Other genes that are commonly thought to be associated with lupus are those in the human leukocyte antigen (HLA) family. There have been several cases wherein a single gene influence appears to be present, but this is rare. When a single gene deficiency does cause lupus, it is usually attributed to the complement protein genes C1, C2, or C4. The influence of sex chromosomes and environmental factors are also noteworthy. Usually, these factors contribute to lupus by influencing the immune system. Several studies also indicate a potential association of lupus with mutations in DNA repair genes. Age difference
Lupus can develop in people at any age, but it does most commonly at ages 15 to 44, with varying results. Typically, the manifestation of the disease tends to be more acute in those of younger age. Women are more likely to get it than men. Patients with juvenile-onset lupus are more vulnerable to mucocutaneous manifestations of the disease (alopecia, skin rash, and ulceration of the mucus membranes) than any other age group, and they are also more susceptible to evaluation of pulmonary artery pressure. However, patients with late-onset lupus have a much higher mortality rate. Nearly 50% of those with late-onset lupus die of their condition. Women who are of childbearing age are also particularly at risk. Differences in ethnicity
Substantial data have been found to indicate that certain ethnic populations could be more at risk for lupus erythematosus and to have a better or worse prognosis.
Asymptomatic humans serve as a significant reservoir for the disease. Little is known about other reservoirs of the disease. Pathogenesis
Mansonelliasis infection has been considered a minor filariasis, remaining asymptomatic in most infected subjects. Larvae develop in the subject and migrate to their respective regions in the skin or body cavities. It is likely that aside from being caused by the worm itself, some of the pathological changes observed are induced by the immune response to the infection leading to some of the various symptoms mentioned above. However, Mansonelliasis is little studied compared to other forms of filariasis so there is not as much information known regarding its specific pathogenesis. Diagnosis
Examination of blood samples will allow identification of microfilariae of M. perstans, and M. ozzardi based. This diagnosis can be made on the basis of the morphology of the nuclei distribution in the tails of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used. These include centrifugation of the blood sample lyzed in 2% formalin (Knotts technique), or filtration through a Nucleopore membrane.Examination of skin snips will identify microfilariae of Onchocerca volvulus and M. streptocerca. Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle. It is important that the sample be allowed to incubate for 30 minutes to 2 hours in saline or culture medium and then examined.