Assessment of the influence of HLA class I and class II loci on the prevalence of keloid disease in Jamaican Afro-Caribbeans.

Keloid disease (KD) is a common abnormal cutaneous fibrotic disorder of unknown aetiopathogenesis. KD is reported to have a strong genetic component as it is often familial and has a high incidence in certain ethnicities, in particular those of Afro-Caribbean origin. Genetic risk factors combined with aberrant lesional inflammatory responses point to the human leukocyte antigen (HLA) system as a viable target for investigating disease aetiology. Sequence specific primer polymerase chain reaction with allele sequencing was used to determine HLA-DQA1 and DQB1 allele frequencies (AF) for 165 KD patients and 119 healthy controls of black Jamaican Afro-Caribbean origin. HLA class I alleles A*01, A*03, A*25, B*07 and Cw*08:02, previously identified as KD associated in a different ethnicity, were also analysed. Allele sequencing confirmed typing accuracy but no statistically significant differences in AF were identified between KD patients and controls. Furthermore, KD subgroups including patient gender, family history and multiple- or single-site scarring did not show significant allele-disease associations.

Tubal occlusion causing infertility due to an excessive inflammatory response in patients with predisposition for keloid formation.

Infertility is a condition that affects approximately 15-25% of couples with the desire to procreate. The integrity of the feminine reproductive tract is essential for this purpose, but the occlusion of the Fallopian tubes occurs in 12-33% of infertile women. The infection by Chlamydia trachomatis is one of the principle causes of tubal injury, which could finally lead to tubal occlusion. The tract infection has also been related to the use of intrauterine device, basically due to the fact that the insertion of the device could carry bacteria to the endometrial cavity. Keloid scars result from alterations in the normal process of wound healing, and it affects principally the population in reproductive age, maybe due to specific hormonal influence. These fibroproliferative alterations may produce significant deformations and alter organ function. The genetic factors have been studied in order to have a better understanding of the pathophysiology of keloid scarring. With these assessments, many other factors have been known to have a relationship with this abnormal healing process. This keloid scarring involves an excess in extracellular matrix production and inhibition of apoptosis, for which a several growth factors and interleukins are needed. One of the most important growth factors is IGF-1, which increases the expression of type I and III procollagen (found in the uterus); the IGF-1 receptor is overexpressed in the fibroblasts of keloids. Based on those previous observations a hypothesis that the chronic and repeated infection, and the use of IUD, generate an exaggerated inflammatory response in patients with a predisposition for keloid formation (which frequently form in childbearing age), in comparison to the patients that do not form this type of scarring, has been proposed. This makes a major frequency of adherences and finally tubal occlusion and infertility. The tendency of excessive scarring could not be exclusive of skin and generate abnormal scarring responses in feminine reproductive tract, leading to a major frequency of infertility. Thus, it could be suggested the use of other contraceptive methods and a more aggressive treatment against infections of the reproductive tract, taking in consideration the pathophysiology of keloid scar formation and its relationship with tubal occlusion.

Functions of polymorphonuclear leukocytes and individuality of Jorge Lobo's disease: absence of the specific leukocyte digestive defect against Paracoccidioides brasiliensis.

Peripheral blood neutrophils (PMNs) from a patient with Jorge Lobo's disease (JLD) digested well phagocytosed Paracoccidioides brasiliensis. We found no circulating antibodies against P. brasiliensis in the patient's serum. Such neutrophils showed myeloperoxidase activity and also digested normally phagocytosed Candida albicans. We had previously reported the presence of a specific digestive deficiency of PMNs from patients with paracoccidioidomycosis (PARA) vis à vis P. brasiliensis. Current findings provide new information about leukocyte functions in JLD and bolster the view that JLD, PARA and their respective causative microorganisms are distinct.