with the rash. toes. is widely variable.Joint edema and tenderness .Pain on movement and morning stiffness b. b. NURSING MANAGEMENT 1. Oral ulcers of the buccal mucosa and hard palate occur in crops and may accompany skin lesions. Musculoskeletal system . c. Antinuclear antibody test result is positive. NSAIDs.pericarditis - papular. Anti-DNA cell test reveals a high titer d. the client may remain undiagnosed for many years. Symptoms result from immune complex invasion of body systems. renal.lymphadenopathy .

the tissue degenerates and becomes nonfunctional. and inspecting the skin for vasculitic lesions Perform a CV. resp. 5. a. - 3. Its incidence is 18-20 people per million per yr. Maintain skin integrity. Use sunscreen with a SPF at least 30. impeding respiration Hardening of the intestinal mucosa causing digestive disturbances Progressive renal failure may occur CREST syndrome may develop (calcinosis – calcium deposits in the tissues) Sclerodactyly (scleroderma of the digits) Teleangiectasia (capillary dilation that forms a vascular leion) Assessment and Diagnostic Findings 1. Encourage protection form the sun and UV light. Advise the client to avoid going out between 10 am and 4 pm. Provide meticulous mouth care. No conclusive test to diagnose scleroderma Skin Biopsy – to identify cellular changes specific to scleroderma Pulmonary Studies – show ventilation – perfusion abnormalities ECG – identifies pericardial perfusion Esophageal Studies – demonstrates decreased motility Blood Tests – detect ANAs (+) result . using mild soaps and lotions. c.2. Eventually. Insoluble collagen is formed and accumulates excessively in the tissues. 8. 7. Advise the client to avoid persons with contagious infections. Initially. Collaborate with the PT Dept and encourage an appropriate exercise program to help maintain mobility and strength. The skin then undergoes fibrotic changes. immobile and expressionless and the mouth becomes rigid Left ventricle of the heart is involved resulting in heart failure Hardening of the esophagus. 6. Condition spreads slowly for years. Provide a client and family teaching.“hard skin”. B. neurologic. PATHOPHYSIOLOGY - commonly begins with skin involvement. 3. 4. and musculoskeletal assessment to identify any systemic problems. 2. also occurs in blood vessels. from inflammation to degenartion. 4. Mononuclear cells cluster on the skin and stimulate lymphokines to stimulate procollagen. major organs and body systems. b. the inflammatory response causes edema formation. This chain of events. Advise the client to consult a health care provider before receiving immunizations or taking birth control pills of OTC drug. 5. Arrange for a dietary consult to ensure optimal nutrition while meeting the client’s need for soft. interfering with swallowing Lungs become scarred. leading to loss of elasticity and movement. easily tolerated foods. Changes may localized in the hands and feet Face appears masklike. smooth and shiny skin appearance. with a resulting taut. Clinical Manifestations starts with Raynaud’s phenomenon ad swelling in the hands skin and subcutaneous tissues become increasingly hard and rigid and cannot be pinched up from the underlying structures wrinkles and lines are obliterated skin is dry because sweat secretion over the involved region is suppressed extremities stiffen and lose mobility. SCLERODERMA . The cause is unknown. keep the skin clean and dry. Apply warm packs as needed to relieve joint pain and stiffness. wear a large hat and tight weave clothing and refrain from using a tanning bed.

Hydroxychloroquine (Plaquenil) – antimalarial – for skin rashes Nursing Management . 3. Serum Studies indicate increased muscle enzyme activity. Clinical Manifestations Proximal muscle weakness is the first symptom Muscle weakness is symmetric and diffuse Dermatomyositis – identified by an erythematous smooth or scaly lesion found over the joint surface. and prevent the effects of Raynaud’d phenomenon. Assessment and Diagnostic Findings No single test confirms polymyositis 1. Cessation of smoking. Avoid cold and protect fingers with mittens in cold weather. Nursing Management 1. (gradual dosage reduction after several months 2. These antibodies do not cause damage to muscle cells. 3. EMG – to rule out degenerative muscle disease 2. Drugs – may and provide general stiffness C. Pharmacologic Therapy Focus is treating organ system involvement 1. Total – body irradiation *2-4 are used if corticosteroids and other immunosuppressive agents are unsuccessful 5. POLYMYOSITIS Incidence estimated 5 to 10 cases per million adults per year Pathophysiology - Autoimmune because autoantibodies are present. Plasmapheresis – 3. 2. Genetic predisposition is likely and some evidence suggests a viral link. High-Dose Corticosteroid Therapy – immunosuppressive. musculoskeletal discomfort. Anti-inflammatory medications – control arthralgia. Provide meticulous skin care. 2.Medical Management Treatment depends on the clinical manifestations Moderate exercise program is encouraged to prevent joint contractures Avoid extreme temperatures and to use lotion to minimize skin dryness. Lymphapheresis 4. Calcium Channel Blockers and other Antihypertensive improvement in symptoms of Raynaud’s phenomenon. Warm socks and properly fitting shoes are helpful in preventing ulcers. Medical Management 1. Muscle Biopsy – reveals inflammatory infiltrate in the tissue.

