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Biomedical subjects

M J Rico

Publications and source records attributed to M J Rico.

At least 37 records · Page 2Linked to original sources
PubMed1993

Neonatal pemphigus vulgaris in a child born to a woman in remission.

We describe the tenth reported case of neonatal pemphigus that mimicked Bart's syndrome and review previously published cases. Unlike previous cases, the child was born with significant blistering to a mother who was in complete remission throughout the pregnancy. High antepartum maternal titers of anti-intercellular space antibodies, increased maternal disease activity, and maternal disease that requires high doses of corticosteroids or use of combined therapy correlate with poor fetal outcome, including intrauterine death.

Adult↗
PubMed1993

Rabbits immunized with a peptide encoded for by the 230-kD bullous pemphigoid antigen cDNA develop an enhanced inflammatory response to UVB irradiation: a potential animal model for bullous pemphigoid.

Previous attempts to develop an animal model of bullous pemphigoid (BP) have failed to result in inflammatory disease in the skin. P1-2 is an 18-amino acid peptide encoded for by the 230-kD BP antigen cDNA that has been shown to contain an epitope recognized by circulating antibodies from patients with BP. The purpose of this study was to determine if ultraviolet B irradiation of rabbits after immunization with the P1-2 peptide would result in an enhanced inflammatory response in the skin to that injury. Three rabbits were immunized with either P1-2 or a control peptide. All rabbits immunized with P1-2, and none of the control rabbits, developed antibodies against P1-2 that bound in vitro to both human and rabbit skin in a linear pattern at the basement membrane zone. Immunized rabbits were irradiated on the flank with ultraviolet light. Rabbits immunized with P1-2 developed an enhanced inflammatory reaction to ultraviolet B irradiation leading to epidermal necrosis and sloughing of some sites in 6-9 d. Control rabbits showed only mild erythema without sloughing, which healed in 4-6 d. Histology in the P1-2 immunized rabbits at 24 h revealed an inflammatory infiltrate of neutrophils at the dermal-epidermal junction, whereas control rabbits showed only mild edema and a sparse inflammatory infiltrate. All the rabbits immunized with P1-2 had linear deposits of immunoglobulin G and C3 at the basement membrane zone of healed skin compared to none of the controls. These findings demonstrate that antibodies against a synthetic peptide encoded by the BP antigen 1 sequence can lead to an enhanced inflammatory response after epithelial injury in rabbit skin.

Animals↗
PubMed1993

IgG antibodies from patients with bullous pemphigoid bind to fusion proteins encoded by BPAg1 cDNA.

Bullous pemphigoid (BP) is an autoimmune blistering skin disease characterized in part by the presence of circulating and tissue-bound IgG antibodies directed against the epidermal basement membrane zone. IgG from over 95% of patients with BP have been shown to immunoprecipitate a 230-kD epidermal protein, BPAg1, which has been cloned and sequenced. Although sera from almost all patients with BP react with the 230-kD BP antigen the specific epitope(s) of BPAg1 that IgG binds is not known. We have generated fusion proteins from the 230-kD BP antigen cDNA and analyzed sera from patients with BP for binding to these fusion proteins by immunoblot. Sera from 21 of 30 (70%) patients with BP reacted with FP3A (amino acid 873-1193) compared to four of 13 (30%) normal subjects (p < 0.02). Sera from 10 of 30 (33%) patients reacted with FP7 (AA1623-1812) and to FP3 (AA1003-1193), compared to one of 22 (5%) and 0 of 19 (0%) controls, respectively. No significant reactivity was noted against two other fusion proteins (FP6, FP9). Twenty-four of 30 (80%) patients with BP reacted to at least one of three fusion proteins (FP3, FP3A, FP7) compared to three of 11 (27%) of the control subjects (p < 0.003). Fusion proteins FP3, FP3A, and FP7 are at the amino- or carboxyl-terminal regions of the putative central alpha-helical coiled-coil rod domain of BPAg1, which has been postulated to be involved in the self-aggregation of BPAg1. These findings demonstrate that patients with bullous pemphigoid react with multiple regions of BPAg1 and suggest that part of the pathologic consequences of these auto-antibodies in patients with bullous pemphigoid may be by the disruption of the normal self-aggregation of the BPAg1.

Animals↗
PubMed1993

Expression of cross-reactive idiotypes at the basement membrane zone in patients with bullous pemphigoid.

