ABSTRACT
Systemic lupus erythematosus [SLE] may affect respiratory muscles. Diaphragmatic weakness in patients with SLE is a controversial issue and is claimed to have a neuropathic, myopathic or unknown pathogenesis. To determine whether the diaphragmatic weakness could be explained on the basis of a phrenic neuropathy in patients with SLE. A total of 21 patients [18 female and 3 male] with systemic lupus erythematosus [SLE] [age range, 16-36yr] were included and studied by physical chest examination, chest radiography, spirometry, as well as serological examinations and bilateral transcutaneous phrenic nerve conduction studies. 14 [66.6%] patients complained of dyspnea, only one patient showed paradoxical abdominal movement. Pulmonary function tests showed proportional reduction of the forced vital capacity [FVC] and forced expiratory volume in 1 second [FEV[1]] in 17 [81%] patients, suggesting a restrictive process which was severe in 5 [23%] patients. Phrenic nerve evaluation using transcutaneous stimulation studies showed delayed latencies of the right, left and both phrenic nerve in 17 [81%], 19 [90%] and 17 [81%] patients respectively, confirm-ingademyelinating neuropathy. Also Phrenic nerve stimulation evoked a low-amplitude response from right, left and both phrenic nerve in 17 [81%], 15 [71%] and 14 [66.6%] of patients respectively, confirming axonal neuropathy. There were no significant differences in serum immune markers between individuals with and those without abnormal electrical phrenic nerve stimulation. All patients presented with dyspnea showed abnormal phrenic nerve conduction studies. There was tendency for small but clear lung fields in CXR of individuals with abnormal electrical phrenic nerve stimulation. Overall FVC% predicted was decreased in individuals with abnormal electrical phrenic nerve stimulation compared to those without. Diaphragmatic weakness in patients with SLE is both common and is very likely to be caused by a phrenic neuropathy with evidence of bilateral involvement in patients with SLE
Subject(s)
Humans , Male , Female , Electrophysiology , Phrenic Nerve , Respiratory Function TestsABSTRACT
End-stage renal disease [ESRD] patients have high incidence of thrombotic events. The pathogenesis of the thrombophilic tendency in those patients is not clearly defined. Endothelial dysfunction and/or platetet activation may have an important role in thrombosis in ESRD. Circulating endothelial microparticles [EMPs] are circulating small fragments of plasma membranes of activated endothelial cells. Increased levels of circulating activated platelets and platelet hyperaggregability have been described in ESRD patients. Circulating platelet microparticles [PMPs] are small vesicles with procoagulant activity released from activated platelets. The aim of this study was to determine the levels of both circulating EMPs and PMPs in ESRD patients under maintenance hemodialysis therapy. Circulating levels of both EMPs and PMPs were measured by flow cytometry in platelet-poor plasma of 25 hemodialysis patients younger than 40 years old [14 females and 11 males] and 20 age-matched healthy controls. The blood samples were taken from the venous line before the start of the dialysis session. All patients were subjected to full history taking and clinical examination. Patients known to have any of the disease conditions that is known to cause endothelium and/ or platelet activation [Diabetes mellitus, systemic lupus erythematosus, cerebrovascular or ischemic heart disease] were excluded. The level of EMPs was higher in dialysis patients [45.20 +/- 11.03] than in the control subjects [25.2 +/- 13.13] with a statistically significant difference between the two groups [p=0.002]. Also, the level of PMPs showed a statistical significant difference [p=0.01] between dialysis patients and the control group [755.0 +/- 187.9 vs 576.0 +/- 117.70]. In the dialysis group, the EMPs counts were negatively correlated with platelet counts [r=-0.41; p=0.04] but were positively correlated with the pre-dialysis diastolic blood pressure [r=0.34; p=0.02], while the levels of PMPs were negatively correlated with the hemoglobin levels in the dialysis group [r=-0.41; p=0.04]. The levels of PMPs were positively correlated with the pre-dialysis systolic blood pressure [r=0.34; p=0.02] and the duration of hemodialysis therapy [r=0.4; p=0.05]. Increased concentrations of both endothelial-derived [EMPs] and platelet-derived [PMPs] were detected in hemodialysis patients. This may indicate endothelium and platelet activation or injury in ESRD patients. Further large scale studies are needed to confirm their roles in thrombotic events and their clinical implications