Data-Medicos 
 Dermagic/Express  No. 2-(94) 
 03 Mayo 2.000 03 May 2.000 

 ~ El fenomeno de Lucio  ~ 
 ~ The Lucio's  Phenomenon ~ 
  

 EDITORIAL ESPANOL 
 ================= 
 Hola amigos de la red. DERMAGIC de nuevo con ustedes, el tema de hoy: EL 
 FENOMENO DE LUCIO. La semana pasada vi una paciente de 14 años en mi 
 consulta privada, era una adolescente con una LEPRA. EL FENOMENO 
 DE LUCIO llamado tambien ERITEMA NECROTIZANTE es uno de los tipos de 
 reaccion leprosa (Reaccion tipo II) , poco comun y descrito por primera
 vez 
 por Lucio y Alvarado en 1852, y reidentificado por Latapi en 1936. Se 
 presenta principalmente en la lepra lepromatosa difusa llamada tambien 
 lepra de Lucio, caracterizada principalmente por la ausencia de NODULOS, 
 este tipo de lepra es bastante comun en Centro America y Mexico. Las 
 lesiones CARACTERISTICAS SON ULCERAS que afectan principalmente miembros 
 inferiores, pero otras partes del cuerpo pueden estar involucradas. 
 Histopatologicamente se trata de una vasculitis leucocitoclastica. El 
 tratamiento, TODO UN RETO. Pareciera una MENTIRA, pero HOY en NUESTROS
 DIAS 
 DE modernismo ENCONTRAMOS AUN ESTE FENOMENO. 

 Espero disfruten estas 41 referencias. 

  
 En el attach el CASO REPORTADO en la referencia No. 2 

 Saludos a todos !!! 

 Dr. Jose Lapenta R.,,, 

 EDITORIAL ENGLISH 
 ================= 
 Hello friends of the net. DERMAGIC again with you, today's topic: THE 
 LUCIO'S PHENOMENON. Last week I saw a 14 year-old patient in my private 
 office, she was a adolescent with a LEPROSY. THE LUCIO'S 
 PHENOMENON also called ERYTHEMA NECROTIC is also one of the types of 
 reaction leprous (Reaction type II), not very common and described for
 the 
 first time by Lucio and Alvarado in 1852, and reidentified by Latapi in 
 1936. It is presented mainly in the diffuse lepromatous leprosy,  call 
 leprosy of Lucio, characterized mainly by the absence of NODULES, this
 leprosy type is quite 
 common in Central America and Mexico. The 
 CHARACTERISTIC lesions are ULCERS that affect mainly inferior members,
 but 
 other parts of the body can be involved. Histopathologically is a 
 leukocytoclastic vasculitis. The treatment, an entire CHALLENGE. It
 seemed 
 a LIE, but TODAY in OUR DAYS OF modernism we EVEN FIND THIS PHENOMENON. 
  
 I wait you enjoy these 41 references. 
  
 In the attach file THE CASE REPORT of the REFERENCE No. 2 

 Greetings to ALL,  !! 
 Dr. Jose Lapenta R.,,, 
 =================================================================== 
 REFERENCIAS BIBLIOGRAFICAS / BIBLIOGRAPHICAL REFERENCES 
 =================================================================== 
 1.) Lepra type reactions 
 2.) Diffuse Painless Ulcerations 
 3.) [Lucio-Latapi leprosy and the Lucio phenomenon] 
 4.) [Lucio's leprosy]. 
 5.) [22 years of leprosy: histopathology] 
 6.) Lucio's phenomenon. 
 7.) Lucio's phenomenon and diffuse nonnodular lepromatous leprosy. 
 8.) Lucio's phenomenon: a comparative histological study. 
 9.) [Diffuse lepromatous leprosy disclosed by cutaneous vasculitis. The 
 Lucio phenomenon]. 
 10.) Immunologic aspects of leprosy as related to leucocytic
 isoantibodies 
 and platelet aggregating factors. 
 11.) The role of protein malnutrition in the pathogenesis of ulcerative 
 "Lazarine" leprosy. 
 12.) Dermal ultrastructure in leprosy. 
 13.) Lepromatous and tuberculoid leprosy: clinical presentation and
 cytokine 
 responses. 
 14.) Leprosy (Hansen's disease) in South Dakota. 
 15.) [Virchowian Hansen's disease, Lucio's phenomenon, cryptococcosis]. 
 16.) Erythema nodosum leprosum in Singapore. 
 17.) Epidermal keratinocyte Ia expression, Langerhans cell hyperplasia
 and 
 lymphocytic infiltration in skin lesions of leprosy. 
 18.) Specific antigen and antibody to Mycobacterium leprae in the 
 cryoprecipitate of a patient with Lucio phenomenon. 
 19.) In situ characterization of T lymphocyte subsets in the reactional 
 states of leprosy. 
 20.) Ultrastructure of the dermal microvasculature in leprosy. 
 21.) Lucio's phenomenon: a comparative histological study. 
 22.) Serum macrophage migration inhibition activity in patients
 with leprosy. 
 23.) [Leprosy tests: diagnostic problems]. 
 24.) Serum and tissue lysozyme in leprosy. 
 25.)[Reactional status of leprosy]. 
 26.) Auricular chondritis as a rheumatologic manifestation of Lucio's 
 phenomenon: clinical improvement after plasmapheresis. 
 27.) Contemplative immune mechanism of Lucio phenomenon and its global 
 status. 
 28.) Plasma exchange therapy in Lucio's phenomenon. 
 29.) [Lepromatous leprosy with extensive ulcerations and cachexia. The 
 Lucio phenomenon? Lazarine leprosy]? 
 30.)[2 cases of Lucio phenomenon in Paraguay]. 
 31.) An unusual case of leprosy with pathological features common to 
 Lucio's phenomenon. 
 32.) Primary diffuse lepromatous leprosy with erythema necrotisans 
 (lucio phenomenon). 
 33.) The "Lucio phenomenon" in diffuse leprosy. 
 34.) [Macular leprosy of Lucio--antimalarials in leprotic reaction]. 
 35.) [Dermatology in the Central American tropics. I. Lucio's spotted 
 leprosy. Antimalarials in the leprous reaction]. 
 36.) [Lucio's leprosy]. 
 37.) [Lucio phenomenon in leprosy reactions]. 
 38.) Lucio's phenomenon: an overview. 
 39.) Lucio's phenomenon: an immune complex deposition syndrome in 
 lepromatous leprosy. 
 40.) [Lucio's leprosy]. 
 41.) Antiphospholipid antibodies thrombotic syndrome misdiagnosed as 
 Lucio's phenomenon. 
 ============================================================= 
 ============================================================= 
 1.) Lepra type reactions 
 ============================================================= 
 Source: Mandell, Douglas and Bennett's 
 Principles and Practice of Infectious Diseases Fourth Edition: 1.995 

 Lepra Type-1 Reactions (Downgrading and Reversal Reactions) 
 ========================================= 
 Borderline leprosy patients (BT to BL) may develop before therapy 
 (downgrading reaction) or after the initiation of therapy (reversal 
 reaction) inflammation within previous skin lesions; neuritis; at times, 
 new, multiple, small "satellite" maculopapular skin lesions; and
 low-grade 
 fever. If neuritis is not treated within the first 24 hours or so, 
 irreversible nerve damage and consequent deformity and muscular
 dysfunction 
 may result. 
 Reversal reactions are associated with histologic shifts toward the 
 tuberculoid end of the spectrum. Lesions demonstrate increased numbers of 
 CD4+ helper cells, increased levels of interferon-g and IL-2, and an 
 abundance of T cells bearing g- and d-receptors. This pattern is shared 
 with Mitsuda-positive skin tests and does not occur spontaneously
 otherwise 
 in leprosy. 