The purpose of the present study was to determine whether tissue-bound anti-basement membrane zone (BMZ) autoantibodies in patients with bullous pemphigoid (BP) express a cross-reactive idiotype. We assayed 34 skin biopsies from 26 patients with BP and nine biopsies from control subjects, including normal subjects and patients with epidermolysis bullosa acquisita for the presence of a cross-reactive idiotype at the BMZ. Perilesional split-skin biopsies were assayed for the presence of immunoreactants, immunoglobulin G, and complement and for reactivity with a monoclonal anti-idiotypic antibody specific for a circulating anti-BMZ antibody, anti-Id 3-17. Anti-Id 3-17 bound in a linear band to the BMZ in 12 of 26 patients with BP (46%) and in 0 of 9 control subjects. In serial biopsy specimens, the presence or absence of cross-reactive idiotype at the BMZ in six patients was stable during the disease course. This cross-reactive idiotype has been previously identified in the serum of 36% of patients with BP; however, in this study, no correlation was noted between the presence of the cross-reactive idiotype in skin and serum of individual patients. Because cross-reactive idiotypes occur as a consequence of restricted variable-region gene utilization, the demonstration of a cross-reactive idiotype at the BMZ previously identified in the serum of patients with BP supports the hypothesis that circulating and tissue-bound autoantibodies in this disease arise from a common genetic origin.

Antibodies, Anti-Idiotypic↗
PubMed1993

Autoimmune blistering diseases: characterization of target antigens.

The development of techniques for identification of antigens has had broad application and success in the field of immunodermatology. During the past 10 years, a variety of skin autoantigens, including those found within the epidermis such as in pemphigus and those defined as extracellular matrix proteins such as in EBA, have been identified as the specific targets for autoantibody binding. The intrinsic function of all the autoantigens identified to date is adhesion, either cell-to-cell or cell-to-substrate. The binding of autoantibodies to these adhesion proteins abrogates this critical function via mechanisms not yet clearly understood. Further investigations will focus not only on the characterization of additional autoantigenic targets, but also on identifying mechanisms for the origin and pathogenesis of autoantibodies in blistering skin diseases.

Autoantigens↗
PubMed1993

Treatment of autoimmune blistering diseases.

This review highlights some of the recent advances and controversies in the treatment of autoimmune blistering diseases, with an emphasis on the practical management of these patients for the clinician. The indications, dosages, and side effects of drugs commonly used to treat these conditions are reviewed. Corticosteroids, administered either topically or systemically, are commonly used in the management of these disorders. Agents that may act as anti-inflammatory agents may offer some benefit, including gold, dapsone, antibiotics, and niacinamide. Immunosuppressants, particularly azathioprine or cyclophosphamide, are used as adjuvants in patients whose condition is not controlled on high-dosage corticosteroids or who cannot tolerate the side effects of steroids.

Anti-Inflammatory Agents↗
PubMed1992

Vancomycin-associated linear IgA dermatosis. A report of three cases.

BACKGROUND: Linear IgA dermatosis is an autoantibody-mediated, subepidermal blistering disease that is rarely associated with drug exposure. OBJECTIVE: We report the development of linear IgA dermatosis in three patients associated with the administration of vancomycin and further characterize the immunopathology. METHODS: Direct and indirect immunofluorescence assays were performed to characterize the immunoreactants, determine the subclass of the IgA deposits, and map the site of antibody deposition. RESULTS: A subepidermal blistering disease developed in all patients shortly after vancomycin was initiated, which resolved on discontinuation of the drug. Immunofluorescence studies revealed linear deposits of IgA1 only at the basement membrane zone, below the lamina lucida. Circulating IgA anti-basement membrane zone antibodies were not detected. CONCLUSION: Three patients had linear IgA dermatosis in association with the administration of vancomycin. All patients had linear deposits of IgA1 localized to the sublamina densa zone. Immunophenotypically, the disease in these patients mimics the pattern of IgA deposits seen in the majority of patients with idiopathic linear IgA dermatosis.

Aged↗
PubMed1991

Detection of cross-reactive idiotypes in the serum of patients with bullous pemphigoid.

