The relationship between circulating C-reactive protein concentrations and potential cytokine and receptor mediators (interleukin-6, leukaemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), soluble IL-6 receptor, soluble gp130, soluble TNF receptor, interleukin-1 receptor antagonist and interleukin-8 (IL-8)) of this acute phase protein were examined in healthy subjects (n ¼ 11) and patients with non-small-cell lung cancer (n ¼ 50). Leukaemia inhibitory factor and CNTF were below detection limits in all controls and patients. C-reactive protein, interleukin-6, soluble gp130, soluble TNF receptor, interleukin-1 receptor antagonist and IL-8 concentrations were significantly elevated in cancer patients (Pp0.001). Cancer patients with elevated C-reactive protein concentrations had greater concentrations of interleukin-6 (Po0.01) and interleukin-1 receptor antagonist (Po0.05). On regression analysis only interleukin-6 was independently associated with C-reactive protein (r ¼ 0.616, Po0.001). Interleukin-6 is an important independent mediator of elevated C-reactive protein concentrations in patients with non-small-cell lung cancer.
A 63 year old woman visits her doctor with a three month history of fatigue and generalised joint pains. Her medical history is unremarkable and she reports no recent stress, infection, or weight loss. There are no abnormalities on clinical examination. Haemoglobin, creatinine, and electrolytes, liver enzymes, glucose, inflammatory markers, and thyroid function tests are normal. Ferritin, iron, transferrin, and transferrin saturation are also requested.This article discusses some situations in which ferritin and iron studies might be helpful and how to avoid common pitfalls in their interpretation. What are the next investigations?The doctor in this case requested iron studies to investigate the possibility of iron overload and to screen for haemochromatosis. Iron studies are also commonly indicated in clinical practice to investigate iron deficiency, or to monitor response to treatment for these conditions (box 1).Conventional laboratory tests of iron status are often referred to as "iron studies." They include tests for serum ferritin, iron, transferrin, or total iron binding capacity (TIBC), and transferrin saturation.Iron is a key component of haemoglobin in red blood cells, myoglobin in muscle, and many metalloproteins and enzymes. It is essential for uptake of oxygen and its delivery to tissues, utilisation of oxygen by muscle cells, and mitochondrial energy production. 3 Normal iron metabolism and regulation is outlined in Figure 1⇓. The adult male body contains 3-5 g of iron. Less than 0.1% of total body iron stores circulate in plasma. Dietary Fe 3+ is reduced to Fe 2+ and transported into the enterocyte by the divalent metal transporter DMT1. Iron is exported across the basolateral membrane via the iron export protein ferroportin 1 or stored as ferritin. Transferrin bound iron binds to transferrin receptor 1 (TFR1) and is taken up into the cell via receptor mediated endocytosis. Expression of TFR1 is regulated locally by the iron demands of the cell, via binding of iron regulatory proteins. Old or damaged erythrocytes are removed from the circulation by splenic macrophages. Iron is removed from haem by haem oxygenase 1, and either stored as ferritin or released into the circulation.Regulation of iron release at a systemic level is mediated by the peptide hormone hepcidin (produced predominantly by hepatocytes) and has an inhibitory effect on iron release from cells and dietary iron absorption. Expression is controlled by complex signalling pathways. 1 What is included in iron studies?Ferritin-is the intracellular storage form of iron. A very small amount is found in serum. In inflammation, liver disease, and malignancy, ferritin levels can rise because ferritin is an acute phase protein. 4 In these patients, ferritin can appear either falsely high or normal, when in reality stores are low.Serum iron-refers to ferric ions (Fe 3+ ) bound to serum transferrin. Serum iron concentration is highly variable and is affected by dietary iron intake, inflammation, and infection. 5Transferrin-is the principal iron...
Background: Primary aldosteronism (PA), the most common secondary cause of hypertension, can be screened for using the aldosterone/renin ratio. This ratio is raised in PA and its accuracy depends on the ability to measure plasma renin at extremely low concentrations. Methods: We compared two different procedures for assessing plasma renin. The conventional method, which measures plasma renin activity (PRA), is technically demanding and laborious, and the Diasorin Liaison w method, which measures plasma renin concentration (PRC), is an automated immunoassay. Results from each method were used to calculate the aldosterone/renin ratio (ARR) and the performance of the Diasorin Liaison w method compared with that of the conventional assay using receiver operator characteristic curves. Results: The analytical and functional sensitivity of the PRC method were 2.1 and 5 mIU/mL, respectively. Intra-and interassay precision were ,7.2% and 10.4%, respectively. There was significant (9%) prorenin interference. Samples with PRA . 1.0 ng/mL/h showed significant correlation with PRC (r ¼ 0.93; P , 0.05; n ¼ 146); however, with PRA , 1.0 ng/mL/h, no significant correlation occurred (r ¼ 0.14; P , 0.05; n ¼ 79). An aldosterone ( pmol/L)/PRC(mIU/mL) ratio of .35, in patients with aldosterone .300 pmol/L, resulted in 100% sensitivity and 93% specificity, when compared with the commonly accepted aldosterone ( pmol/L)/PRA (ng/mL/h) ratio of .750, in identifying patients who may suffer from PA. Conclusion: This study indicates the feasibility of using the automated PRC assay as a replacement for the conventional manual PRA assay in calculating the ARR as a first-line screen for PA.
SummaryBACKGROUND Conventional hormone replacement therapy (HRT) containing conjugated equine oestrogen (CEE) and medroxyprogesterone acetate (MPA) increases triglyceride, C-reactive protein (CRP) and coagulation Factor VII concentrations, potentially explaining their increased coronary heart disease (CHD) and stroke risk.
Serum PTH-(1-84), PRL, and adjusted calcium concentrations were determined at 30-min intervals for a 24-h period in six normal adult men. PTH-(1-84) and PRL both exhibited two peaks of increased secretion [1600-1900 and 0200-0600 h for PTH-(1-84); 2000-2200 and 0400-0800 h for PRL]. For each subject there was a striking similarity in the magnitude of secretion of the two hormones and a consistent temporal relationship. Thus, the maximum correlation coefficients of 0.62-0.83 were obtained for the six subjects when the PRL surge lagged that of PTH-(1-84) by 0.5-3.5 h. In contrast, the correlation between PTH-(1-84) and adjusted calcium was weaker (r = -0.36 to -0.66) and showed no consistent temporal relationship (0.0-10.5 h). These data support the concept of higher center control of PTH-(1-84) secretion with the possible involvement of factors common to the control of PRL secretion.
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