 Lepra Type-2 Reaction (Erythema Nodosum Leprosum) 
 ======================================== 
 Erythema nodosum leprosum (ENL) is a syndrome affecting nearly half of 
 lepromatous leprosy patients, 90 percent of the time occurring after the 
 initiation of antimicrobial therapy and generally within the first 2
 years 
 of treatment. Clinical manifestations include, in order of frequency, 
 painful papules, generally on the extensor surfaces of extremities, which 
 may pustulate and ulcerate and may appear as recurrent crops; neuritis 
 (most frequently the ulnar nerve); fever; uveitis; lymphadenitis;
 orchitis; 
 and glomerulonephritis. Lepromatous leprosy patients should be forewarned 
 of signs and symptoms of ENL, lest their appearance result in loss of 
 confidence with antimicrobial therapy and noncompliance. ENL is 
 histologically an acute vasculitis or paniculitis primarily thought to be 
 secondary to immune complex deposition. It is also thought to be
 associated 
 with a local increase in cell-mediated immunity: increased numbers of T 
 helper cells and levels of IL-2 and interferon-g, and loss of suppresor 
 T-cell activity. 61 
  
 Lucio's Reaction and Nerve Abscesses 
 ============================ 
 Patients with diffuse lepromatosis may develop shallow, often large 
 polygonal sloughing ulcerations on the lower extremities that heal
 poorly, 
 are frequently recurrent, and may be generalized. Histopathologically, 
 these lesions appear to be either a variant of ENL or a result of 
 arteriolar infarction. When generalized, Lucio's reaction is frequently 
 fatal, generally a result of secondary bacterial infection and sepsis. 
 Also, leprosy patients, particularly BT or neural leprosy patients, may 
 develop nerve abscesses requiring urgent surgical decompression
 and drainage. 

 Therapy of Reactions 
 ================ 
 Lepra type-1 
 ================ 
 reactions can be effectively treated only with corticosteroids. We 
 generally initiate therapy with prednisone, 40-60 mg daily. Because 
 relapses commonly occur if steroids are rapidly discontinued, steroids at 
 reduced doses as signs and symptoms allow must be maintained for 2-3 
 months. Because of the requirement that steroids be maintained for long 
 durations, strict indications are neuritis, lesions that threaten to 
 ulcerate, and lesions that appear on cosmetically important places such
 as 
 the face. 

 Lepra type-2 
 ============= 
 reactions (ENL) can also be effectively treated with corticosteroids, and 
 short durations are often sufficient. If ENL is recurrent, thalidomide in
 a 
 nightly dose of 100-300 mg is the treatment of choice. In the United 
 States, thalidomide cannot be prescribed to fertile women on an
 outpatient 
 basis and remains classified as an investigational new drug (IND) with 
 investigators at the G.W. Long Hansen's Disease Center and a number of
 U.S. 
 Public Health Service-sponsored Regional Ambulatory Hansen's Disease
 Programs. 
 The mechanism of action of thalidomide for ENL is not fully understood
 but 
 may be a result of its action to reduce IgM synthesis, 62 retard 
 polymorphonuclear leucocyte migration, 63 and reduce tumor necrosis
 factor 
 (TNF) levels. 64 Other than resultant birth defects when administered to 
 pregnant women in the first trimester, thalidomide is nontoxic, its only 
 side effects being tranquilization, to which tolerance develops quickly,
 as 
 well as mild leukopenia, and constipation. 

 Lucio's Reaction 
 ================ 
 Neither thalidomide nor corticosteroid therapy has proved effective 
 therapy for Lucio's reaction. In severe cases, exchange transfusion may
 be 
 effective. In general, however, the principals of good wound care and 
 appropriate antibiotics for sepsis are recommended. 

 ============================================================= 
 2.) Diffuse Painless Ulcerations 
 ============================================================= 
 Fernando Gallardo Hernández, MD; Jaime Notario Rosa, MD; Anna
 Jucglà Serra, 
 MD; Jordi Peyri Rey, MD 
  
 Ciutat Sanitària i Universitària de Bellvitge, Barcelona, Spain 
 Arch Dermatol, Vol. 135 No. 8, August 1999 
  

 REPORT OF A CASE 

 A 62-year-old man presented with a 3-month history of severe, ulcerating 
 skin lesions over the extremities. Painless violaceous macules, livedo,
 and 
 occasional bullae gave rise to ulcerations after a few weeks. The lower 
 extremities were predominantly involved, with spontaneous amputation of 
 some necrotic digits. The lesions extended proximally over the buttocks. 
 The patient had a 4- to 5-year history of frequent painless traumatic 
 wounds that healed after 2 to 3 weeks, leaving atrophic scars. The
 patient 
 also noted progressive thickening of the skin, with loss of body hair, 
 especially the eyebrows. Physical examination revealed a chronically ill 
 man with waxy diffuse skin infiltration and a total loss of body hair. 
 Numerous angular ulcerations were located over the extremities (Figure 1) 
 and surrounded by a livedoid pattern. The findings of the rest of his 
 examination were unremarkable except for a sensitive polyneuropathy. 
 Laboratory evaluation showed the following abnormal values: hemoglobin,
 90 
 g/L; mean corpuscular volume, 67 pg; erythrocyte sedimentation rate, 120 
 mm/h; and serum albumin, 16 g/L. The serum concentration of -globulin was 
 increased in a polyclonal pattern. A skin biopsy specimen was obtained 
 (Figure 2), and Ziehl-Neelsen staining was performed (Figure 3). (see the 
 attach file) 

 Diagnosis: Lucio phenomenon. 
  
 HISTOPATHOLOGIC FINDINGS AND CLINICAL COURSE 
 A punch biopsy specimen from the border of an ulcer revealed a patchy 
 infiltrate of foamy histiocytes and scattered lymphocytes in the dermis
 and 
 subcutaneous fat, tending to be clustered around blood vessels. Large 
 number of acid-fast bacilli were present in the Ziehl-Neelsen stain of
 the 
 specimen. Foamy histiocytes and acid-fast bacilli were also noted in the 
 wall of the medium-sized arteries, with narrowing of the vessel lumen. No 
 nuclear dust was observed. Slit-skin smears showed single and clustered 
 acid-fast bacilli. 

 Multidrug therapy was initiated with 100 mg/d of oral dapsone, 50 mg/d of 
 clofazimine, 600 mg/d of rifampin, and a single 300-mg dose of
 clofazimine 
 per month, with good response to date. Prednisone (40 mg) was also 
 prescribed at decreasing doses for Lucio phenomenon and has been required 
 for months at low doses. Our patient's ulcers healed with irregular 
 atrophic scars in 10 to 12 weeks. 