To further characterize the circulating antibasement membrane zone (antiBMZ) antibodies present in the sera of patients with bullous pemphigoid (BP), we have generated a mouse monoclonal anti-idiotypic antibody (antiId 3-17) specific for an IgG antiBMZ antibody. AntiId 3-17 is specific for an idiotype expressed on antiBMZ IgG in the serum of a patient with BP, and not expressed on pooled normal human IgG or IgG from patients with other autoimmune skin diseases. AntiId 3-17 binds to non-reduced, but not reduced, antiBMZ IgG on immunoblot, suggesting that the idiotype is composed of a conformational epitope expressed on native antibody. By a competitive inhibition ELISA, antiId 3-17 detects a cross-reactive idiotype (CRI) expressed in 18 of 50 (36%) of the sera of patients with BP, but in the sera of only 1 of 50 (2%) normal blood bank controls (p less than 0.001, Fisher's exact test) and 1 of 12 (8%) patients with pemphigus (p = 0.005). Thus, antiId 3-17 recognizes a public idiotype on a native antiBMZ antibody from a patient with BP, which is expressed in the sera of 36% of the unrelated patients with BP studied.

Antibodies, Anti-Idiotypic↗
PubMed1990

IgG antibodies from patients with bullous pemphigoid bind to localized epitopes on synthetic peptides encoded by bullous pemphigoid antigen cDNA.

Bullous pemphigoid (BP) is an autoimmune blistering disease characterized in part by the presence of tissue-bound and circulating antibodies specific for basement membrane zone proteins, the BP Ag. The purpose of the present study was to determine seroreactivity of patients with BP to six nonoverlapping synthetic peptides representing sequences in the carboxyl domain of the recently cloned 230-kDa BP Ag. Sera from 40 patients with BP, 57 normal subjects, and 18 patients with other autoimmune blistering skin diseases were examined in an ELISA for binding to six synthetic peptides varying between 17 and 19 amino acids in length. The binding of IgG from patients with BP to three synthetic peptides, P1-2, P1-1, and P3-1, was significantly different from that seen in the normal controls (p less than 0.001, Fisher's exact test). Affinity-purified anti-P1-2 antibody from a patient with BP bound in a characteristic linear band to the epidermal side of 1 M NaCl split skin and immunoprecipitated the native 230-kDa BP Ag. Serum IgG antibodies from a rabbit immunized with a BP fusion protein that contains the sequences for P1-1 and P1-2, bound on ELISA to P1-2 but not to P1-1. These data suggest that multiple epitopes on the 230-kDa BP Ag are recognized by circulating autoantibodies in patients with this disease, and that an epitope encoded within the synthetic peptide P1-2 is expressed on the native molecule and may be relevant in the generation of an immune response both in man and in an animal model.

Amino Acid Sequence↗
PubMed1990

Eight years' experience with the Medtronic-Hall valve prosthesis.

During the period January 1981 to September 1986, 444 Medtronic-Hall heart valve prostheses were implanted in 351 patients (mean age, 45 +/- 10 years) mainly for rheumatic valve disease (63.2%). Most of the patients were in New York Heart Association functional class III. Concomitant surgical procedures, mainly conservative tricuspid or mitral procedures or coronary artery bypass grafting, were performed in 101 patients (28.7%). Single-valve replacement was performed in 262 patients (74.6%) (aortic in 117 patients, mitral in 143, and tricuspid in 2), double-valve replacement in 85 (24.2%) (mitral and aortic in 83 and mitral and tricuspid in 2), and triple-valve replacement in 4 (1.1%). Hospital mortality was 6.2%. Follow-up was 97.7% complete. The overall actuarial 8-year survival rate was 77.2%. The linearized incidence of valve-related complications was as follows: thromboembolism, 1.5%/patient-year; reoperation, 1.5%/patient-year; endocarditis, 1.25%/patient-year; hemolysis, 0.52%/patient-year; anticoagulant-related hemorrhage, 0.39%/patient-year; and noninfection-related paraprosthetic leak, 0.33%/patient-year. There were no instances of structural failure. We conclude that after 8 years of follow-up, the Medtronic-Hall valve prosthesis has an excellent clinical performance and a low range of valve-related complications.

Adolescent↗
PubMed1989

Anti-idiotypic antibodies as vaccine candidates. The immune network.

Antibodies specific for determinants within the variable region of an antibody molecule are known as anti-idiotypic antibodies. Anti-idiotypic antibodies specific for determinants within the antigen binding site of the antibody may mimic the original antigen and are said to bear an "internal image" of the antigen. These anti-idiotypic antibodies have been shown in animal studies to function as surrogate antigens in stimulating an immune response and may ultimately be useful therapeutically as vaccines to prevent infectious diseases, to enhance the immune response to neoplasms, and to modulate autoantibody production in autoimmune diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Idiotypes, anti-idiotypes, and autoimmunity.

