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Multibacillary leprosy patients with high and persistent serum antibodies to leprosy IDRI diagnostic-1/LID-1: higher susceptibility to develop type 2 reactions.

Mizoguti Dde F, Hungria EM, Freitas AA, Oliveira RM, Cardoso LP, Costa MB, Sousa AL, Duthie MS, Stefani MM - Mem. Inst. Oswaldo Cruz (2015)

Bottom Line: Patients who presented T2R had a median BI of 3+, while MB patients with T1R and nonreactional patients had median BI of 2.5+ (p > 0.05).Anti-LID-1 levels waned in MB with T2R at diagnosis and nonreactional MB patients (p < 0.05).Higher anti-LID-1 levels were seen in patients with T2R at diagnosis (vs. patients with T1R at diagnosis, p = 0.008; vs. nonreactional patients, p = 0.020) and in patients with T2R during MDT (vs. nonreactional MB, p = 0.020).

View Article: PubMed Central - PubMed

Affiliation: Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, GO, Brasil.

ABSTRACT
Leprosy inflammatory episodes [type 1 (T1R) and type 2 (T2R) reactions] represent the major cause of irreversible nerve damage. Leprosy serology is known to be influenced by the patient's bacterial index (BI) with higher positivity in multibacillary patients (MB) and specific multidrug therapy (MDT) reduces antibody production. This study evaluated by ELISA antibody responses to leprosy Infectious Disease Research Institute diagnostic-1 (LID-1) fusion protein and phenolic glycolipid I (PGL-I) in 100 paired serum samples of 50 MB patients collected in the presence/absence of reactions and in nonreactional patients before/after MDT. Patients who presented T2R had a median BI of 3+, while MB patients with T1R and nonreactional patients had median BI of 2.5+ (p > 0.05). Anti-LID-1 and anti-PGL-I antibodies declined in patients diagnosed during T1R (p < 0.05). Anti-LID-1 levels waned in MB with T2R at diagnosis and nonreactional MB patients (p < 0.05). Higher anti-LID-1 levels were seen in patients with T2R at diagnosis (vs. patients with T1R at diagnosis, p = 0.008; vs. nonreactional patients, p = 0.020) and in patients with T2R during MDT (vs. nonreactional MB, p = 0.020). In MB patients, high and persistent anti-LID-1 antibody levels might be a useful tool for clinicians to predict which patients are more susceptible to develop leprosy T2R.

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serological reactivity to leprosy Infectious Disease Research Institutediagnostic-1 (LID-1) and to phenolic glycolipid I (PGL-I) in paired serumsamples from multibacillary (MB) patients who developed type 1 (T1R) and type 2(T2R) reactions at diagnosis or during multidrug therapy (MDT) and amongnonreactional MB (nonreactional MB patients: n = 12). A; seroreactivity toLID-1; B: seroreactivity to PGL-I (MB patients who developed T1R at diagnosis:n = 18); C: seroreactivity to LID-1; D: seroreactivity to PGL-I MB patients whodeveloped T1R during MDT (n = 5); E: seroreactivity to LID-1; F: seroreactivityto PGL-I (MB patients who developed T2R at diagnosis: n = 7); G: seroreactivityto LID-1; H: seroreactivity to PGL-I (MB patients who developed T2R during MDT:n = 5); I; seroreactivity to LID-1; J: seroreactivity to PGL-I. Fornonreactional patients paired samples were collected at diagnosis and afterMDT. For reactional patients, each point represents the optical density (OD) ineach sample taken from the same patient in the presence and in the absence ofthe reaction. The dashed line represents the cut-off: OD > 0.3 to anti-LID-1and OD > 0.25 to anti-PGL-I serology. Asterisks mean p < 0.05. ns: notstatistically significant.
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f02: serological reactivity to leprosy Infectious Disease Research Institutediagnostic-1 (LID-1) and to phenolic glycolipid I (PGL-I) in paired serumsamples from multibacillary (MB) patients who developed type 1 (T1R) and type 2(T2R) reactions at diagnosis or during multidrug therapy (MDT) and amongnonreactional MB (nonreactional MB patients: n = 12). A; seroreactivity toLID-1; B: seroreactivity to PGL-I (MB patients who developed T1R at diagnosis:n = 18); C: seroreactivity to LID-1; D: seroreactivity to PGL-I MB patients whodeveloped T1R during MDT (n = 5); E: seroreactivity to LID-1; F: seroreactivityto PGL-I (MB patients who developed T2R at diagnosis: n = 7); G: seroreactivityto LID-1; H: seroreactivity to PGL-I (MB patients who developed T2R during MDT:n = 5); I; seroreactivity to LID-1; J: seroreactivity to PGL-I. Fornonreactional patients paired samples were collected at diagnosis and afterMDT. For reactional patients, each point represents the optical density (OD) ineach sample taken from the same patient in the presence and in the absence ofthe reaction. The dashed line represents the cut-off: OD > 0.3 to anti-LID-1and OD > 0.25 to anti-PGL-I serology. Asterisks mean p < 0.05. ns: notstatistically significant.

