Reference interval of pregnancy-associated plasma protein-a in healthy men and non-pregnant women.

OBJECTIVE: The serum pregnancy-associated plasma protein-A (PAPP-A) concentration is a predictor of ischemic cardiac events and renal impairment. However, the reference interval of PAPP-A has not been determined. This study determined the reference interval of PAPP-A in men and non-pregnant women. METHODS: The study enrolled 126 apparently healthy individuals (52 males and 74 females). The mean age of the men and women was 34.7 (range 20-66) years and 34.6 (range 18-65) years, respectively. Serum PAPP-A concentrations were determined using an ultrasensitive enzyme-linked immunoassay kit. Reference intervals were calculated using the bootstrap method. RESULTS: The results for three subjects were outliers, so the reference interval of PAPP-A was calculated using the data for 123 subjects. PAPP-A was undetectable in 26 subjects. The reference interval of PAPP-A for men and women (with the 90% confidence interval) was <22.9 ng/mL (19.7-23.3) and <33.6 ng/mL (25.2-36.7), respectively. In male subjects, serum PAPP-A levels of smokers [3.10 (UD, 7.30)ng/mL] were significantly lower than that of non-smokers [11.00 (UD, 24.4)ng/mL] (p<0.001) and there was a positive correlation between serum PAPP-A levels and subjects' age (r=0.439; p<0.001). CONCLUSIONS: The reference interval of PAPP-A differed for men and non-pregnant women. In clinical practice, <22.9 ng/mL for men and <33.6 ng/mL for non-pregnant women may be used as reference intervals for PAPP-A.

Does pregnancy-associated plasma protein A have a role in allergic rhinitis?

BACKGROUND: Pregnancy-associated plasma protein A (PAPP-A), also known as insulin-like growth factor binding protein 4 protease, is postulated to be a new inflammatory marker in various clinical situations such as cardiovascular events, dialysis, renal transplantation, and asthma. PAPP-A also is produced in high concentrations by trophoblasts during pregnancy. METHODS: We evaluated PAPP-A levels in allergic rhinitis patients and compared these with levels in healthy subjects. Thirty-one newly diagnosed allergic rhinitis patients and 29 healthy controls were included in the study. Serum PAPP-A, IgE, urea, creatinine, aspartate aminotransferase, creatine kinase (CK), CK-MB isoenzyme, total cholesterol, and triglyceride levels were determined. RESULTS: The serum PAPP-A level was significantly higher (p = 0.013) in the allergic rhinitis group (6.1 +/- 2.9 mU/L) than in the control group (4.5 +/- 1.7 mU/L). The PAPP-A level in patients with allergic rhinitis and asthma (6.1 +/- 2.3 mU/L) was not significantly different (p = 0.959) from that in patients with allergic rhinitis alone (6.1 +/- 3.3 mU/L). The serum PAPP-A level in allergic rhinitis patients who had turbinate hypertrophy (6.9 +/- 2.2 mU/L) had a tendency to be higher than that in patients who had no turbinate hypertrophy (5.5 +/- 3.2 mU/L); however, this difference was not statistically significant (p = 0.151). CONCLUSION: Increased PAPP-A activity may be involved in the inflammation and tissue remodelling that occurs in allergic rhinitis.

Do Turkish adults really have lower serum levels of high-density lipoprotein cholesterol?

