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Dermatologic Manifestations of Leprosy Treatment & Management

  • Author: Felisa S Lewis, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Apr 12, 2016
 

Medical Care

The management of leprosy includes early pharmacotherapy and physical, social, and psychological rehabilitation. The goals of pharmacotherapy are to stop the infection, reduce morbidity, prevent complications, and eradicate the disease. Since 1981, multidrug therapy (MDT) has been advocated by the World Health Organization (WHO)[64] and the United States government. MDT prevents dapsone resistance, quickly reduces contagiousness, and reduces relapses, reactions, and disabilities. If a patient has been previously treated with dapsone monotherapy, re-treatment with a modified MDT regimen of rifampin, clofazimine, and dapsone can reduce or delay the risk of relapse.[65]

The length of treatment ranges from 6 months to 2 years. Patients are considered noninfectious within 1-2 weeks of treatment (usually after the first dose). These drugs are conveniently packaged in monthly calendar blister packs. Monitor for drug resistance and adverse reactions to medications.

Paucibacillary disease can be treated with a combination of 2 drugs, whereas multibacillary disease requires triple-drug therapy. Single skin lesions (paucibacillary) can be treated with a single dose of 3 drugs. The length of treatment depends on the type of disease and on the access to drugs.

WHO and US treatment regimens for paucibacillary and multibacillary disease are listed below. Therapy for single skin lesions is not universal, because 80% of single skin lesions heal spontaneously. Therefore, only the WHO has a recommended treatment.

Current WHO recommendations for treatment of leprosy are as follows[66] :

  • Paucibacillary disease - Dapsone at 100 mg/d plus rifampin at 600 mg once a month for 6 months; children aged 10-14 years – Dapsone at 50 mg/d plus rifampin at 450 mg once a month for 6 months
  • Multibacillary disease - Dapsone at 100 mg/d plus rifampin at 600 mg once a month plus clofazimine at 300 mg once a month and 50 mg/d for 1 year; children aged 10-14 years - Dapsone at 50 mg/d plus rifampin at 450 mg once a month plus clofazimine at 150 mg once a month and 50 mg/d for 1 year
  • Single skin lesion - A single dose of rifampin at 600 mg, ofloxacin at 400 mg, and minocycline at 100 mg; children aged 10-14 years - Single dose of rifampin at 300 mg, ofloxacin at 200 mg, and minocycline at 50 mg; treatment of single skin lesions not recommended for pregnant women and children younger than 5 years

Current US recommendations for the treatment of leprosy are as follows[67] :

  • Paucibacillary disease - Dapsone at 100 mg/d plus rifampin at 600 mg/d for 1 year
  • Multibacillary disease - Dapsone at 100 mg/d plus rifampin at 600 mg/d plus clofazimine at 50 mg/d for 2 years

Resistance to rifampin and dapsone has been reported. WHO treatment recommendations are as follows[66] :

  • Rifampin resistance: 24-month treatment broken down as 6 months of 50-mg/d clofazimine, 400-mg/d ofloxacin, and 100-mg/d minocycline, followed by  18 mo of 50-mg/d clofazimine plus  400-mg/d ofloxacin or 100-mg/d minocycline
  • Dapsone resistance in paucibacillary disease - Clofazimine is substituted for dapsone; clofazimine at 300 mg once a month and 50 mg/d plus rifampin at 600 mg once a month for 6 months
  • Dapsone resistance in multibacillary disease: Treat as described above with only clofazimine and rifampin, omitting the dapsone
  • Other drugs that have been proposed as alternatives include moxifloxacin and rifapentine, but no specific regimens have been validated as effective.

In patients taking dapsone, the CBC count should be checked frequently early during the therapy and then less frequently later during therapy.

A modified course of MDT using rifampin and clofazimine was used effectively in patients with dapsone hypersensitivity syndrome.[68]

A small study also demonstrated the efficacy of a 4-week regimen of 600 mg of rifampin and 400 mg ofloxacin for paucibacillary disease.[69]

Treatment of pure neural leprosy often follows that of multibacillary disease.

Skin lesions usually resolve within the first year of treatment, although some may persist for up to 5 years in multibacillary disease.

