Khat is a natural stimulant from the Catha edulis plant, which grows mainly in Yemen. The liver has been suspected to be vulnerable to the harmful effects of khat use.
The aim of the study was to investigate the effect of khat chewing on the liver function in healthy Yemeni individuals.
Liver function tests were performed on 30 chronic khat chewers (group I) and 20 individuals who did not chew khat (group II).
Twenty percent of group I and only 5% of group II reported abnormally elevated alanine transaminase (ALT) levels, with no statistically significant difference between the mean ALT values (P=0.208); 13.3% of group I showed elevated aspartate aminotransferase levels (P=0.058). With regard to other liver function tests there was no statistically significant difference between the two groups. ALT levels increased with increasing duration of khat chewing.
Chronic khat chewing causes subclinical hepatocellular damage, whereas transient khat chewing has no effect on the liver function.
Obesity is commonly associated with insulin resistance and hyperinsulinemia and is the most important risk factor for type 2 diabetes. Visfatin is an adipokine that exerts insulin-mimetic effects that stimulate muscle and adipocyte glucose transport and inhibit hepatocyte glucose production.
The aim of this study was to assess levels of visfatin and its relationship to obesity and insulin resistance in type 2 diabetes mellitus.
This study included 40 patients with type 2 diabetes as the patient group: 20 of them were obese (BMI≥30) and 20 were not (BMI<25). Forty apparently healthy individuals matched for age and sex were included as the control group: 20 of them were obese (BMI≥30) and the other 20 were not (BMI<25). All patients and controls underwent history taking, physical examination including determination of BMI, and the following laboratory investigations: determination of levels of fasting blood glucose, 2 h postprandial blood glucose, serum cholesterol, triglycerides, fasting insulin, and fasting visfatin; kidney and liver function tests and calculation of homeostasis model of assessment-insulin resistance (HOMA-IR) were also performed. Neither the patients nor controls suffered from any chronic disease other than diabetes.
The results of this study revealed a highly significant increase in the fasting serum insulin level, HOMA-IR, and fasting serum visfatin level among diabetic patients (26.10±6.04 µIU/ml, 12.18±5.24, 36.70±6.86 ng/ml, respectively) when compared with controls (12.10±3.45 µIU/ml, 2.42±0.79, 13.63±3.98 ng/ml, respectively; P<0.01). Fasting insulin levels, HOMA-IR, and visfatin levels were significantly higher in obese diabetic patients (31.13±4.34 μIU/ml, 14.71±6.22, 42.36±4.11 ng/ml, respectively) than in obese controls (14.31±3.11 µIU/ml, 2.89±0.77, 16.72±3.16 ng/ml, respectively; P<0.01). Visfatin levels were higher in nonobese diabetic patients than in nonobese controls. Moreover, visfatin levels were higher in obese diabetic patients (31.04±3.49 ng/ml) than in nonobese diabetic patients (10.54±1.53 ng/ml; P<0.01). The present study revealed a highly significant positive correlation between levels of visfatin and fasting insulin in both obese and nonobese diabetic patients. Although there was a significant positive correlation between visfatin levels and HOMA-IR, there was no significant correlation between visfatin levels and BMI in obese diabetic patients.
Visfatin levels are increased in patients with type 2 diabetes regardless the degree of adiposity.
Diabetic nephropathy is one of the debilitating complications of type 2 diabetes and the leading cause for end-stage renal disease requiring renal replacement therapy. Currently identified risk factors do not fully explain the susceptibility of some patients to diabetic nephropathy. Peroxisome proliferator-activated receptor γ (PPARγ) Pro12Ala gene polymorphisms modulate insulin sensitivity and oxidative stress in diabetic patients, and conflicting data exist on its association with kidney disease in diabetes. Several polymorphisms in another immune modulator set of genes, the C–C chemokine receptor 5 (CCR5) genes, were associated with diabetic nephropathy. However, CCR5δ 32 gene polymorphisms were not studied in patients with diabetic nephropathy. The aim of this study was to assess the association between polymorphisms in both PPARγ Pro12Ala and CCR5δ 32 genes and the presence of diabetic nephropathy in Egyptian patients with type 2 diabetes.
