Professional/CME. Targeting residual cardiovascular risk: raising high-density lipoprotein cholesterol levels. Management of dyslipidaemias. Peri-articular ‘hard tumours’ in soft tissues. A 17-year-old man presented with painless, progressively increasing, non-simultaneous, peri-articular swellings evolving for the last 7 years.
He had undergone repeated drainage of white chalky material and received adequate antitubercular therapy without any relief. He subsequently developed multiple non-healing sinuses. There was no history of colicky pain, graveluria, dyspnoea, excessive intake of antacids and vitamin D preparations, trauma or family history of similar disorder. Examination revealed pallor, axillary and inguinal lymphadenopathy and multiple, soft-to-firm, non-tender swellings of varying sizes (2–5 × 3–8 cm) with non healing sinuses at left shoulder, both hips and right elbow (figure 1). The mobility of the left shoulder and right elbow joints was markedly restricted.
Figure 1 The patient (reproduced with his permission) On investigation he had a haemoglobin of 9.2 g/dl and total leucocyte count of 10 × 109/l with 90% polymorphs. Figure 2 Corresponding CT scans Questions. Review: once daily LMWH is as effective as twice daily LMWH for initial treatment of venous thromboembolism. A negative quantitative latex d-dimer assay helped to rule out venous thromboembolism.
QUESTION: In patients with suspected venous thromboembolism (VTE) (ie, deep venous thrombosis [DVT] or pulmonary embolism [PE]), can a quantitative latex d-dimer assay rule out VTE?
Design Blinded comparison of the results of the latex d-dimer test (MDA d-Dimer, Organon Teknika Corporation, Durham, NC, USA) with objective testing done at presentation and during follow up (3 mo). Setting 4 tertiary care university medical centres in Ontario, Canada. Patients 595 patients (60% women) with suspected VTE (317 with suspected DVT and 278 with suspected PE). Description of tests and diagnostic standards All patients had a clinical examination and were classified into low, intermediate, or high probability categories according to a previously validated model. Main outcome measures. Prophylaxis of venous thromboembolism in patients with lower limb plaster cast immobilisation. Molecular developments in renal tubulopathies. The renal tubule is responsible for the reabsorption of more than 99% of the water and sodium in the glomerular ultrafiltrate.
Congenital or acquired tubular dysfunction can therefore readily cause profound electrolyte and volume disturbance. The tubule also has to regulate acid–base balance, mineral homoeostasis, and the excretion of organic anions and drugs. To fulfil these functions, a large number of specialised transporters and channels are specifically localised in the tubular cell membranes, some in the luminal border and others in the plasma membrane border (basolateral membrane).
In the past decade (and especially in the past five years) advances in molecular genetic research have revealed the structure, function, and effects of mutations in these transporters, thereby greatly increasing our understanding of the function and dysfunction of the renal tubule. Presentation The initial assessment of tubular function is based on the results of routine biochemical investigations. Peripheral blood culture contamination in adults and venepuncture technique: prospective cohort study. ADC - Education and Practice. Postgraduate Medical Journal. + Author Affiliations Correspondence to: Professor David Oliveira, Department of Renal Medicine, St George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK; d.oliveira@sghms.ac.uk Received 17 May 2002 Accepted 5 November 2002 Abstract Glomerulonephritis is an important cause of renal failure thought to be caused by autoimmune damage to the kidney.
While each type of glomerulonephritis begins with a unique initiating stimulus, subsequent common inflammatory and fibrotic events lead to a final pathway of progressive renal damage. In this article the different forms of inflammatory glomerulonephritis and their diagnosis are discussed. Although our understanding of the causes of glomerulonephritis is still at a basic level, inflammation is thought to be autoimmune mediated and involve both cellular and humoral immune systems. To understand the histology of glomerulonephritis, we need to revisit the basic structure of the normal kidney (see fig 1).
Table 1 Table 2 Figure 1. Alveolar haemorrhage in anti-glomerular basement membrane disease without detectable antibodies by conventional assays. + Author Affiliations Correspondence to: Dr D J Serisier Department of Respiratory Medicine, Mater Adult Hospital, Raymond Tce, South Brisbane, Queensland 4101, Australia; david_serisier@mater.org.au Received 21 May 2004 Accepted 8 October 2004 Abstract Anti-glomerular basement membrane (anti-GBM) disease represents the spectrum of disease attributable to circulating anti-GBM antibodies.
While active anti-GBM disease in the absence of circulating anti-GBM antibodies has been described, it is considered rare with the use of current routinely available assays. We report four subjects with features consistent with active anti-GBM antibody disease without detectable antibodies by routinely available enzyme linked immunosorbent assay (ELISA) and immunoblot techniques.
Reduced mucosal antimicrobial activity in Crohn’s disease of the colon. Treatment of refractory antibody mediated autoimmune disorders with an anti-CD20 monoclonal antibody (rituximab) + Author Affiliations Correspondence to: Dr H A Liebman, Division of Hematology, Kenneth Norris Jr Cancer Center, MS 34, 1441 Eastlake Ave, Los Angeles, CA 90033, USA; liebman@hsc.usc.edu Accepted 12 February 2002 Abstract Background: Rituximab, a chimeric monoclonal anti-CD20 antibody, has recently been used for the treatment of refractory antibody mediated autoimmune diseases such as immune mediated thrombocytopenia and haemolytic anaemia.
Patients: Because of its novel mechanism of action, rituximab was used to treat three patients with refractory systemic antibody mediated autoimmune disorders. The first patient, a 71 year old woman with idiopathic type II mixed essential cryoglobulinaemia, had both dermatological and neurological manifestations with marked renal disease attributed to her cryoglobulinaemia. Results: Treatment with rituximab resolved all clinical and laboratory manifestations in the three patients. Case 1 Table 1 Patient characteristics and treatment summary Case 2 Case 3.