 DISCUSSION 
 Our patient manifested the clinical and histopathologic features of a 
 diffuse, lepromatous leprosy with skin ulcerations characteristic of
 Lucio 
 phenomenon, a severe, necrotizing reaction described by Lucio and
 Alvarado1 
 in 1852. The reactional states in leprosy are characterized by acute 
 inflammatory changes, and they occur more commonly toward the borderline 
 and lepromatous end of the clinical spectrum. Lucio phenomenon is an 
 infrequent reaction in leprosy. It has usually been described in diffuse 
 lepromatous leprosy, so-called Lucio leprosy, which is unique because of 
 the absence of cutaneous nodules. This type of leprosy is almost 
 exclusively seen in Mexico and Central America. Lucio phenomenon is a 
 cutaneous necrotizing reaction that most commonly involves the
 extremities 
 but may also affect the buttocks and trunk. The acute constitutional 
 symptoms of Lucio phenomenon are variable and, occasionally, may be 
 fatal.2, 3 It is believed to be an immune complex–mediated disease
 like the 
 Arthus phenomenon and is included as a type 2 reaction in leprosy.4, 5 
 Lucio phenomenon shows histopathologic findings of leukocytoclastic 
 vasculitis along with a superficial and deep mixed infiltrate of foamy 
 histiocytes in a perineural and perivascular distribution. In some
 reported 
 cases, the vascular damage may have been the result of direct invasion of 
 Mycobacterium leprae, with endothelial cell proliferation, thrombosis,
 and 
 tissue necrosis.6 

 The treatment of Lucio phenomenon is the same as that for other type 2 
 reactions in leprosy. Local care and supportive therapy are important to 
 prevent secondary infections and loss of proteins. Prednisone therapy, 
 which is initially administered at dosages of 20 to 60 mg/d and then 
 tapered, may be required for weeks to months. Thalidomide (400 mg/d with 
 reduction to maintenance doses of 100 mg/d) may be prescribed as an 
 alternative to prednisone. Clofazimine administered at a dosage of 300
 mg/d 
 has a useful anti-inflammatory effect. It is not necessary to discontinue 
 multidrug therapy for leprosy. 

 REFERENCES 

 1. Lucio R, Alvarado Y, Latapi F, Cited by, Zamora AC, Cited by. The 
 spotted leprosy of Lucio. Int J Lepr. 1948;16:421-430. 

 2. Pursley TV, Jacobson RR. Lucio's phenomenon. Arch Dermatol. 1980;116: 
 201-204. MEDLINE 

 3. Bernadat JP, Faucher JF, Huerre M. Lèpre lépromateuse diffuse
 révélée 
 par une vasculite cutanée: le phenomene de Lucio. Ann Dermatol
 Venereol. 
 1996;123:21-23. MEDLINE 

 4. Touma DJ, Phillips TJ, Kurban AK, Goldberg L. Recurrent rapidly 
 progressive infiltrated plaques and bullae. Arch Dermatol. 
 1996;132:1432-1434. MEDLINE 

 5. Murphy GF, Sánchez NP, Flynn TC, Sánchez JL, Mihm MC, Soter
 NA. Erythema 
 nodosum leprosum. J Am Acad Dermatol. 1986;14:59-69. MEDLINE 

 6. Rea TH, Levan NE. Lucio's phenomenon and diffuse nonnodular
 lepromatous 
 leprosy. Arch Dermatol. 1978;114:1023-1028. MEDLINE 
  
  
 ============================================================= 
 3.) [Lucio-Latapi leprosy and the Lucio phenomenon] 
 ============================================================ 
 ARTICLE SOURCE:  Acta Leprol  (Switzerland), Jul-Sep 1983, 1(3) p115-32 
 AUTHOR(S):  Saul A; Novales J 
 PUBLICATION TYPE:  JOURNAL ARTICLE; REVIEW (18 references) 
 ABSTRACT:  The Lucio-Latapi's leprosy or diffuse lepromatous leprosy is a 
 clinical variety of lepromatous leprosy first described by Lucio and 
 Alvarado in 1852 and reidentified by Latapi in 1936. It is frequent in 
 Mexico (23%) and in Costa Rica and very rare in other countries. It is 
 characterized by a diffuse infiltration of all the skin which never is 
 transformed into nodule, by a complete alopecia of eyebrows and eyelashes 
 and body hair, by anhydrotic and dysesthesic zones of the skin and by a 
 peculiar type of lepra reaction named Lucio's phenomenon or necrotic 
 erythema which is a vascularitis of vessels especially of the 
 dermohypodermic union and of the hypodermis. Clinically this vascularitis 
 is represented by well-shaped erythematous spots, later becoming necrotic 
 with scabs, ulcerations and scars. Three points of confusion are
 stressed: 
 the differences between nodules and nudosities, Lucio's leprosy and
 Lucio's 
 phenomenon and necrotic erythema and necrotic erythema nodosum leprosum. 
 The differences between the pure and primitive form of Lucio's leprosy
 and 
 the secondary one is also discussed such as the laboratory findings, 
 histopathological data, pronostic and treatment. Lucio's leprosy is 
 considered the most anergic one of the all immunological spectrum
 of leprosy. 

 ============================================================= 
 4.) [Lucio's leprosy]. 
 ============================================================= 
 Med Cutan Ibero Lat Am 1982;10(1):41-6 Related Articles, Books, LinkOut 

 Gibert E, Cubria JL, Gratacos R, Castro J, Monfort J, Castel T, Lecha M 

 A case of diffuse lepromatous leprosy with lepra reaction type II-Lucio's 
 phenomenon-in a 24 years old male patient is reported. The histological 
 examination of the necrotic lesions and of the apparently normal skin 
 showed the presence of dense perivascular and perianexial
 lymphohystiocitic 
 infiltrates with great quantities of bacilli. The first biopsy did not
 show 
 a picture a leuccocytoclastic vasculitis but only areas of necrosis. The 
 immunofluorescence studies revealed on direct examination complement 
 deposits on vessel walls. The complement levels in blood were lowered and 
 circulating inmunecomplexes were also detected. These data confirm the 
 opinion that Lucio's phenomenon is caused by circulating inmunecomplexes 
 fixed on dermal vessel walls causing skin necrotic lesions. 

 ============================================================= 
 5.) [22 years of leprosy: histopathology] 
 ============================================================= 
 AU: Dionisio-de-Cabalier-ME; Perez-HJ 
 AD: Ia. Catedra de Patologia, Facultad de Ciencias Medicas, Hospital Nac, 
 de Clinicas, U.N.C. 
 SO: Rev-Fac-Cien-Med-Univ-Nac-Cordoba. 1995; 53(1): 17-21 
 AB: In the present study, the frequency of histopathological reports of 
 leprosy carried out in the last 22 years at the Fst Chair of Pathology 
 (Medical School, U. N.C) was determined. Our findings on the frequency of 
 pure forms of leprosy agree with those reported by the O.M.S. On the 
 contrary, that was not the case with respect to reactive forms, since the 
 phenomenon of Lucio and Alvarado was more frequent in endemic zones. 

