This study looks at the possible role of some non-traditional risk factors for premature coronary artery disease (CAD) and assesses the presence of relationship between these factors and the traditional cardiovascular risk factors. The study subjects (n=45) are divided into three groups comprising 15 premature CAD patients without traditional cardiovascular risk factors (group I); 15 premature CAD patients with one or more traditional cardiovascular risk factors (group II); and 15 healthy normal control subjects matched for age and sex (group III). Estimation of plasma homocysteine (Hcy) and plasminogen activator inhibitor-1 (PAI-1) is performed by enzyme-linked immunosorbent assay (ELISA); plasma folic acid by radioimmunoassay; plasma lipoprotein a (Lpa) by turbidimetry; and plasma lipids by colorimetry. Results showed a significant association between elevated Hcy and low folate levels and premature CAD in both patient groups. Also, a significant association was seen between elevated PAI-1 and CAD in the two patient groups, and between CAD and high levels of Hcy and triglycerides, as well as a low level of high-density lipoprotein cholesterol. Lpa showed significant association with premature CAD only in group II. Thus, Hcy, folic acid and PAI-1 might serve as independent risk factors for premature CAD in patients both with and without traditional coronary risk factors. However, Lpa might confer an additional coronary risk factor only in the presence of traditional risk factors.
The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-alpha (TNF alpha) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group 1 was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNF alpha, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNF alpha levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNF alpha levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNF alpha levels. Thus, elevated serum TNF alpha in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.
Introduction:
Hypoxia is a major feature of hepatocellular carcinoma (HCC). The master hypoxamir, MIRNA-210, controls many carcinogenic pathways. Hypoxia can affect mitochondrial DNA copy number (MTCN), which could impair many mitochondrial functions, including electron transport chain (ETC). Vitamin K2 (VK2) is crucial for preserving ETC integrity.
Aim of the study:
To evaluate the role of MTCN, MIRNA-210 and VK2 in HCC prediction, prevention and personalized treatment.
Methodology:
60 cirrhotic patients with HCC (group I) classified into three sub-groups according to BCLC staging (20 patients each); Group (IA): Stages 0/A, (IB): stage B and (IC): stages C/D. Group II comprised 60 cirrhotic patients without HCC. Group III included 60 healthy controls. All participants were evaluated clinically, circulating MIRNA-210 expression and MTCN were assessed by real time polymerase chain reaction and VK2 levels were measured by ELISA.
Results
MIRNA-210 was higher in group I compared to other groups (P < 0.001). VK2 and MTCN were lower in group I than in other groups (P = 0.001 in both parameters). MIRNA-210 was higher in subgroup 1C than other sub-groups (P < 0.001). Both VK2 and MTCN were lower in subgroup IC than in subgroups IA and IB (P = 0.042, P < 0.001 respectively). In group I, Both VK2 and MTCN were negatively correlated with MIRNA-210 (p = 0.001, p < 0.001 respectively), but positively correlated with each other (p < 0.001). Same pattern followed in subgroups of group I and in group II.
Conclusion
Results suggest a potential predictive role of the studied markers in HCC, hence the possibility of early prevention and personalized treatment.
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