Help patient prevent and monitor side effects of medication (infections. GI problems. changes in vision and jaw claudication. 3. D.Smoking cessation . NSAIDs sometimes used for mild disease Nursing Management 1.1. Stiffness in the morning and after periods of inactivity. Severe aching in the neck. DEGENERATIVE JOINT DISEASE . POLYMYALGIA RHEUMATICA Pathophysiology Occurs in Caucasians Associated with the genetic marker HLA – DR4 suggests a familial predisposition. Assist in self-care activities. Medical Management 1. Systemic features Low-grade fever Weight loss Malaise Anorexia Depression Giant Cell Arteritis – may cause headaches. May cause permanent loss of vision if not evaluated immediately. .Reduction of alcohol consumption.Weight – bearing exercise . Recommend use of assistive devices 2. If without arteritis.Adequate dietary calcium and Vitamin D. Initiate PT with ROM exercise to maintain joint ability followed by gradual strengthening exercises. . and depression) 2. moderate dose of corticosteroid 2. Immunoglobulin deposits in the walls of inflamed temporal arteries also suggest and autoimmune process.000 1. High ESR – a screening test but is not definitive.Measurement of bone mineral density. III. Response to treatment with corticosteroids is considered by some to be diagnostic. Interventions to promote bone health. if indicated. - Clinical Manifestations - Characterized by severe proximal muscle discomfort with mild joint swelling. 2. Annual incidence rate of 52 cases/100. DM. . shoulder and pelvic muscles is common. - Assessment and Diagnostic Findings Found almost exclusively in people older than 50 years of age.

It causes deterioration of the joint cartilage and formation of reactive new bone at joint margins and in subchondral areas. or pillows as needed. It starts with asymmetric cartilage loss.- Osteoarthritis is a slowly. A physical therapist may prescribe and implement modified weight bearing exercises within the client’s tolerance level. An OT may help with self-management strategies. b. Soft tissue imbalance. 3. genetic predisposition and congenital abnormalities. if used. Remove splints routinely. d. Pain and muscle spasms. trauma. Administer prescribed medications. Promote adequate rest and reduction of stress. degenerative joint disease characterized by variable changes in weight-bearing joints. Disability ovaries from the limitation of finger movement to severe hip and knee degeneration. aging. e. Limited motion in affected joints. as indicated. 6. Prepare the client for surgical treatment. Ankylosing Spondylitis . Joint tenderness and Heberden’s nodes in interphalangeal joints. at night and in the early morning. PATHOPHYSIOLOGY 1. a. Joint “grating” with movement. sandbags. which leads to abnormal forces on the joint. joints with minor deterioration may remain stable for years. and bony hypertrophy can result. 2. Massage surrounding muscles. which may include analgesics and NSAIDs such as COX-2 inhibitors. 2. to exercise joints. 3. which are more pronounced after exercise. b. SPONDYLOARTHROPATHIES A category of systemic disorders of the skeleton. NURSING MANAGEMENT 1. The most common form of arthritis. 5. c. Provide nonpharmacologic comfort measures. as indicated. ETIOLOGY – it is associated with obesity. Refer the client to PT and OT. Types of Spondyloarthropathies 1. progressive. Apply warm compress or diathermy to sore joints. Position the client to prevent flexion deformity using a foot board. d. Plan activities that promote optimal function and independence. not over inflamed joints. c. LABORATORY AND DIAGNOSTIC STUDY FINDINGS Radiographs may reveal a narrowing of joint space (because cartilage is not radiographic). osteoarthritis affects both sexes about equally. splints. IV. joint malalignment. 4. wedges. primarily in the hip and knee. ASSESSMENT FINDINGS CLINICAL MANIFESTATTIONS a. Maintain nonjudgmental attitude and respect the client’s right to choose any alternative treatment for pain relief. Progression is also variable. Flexion contractures. wit h onset usually at age 40.