Lack of improvement despite MDT may be due to anergy. This may be proven by a negative Mantoux test prior to administering the BCG injection. When given with MDT, BCG stimulates the suppressed cell-mediated immunity to produce a delayed hypersensitivity reaction, and induces clearance of bacilli.[70]

One promising avenue to measure treatment efficacy may be to follow immunoglobulin G levels of LID-1 fusion protein, and ML0405 and ML2331, both recombinant proteins. One study of Brazilian and Venezuelan patients demonstrated a decrease in reactivity across the clinical spectrum (highest levels in lepromatous leprosy → lowest levels in paucibacillary leprosy) and with MDT.[71]

Potential deformities can be prevented by educating patients about how to minimize existing nerve damage and by treating any sequelae of this damage. Close follow-up is important to ensure patient compliance (see Complications).

Further inpatient care

Patients with leprosy may need hospitalization for acute complications. Sanatoria, which were widely used in the past, are no longer necessary. Most patients can be treated in an outpatient setting.

Community-based rehabilitation programs are important to integrate and support people with leprosy and their families. A current list of Hansen disease clinics in the United States can be obtained from the National Hansen's Disease (Leprosy) Program.

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Surgical Care

Emergency surgery may be necessary if a patient with profound nerve inflammation presents with a nerve abscess or loss of nerve function secondary to compression. Prompt recognition and surgical drainage of the abscess can often restore nerve function.

Elective surgery may be required for correction of lagophthalmos (ie, inability to close the eye).

Reconstructive surgery can be used to repair nasal collapse in patients with lepromatous leprosy, but it is not recommended until the disease has been inactive for a minimum of 1 year.

Other surgery may be needed to improve function or for cosmesis.

Contractures can be surgically repaired.

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Consultations

Consultations with an ophthalmologist, a plastic surgeon, an orthopedic surgeon, an otolaryngologist, a neurosurgeon, and/or a neurologist may be necessary.

Reasons for a consultation with an ophthalmologist include the following:

  • Lagophthalmos
  • Erythema nodosum leprosum (ENL)–induced iritis
  • Direct invasion of the anterior chamber of the eye by Mycobacterium leprae
  • Corneal and conjunctival insensitivity
  • Infection or scarring from involvement of CN V and CN VII
  • Cataracts

Specialists in rehabilitation medicine, including physical and occupational therapists, can help in reducing morbidity.

Consultation with a prosthetics specialist also may be appropriate.

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Activity

Restrictions on activity depend on the extent of nerve damage.

In patients with bone or joint destruction, weight bearing should be minimized.

Patients with anesthesia of the limbs must be educated about their condition, and they should wear appropriate protection (especially footwear).

Plantar ulceration requires rest and avoidance of weight bearing.

Weakness or paralysis requires physical therapy to prevent contractures.

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Complications

Reactional states occur in approximately 20-50% of patients and are acute inflammations of the disease. They may be induced by MDT, physical or mental stress, puberty, childbirth, trauma, pregnancy, or surgical procedures. A leprous reaction should be considered a medical emergency and mandates immediate care. These states can result in permanent neurologic sequelae and are the leading causes of grade 2 disability. Patients at the highest risk are those with multibacillary leprosy, those with preexisting/persistent nerve impairment, those with positive anti-PGL-I, and those with positive bacillary indexes in skin smears.[72] MDT should be continued through the reactional episode.

Lepra type I (reversal) reactions usually affect patients with borderline disease. Reversal reactions are a shift toward the tuberculoid pole after the start of therapy, and they are type IV cell-mediated allergic hypersensitivities, with CD4+ lymphocytes infiltrate lesions with high levels of IFN-gamma and TNF-alpha, indicating an improvement in cell-mediated immunity. These reactions are characterized by increased inflammation of preexisting lesions and edema of the face and extremities, with edema and tenderness of peripheral nerves. New skin lesions are common, and the patient may have an acute febrile illness. The peak time for type I reactions is during the first 6 months of therapy and for up to 12 months. Corticosteroid treatment is aimed at controlling acute inflammation, relieving pain, and reversing nerve and eye damage. With treatment, approximately 60-70% of the patient's nerve function is recovered.[73] If neuritis is absent, NSAIDs may be helpful. Skin lesions have been successfully treated with the addition of topical tacrolimus.[74]

