Hypertension in Jordanian children: a retrospective analysis of 70 cases

Seventy patients, aged 1–20 years, were seen at Jordan University Hospital with high blood pressure (BP) over a 3-year period. BP values ranged from 140 to 230 mmHg for systolic pressure and from 90 to 130 mmHg for diastolic pressure. Essential hypertension was seen in only 6 patients (8.6%); secondary hypertension (n=64 or 91.4%) was due to renal parenchymal diseases (RPD) in 46 patients (65.7%), reno-vascular lesions in 8 (11.4%), renal transplantation in 5 (7.2%), teenage pregnancy in 4 (5.7%), and phaeochromocytoma in 1 patient (1.4%). The aetiologies of RPD were as follows: end-stage renal disease requiring dialysis in 14 patients, acute glomerulonephritis in 14, idiopathic nephrotic syndrome in 10, chronic renal insufficiency in 5, and polycystic kidney in 3 patients. Surgical cure of hypertension was achieved in 5 of the children with reno-vascular lesions and in the patient with phaeochromocytoma.     

The αvβ6 integrin plays a role in compromised epidermal wound healing

The alphavbeta6 integrin is an exclusively epithelial integrin that is highly expressed during fetal development. In adult tissue, alphavbeta6 integrin is expressed during inflammation, carcinogenesis, and in wound healing. We previously reported that alphavbeta6 integrin is highly expressed in poorly healing human wounds and its over-expression is associated with chronic wounds in a mouse model. The objective of this study was to investigate the role of alphavbeta6 integrin in compromised wound healing induced by hydrocortisone treatment or aging by using young and old mice deficient in or overexpressing the beta6 integrin subunit in the epidermis. Untreated aged beta6 integrin-deficient (beta6-/-) animals showed a significant delay in wound healing when compared to their age-matched controls or younger beta6-/- mice. The most significant delay was observed at the stages where granulation tissue deposition was occurring. Hydrocortisone treatment significantly delayed wound healing in wild-type and beta6 integrin-deficient mice in comparison with the untreated controls. However, hydrocortisone treatment in beta6 integrin overexpressing animals did not cause a significant delay in wound healing. The results of this study suggest that alphavbeta6 integrin plays an important role in wound healing in animals compromised by either age or stress mimicked by hydrocortisone.     

Natural killer cells in Behçet''s disease.

We studied natural killer (NK) cell activity and numbers in the peripheral blood obtained from patients with Behçet''s disease (BD) in inactive and convalescent stage, and from healthy controls. Ratios of helper/suppressor cells (OKT4/OKT8) were below 1.0 in patients with active stage and were normal in the convalescent stage of BD. A relative increase of OKT8+ cells and at the same time of Leu 7+ cells was obtained in the active and convalescent BD stages. Double marker analysis revealed that the sub-population of cells expressing both the T8+ and the Leu 7+ antigen (T8+/Leu 7+) was increased in patients with active stage, and normal in the convalescent stage. The frequency of cells reactive with Leu 11 monoclonal antibody (active NK cells) was evaluated in patients with BD. Data from peripheral blood showed an increased sub-population of T8+/Leu 7+ double marker cells, and a decreased Leu 11+ cell sub-population in patients with active BD, but the majority of Leu 7+ cells in patients with convalescent stage lacked OKT8 antigen when investigated in a double marker system. A parallel increase of Leu 11+ cells was observed in the convalescent stage. This phenotypic analysis was carried out with the NK in vitro functional evaluation of cell populations from peripheral blood. NK cell activity in the clinically active stage of BD was significantly lower than that of healthy controls and patients in the convalescent stage. The decrease of peripheral blood NK function in patients with active BD may be related to the presence of immature forms of NK cells and/or to the increased percentage of T8+/Leu 7+ cells.     

The effect of adherent peritoneal exudate cells (APECs) and their products on the RPC-5 plasmacytoma growth in vitro

The ability of peritoneal exudate cells (PECs) and their adherent (APECs) and nonadherent (NAPECs) fractions to enhance RPC-5 plasmacytoma growth in vitro was studied. The capability of these cells to bind RPC-5 cells and influence of the binding on cytolysis tumor cells by activated with C. parvum macrophages was also determined. The effector cells were harvested from mice injected i.p. with pristane, thioglicollate medium or C. parvum or from intact mice. The effect of supernatants from the in vitro cultured PECs, APECs or NAPECs on growth RPC-5 cells were also tested. It was found that the RPC-5 plasmacytoma growth was enhanced only by cells obtained from mice treated with pristane, or by supernatants from cultured PECs and APECs derived from pristane treated mice. The adherent cells from pristane treated mice were able to bind tumor cells. The tumor cells preexposed to adherent cells from pristane stimulated mice were resistant to lysis by activated with C. parvum macrophages.     