Mentions: Antibody responses at time of initial diagnosis - As expected, at thetime of diagnosis, the vast majority of MB patients presented with positive anti-LID-1and anti-PGL-I responses (81% and 54 %, respectively). The rate of seropositivity amongnonreactional MB patients was 75% (9/12) for anti-LID-1 and 67% (8/12) for anti-PGL-Iantibodies (Fig. 2A,B). Similarly, among MB patients 78% (14 of 18) exhibiting T1R at the time ofdiagnosis recognised LID-1 antigen and 50% (9 of 18) was anti-PGL-I positive (Fig. 2C, D).The highest rate of anti-LID-1 seropositivity was observed in patients presenting withT2R, with all seven (100%) seropositive for LID-1 (Fig.2G) while anti-PGL-I responses in patients presenting with T2R was 43% (3/7).In addition to the rate of anti-LID-1 positivity being greater, patients presenting withT2R also had higher levels of anti-LID-1 antibodies when compared to both nonreactionaland T1R patients (Fig. 3A) (p = 0.020 and 0.008,respectively). Anti-PGL-I responses were similar in these same groups of MB patients(Fig. 3B). Thus, high levels of anti-LID-1 atthe time of diagnosis were indicative of a T2R.


Multibacillary leprosy patients with high and persistent serum antibodies to leprosy IDRI diagnostic-1/LID-1: higher susceptibility to develop type 2 reactions.

Mizoguti Dde F, Hungria EM, Freitas AA, Oliveira RM, Cardoso LP, Costa MB, Sousa AL, Duthie MS, Stefani MM - Mem. Inst. Oswaldo Cruz (2015)

serological reactivity to leprosy Infectious Disease Research Institutediagnostic-1 (LID-1) and to phenolic glycolipid I (PGL-I) in paired serumsamples from multibacillary (MB) patients who developed type 1 (T1R) and type 2(T2R) reactions at diagnosis or during multidrug therapy (MDT) and amongnonreactional MB (nonreactional MB patients: n = 12). A; seroreactivity toLID-1; B: seroreactivity to PGL-I (MB patients who developed T1R at diagnosis:n = 18); C: seroreactivity to LID-1; D: seroreactivity to PGL-I MB patients whodeveloped T1R during MDT (n = 5); E: seroreactivity to LID-1; F: seroreactivityto PGL-I (MB patients who developed T2R at diagnosis: n = 7); G: seroreactivityto LID-1; H: seroreactivity to PGL-I (MB patients who developed T2R during MDT:n = 5); I; seroreactivity to LID-1; J: seroreactivity to PGL-I. Fornonreactional patients paired samples were collected at diagnosis and afterMDT. For reactional patients, each point represents the optical density (OD) ineach sample taken from the same patient in the presence and in the absence ofthe reaction. The dashed line represents the cut-off: OD > 0.3 to anti-LID-1and OD > 0.25 to anti-PGL-I serology. Asterisks mean p < 0.05. ns: notstatistically significant.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4660621&req=5