Lepra type II reactions, or erythema nodosum leprosum (ENL), occur in approximately 10% of patients with borderline lepromatous leprosy and in 20% of patients with lepromatous leprosy. These reactions are type III humoral (antibody-antigen) hypersensitivities, with a systemic inflammatory response to immune complex deposition. The most common presenting symptoms are crops of painful erythematous nodules of the skin and subcutaneous tissue. Sweet syndrome –like lesions have also occurred.[75] Bullae, ulcers, and necrosis also may occur.[76] Nerve damage is slower than in reversal reactions. The reaction usually manifests after a few years of therapy, and, although a single acute episode is possible, relapses occur intermittently over several years. Associated fever, malaise, arthralgias, neuralgia, iridocyclitis, dactylitis, orchitis, and proteinuria may be present. The use of clofazimine in MDT substantially reduces the incidence of ENL to 5%. Clofazimine has also been used to treat ENL. Mild cases can be treated with NSAIDs. Thalidomide is effective except in the case of neuritis or iritis, in which case corticosteroids should be used. Thromboembolic events are reported with thalidomide use.[77]  Other treatment therapies reported to be effective include colchicine, pentoxifylline, cyclosporine A, azathioprine,[78] methotrexate,[79] intravenous immunoglobulin, infliximab,[80] and etanercept.[81]

Lowering the dose of dapsone may decrease the severity of bullae and ulcers.

Lucio phenomenon[82] is a cutaneous necrotizing vasculitis that is sometimes designated a type II reaction. It is common in Mexico and Central America and is characterized by erythematous, geometric, irregular-shaped macules that rapidly progress to ulceration and necrosis on acral areas or extremities of patients with diffuse lepromatous leprosy. Systemic symptoms such as hepatosplenomegaly, fever, arthritis, and nephritis are usually present. Thalidomide is ineffective in treating this type of reaction; however, no consensus on treatment had been determined.[83] Most patients with Lucio phenomenon have not received MDT or were treated irregularly; therefore, MDT is recommended. Azathioprine or cyclophosphamide with corticosteroids with or without plasmapheresis has also been used.

The real challenge in managing leprosy is the treatment of reactional states.

If the course of MDT is not complete, continue taking those medications as directed.

Systemic steroids are effective in reducing inflammation and edema in reversal reactions; therefore, they are the most helpful medications in preventing nerve damage.

Prednisone at 1-2 mg/kg/d should be given until clinical improvement is seen, then tapered slowly over 3-6 months (and possibly longer).[63] One study suggests a course of at least 8 months.[84] This long course is necessary to decrease the severity of disabilities and deformities.

Clofazimine can also be used as a steroid-sparing agent for reversal reactions, alone or with corticosteroids.

Although the World Health Organization (WHO) does not support its use for ENL, thalidomide is highly effective with ENL. It is ineffective for the treatment of reversal reactions.

It is not unusual for an immunosuppressive therapy for a reactional state to cause a re-activation of a latent comorbid infection. Consider screening for chronic hepatitis B, chronic strongyloidiasis, latent tuberculosis, Chagas disease, and human immunodeficiency virus (HIV) infections before starting MDT, in patients who come from geographic areas where any of these conditions are endemic.[85]

Neuropathy induced by leprosy can result in trauma, pressure necrosis, or secondary infection that goes unnoticed, leading to amputation of digits or limbs. Wrist and foot drop are also common. Silent neuropathy can occur in the absence of overt signs of nerve or skin inflammation. Even with corticosteroid treatment, only approximately 60% of nerve function is recovered. Cyclosporine A may be useful in controlling nerve impairment and pain.[86] Intraneural corticosteroid injection in one case resulted in nerve regeneration and improved sensory and motor function.[87] Tibialis posterior transfer by the interosseus route with early postoperative mobilization can correct foot drop in leprosy.[88, 89]

Injuries can result in ulcerations, cellulitis, scarring, and bony destruction. Foot ulcers discovered early should be treated with rest because they heal if they are not subject to weight bearing.

Osteoporosis and fractures can result from bony changes due to leprosy. Risedronate and other bisphosphates may help improve lumbar bone mineral density.[90]

Contractures can develop and may result in fixation. Common sequelae include clawing of hands and feet.