We included 51 patients having type 2 diabetes for at least 5 years. They were all normotensive patients selected from the outpatient clinic with no other clinically identifiable risk factor for kidney disease. Genotype detection for PPARγ Pro12Ala and CCR5δ 32 gene polymorphisms was carried out using the PCR technique. Clinical data, HbA1c levels, lipid profile, and fasting and postprandial blood sugar levels were recorded. Serum creatinine levels and the urinary albumin/creatinine ratio were measured to stratify the participants according to the presence or absence of diabetic nephropathy.
Age, sex, BMI, HbA1c, and duration of diabetes were not significantly different among patients with and those without diabetic nephropathy. Diabetic nephropathy patients had a significantly higher urinary albumin/creatinine ratio and lower estimated glomerular filtration rate levels (P<0.0001). Homozygotes for the PPARγ Pro12Ala Pro–Pro allele constituted 82% of our total study population and 86.4% of patients with diabetic nephropathy; the remaining were Pro–Ala heterozygotes, and we had no Ala–Ala homozygotes. The odds ratio for diabetic nephropathy in Pro–Pro homozygotes was 3.5 (P=0.075, 95% confidence interval, 0.8–15). The Pro allele was present in 75% of patients with nephropathy and 50% of those without nephropathy. The Pro allele was significantly associated with diabetic nephropathy compared with the Ala allele (odds ratio=3.5, P=0.012, 95% confidence interval, 1.3–15). With regard to the CCR5δ 32 insertion/deletion genotype, 24 patients were homozygous for the insertion polymorphism, two were homozygous for the deletion polymorphism, and the remaining 25 were insertion/deletion heterozygotes. There was no significant difference between nephropathic and non-nephropathic patients as regards the CCR5δ 32 genotype (P=0.3) or the frequency of allele distribution (P=0.6).
The Pro allele of PPARγ Pro12Ala was associated with diabetic nephropathy. Polymorphisms in the CCR5δ 32 gene did not show an association with diabetic nephropathy.
Renal failure is a common and serious complication of long-standing diabetes mellitus. Diabetes is the most common cause of end-stage renal failure. Transforming growth factor-β (TGF-β) is one of the major growth factors involved in extracellular matrix accumulation in fibrotic disorders including diabetic nephropathy.
The aim of the present study was to evaluate the serum level of TGF-β as a marker for the development and progression of diabetic nephropathy.
This work included 40 patients with diabetes and 40 healthy controls with matched age and sex. Individuals with diabetes included 25 patients with type 2 diabetes and 15 with type 1 diabetes. We considered the presence of hypertension, use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, and the degree of proteinuria. All patients were subjected to careful history taking, thorough physical examinations, and fundus examination. Routine laboratory tests such as analysis of complete blood count and determination of erythrocyte sedimentation rate were carried out to rule out patients with malignancy or autoimmune disease. Kidney function tests (blood urea and serum creatinine), complete urine analysis, and estimation of 24-h urinary protein or albumin, creatinine clearance, blood glucose measurement (fasting and 2 h postprandial), serum TGF-β level, and microalbuminuria were also carried out.
The serum levels of TGF-β were statistically significantly higher in patients with diabetes compared with normal healthy people. The serum TGF-β level was statistically significantly higher in patients with diabetes with overt nephropathy compared with those without it. There was a statistically significant decrease in TGF-β levels in patients with diabetes who were taking angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers compared with those who were not taking such medications.
Serum TGF-β level increases in patients of both type 1 and type 2 diabetes and in those with diabetic nephropathy. TGF-β is considered one of the major mediators of diabetic renal fibrogenesis that results in end-stage renal disease.
The aim of this study was to report a rare case of a leaking thoracic aorta aneurysm in a female patient with massive pulmonary embolism. A 70-year-old woman with hypertension who had suffered a cerebral vascular accident 2 years ago presented with urinary tract infection, dehydration, and anemia. While in hospital, she was diagnosed with pulmonary embolism, and anticoagulation therapy was started using heparin. As the tachycardia persisted with a further drop in hemoglobin levels, and because a new left-sided pleural effusion was revealed on chest radiograph, a chest CT with a CT angiography was performed. It revealed a large leaking aneurysm of the descending thoracic aorta. This was treated by inserting an endovascular stent. This rare case shows the importance of investigating for other serious coexistent causes of tachycardia in patients with pulmonary embolism during treatment.
Systemic inflammatory response syndrome (SIRS), sepsis, and severe sepsis influence total hepatic blood flow. However there are conflicting data on the time of its assessment, methodology, study design, and differentiation in terms of whether the condition is an experimental SIRS, sepsis, or a human clinical syndrome.
