Israel Medical Association Journal

Background: Human parvovirus B19 is responsible for a variety of clinical syndromes, such as erythema infectiosum, non-immune hydrops fetalis, transient aplastic anemia, and arthropathies. HPV is also suspected of playing a role in the pathogenesis of various chronic inflammatory and autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, Kawasaki disease and multiple sclerosis.

Objectives: To study the age distribution and clinical presentation of patients hospitalized for human parvovirus B19 infection.

Method: We reviewed the case records of all pediatric patients with serologic evidence of HPV infection who were admitted during a 20 month period to a major community hospital

Results: Of 128 children tested for HPV, 48 had evidence of acute infection based on the presence of immunoglobulin M antibodies; 8 patients who also had positive IgM for other viruses were excluded, thus 40 case records were studied. The mean age of the patients was 5.21 years, but 22 patients were under 4: The clinical presentations included 25 patients with fever, either recurrent or prolonged, accompanied in some by enlarged spleen, liver and lymph nodes, skin rash and arthropathy; the remaining patients were investigated for anemia, skin rash, joint complaints and hepatitis. In addition; HPV infection was documented in several well-defihed clinical conditions, such as SLE, vasculitic skin lesions, acute lymphoblastic leukemia, pure red cell aplasia, and optic neuritis.

Conclusions: In a group of 40 pediatric patients exhibiting anti-HPV IgM antibodies, a younger age and less common clinical presentations were observed, furthermore 5 patients had clinical syndromes in which the causative role of HPV infection was not clear.

Background: The prevalence of clinical manifestations and laboratory parameters in systemic lupus erythematosus differ among various ethnic groups. Few studies have reported on SLE[1] in Arabs.

Objectives: To summarize the demographic, clinical and laboratory features of Arab SLE patients and to compare them with other series from different Arab countries.

Methods: We reviewed the charts of all Arab SLE patients who had been seen at the Carmel Medical Center in Haifa, the Nazareth Hospital and the Holy Family Hospital in Nazareth, and a professional clinic (a referral outpatient clinic of the largest health maintenance organization in Israel) in Acre – all cities in northern Israel. Only patients with symptoms of more than one year were included. Demographic, clinical and laboratory parameters were documented and compared with those of four series from different Arab countries.

Results: The study group comprised 34 patients. The majority of the patients was Moslem; there were a few Druze and one Christian. There was no statistical difference between our patients and any of the other Arab series in terms of arthritis, neuropsychiatric manifestations and VDRL. The presence of serositis and mucocutaneous manifestations was significantly lower in our series compared to some of the other series. However, there was significantly less renal involvement in our patients compared to each of the other series.

Conclusions: The prevalence of most clinical and laboratory parameters in Israeli Arab SLE patients is comparable to that of other series of SLE patients from different Arab countries. The prevalence of renal involvement in Israeli Arab SLE patients seems to be lower than in SLE patients from different Arab countries.

Recent studies have implicated the dying cell as a potential reservoir of modified autoantigens that may initiate and drive systemic autoimmunity in susceptible hosts. The uridine-rich small nuclear ribonucleoprotein complex is a common target for autoantibodies present in the serum of patients with systemic lupus erythematosus and SLE[1]-overlap syndromes. Four modifications occurring in this complex during apoptosis have been described to date: the caspase-mediated cleavage of the U1-70K protein, the U1 RNA and the Sm-F protein, and the association with hyperphosphorylated SR proteins. In addition, the U1 snRNP[2] complex has been shown to translocate from its normal subcellular localization to apoptotic bodies near the surface of cells undergoing apoptosis. This redistribution might facilitate exposure of the modified components of the U1 snRNP complex to the immune system when the clearance of apoptotic cell remnants is somehow disturbed. The modifications in the U1 snRNP components during apoptosis might represent the initial epitopes to which an immune response is generated and may be the trigger for the production of autoantibodies to this complex in patients with SLE or SLE-overlap syndromes. Therefore, it can be hypothesized that the exposure of elevated levels of apoptotically modified U1 snRNP to the immune system of a genetically susceptible individual might lead to the breaking of immunologic tolerance towards the U1 snRNP complex.

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