 ============================================================= 
 6.) Lucio's phenomenon. 
 ============================================================= 
 ARTICLE SOURCE:  Arch Dermatol  (United States), Feb 1980, 116(2) p201-4 
 AUTHOR(S):  Pursley TV; Jacobson RR 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  A 38-year-old woman had diffuse, nonnodular, lepromatous
 leprosy 
 and Lucio's phenomenon. Most cases of Lucio's phenomenon have been
 reported 
 to have a leukocytoclastic vasculitis as the underlying pathologic 
 abnormality. In this patient, however, the histologic picture of an early 
 lesion of Lucio's phenomenon showed a milk, mononuclear cell
 infiltration, 
 endothelial swelling, vascular thrombosis, and ischemic necrosis. Lepra 
 bacilli were abundant around nerves and blood vessels, and many were
 noted 
 in vascular walls and endothelium. Our findings raise the possibility
 that 
 some cases of Lucio's phenomenon may be caused by vascular damage due to 
 direct invasion of Mycobacterium leprae and not necessarily by 
 leukocytoclastic vasculitis. 

 ============================================================= 
 7.) Lucio's phenomenon and diffuse nonnodular lepromatous leprosy. 
 ============================================================= 
 ARTICLE SOURCE:  Arch Dermatol  (United States), Jul 1978, 114(7) p1023-8 
 AUTHOR(S):  Rea TH; Levan NE 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  The records of ten patients with Lucio's phenomenon showed 
 clinical and histopathological changes similar to those described by 
 others. Lucio's phenomenon is a syndrome distinct from erythema nodosum 
 leprosum as indicated by an absence of fever, leukocytosis and
 tenderness, 
 a failure to respond to thalidomide, and a restriction to patients with 
 diffuse nonnodular lepromatous leprosy. Lymphopenia associated with 
 splenomegaly in three patients and glomerulonephritis in one patient were 
 unexpected findings of unknown relevance. 

 ============================================================= 
 8.) Lucio's phenomenon: a comparative histological study. 
 ============================================================= 
 ARTICLE SOURCE:  Int J Lepr Other Mycobact Dis  (United States), Jun
 1979, 
 47(2) p161-6 
 AUTHOR(S):  Rea TH; Ridley DS 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  To study further the pathogenesis of Lucio's phenomenon, we
 have 
 made a comparative histological study of 11 patients with Lucio's 
 phenomenon and 12 with ENL. Confirming the findings of others, Lucio's 
 reaction could be distinguished from ENL by epidermal necrosis and by 
 necrotizing vasculitis manifesting necrosis in the walls of superficial 
 vessels and severe, focal endothelial proliferation of mid-dermal
 vessels. 
 Furthermore, in Lucio's phenomenon large numbers of AFB were found in 
 evidently normal and in swollen or proliferating endothelial cells. We 
 hypothesize that patients with Lucio's phenomenon have an exceptionally 
 deficient defense mechanism, allowing unrestricted proliferation of AFB
 in 
 endothelial cells, facilitating contact between bacterial antigen and 
 circulating antibody and leading to infarction; also, this nadir of 
 resistance allows unimpeded dissemination of AFB, accounting for the 
 clinical features of diffuse non-nodular leprosy. Thus, an explanation is 
 offered for the restriction of Lucio's phenomenon to patients with
 diffuse 
 non-nodular lepromatous leprosy. 

 ============================================================= 
 9.) [Diffuse lepromatous leprosy disclosed by cutaneous vasculitis. The 
 Lucio phenomenon]. 
 ============================================================= 
 Ann Dermatol Venereol 1996;123(1):21-3 

 Bernadat JP, Faucher JF, Huerre M 

 Clinique Paofai, Papeete, Tahiti, Polynesie francaise. 

 INTRODUCTION: Lucio's phenomenon, also called necrotizing erythema, is a 
 rare acute manifestation which sometimes introduces diffuse lepromatous 
 leprosy, almost exclusively in Central American populations. CASE REPORT:
 A 
 76-year-old polynesian man of chinese ethnic origin had necrotizing 
 erythema for several months before development of Lucio's leprosy. The 
 patient had necrotizing lesions of the lower limbs with large polygonal 
 scars and poor general health status. Diagnosis was based on the
 discovery 
 of acid-fast bacilli at the pathology examination of skin biopsies. The 
 necrotizing zones appeared as cutaneous vasculitis with angiogenesis of
 the 
 superficial dermis and presence of Hansen bacilli within the endothelium. 
 DISCUSSION: This case of diffuse lepromatous leprosy, the first reported
 in 
 the South Pacific, emphasizes the polymorphism of leprosy and the 
 importance of recognizing rare clinical forms, especially in the tropics. 
 Anti-Hansen drugs are effective. 

 ============================================================= 
 10.) Immunologic aspects of leprosy as related to leucocytic
 isoantibodies 
 and platelet aggregating factors. 
 ============================================================= 
 ARTICLE SOURCE:  Int J Lepr Other Mycobact Dis  (United States), Jul-Sep 
 1975, 43(3) p239-48 
 AUTHOR(S):  Saha K; Dutta RN; Mittal MM 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  The incidences of various iso- and autoantibodies in a random 
 population of 112 unselected leprosy patients is presented. Low titers of 
 leucocytic isoantibodies and platelet aggregating factor were detected in 
 the sera of a variable number of such patients. The leucoisoagglutinins 
 were found in 8% of the sera of tuberculoid as well as lepromatous
 leprosy 
 patients, whereas the leucoisocytotoxins were detected in a larger 
 percentage of the lepromatous (40%) as well as tuberculoid (28%) cases.
 The 
 platelet aggregating factors (PAF) were positive in 51.2% and 45% of 
 lepromatous and tuberculoid cases respectively. Of the 21 positive sera
 for 
 PAF, the antiplatelet factor by antihuman globulin consumption test could 
 be demonstrated only in 66.6% and 50% of lepromatous and tuberculoid sera 
 respectively. To study the frequencies of these newly detected antibodies 
 or antibody-like factor and to compare their occurrences with other 
 well-documented autoantibodies present in the sera of leprosy patients: 
 cryoglobulins, antinucleoprotein antibody and thyroglobulin
 autoprecipitin 
 were also studied in the sera of the same population of leprosy patients. 
 It has been observed that the simultaneous occurrence of all these auto- 
 and isoantibodies in the serum of one patient is a rare phenomenon. 
 Leucocytic and platelet counts of these patients having antibodies
 against 
 leucocytes and platelets were found to be within normal limits. 
 Accordingly, it is suggested that the low levels of antileucocyte
 antibody 
 and antiplatelet factor are probably harmless to the hosts. On the other 
 hand, it is postulated that these antibodies may act as enhancing factors 
 by being specifically adsorbed on the lymphoid cells, thus rendering them 
 unresponsive to mitogenic stimulus in vitro. From these studies it seems 
 that leprosy, especially the lepromatous type, is associated with some of 
 the serological features suggestive of an autoimmune aberration. 