the large synovial joints. NSAIDs and Corticosteroids – improve back. Anti-TNF therapy is under investigation for treatment of the spondyloarthorpathies. If patient responds to an itch by scratching. leading to respiratory compromise and complications. skin and joint symptoms b.6 to 7% - Pharmacologic Management a. Reactive Arthritis (Reiter’s Syndrome) Reactive because the arthritis occurs after an infection Affects young adult males and is characterized primarily by urethritis. Medical Management 1. NURSING CARE MANAGEMENT OF PATIENTS WITH DERMATOLOGIC PROBLEMS I. Dermatitis and ulcerations of the mouth and penis Low back pain 3. c. Job modification. 2. infection or changes in pigmentation may result. especially among those who perform physical work. At night there are few distractions. hepatic and thyroid diseases. Pruritus may be the first indication of a systemic internal disease such as DM. raised areas. Pruritus occurs frequently in elderly people as a result of dry skin. mucous membranes and cornea. knees or shoulders may be involved. arthritis and conjunctivitis. radiation therapy. which produces more pruritus. the integrity of the skin may be altered and excoriation. should be identified. Nursing Management 1. redness. polyarthritis and spondylitis Prevalence of arthritis in patients with psoriasis is 7 to 42% Prevalence of psoriasis in persons with arthritis is 2. More prevalent in males than females and is usually diagnosed in he second or third decade of life Ankylosis of the entire spine may occur. Good body positioning and posture are essential. Certain soaps and chemicals. blood disorders or cancer. Methotrexate (Rheumatrex) and Sulfasalazine (Azulfidine) – may help with peripheral disease Methotrexate is also used to control psoriasis. generating a vicious itch – scratch cycle. antibiotics. More frequently at night and is less frequent during waking hours. probably because the person is distracted by daily activities. hormones and opioids may cause pruritus indirectly or by increasing sensitivity to UV light. dry air or irritating bed linens. Psoriatic Arthritis Characterized by synovitis. such as the hips. Warm. prickly heat and contact with woolen garments are also associated with pruritus. Maintain ROM with regular exercise and muscle – strengthening program. 2. PRURITUS (General Pruritus) Itch receptors are unmyelinated. Pathophysiology Scratching the pruritic area causes the inflamed cells and nerve endings to release histamine. It may also accompany renal. . penicillate (brush-like) nerve endings that are found exclusively in the skin.- Affects the cartilaginous joints of the spine and surrounding tissues Occasionally. 3. Some oral medications such as aapirin.

[2] HS often goes undiagnosed for years because patients are too ashamed to speak with anyone.[1]:710 It is more commonly found in women and can be present under the breasts. however. 2. culminating in drainage of pus.1. 3. Applying a cold compress. 5. Avoid rubbing vigorously with a towel because this overstimulates the skin and causes more itching. Tricyclic Antidepressant like Doxepin (Sinequan) – for pruritus of neuropsychogenic origin. hormonal changes (such as monthly cycles in women). At this stage.1%) and 1:600 (0. but has been estimated as being between 1:24 (4. HS pain can be difficult to manage.2%). others may worsen and require surgery in order to live comfortably. Because HS is considered a rare disease. often leaving open wounds that will not heal. 4. A warm bath with a mild soap followed by application of emollient to moist skin can aontrol xerosis (dry skin). The disease manifests as clusters of chronic abscesses or boils. where the affected areas are excised. SECRETORY DISORDERS 2. Pharmacologic Management 1. 4.[2] When they do see a doctor. There is no known cure nor any consistently effective treatment. Nursing Management 1. 3. that are extremely painful to the touch and may persist for years with occasional to frequent periods of inflammation. pressure pain. Carbon dioxide laser surgery is currently considered the last resort for those who have advanced to its highest stage. Oral Antihistamines – can overcome the effects of histamine release from damaged mast cells 2. and can be very expensive. HYDRADENITIS SUPPURATIVA Hidradenitis suppurativa or HS is a skin disease that affects areas bearing apocrine sweat glands and hair follicles. HS is often called an 'orphan illness'. the disease is frequently misdiagnosed or prescribed treatments are ineffective. Fexofenadine (Allegra) – relieves daytime pruritus 3. and the skin is grafted. Surgery doesn't always alleviate the condition. and progression varies from person to person.1. Topical Corticosteroids – anti – inflammatory agents to decrease itching. It is possible that there is genetic predisposition to the disease. Bath oils containing surfactant that makes oil mix with bath water may be sufficient for cleaning.[3] HS is not contagious.2. 5. Occurrences of bacterial infections and cellulitis (deep tissue inflammation) may occur at these sites. perspiration. and clothing friction. with some experiencing remission anywhere from months to years at a time. the skin should be lubricated with an emollient to trap moisture. complete healing is usually not possible.[4] . groin and buttocks. due to little research being conducted on the disease at this time. 2. Flare-ups may be triggered by stress. ice cube or cool agents that contain menthol and camphor (which constrict blood vessels) may also help relieve pruritus. Persistent lesions may lead to scarring and the formation of sinus tracts. such as the underarms. Diphenhydramine (Benadryl) or Hydroxyzine (Atarax) – prescribed in a sedative dose at bedtime and effective in producing a restful and comfortable sleep. humid heat. Immediately after bathing. its incidence rate is not well known. II.2. or tunnels connecting the abscesses under the skin. Avoid situations that cause vasodilation. and is not affected nor caused by good or bad hygiene. Drainage provides some relief from severe. Washing with soap and hot water is avoided. Remind patient to use tepid (not hot) water to shake off excess water and blot between intertriginous areas (body folds) with a towel. 2. often debilitating. which can be as large as baseballs or as small as a pea. temporary and sometimes even harmful.