f02: serological reactivity to leprosy Infectious Disease Research Institutediagnostic-1 (LID-1) and to phenolic glycolipid I (PGL-I) in paired serumsamples from multibacillary (MB) patients who developed type 1 (T1R) and type 2(T2R) reactions at diagnosis or during multidrug therapy (MDT) and amongnonreactional MB (nonreactional MB patients: n = 12). A; seroreactivity toLID-1; B: seroreactivity to PGL-I (MB patients who developed T1R at diagnosis:n = 18); C: seroreactivity to LID-1; D: seroreactivity to PGL-I MB patients whodeveloped T1R during MDT (n = 5); E: seroreactivity to LID-1; F: seroreactivityto PGL-I (MB patients who developed T2R at diagnosis: n = 7); G: seroreactivityto LID-1; H: seroreactivity to PGL-I (MB patients who developed T2R during MDT:n = 5); I; seroreactivity to LID-1; J: seroreactivity to PGL-I. Fornonreactional patients paired samples were collected at diagnosis and afterMDT. For reactional patients, each point represents the optical density (OD) ineach sample taken from the same patient in the presence and in the absence ofthe reaction. The dashed line represents the cut-off: OD > 0.3 to anti-LID-1and OD > 0.25 to anti-PGL-I serology. Asterisks mean p < 0.05. ns: notstatistically significant.
Mentions: Antibody responses at time of initial diagnosis - As expected, at thetime of diagnosis, the vast majority of MB patients presented with positive anti-LID-1and anti-PGL-I responses (81% and 54 %, respectively). The rate of seropositivity amongnonreactional MB patients was 75% (9/12) for anti-LID-1 and 67% (8/12) for anti-PGL-Iantibodies (Fig. 2A,B). Similarly, among MB patients 78% (14 of 18) exhibiting T1R at the time ofdiagnosis recognised LID-1 antigen and 50% (9 of 18) was anti-PGL-I positive (Fig. 2C, D).The highest rate of anti-LID-1 seropositivity was observed in patients presenting withT2R, with all seven (100%) seropositive for LID-1 (Fig.2G) while anti-PGL-I responses in patients presenting with T2R was 43% (3/7).In addition to the rate of anti-LID-1 positivity being greater, patients presenting withT2R also had higher levels of anti-LID-1 antibodies when compared to both nonreactionaland T1R patients (Fig. 3A) (p = 0.020 and 0.008,respectively). Anti-PGL-I responses were similar in these same groups of MB patients(Fig. 3B). Thus, high levels of anti-LID-1 atthe time of diagnosis were indicative of a T2R.

Bottom Line: Patients who presented T2R had a median BI of 3+, while MB patients with T1R and nonreactional patients had median BI of 2.5+ (p > 0.05).Anti-LID-1 levels waned in MB with T2R at diagnosis and nonreactional MB patients (p < 0.05).Higher anti-LID-1 levels were seen in patients with T2R at diagnosis (vs. patients with T1R at diagnosis, p = 0.008; vs. nonreactional patients, p = 0.020) and in patients with T2R during MDT (vs. nonreactional MB, p = 0.020).

View Article: PubMed Central - PubMed

Affiliation: Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, GO, Brasil.

ABSTRACT
Leprosy inflammatory episodes [type 1 (T1R) and type 2 (T2R) reactions] represent the major cause of irreversible nerve damage. Leprosy serology is known to be influenced by the patient's bacterial index (BI) with higher positivity in multibacillary patients (MB) and specific multidrug therapy (MDT) reduces antibody production. This study evaluated by ELISA antibody responses to leprosy Infectious Disease Research Institute diagnostic-1 (LID-1) fusion protein and phenolic glycolipid I (PGL-I) in 100 paired serum samples of 50 MB patients collected in the presence/absence of reactions and in nonreactional patients before/after MDT. Patients who presented T2R had a median BI of 3+, while MB patients with T1R and nonreactional patients had median BI of 2.5+ (p > 0.05). Anti-LID-1 and anti-PGL-I antibodies declined in patients diagnosed during T1R (p < 0.05). Anti-LID-1 levels waned in MB with T2R at diagnosis and nonreactional MB patients (p < 0.05). Higher anti-LID-1 levels were seen in patients with T2R at diagnosis (vs. patients with T1R at diagnosis, p = 0.008; vs. nonreactional patients, p = 0.020) and in patients with T2R during MDT (vs. nonreactional MB, p = 0.020). In MB patients, high and persistent anti-LID-1 antibody levels might be a useful tool for clinicians to predict which patients are more susceptible to develop leprosy T2R.

Show MeSH
Related in: MedlinePlus