 ============================================================= 
 11.) The role of protein malnutrition in the pathogenesis of ulcerative 
 "Lazarine" leprosy. 
 ============================================================= 
 ARTICLE SOURCE:  Int J Lepr Other Mycobact Dis  (United States), Jul-Sep 
 1976, 44(3) p346-58 
 AUTHOR(S):  Skinsnes LK; Higa LH 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  1. Clinical and necropsy observations in lepromatous leprosy 
 associated with severe emaciation and accompanying hypoproteinemia
 suggest 
 that protein deprivation may be of pathogenic significance in the 
 ulcerative phenomenon that is designated "Lazarine leprosy". 2. An 
 experimental utilizing Wiersung rats infected with Mycobacterium 
 lepraemurium and maintained on a protein-free diet was developed for the 
 purpose of studying the effect of protein starvation on the course of 
 chronic mycobacterial disease similar to lepromatous leprosy with respect 
 to pathogen and host inflammatory response. 3. It was possible to
 maintain 
 the experimental animals on a protein-free diet for up to 18 weeks of 
 concomitant M. lepraemurium infection. This was long enough for the 
 infection to disseminate to a degree that was evident in control animals 
 only several weeks later. 4. The protein-deprived animals showed
 decreased 
 inflammatory response to the pathogen, presented more rapid dissemination 
 of the infection and harbored more bacilli per macrophage than did
 animals 
 similarly infected but maintained on a protein adequate diet. This 
 indicates impairment of native cellular immunity by protein deprivation 
 through decrease in ability of macrophages to inhibit bacillary 
 multiplication. 5. There was no evidence of impairment of macrophage 
 ability to phagocytose the pathogens. 6. Morphologically the increased 
 dissemination of pathogens and decrease in inflammatory response was 
 similar to the increase in number and extent of visceral lesions seen in 
 Lazarine leprosy. Decreased ability to dispose of the infecting bacilli
 was 
 similar in the two models, human and animal. The animal model does not,
 as 
 does lepromatous leprosy, involve the skin in the infection. Hence 
 comparable ulcerative phenomena were not replicated in the animals. 7. It 
 is suggested that Lazarine leprosy may result from enhanced lepromatous 
 leprous infection occurring as a result of protein malnutrition. The 
 pathogenic mechanism appears to be impairment of cellular immunity
 probably 
 enhanced by concomitant impairment of humoral antibody immunity resulting 
 also in decreased resistance to pyogenic and other secondary pathogens.
 The 
 tissue edema attendant on decreased serum osmotic pressure due to
 lowering 
 of the serum protein fractions enhances the probability of ulceration. 

 ============================================================= 
 12.) Dermal ultrastructure in leprosy. 
 ============================================================= 
 ARTICLE SOURCE:  Arch Pathol Lab Med  (United States), May 1984, 108(5) 
 p383-6 
 AUTHOR(S):  Van Hale HM; Turkel SB; Rea TH 
 PUBLICATION TYPE:  JOURNAL ARTICLE 
 ABSTRACT:  We studied the ultrastructure of the dermal inflammatory 
 response in 18 patients with leprosy. Biopsy specimens from 14
 lepromatous 
 patients, including four with Lucio's phenomenon and four with erythema 
 nodosum leprosum, were compared with biopsy specimens from one borderline 
 lepromatous and three borderline tuberculoid patients. In all, the dermal 
 infiltrate consisted of macrophages, lymphocytes, and mast cells. This 
 infiltrate was predominantly perivascular, and chronic reactive changes 
 were found in the small dermal vessels. The macrophages contained 
 phagocytized organisms within membrane-bound vacuoles and a wide variety
 of 
 lysosomal residual dense bodies. Intraendothelial organisms were 
 occasionally seen, especially in biopsy specimens from the patients with 
 Lucio's phenomenon. The greatest number of mast cells were also seen in
 the 
 infiltrate in those cases. The frequent close association of macrophages 
 with lymphocytes and mast cells suggests an interrelationship between
 these 
 cells that appears typical of the host response to leprosy. 

 ============================================================= 
 13.) Lepromatous and tuberculoid leprosy: clinical presentation and
 cytokine 
 responses. 
 ============================================================= 
 Ochoa MT; Valderrama L; Ochoa A; Zea A; Escobar CE; Moreno LH; Falabella 
 Dermatology Service, Universidad del Valle, Cali, Colombia. 
 Int J Dermatol  (UNITED STATES)  Nov 1996  35 (11) p786-90 
 OBJECTIVE: This study analyzes the major clinical characteristics of 
 patients with active leprosy in relation to the in vitro immune response 
 to the T-lymphocyte activator anti-CD3.  METHODS: Thirty-eight patients 
 with an established diagnosis of leprosy were classified according to the 
 Ridley and Jopling table.  Peripheral blood mononuclear cells from both 
 lepromatous leprosy (LL) and tuberculoid leprosy (TL) patients and
 healthy 
 controls were used to evaluate lymphocyte proliferation; immunoenzymatic 
 assays were used to evaluate cytokine production (IL-1, IL-2, IL-4, IL-6, 
 IL-10, IFN-gamma).  RESULTS: Peripheral blood mononuclear cells from both 
 LL and TL patients displayed blastogenic responses to anti-CD3.  The 
 cytokines IL-1 beta, IL-6, IL-10, and IFN-gamma were detected in culture 
 supernatants.  Endogenous production of IL-1 beta was significantly
 higher 
 in cell cultures from patients with the lepromatous form of the disease 
 compared to those with tuberculoid leprosy.  Production of IL-6 in 
 response to anti-CD3 was observed in a significantly higher proportion of 
 LL than TL patients (P = 0.0025).  Gamma-interferon production did not 
 differ between TL and LL, but a direct correlation was observed between 
 time of multidrug treatment and IFN production in vitro (P = 0.016). 
 Interleukin-10 was detected in culture supernatants of lymphocytes 
 activated by anti-CD3 from both patient groups, but not from healthy 
 controls.  CONCLUSIONS: The findings of this study suggest that patients 
 with the two distinct forms of leprosy are capable of responding to a 
 polyclonal T-lymphocyte stimulus such as anti-CD3 and provide evidence 
 suggestive of alterations in the immune responses mediated by cytokines 
 that may contribute to the spectrum of disease and response to treatment. 

 ============================================================= 
 14.) Leprosy (Hansen's disease) in South Dakota. 
 ============================================================= 
 S D J Med 1996 Jun;49(6):185-7 Related Articles, Books, LinkOut 

 Burrish G, Hartmann A, Lockwood W 

 Department of Dermatology, Central Plains Clinic, Sioux Falls, SD, USA. 

 Worldwide Hansen's disease is an important and relatively common disease, 
 but is still very rare in South Dakota. Two patients are described to
 help 
 demonstrate the wide variety of clinical manifestations associated with 
 Hansen's disease. Since the clinical appearance of Hansen's disease is 
 highly variable, the following six forms of Hansen's disease are
 described: 
 Indeterminate, tuberculoid (TT), borderline tuberculoid (BT), borderline 
 (BB), borderline lepromatous (BL), and lepromatous leprosy (LL). In 
 addition, three well-recognized reactional forms of leprosy are also 
 described: Type 1 (lepra reaction), type 2 (erythema nodosum leprosum),
 and 
 type 3 (Lucio's phenomenon). While the disease affects primarily the skin 
 and nerves, health care providers of all disciplines should remain alert 
 for this disease which can present with a high degree of clinical
 variability. 