Over the past two decades it has become clear that the ability of a host to generate antibodies against a wide variety of potential antigens is due to structural diversity in the antibody molecule within the variable region. This diversity results in sites within the molecule that are themselves immunogenic. These immunogenic sites are called idiotopes, and the collection of idiotopes on a single antibody molecule determines that antibody's idiotype. The idiotype of an antibody molecule is defined serologically by a second antibody termed an anti-idiotype. Anti-idiotypic antibodies can recognize antibody molecules bearing similar or identical structures within the variable regions, which are often on or near sites of antigen binding. Investigation into the nature of idiotype and anti-idiotype interactions has increased our knowledge of antibody structure, antigen-antibody interactions, the regulation of antibody production, and the nature of autoimmune disorders. This review will discuss the nature of idiotypes and anti-idiotypes and their potential role in the diagnosis, management, and treatment of autoimmune, infectious, and malignant diseases.

Antibodies, Anti-Idiotypic↗
PubMed1987

Interface dermatitis in patients with the acquired immunodeficiency syndrome.

We report twenty-five patients with the acquired immunodeficiency syndrome (AIDS) and interface dermatitis. Patients with AIDS and interface dermatitis had numerous opportunistic and herpetic infections. Nearly all patients were receiving at least one medication prior to the development of their rash and many were clinically thought to have a drug eruption. When compared to skin biopsy specimens from non-AIDS patients with drug eruptions, specimens from patients with AIDS and interface dermatitis demonstrated a greater degree of vacuolar change, the frequent occurrence of necrotic keratinocytes, often in clumps, and the absence of eosinophils and polymorphonuclear leukocytes in the dermal infiltrates. Histologic and clinical features of our patients with AIDS and interface dermatitis are presented and contrasted with other interface dermatitides. Systemic and cutaneous immune abnormalities in patients with AIDS may be relevant to the pathogenesis of this interface process.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Dermatopathologic findings in patients with acquired immunodeficiency syndrome.

We recently undertook a survey of all patients with acquired immunodeficiency syndrome (AIDS) seen at the University of Miami/Jackson Memorial Medical Center (UM/JMMC) and reviewed all skin biopsies received from these patients. Skin was the second most common organ biopsied; 36% of all patients (78/217) with AIDS had at least one skin biopsy. Kaposi's sarcoma (KS), the most frequent diagnosis, was seen in 47% of the biopsy specimens. Cutaneous infection, most commonly herpes simplex infection, was present in 19%. Atypical presentations of common dermatologic infections were also seen. Among the patients with neither KS nor infection, 16 had a vacuolar type of interface dermatitis.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Comparison of alloimmunogenicity of Langerhans cells and keratinocytes from mouse epidermis.

Among lymphoreticular cells, Langerhans cells and splenic dendritic cells stand alone in their capacity, when hapten-derivatized, to induce vigorous immune responses, irrespective of route of inoculation, including intravenous. We have examined the comparative efficiency of relatively purified populations of Langerhans cells and their epidermal companions, keratinocytes, to induce alloimmunity when injected intravenously into adult mice. It was found that as few as 100 BALB/c Langerhans cells injected intravenously into C3H mice are capable of inducing specific sensitization as evidenced by subsequent accelerated rejection of BALB/c skin grafts. By contrast, 10,000 BALB/c keratinocytes failed to immunize similarly injected C3H recipients. These results emphasize the unparalleled capacity of Langerhans cells to induce sensitization, and they point to Langerhans cells, among cells within the epidermal compartment, as dominant in the alloimmunogenic potential of skin grafts.

Animals↗
PubMed1986

Thrombosis of a mechanical valve prosthesis late in pregnancy. Case report and review of the literature.

A case of acute thrombosis of a mechanical mitral valve prosthesis (Medtronic-Hall) in a 34 weeks pregnant woman is reported. The clinical diagnosis was confirmed by Doppler echocardiography. Emergency surgery was performed starting with a cesarean section to save the fetus, followed by an obstetric hysterectomy. Valve thrombectomy could then be safely carried out. Both, the mother and child could be rescued by this combined intervention and were discharged from the hospital without further complications.

Adult↗