Rab 32 Gene Polymorphisms as a Prognostic Factor in Leprosy Patients

NCT ID: NCT06819449

Last Updated: 2025-02-11

Basic Information

• Recruitment Status: RECRUITING
• Clinical Phase: NA
• Total Enrollment: 50 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2024-12-20
• Study Completion Date: 2025-12-20

Brief Summary

Mycobacterium leprae is a slow-growing bacillus that causes leprosy. the infection may take two to ten years to incubate. While the exact mechanism of infection transmission is unknown, direct bacillus absorption through the nasal or respiratory mucosa and aerosolized nasal secretions are the most common theories. The bacteria is subsequently transported by the bloodstream to the peripheral nerves, where it can result in tissue damage from painless burns and ulcers as well as irreparable nerve damage that results in a loss of protective feeling.

Detailed Description

One of the most common host cells that mycobacteria encounter is macrophages. The process of monocyte-derived macrophages phagocytosing M. leprae is controlled by protein kinase and can be facilitated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18). A Th2 cytokine profile appears to be correlated with nonreactivity to M.Leprea.

The Ridley-Jopling classification (1962) divides leprosy into six forms: Tuberculoid (TT), Borderline Tuberculoid (BT), Borderline-borderline Mid-borderline (BB), Borderline-Lepromatous (BL), Subpolar Lepromatous (LLs), and Polar Lepromatous (LLp). These categories are based on clinical, histopathological, and immunological criteria. According to WHO, leprosy is classified into two groups: the paucibacillary (PB) and multibacillary (MB) types, to aid in treatment.

Leprosy is treated as an outpatient procedure using WHO-standardized regimens from 1982, which essentially consist of three first-line medications: clofazimine, rifampicin, and dapsone. This relationship is referred to as polychemotherapy, or MDT (PCT). With minimal bactericidal activity, sulfone (diaminodiphenyl sulfone, or DDS), commonly referred to as dapsone, primarily acts as a bacteriostatic agent.

It most likely functions as an antagonist of para- aminobenzoic acid (PABA), preventing M. leprae from using it to synthesize folic acid. It is well-tolerated and has a number of adverse effects, most of which do not require stopping treatment.

The primary bactericidal effect of rifampicin (RMP), a semi-synthetic derivative of rifamycin B, is observed. It functions by preventing the RNA-polymerase enzyme in the bacillus from growing. RMP has been used to treat leprosy since 1963. Most of the bacilli become non-viable after a few days of therapy, and its use is crucial in all clinical types of leprosy. Clofazimine (CLF) is an iminophenazine dye . It has a mild bactericidal action, acting slowly on M. leprae and destroying 99% of the bacteria in approximately five months. Its efficacy is similar to DDS. CLF has an important anti-inflammatory action.

With an estimated heritability of up to 57%, family studies and community epidemiological surveys have amply established the significant role that host genetics plays in an individual's vulnerability to leprosy.

RAB32 is a low molecular weight G protein belonging to the Ras superfamily. It is necessary for the production of autophagic vacuoles and the control of autophagy's removal of aggregated proteins. Rab32 may play a similar role in the pathogenesis of leprosy, according to a recent study that found the protein controls the recruitment of cathepsin D to phagosomes containing Mycobacterium tuberculosis.

Conditions

Leprosy; Mycobacterium Leprae Infection

Study Design

• Allocation Method: RANDOMIZED
• Intervention Model: PARALLEL
• Primary Study Purpose: TREATMENT
• Blinding Strategy: NONE

Study Groups

Group A: Leprosy Patients

About 40 patients suffering from Leprosy and will treated by Multi drug therapy as ( dapsone \_ clofazimine \_ rifampcin) then to assess the role of Rab 32 gene.by taking Two millimetres of venous blood from each participant At the end of third month therapy.

Group Type: ACTIVE_COMPARATOR

Dapsone

Intervention Type: DRUG

To evaluate the effect of the multi drug therapy in leprotic patients and their side effects and to assess the role of Rab 32 gene in leprosy prognosis and to know its association with the multi drug therapy.

Group B: Healthy People

About 10 Healthy People. no drugs used and then to assess the role of Rab 32 gene.by taking Two millimetres of venous blood from each participant

Group Type: ACTIVE_COMPARATOR

Dapsone

Intervention Type: DRUG

To evaluate the effect of the multi drug therapy in leprotic patients and their side effects and to assess the role of Rab 32 gene in leprosy prognosis and to know its association with the multi drug therapy.

Interventions

Dapsone

To evaluate the effect of the multi drug therapy in leprotic patients and their side effects and to assess the role of Rab 32 gene in leprosy prognosis and to know its association with the multi drug therapy.

Intervention Type: DRUG

Other Intervention Names

clofazimine; rifampcin

Eligibility Criteria

Inclusion Criteria

• Patients of both sexes with positive slit skin smear for m.leprae .

Exclusion Criteria

• Contraindications to Multi drug therapy :
• Patients with hypersensitivity to sulfa .
• Patients with hypersensitivity to clofazimine or rifampcin.
• pregnant or lactating women.

• Minimum Eligible Age: 5 Years
• Maximum Eligible Age: 60 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

South Valley University

OTHER

Sponsor Role: lead

Responsible Party

Lydia Atef Nassief

Resident of Dermatology , venereology and andrology at Faculty of medicine

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Eisa Mohammed Hegazy, Assist. Prof

Role: STUDY_CHAIR

Dermatology, Venereology and Andrology. Faculty of Medicine,South Valley University

Locations

Qina University hospital, South Valley University Hospital

Qina, , Egypt

Site Status: RECRUITING

Countries

Egypt

Central Contacts

Lydia Atef Nassief, MSc

Role: CONTACT

lydiaatef67@gmail.com

+201289416276

Eisa Mohammed Hegazy, Assist. Prof

Role: CONTACT

eisa_mohamed4152@med.svu.edu.eg

+201094337795

Facility Contacts

Mohammed Hosny Hassan, Professor

Role: primary

mohammedhosnyhassaan@med.svu.edu.eg

+201098473605

Soheir Abdel-hamid Ali, M.D

Role: backup

Soher.abdel-hamid@med.svu.edu.eg

+201066877343

Other Identifiers

Rab 32 gene polymorphisms

Identifier Type: -

Identifier Source: org_study_id