 ============================================================= 
 15.) [Virchowian Hansen's disease, Lucio's phenomenon, cryptococcosis]. 
 ============================================================= 
 Hansenol Int 1988 Dec;13(2):47-56 Related Articles, Books, LinkOut 

 [Article in Portugese] 

 A 75 years old white male, for 3 years on treatment for virchowian 
 hanseniasis, was admitted with active HD lesions, infiltration on the
 base 
 of right lung, leg ulcer and malaise. After two days he developed purpura 
 and hemorrhagic blisters in the limbs. The biopsy of these lesions
 revealed 
 Lucio phenomenon. The patient worsened with mental confusion, psychomotor 
 agitation and anisocoric pupils. In the 18th day of internation the
 patient 
 died. Necropsy revealed virchowian infiltration plenty of bacilli in the 
 skin and viscera as well as tuberculoid granuloma with acid-fast bacilli
 in 
 the liver, spleen and bone marrow. These findings lead us to review the 
 patient's classification from virchowian to borderline. In the lungs, 
 leptomeninge, renal papile, prostate and thyroid it was found loose 
 tuberculoid granuloma with a great amount of fungi surrounded by a gelly 
 halo resembling Criptococcus neoformans. These findings and the onset of 
 Lucio phenomenon are discussed in a patient that has been treated for 3 
 years and still having several virchowian lesions and a great amount of 
 acid-fast bacilli. 

 ============================================================= 
 16.) Erythema nodosum leprosum in Singapore. 
 ============================================================= 
 Ann Acad Med Singapore 1987 Oct;16(4):658-62 

 Giam YC, Ong BH, Tan T 

 Middle Road Hospital, Singapore. 

 Erythema Nodosum Leprosum (ENL) or Type II reaction is an immune complex 
 syndrome seen in multibacillary leprosy. 20 patients with histological 
 confirmation of ENL in leprosy were studied from 1982 to 1986. These 
 patients had a range of clinical signs, from fever, tender dusky nodules, 
 bullae, ulcers to lymphadenopathy, arthralgia and neuritis. The four
 major 
 histological patterns are: a) classical pattern showing heavy
 infiltrations 
 of neutrophils in three cases, b) sub-epidermal bulla pattern with marked 
 oedema of the upper dermis, and collections of neutrophils in five cases, 
 c) vasculitis pattern, affecting superficial and mid-dermal vessels, 
 leading to epidermal necrosis, bulla formation and ulceration. Dilated 
 vessels, congestion, lumenal fibrin clots and fibrinoid necrosis of
 vessels 
 were seen, d) non-specific picture in nine cases with mild oedema, 
 infiltration with neutrophils, and two cases with minimal reaction had 
 chronic ENL with clinical vasculitis. All the five cases with vasculitis 
 showed C1q, C3 and fibrinogen in the vessels. Comparing ENL reactions 
 reported in Asia, our pattern is similar to that of Malaysians with the 
 majority showing sub-epidermal oedema. Vasculitis is more common in
 India. 
 Oedema with collagen necrosis as seen in acute ENL with iritis in New 
 Guinea. The Lucio's phenomenon was not seen in any of the countries in
 Asia. 

 ============================================================= 
 17.) Epidermal keratinocyte Ia expression, Langerhans cell hyperplasia
 and 
 lymphocytic infiltration in skin lesions of leprosy. 
 ============================================================= 
 Clin Exp Immunol 1986 Aug;65(2):253-9 Related Articles, Books, LinkOut 

 Rea TH, Shen JY, Modlin RL 

 Epidermal changes, Ia expression on keratinocytes, Langerhans cell 
 hyperplasia and lymphocyte infiltration were sought in skin lesions of 
 leprosy: 15 borderline tuberculoid (BT), six borderline lepromatous (BL), 
 17 lepromatous (LL), 13 erythema nodosum leprosum (ENL), six Lucio 
 reactions and nine reversal reactions. All three changes were well 
 developed in BT and reversal reactions. ENL showed well developed 
 keratinocyte Ia and Langerhans cell hyperplasia, but little lymphocytic 
 infiltration. LL and Lucio tissues had some Langerhans cell hyperplasia
 but 
 little or no keratinocyte Ia or lymphocytic infiltration. BL tissues were 
 so diverse as to suggest two distinct subgroups. These findings are 
 consistent with the hypothesis that keratinocyte Ia expression is an 
 immunohistological sign of a cell-mediated immune (CMI) response.
 However, 
 the Ia keratinocyte expression found in BL and ENL tissues appears
 contrary 
 to the undifferentiated macrophages and numerous bacilli found in the 
 lesions. Thus, if a sign of CMI, keratinocyte Ia expression is not a 
 measure of the effectiveness of the response. 

 ============================================================= 
 18.) Specific antigen and antibody to Mycobacterium leprae in the 
 cryoprecipitate of a patient with Lucio phenomenon. 
 ============================================================= 
 Rheumatol Int 1986;6(2):93-4 Related Articles, Books, LinkOut 

 Drosos AA, Brennan PJ, Elisaf MS, Stefanou SG, Papadimitriou CS, 
 Moutsopoulos HM 

 Using a sensitive and specific enzyme-linked immunosorbent assay (ELISA) 
 assay we showed that the cryoglobulins of a patient with Lucio phenomenon 
 contain phenolic glycolipid I antigen and a specific antibody. 

 ============================================================= 
 19.) In situ characterization of T lymphocyte subsets in the reactional 
 states of leprosy. 
 ============================================================= 
 Clin Exp Immunol 1983 Jul;53(1):17-24 Related Articles, Books, LinkOut 

 Modlin RL, Gebhard JF, Taylor CR, Rea TH 

 Using monoclonal antibodies and the immunoperoxidase technique, the
 numbers 
 and distribution of T lymphocyte subsets in the tissues of reactional 
 states of leprosy (six reversal reaction, nine erythema nodosum leprosum 
 (ENL) and two Lucio's reaction) were determined and compared with those 
 found in stable, non-reactional patients (six tuberculoid, two borderline 
 lepromatous and seven lepromatous). The pattern of segregation of the 
 suppressor/cytotoxic phenotype at the periphery of the granuloma was
 found 
 in both non-reactional tuberculoid lesions and reversal reactions, but
 was 
 better developed in the former. In ENL and Lucio's reaction, as well as
 in 
 non-reactional lepromatous tissue, the helper/inducer and 
 suppressor/cytotoxic phenotypes were both admixed with the aggregated 
 histiocytes. However, the helper/suppressor ratio in ENL (2.1 +/- 0.4)
 was 
 significantly larger than that in non-reactional lepromatous tissue (0.7 
 +/- 0.4, P less than 0.001). The immature thymocyte antigen OKT6 was
 found 
 on scattered large non-lymphoid cells, most commonly in tuberculoid and 
 reversal reaction tissues, less commonly in ENL, but only irregularly in 
 non-reactional lepromatous tissue. The peripheral pattern of the 
 suppressor/cytotoxic phenotype may be an immunohistological reflection of
 a 
 cell-mediated immune response common to both non-reactional tuberculoid
 and 
 reversal reaction patients. The reversal of the helper/suppressor ratio
 in 
 ENL as compared to non-reactional lepromatous disease suggests some role 
 for cell-mediated immunity in the pathogenesis of ENL. The OKT6 positive 
 cell is of unknown origin and function. 

