REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES

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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. 

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 1.) Lepra type reactions 

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 Source: Mandell, Douglas and Bennett's 

 Principles and Practice of Infectious Diseases Fourth Edition: 1.995 

 Lepra Type-1 Reactions (Downgrading and Reversal Reactions) 

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 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. 

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 Lepra Type-2 Reaction (Erythema Nodosum Leprosum) 

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  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 

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 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   

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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. 

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2.) Diffuse Painless Ulcerations 

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 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 

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 3.) [Lucio-Latapi leprosy and the Lucio phenomenon] 

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 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. 

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 4.) [Lucio's leprosy]. 

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 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. 

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 5.) [22 years of leprosy: histopathology] 

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 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. 

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 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. 

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 7.) Lucio's phenomenon and diffuse nonnodular lepromatous leprosy. 

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 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. 

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8.) Lucio's phenomenon: a comparative histological study. 

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 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. 

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 9.) [Diffuse lepromatous leprosy disclosed by cutaneous vasculitis. The   Lucio phenomenon]. 

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 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. 

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 10.) Immunologic aspects of leprosy as related to leucocytic  isoantibodies   and platelet aggregating factors. 

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 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. 

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 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. 

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12.) Dermal ultrastructure in leprosy. 

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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. 

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 13.) Lepromatous and tuberculoid leprosy: clinical presentation and  cytokine   responses. 

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 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. 

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 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. 

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 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. 

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 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. 

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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. 

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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. 

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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-MÉDICOS/DERMAGIC-EXPRESS No 2-(94)  03/05/2.000 DR. JOSÉ LAPENTA

                                               UPDATED 11 SEPTEMBER 2025

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Produced by Dr. José Lapenta R. Dermatologist

Venezuela 1.998-2.025