Pseudo-tumoral osteomyelitis. Immunologic study and etiopathogenic approach. Apropos of 2 cases]

Two cases of pseudo-tumoral osteomyelitis are reported. The first concerns a 12 year-old boy who presented with pain of the left knee during 8 months and, later on, with swelling of the upper extremity of the left leg, without fever or local inflammatory signs. The radiological aspect of condensation with a filling defect and "chimney" crossing the cartilage led to osteotomy. Local bacteriological samplings were normal. The second case concerns a 11 year-old boy who, after having complained from pain of the right wrist during 2 weeks, presented with swelling and on X-ray films a picture of metaphyso-epiphyseal lysis and an aspect of sequestrum in its center. There was no biological sign of inflammation. Evolution was favorable after antibiotic treatment and immobilization. In both cases, an immunological study showed an activation syndrome of the immune system with increased serum IL-1, IL-2 receptors and class II antigen receptors on the surface of T cells, suggesting a previous immunization of both children towards staphylococcus and, thereby, the subacute nature of evolution.     

Unusual bone localization of sarcoidosis mimicking metastatic lesions: case report and review of literature

Sarcoidosis is a multisystem disease of unknown origin. Diagnosis remains challenging, based on organ site involvement, histological confirmation of non-caseating granuloma and an appropriate clinical syndrome. Granulomatous bone involvement is rare and may be ignored because it is usually asymptomatic. Vertebrae, ribs and skull localizations are rarely reported. We described an interesting case of a woman with chronic and multiorgan sarcoidosis with unusual bone localizations.     

CXC ligand 13 in rheumatoid arthritis and its relation to secondary Sjögren’s syndrome

Aim of the workThe aim of the present study was to measure the level of the chemokine CXC ligand 13 protein (CXCL13) in the plasma and unstimulated saliva of rheumatoid arthritis (RA) patients in order to find out its role in the disease activity and its relation to secondary Sjögren’s syndrome (sSS).Patients and methodsThe study was conducted on thirty rheumatoid arthritis patients attending the Outpatient Clinic of Rheumatology and Rehabilitation department of Ain shams University Hospitals. The patients’ group had been classified into group (1) which included fifteen RA patients associated with sSS diagnosed according to the American–European Consensus Group Classification Criteria and group (2) which included fifteen RA patients not associated with sSS. Ten healthy subjects were included as a control group. Patients were subjected to full history taking, clinical examination, and laboratory detection of CXCL13 level in the plasma and saliva of patients as well as the control groups using ELISA technique. Assessment of disease activity in RA patients was done using the disease activity score (DAS28).ResultsPlasma levels of CXCL13 were significantly higher in RA patients than control group (p < 0.001). Plasma levels of CXCL13 were significantly correlated with the RA disease activity (r = 0.677, p < 0.001) and disease duration (r = 0.406, p < 0.05), while the salivary levels were higher in those with sSS and correlated with sSS disease duration (r = 0.536, p < 0.05). A highly significant correlation was found between salivary CXCL13 and severity of sSS (r = 0.816, p < 0.001). Salivary levels of CXCL13 above 110 pg/ml may diagnose sSS with sensitivity 80% and specificity 84%.ConclusionThe results of this preliminary study point out the importance of CXCL13 as a marker for RA disease activity, its role in diagnosing sSS, and estimation of sSS severity.     

B cells mediate chronic allograft rejection independently of antibody production

Chronic rejection is the primary cause of long-term failure of transplanted organs and is often viewed as an antibody-dependent process. Chronic rejection, however, is also observed in mice and humans with no detectable circulating alloantibodies, suggesting that antibody-independent pathways may also contribute to pathogenesis of transplant rejection. Here, we have provided direct evidence that chronic rejection of vascularized heart allografts occurs in the complete absence of antibodies, but requires the presence of B cells. Mice that were deficient for antibodies but not B cells experienced the same chronic allograft vasculopathy (CAV), which is a pathognomonic feature of chronic rejection, as WT mice; however, mice that were deficient for both B cells and antibodies were protected from CAV. B cells contributed to CAV by supporting splenic lymphoid architecture, T cell cytokine production, and infiltration of T cells into graft vessels. In chimeric mice, in which B cells were present but could not present antigen, both T cell responses and CAV were markedly reduced. These findings establish that chronic rejection can occur in the complete absence of antibodies and that B cells contribute to this process by supporting T cell responses through antigen presentation and maintenance of lymphoid architecture.