 ============================================================= 
 20.) Ultrastructure of the dermal microvasculature in leprosy. 
 ============================================================= 
 Int J Lepr Other Mycobact Dis 1982 Jun;50(2):164-71 

 Turkel SB, Van Hale HM, Rea TH 

 Infection with M. leprae may lead to the presence of the organism within 
 the dermal vascular endothelium, a phenomenon most pronounced in 
 lepromatous leprosy. In order to study the ultrastructural features of
 the 
 dermal microvasculature in leprosy, biopsies from 18 patients with 
 lepromatous (14), borderline lepromatous (1) and borderline tuberculoid
 (3) 
 leprosy were examined. Four patients with Lucio's phenomenon and four
 with 
 erythema nodosum leprosum were included. The ultrastructural changes in
 the 
 dermal microvasculature included endothelial swelling and hypertrophy, 
 increased endothelial and pericytic cytoplasmic processes, and pronounced 
 basal lamina reduplication. Occasional large, pale, endothelial cells
 with 
 widely dispersed organelles were encountered. Phagocytized,
 membrane-bound 
 intraendothelial organisms were found, similar in appearance to those 
 within dermal macrophages. The predominantly perivascular dermal 
 inflammatory infiltrate consisted of lymphocytes, macrophages and mast 
 cells. The observed ultrastructural changes in the dermal
 microvasculature 
 are similar to those previously described in the endoneurial vessels.
 While 
 reflecting nonspecific responses of the dermal microvasculature in
 chronic 
 inflammation, the findings support a possible role of the small dermal 
 vessels in the chronic nature of the host's response to infection with M. 
 leprae. 

 ============================================================= 
 21.) Lucio's phenomenon: a comparative histological study. 
 ============================================================= 
 Int J Lepr Other Mycobact Dis 1979 Jun;47(2):161-6 

 Rea TH, Ridley DS 

 To study further the pathogenesis of Lucio's phenomenon, we have made a 
 comparative histological study of 11 patients with Lucio's phenomenon and 
 12 with ENL. Confirming the findings of others, Lucio's reaction could be 
 distinguished from ENL by epidermal necrosis and by necrotizing
 vasculitis 
 manifesting necrosis in the walls of superficial vessels and severe,
 focal 
 endothelial proliferation of mid-dermal vessels. Furthermore, in Lucio's 
 phenomenon large numbers of AFB were found in evidently normal and in 
 swollen or proliferating endothelial cells. We hypothesize that patients 
 with Lucio's phenomenon have an exceptionally deficient defense
 mechanism, 
 allowing unrestricted proliferation of AFB in endothelial cells, 
 facilitating contact between bacterial antigen and circulating antibody
 and 
 leading to infarction; also, this nadir of resistance allows unimpeded 
 dissemination of AFB, accounting for the clinical features of diffuse 
 non-nodular leprosy. Thus, an explanation is offered for the restriction
 of 
 Lucio's phenomenon to patients with diffuse non-nodular lepromatous
 leprosy. 

 ============================================================= 
 22.) Serum macrophage migration inhibition activity in patients
 with leprosy. 
 ============================================================= 
 J Invest Dermatol 1982 Nov;79(5):336-9 

 Rea TH, Yoshida T 

 We have found that 26 of 54 (48%) untreated patients with leprosy had
 serum 
 migration inhibitory activity, and that this was present in tuberculoid, 
 borderline, and lepromatous forms of the disease. Patients with active 
 recreational states; i.e., reversal reactions, Lucio's reaction, or 
 erythema nodosum leprosum, were particularly apt to have this inhibitory 
 activity. The prevalence of inhibitory activity did not vary
 significantly 
 with treatment, dinitrochlorobenzene responsiveness, tuberculin 
 responsiveness, or serum lysozyme levels. 

 ============================================================= 
 23.) [Leprosy tests: diagnostic problems]. 
 ============================================================= 
 Acta Leprol 1981 Apr-Jun;(83):11-9 Related Articles, Books, LinkOut 

 [Article in French] 

 Strobel M, Ndiaye B, Marchand JP, Stach JL, Foumoux F 

 Two cases of reactional leprosy leading to wrong diagnosis are reported. 
 The first one concerns a reversal reaction predominantly neuritic, 
 initially taken for polyarthritis. The second one concerns an erythema 
 nodosum leprosum with extensive cutaneous necrosis (Lucio's phenomenon or 
 ulcerative lazarine leprosy). Main aspects and mechanisms of leprosy 
 reactional states are reviewed. It is emphasized that errors or delays in 
 diagnosis are often caused by failing to recognize cutaneous or neuritic 
 symptoms. 

 ============================================================= 
 24.) Serum and tissue lysozyme in leprosy. 
 ============================================================= 
 Infect Immun 1977 Dec;18(3):847-56 Related Articles, Books, LinkOut 

 Rea TH, Taylor CR 

 Mean serum lysozyme values were found to be elevated in untreated leprosy 
 patients. Statistically significant elevations were present in each of
 the 
 three major categories of leprosy, tuberculoid, borderline, and 
 lepromatous. Values were particularly high in patients with severe
 reversal 
 reactions or Lucio's phenomenon. Prolonged sulfone therapy was associated 
 with a fall in serum lysozyme values. With an immunoperoxidase method to 
 localize lysozyme in leprous tissues, two distinct staining patterns were 
 found, granular and saccular. The grandular pattern of lysozymal staining 
 was found in epithelioid cells and in giant cells, and the intensity of 
 staining showed a positive correlation with serum lysozyme levels. 
 Conversely, a saccular pattern of lysozymal staining was found in 
 lepromatous histiocytes, buth the intensity of staining was unrelated to 
 serum lysozyme levels; the saccular structures contained dense aggregates 
 of Mycobacterium leprae. These two patterns of staining probably
 represent 
 different functional responses of monocyte-derived granuloma cells,
 whereas 
 the serum levels reflect, to a varying degree, both the absolute number
 of 
 such cells and the rate of secretory activity of this cell population as
 a 
 whole. 