a proposed new term[5][6] which has not gained widespread favour. Some of these are also used to describe different diseases. More recent studies imply there is an autoimmune component.[11] possibly triggered by a blocked gland. which may increase the rate of obesity among sufferers.another misnomer. based on the deep fox den / burrow . the causes are controversial and experts disagree. however this condition is not caused by obesity and weight loss will improve but not cure it. However.[2] • • • • • • • • • Acne conglobata .not really a synonym .[citation needed] .a misnomer. (Inflammation of sites to the size of golf balls.[7] Apocrine Acne . scarring develops.) Diffuse or broad involvement across a regional area with multiple interconnected sinus tracts and abscesses. patients at this stage may be unable to function. or sometimes baseballs.a misspelling Pyodermia sinifica fistulans . pain. single or multiple widely separated lesions.an older term. (Frequent inflammations restrict movement and may require minor surgery such as incision and drainage.[2][9] Stage I II Characteristics Solitary or multiple isolated abscess formation without scarring or sinus tracts.commemorating the French surgeon who first described the disease in 1833 Verneuil's disease . with sinus tract formation.a catchy term not used in medical literature. based on the disproven concept that apocrine glands are primarily involved Apocrinitis . out-dated.like sinuses Hidradenitis Supportiva . The historical understanding of the disease is that there is a dysfunctional apocrine glands[9] or dysfunctional hair follicles. or specific instances of this disease. based on the disproven concept that apocrine glands are primarily involved Fox-den disease . out-dated. may be mistaken for acne.see fistula. as well as in various cultures.this is a similar process but in classic acne areas of chest and back Acne Inversa (AI) . and a swollen lesion. Obviously.) III Causes As this disease is poorly studied. including subcutaneous tracts of infection . creating inflammation. (A few minor sites with rare inflammation. Patients with more advanced cases may find exercise intolerably painful.recognizing the French surgeon whose name is most often associated with the disorder as a result of his 1854-1865 studies[8] Stages HS presents itself in three stages.) Recurrent abscesses. potential indicators include: • • • • • • • • • • • post-pubescent individuals are more likely to exhibit HS females are more likely than males genetic predisposition among families plugged apocrine (sweat) gland or hair follicle excessive sweating bacterial infection sometimes linked with other auto-immune conditions[10] androgen dysfunction genetic disorders that alter cell structure stress can bring on outbreaks being overweight makes it worse. misspelled here Velpeau's disease .Other names for HS Hidradenitis suppurativa has been referred to by multiple names in the literature. considered archaic now.