Arthritis/arthralgias may occur in approximately 10% of patients with leprosy and joint symptoms, and in conjunction with reactional states. Most have polyarticular symmetric arthritis. The arthritis is generally not responsive to conventional therapy, but 50% become asymptomatic within 24 months of diagnosis.[91]

Eye damage, especially in the anterior portion of the eye, can result in loss of the corneal reflex, lagophthalmos, ectropion, entropion, and blindness. One study found the risk of ocular complications in patients with multibacillary disease, after completion of MDT, to be 5.6%, with eye-threatening complications at 3.9%.

Skin drying and fissures can be caused by autonomic disruption.

Hypogonadism and testicular atrophy can lead to sterility and gynecomastia. Testosterone replacement is the treatment of choice.

Renal involvement in leprosy, particularly lepromatous leprosy and ENL, have been described. Findings may range from hematuria and proteinuria to acute and chronic glomerulonephritis, interstitial nephritis, and pyelonephritis.[92]

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Prevention

No skin or serologic tests are available to identify a carrier of leprosy.

In the southern United States, close contact with armadillos should be avoided.[2]

Household contacts of patients with lepromatous disease should be monitored annually for 5 years after diagnosis. There are no universal recommendations for chemoprophylaxis. Children especially should be observed for the development of disease. In endemic countries, chemoprophylaxis may be useful in controlling leprosy. The Prospective (sero-)Epidemiological Study on Contact Transmission and Chemoprophylaxis in Leprosy (COLEP) found that a single dose of rifampin was 57% effective in preventing leprosy in contacts for the first 2 years after diagnosis of a new index case.[93] A 6-year follow-up reported sustained lack of additional prevention beyond 2 years. However, this remained statistically significant. It also found that the most effective groups affected were in the contact groups of female index cases and in those who were in the contact groups of 2 or more leprosy patients.[94] In the United Kingdom, close contacts of lepromatous leprosy patients younger than 12 years are given rifampin at 15 mg/kg once a month for 6 months as prophylaxis.[95]

Attempts have been made to develop a vaccine against leprosy. Although not widely used, antileprosy vaccination can be immunoprophylactic and therapeutic. Current vaccines with various degrees of use are the BCG vaccine; the Mycobacterium w vaccine; the Mycobacterium avium-intracellulare complex (Mycobacterium ICRC) vaccine; and the BCG plus heat-killed Mycobacterium leprae, Mycobacterium tufu, and Mycobacterium habana vaccine.

The BCG vaccine has variable results in protecting certain populations; therefore, it is not widely prescribed. However, repeat immunization with the BCG vaccine may result in further protection. In the United Kingdom, the BCG vaccine is given to household contacts younger than 12 years.

In India, the Mycobacterium w and Mycobacterium ICRC vaccines are given. Mycobacterium w has a synergistic effect with chemotherapy, with accelerated clearing of the infection and shortening of treatment.

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Long-Term Monitoring

Follow-up to monitor post-MDT reactions is no longer necessary because these reactions are rare. Nonetheless, prevention of disability and rehabilitation is important; therefore, suggested follow-up is 5-10 years after treatment is completed. Patients should be educated about the clinical signs of reoccurrence and should be instructed to return for an evaluation if they have any skin, eye, or nerve changes. Periodic assessments for neural impairment are recommended, and prompt treatment of reactions substantially reduces and prevents further damage and disability. Previous nerve involvement is predictive of further nerve function impairment.

Sensation and muscle strength in the hands, feet, and eyes should be checked on a regular basis. The eyes, nerves, and nose should be examined at follow-up to ensure timely recognition of reactivated disease.

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Contributor Information and Disclosures
Author

Felisa S Lewis, MD Chief, Dermatology, Fort Belvoir Community Hospital

Felisa S Lewis, MD is a member of the following medical societies: American Academy of Dermatology, International Society of Dermatology, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Elyse Harrop, MD Clinical Instructor, Department of Dermatology, Metrohealth Medical Center

Elyse Harrop, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology

Disclosure: Nothing to disclose.

Theresa Dressler Conologue, DO, FAAD Physician, Department of Dermatology, Geisinger Medical Center

Theresa Dressler Conologue, DO, FAAD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Hands with Z-thumbs, clawing, contractures, and shortening of fingers due to repetitive injury and healing. Ho Chi Minh City, Vietnam. (Courtesy of D. Scott Smith, MD)
 
 
 
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