 ============================================================= 
 25.)[Reactional status of leprosy]. 
 ============================================================= 
 Med Cutan Ibero Lat Am 1975;3(3):199-208 Related Articles, Books 

 Alonso AM 

 Reactional leprosy is studied according to its clinical forms A) 
 Lepromatous a) Acute lepromatization: encroaching and invasive nature;
 the 
 patient becomes more and more lepromatous ; bad prognosis. b) Erythema 
 nodosum: "contusiform dermatitis"; variable prognosis not so bad as it is 
 in the preceding case; allergic nature and its evolution is usually 
 detained and therapeutics efficient. c) Erythema multiform. d) Lucio's 
 phenomenon: vascular lesions and consequently necrosis as a complication
 of 
 the "erythema necrotisans" (beautiful leprosy). B) Tuberculoid Reactional 
 tuberculoid is the only one in this benign type, the Mitsuda's test must 
 always be positive and prognosis consequently good. C) Dimorphous or 
 "Borderline" whose Mitsuda's test is mostly negative, sometimes positive, 
 but not stable. The lesions may stimulate the tuberculoid leprids but
 they 
 invade mucous membranes, are impregnated by pigmentation, may present the 
 Unna's band, and other characteristics of the Lepromatous type. Are 
 associated (fever, asthenia and emaciation). Prognosis not very good, 
 because of the possibility of lepromatization, according to its tendency. 
 Evolution slower and frequent relapses. Besides there are nodular
 lesions. 
 Pathogeny 1) Perifocal allergic reaction (Jadassohn). Similar to 
 epituberculosis and Herxheimer reaction. 2) Septicemia. Sensitized
 tissues 
 inside or outside the lesions, are invaded by the bacilli and so the 
 allergic reaction takes place. Even without culture resources, 
 Mycobacterium leprae has been found in the blood by direct examination.
 3) 
 Autoimmunization (Waldenstrom, Matthews and Trantman, 1965). Based upon
 the 
 similarity between both humoral syndromes, in leprosy reactions and 
 collagenous, diseases, as to: hypergammaglobulins, hypercryoproteins, 
 antigammaglobulins, serological reactions (Wassermann, Kahn, Kline, VDRL) 
 positives, Antistreptolysin O, protein C reactive, antinuclear factors, 
 latex and Wadler-Rose test positives (rheumatoid tests) lowering of 
 complement. If leprosy reaction is like this, it should be the less 
 agressive of the autoimmune diseases. a) Its eruptions are cyclic not of 
 long standing duration, as a general rule. b) Its prognosis has been 
 recognized as good, except lately, because of the use of corticoid
 therapy 
 which has been fatal, in many cases. After some years the leprosy
 reaction 
 cures spontaneously. Treatment (see article) 

 ============================================================= 
 26.) Auricular chondritis as a rheumatologic manifestation of Lucio's 
 phenomenon: clinical improvement after plasmapheresis. 
 ============================================================= 
 Ann Intern Med 1983 Jan;98(1):49-51 

 Piepkorn M, Brown C, Zone J 

 ============================================================= 
 ============================================================= 
 27.) Contemplative immune mechanism of Lucio phenomenon and its global 
 status. 
 ============================================================= 
 J Dermatol 1987 Dec;14(6):580-5 

 Sehgal VN, Srivastava G, Sharma VK 
 ============================================================= 
 ============================================================= 
 28.) Plasma exchange therapy in Lucio's phenomenon. 
 ============================================================= 
 Arch Dermatol 1980 Oct;116(10):1101 Related Articles, Books, LinkOut 

 Wallach D, Cottenot F, Bussel A, Palangie A, Pennec J 

 Publication Types: 
 Letter 
 ============================================================= 
 ============================================================= 
 29.) [Lepromatous leprosy with extensive ulcerations and cachexia. The 
 Lucio phenomenon? Lazarine leprosy]? 
 ============================================================= 
 Acta Leprol 1979 Sep-Dec;(76-77):331-3 

 [Article in French] 

 Strobel M, Ndiaye B, Carayon A 
 ============================================================= 
 30.)[2 cases of Lucio phenomenon in Paraguay]. 
 ============================================================= 
 Repura 1973 Jan-Mar;42(1):12-5 

 Innami S, Legiuzamon OR, Alvarenga AE 
 ============================================================= 
 ============================================================= 
 31.) An unusual case of leprosy with pathological features common to 
 Lucio's phenomenon. 
 ============================================================= 
 Cent Afr J Med 1971 Jun;17(6):119-22 

 Taube E, Ellis BP 
 ============================================================= 
 ============================================================= 
 32.) Primary diffuse lepromatous leprosy with erythema necrotisans 
 (lucio phenomenon). 
 ============================================================= 
 Arch Dermatol 1968 May;97(5):593-4 

 Moschella SL 
 ============================================================= 
 ============================================================= 
 33.) The "Lucio phenomenon" in diffuse leprosy. 
 ============================================================= 
 Ann Intern Med 1967 Oct;67(4):831-6 

 Donner RS, Shively JA 
 ============================================================= 
 ============================================================= 
 34.) [Macular leprosy of Lucio--antimalarials in leprotic reaction]. 
 ============================================================= 
 Dermatol Int 1965 Jul-Sep;4(3):147-50 

 Padilla HC 
 ============================================================= 
 ============================================================= 
 35.) [Dermatology in the Central American tropics. I. Lucio's spotted 
 leprosy. Antimalarials in the leprous reaction]. 
 ============================================================= 
 Rev Med Hondur 1965 Jul-Sep;33(3):129-35 

 Corrales Padilla H 
 ============================================================= 
 ============================================================= 
 36.) [Lucio's leprosy]. 
 ============================================================= 
 Division de Estudios de Posgrado e Investigacion, Facultad de Medicina, 
 UNAM, Mexico, D.F. 
 Gac Med Mex 1996 May-Jun;132(3):333-4 

 Quijano-Pitman F 

 Publication Types: 
 Biography 
 Historical article 
 ============================================================= 
 ============================================================= 
 37.) [Lucio phenomenon in leprosy reactions]. 
 ============================================================= 
 Nippon Rai Gakkai Zasshi 1980 Apr-Jun;49(2):113-6 

 Mayama A 
 ============================================================= 
 ============================================================= 
 38.) Lucio's phenomenon: an overview. 
 ============================================================= 
 Lepr Rev 1979 Jun;50(2):107-12 

 Rea TH 
 ============================================================= 
 ============================================================= 
 39.) Lucio's phenomenon: an immune complex deposition syndrome in 
 lepromatous leprosy. 
 ============================================================= 
 Clin Immunol Immunopathol 1978 Feb;9(2):184-93 

 Quismorio FP Jr, Rea T, Chandor S, Levan N, Friou GJ 
 ============================================================= 
 ============================================================= 
 40.) [Lucio's leprosy]. 
 ============================================================= 
 Actas Dermosifiliogr 1976 Jan-Feb;67(1-2):31-6 

 Nunez Moreno A, Sotillo Gago I, Castro Romero A, Lopez Molina M 
 ============================================================= 
 =========================================================== 
 41.) Antiphospholipid antibodies thrombotic syndrome misdiagnosed as 
 Lucio's phenomenon. 
 ============================================================= 
 Int J Lepr Other Mycobact Dis 1996 Sep;64(3):320-3 

 Bakos L, Correa CC, Bergmann L, Bonamigo RR, Muller LF 

 Department of Internal Medicine, Hospital de Clinicas de Porto Alegre, 
 Federal University of Rio Grande do Sul, Porto Alegre, Brazil. 
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 DATA-MEDICOS/DERMAGIC-EXPRESS No 2-(94)  03/05/2.000 DR. JOSE LAPENTA R. 
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