undiagnosed. inflammatory. Nearly a quarter of patients state that nothing relieves their symptoms. Lifestyle o o o • Changes in diet avoiding inflammatory foods.[16] This use of the drugs is not currently Food and Drug Administration (FDA) approved and is somewhat controversial. Most cultures done on HS lesions come back negative for bacteria. scaling eruption characterized by periodic remissions and exacerbations. The area becomes inflamed. hydrotherapy.HS is not caused by any bacterial infection—any infection is secondary—and is therefore not contagious. foods high in refined carbohydrates. and patients should discuss all options with their doctor or dermatologist. balneotherapy Icing the inflamed area daily until pain reduction is noticed Medication o Hexachlorophene shower with liquid soap like Phisohex. o Antibiotics orally (only in presence of bacterial infection) o Vitamin A supplementation o Anti-androgen therapy o IV or subcutaneous infusion of anti-inflammatory (anti-TNF-alpha) drugs such as infliximab (Remicade). It most commonly develops in middle-aged or older people as multiple lesions occurring chiefly on the scalp. Due to the poorly-studied nature of this disease. Warm compresses. These areas have a predilection to seborrheic dermatitis because they have a high bacterial count. covering sores with Metrolotion after medicated showers.[citation needed] Severe complications Left undiscovered. and therefore may not be covered by insurance. so antibiotics should be used only when a bacterial infection has been confirmed by a physician. [12][13] Treatments Treatments may vary depending upon presentation and severity of the disease.2. the effectiveness of the drugs and therapies listed below is not yet clear. SEBORRHEIC DERMATOSES . o Acitretin o Zinc gluconate taken orally has been shown to induce remission o Hibiclens + Gold Dial antibiotic soap Hibiclens is an antiseptic/antibiotic found in walgreens Surgery o Incision and drainage or lancing o Wide local excision (with or without skin grafting) o Laser surgery Radiation therapy • • 2. o Corticosteroid injections. etanercept (Enbrel).[15] and adalimumab.is a chronic.[14] A list of treatments that are possible treatments for some patients is as follows. or untreated. face or trunk. PATHOPHYSIOKOGY Seborrhea refers to excessive production of sebum by sebaceous glands in areas where glands are normally found in large numbers. resulting in an oily form or . ETIOLOGY – associated with genetic predisposition and aggravated by physical or emotional stress. the fistulas from severe stage-3 HS can lead to the development of squamous cell carcinoma in the anus or other affected areas.

The inflamed area may develop a secondary Candida (yeast) infection in body creases and folds. Instruct the client to avid excessive heat and perspiration. Diet does not affect incidence or severity. ETIOLOGY – genetics. INFECTIOUS DERMATOSES 3. d. The bacteria secrete the enzyme lipase. ULCERATION . PEMPHIGUS 6. Provide client and family teaching. PARASITIC SKIN INFESTATIONS IV. BACTERIAL SKIN INFECTION 3. predominantly in areas where glands are normally found in large numbers and in skin folds. BLISTERING DISEASE 6. Pathophysiology Acne eruptions are initiated by increased sebum production activated by androgenic hormones. greasy-appearing skin with or without scaling and slight erythema c.4.3. scaling (dry. open comedones (black heads) III. which reacts to sebum to produce free fatty acids to trigger inflammation.2. Sebum is secreted into dilated hair follicles containing normal skin bacteria such as P.dry form of seborrheic dermatitis. b. BULLOUS PEMPHIGOID 6. Caution the client that this is a chronic problem with remissions and exacerbations.4. EXFOLIATIVE DERMATITIS VI. ASSESSMENT FINDINGS a. PSORIASIS 5.2. FUNGAL SKIN INFECTIONS 3. Acne. NON-INFECTIOUS INFLAMMATORY DERMATOSES 5.1. Instruct the client to treat dandruff by properly shampooing with medicated shampoo. moist or greasy). The incidence is highest at puberty. b.1. CONTACT DERMATITIS V. Patches of sallow. a. keratin produced by the hair follicles combines with sebum to form plugs in dilated follicles. although it may occur as early as age 8 and can persist into adulthood. c. DERMATITIS HERPETEFORMIS 6. Administer prescribed medications. At the same time. Pruritus and pain NURSING MANAGEMENT 1. Advise the client to remove any external irritants. Assessment Findings: Clinical Manifestations include closed comedones (white heads). STEVEN JHONSON VII.3. hormonal factors and bacterial infection. which may include topical corticosteroids or antibiotics to allay the secondary inflammatory response. 3. VIRAL SKIN INFECTIONS 3. 2. ACNE VULGARIS an inflammatory disease of the sebaceous follicles.1.2.

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