The aim of this study was to assess the total hepatic blood flow and the contribution of hepatic arterial blood flow (HABF) and portal venous blood flow using a Doppler vascular ultrasound in SIRS, sepsis, and severe sepsis patients, aiming at a clear prognostic parameter that can predict the patient’s outcome.
There was a clear cutoff point of 16.09 ml/min for HABF, above which the hazard ratio for death was 5.6046, with a 95% confidence interval of 2.0078–15.6451 and a P-value of 0.0011 in late sepsis patients. The predictive potential for this HABF cutoff for patient mortality showed a sensitivity of 80%, specificity of 73.7%, positive predictive value of 70.6%, negative predictive value of 82.4%, 95% confidence interval of 0.612–0.907, and P-value of less than 0.0004. There was a significant positive correlation between the HABF and APACHE II scores (P=0.023). Cox regression analysis showed that only the APACHE II score and HABF were independent predictors for patients’ outcome.
Duplex ultrasound assessment was a useful bedside method for predicting mortality in late sepsis patients through estimation of HABF, with a reasonable predictive potential at a definite cutoff level.
The clinical implication of insulin resistance has extended beyond diabetes mellitus to include ischemic heart disease, dyslipidemia, hypertension, and features of metabolic syndrome. Nondiabetic patients with acute coronary syndrome and elevated admission insulin resistance index (AIRI) may have certain clinical angiographic and therapeutic strategies.
The study aimed to illustrate the value of AIRI in nondiabetic patients with acute coronary syndrome and identify the angiographic coronary artery disease severity in relation to AIRI.
This study was cross-sectional in design.
This study included 120 nondiabetic patients presenting with acute chest pain who were admitted to the coronary care unit. Admission glucose and insulin concentrations were measured and the AIRI was calculated. ECG was carried out and the patients were grouped as follows: those with unstable angina (UA) (40 cases) and those with acute myocardial infarction (AMI) (40 cases). They were compared with 40 patients with stable angina (SA) and a group of controls (40 individuals). The studied participants were examined clinically stressing on the other criteria for insulin resistance syndrome. The following laboratory tests were undertaken, including random plasma glucose, HBA1-c, lipid profile, cardiac enzymes (CK-MB, LDH), and troponin T. An angiographic study was carried out for patients from each diseased group and for 20 patients who had suffered a first attack in the SA group.
AIRI was significantly elevated in the AMI (3.9±0.1) and UA (3.01±0.2) groups when compared with the SA and control groups. AIRI was significantly higher in the AMI group when compared with the UA group. Coronary angiography revealed one coronary vessel involvement in 10, 20, and 10% of patients in the SA, UA, and AMI groups, respectively, whereas two-vessel involvement was detected in 0, 30, and 60% of patients in the SA, UA, and AMI groups, respectively. Three-coronary-vessel disease was not detected in the SA group but was evident in 5% of UA and 30% of AMI patients. The relation of AIRI in the studied groups on the basis of the &khgr;2-test revealed significant elevation of AIRI in the AMI and UA groups. Cases with three-vessel affection demonstrated higher AIRI.
Elevated AIRI can predict coronary artery events in nondiabetic patients with acute chest pain. Multiple coronary vessel involvement is common in such cases and suitable planned invasive therapeutic strategies have to be considered.
Changes in renal nitric oxide (NO) production have been associated with glomerular hyperfiltration, vascular permeability, albuminuria, glomerulosclerosis, and tubulointerstitial fibrosis. This study aimed at detection of the role of both inducible nitric oxide synthases (iNOS) and endothelial nitric oxide synthases (eNOS) expression in diabetic and nondiabetic nephropathy patients.
Renal biopsies and clinical data of 30 diabetic patients, 10 nondiabetic patients with renal impairment, and 10 control individuals were assessed for eNOS and iNOS expression.
Both glomerular eNOS and iNOS expression levels were increased in diabetic nephropathy patients and this was associated with peripheral arterial occlusive disease. In nondiabetic patients, increased serum creatinine was found to be associated with increased iNOS and eNOS expression, and, together with the control group, they showed increased iNOS expression in tubular and interstitial cells. An association between cigarette smoking and increased expression of both iNOS and eNOS was detected in diabetic patients.
The presence of iNOS is associated with tubular damage resulting in renal failure. The upregulation of NO in diabetes mellitus type 2 may explain the endothelial dysfunction that is associated with almost all diabetic complications.