BACKGROUND: Coronary heart disease is the leading cause of death in Turkey. The Turkish Heart Study and TEKHARF study have been carried out at various times and in different parts of Turkey and have suggested that the Turkish population has a low high-density lipoprotein-cholesterol (HDL-C) level. However, in our daily practice, mean HDL-C levels were not as low as previously reported. Here, we investigated the lipid profile, especially the HDL-C level, in the population of the Duzce region of northwest Turkey. METHODS: Serum triglyceride, total cholesterol, and HDL-C levels were measured in 674 healthy volunteers (398 women and 276 men); low-density lipoprotein cholesterol (LDL-C) levels were calculated using the Friedewald equation. RESULTS: The mean serum HDL-C level was 46.1 +/- 9.8 mg/dl in men and 53.2 +/- 10.7 mg/dl in women; these values are higher than expected based on the Turkish Heart Study. The mean serum total cholesterol level was 196.7 +/- 43.2 mg/dL in men and 198.4 +/- 43.9 mg/dL in women; the mean LDL-C level was 119.6 +/- 34.9 mg/dL in men and 118.7 +/- 34.1 mg/dL in women; and the mean serum triglyceride level was 151.4 +/- 80.9 mg/dL in men and 132.1 +/- 68.9 mg/dL in women. CONCLUSIONS: Our finding that the HDL-C level in this population was higher than the previously reported levels in Turkey indicates that HDL-C levels may not be as low as previously thought. We believe that lower HDL-C levels that were previously reported might be due to the difference between techniques of analysis, nutritional status, and percent of subjects who were fasting in the day of analysis or improper subject inclusion which did not reflect the Turkish population causing selection bias.

Pregnancy-associated plasma protein-A and asthma.

Pregnancy-associated plasma protein-A (PAPP-A) is potentially a proatherosclerotic metalloproteinase and a new inflammatory marker. Investigators sought to evaluate the significance of PAPP-A in patients with asthma. Blood samples were collected from 35 patients and 20 control subjects. Serum PAPP-A was determined by enzyme-linked immunosorbent assay. PAPP-A levels of patients with asthma (8.1+/-5.0 mU/L) were higher than those of the control group (4.9+/-2.1 mU/L) (P<.01). A significant correlation was noted between serum PAPP-A concentration and asthma severity (r=.581; P<.01). Investigators concluded that PAPP-A may contribute to airway smooth muscle hyperplasia as an insulin-like growth factor-dependent insulin-like growth factor-binding protein-4 protease in patients with asthma.

Pregnancy-associated plasma protein A in dialysis patients.

BACKGROUND: Pregnancy-associated plasma protein A (PAPP-A) was recently described as a new marker of cardiovascular events and of inflammation in uremic patients. The aim of this study was to determine levels of PAPP-A in chronic dialysis patients and its possible relationships with renal osteodystrophy. METHODS: A total of 99 adult chronic hemodialysis patients, 14 peritoneal dialysis patients and 41 control subjects were included in the study. Serum PAPP-A, intact parathormone (iPTH), calcium, phosphorus and alkaline phosphatase (ALP) were measured. The correlations between PAPP-A and iPTH, calcium, phosphorus and ALP were determined. RESULTS: PAPP-A levels were significantly higher in peritoneal dialysis [4.5 (3.2-6.7) mU/L, median (interquartile range)], and hemodialysis patients [4.7 (3.8-6.5) mU/L] in comparison to control subjects [3.4 (3.0-5.0) mU/L] (p<0.05). In hemodialysis patients, post-dialysis PAPP-A levels [6.2 (4.7-9.4) mU/L] were significantly higher than pre-dialysis levels [4.7 (3.8-6.5) mU/L] (p<0.05). There was a weak but statistically significant positive correlation between serum PAPP-A and iPTH (r=0.216; p=0.041) and ALP (r=0.205; p=0.044) in the hemodialysis group. Correlation between the duration of dialysis therapy and PAPP-A levels was also significant (r=0.267; p=0.008) in the hemodialysis group. CONCLUSIONS: PAPP-A levels are elevated in acute coronary syndromes and are closely related to inflammation and oxidative stress. We conclude that PAPP-A levels are increased in dialysis patients and may reflect a greater degree of chronic inflammation than osteodystrophy in uremic patients.

Is there a relationship between cord blood pregnancy-associated plasma protein-A and birth weight and length?

BACKGROUND: Infants whose mothers had low serum pregnancy-associated plasma protein-A (PAPP-A) in the first trimester were observed to have intrauterine growth retardation. AIM: Suggesting that PAPP-A plays an important role in the availability and activity of insulin-like growth factors (IGFs), which affect growth, we aimed to investigate cord blood PAPP-A levels of infants with different birth lengths and weights. STUDY DESIGN AND OUTCOME MEASURES: The study included 97 full-term, live-birth neonates. After birth, their lengths and weights were measured. Cord blood PAPP-A levels were measured with an ultra sensitive enzyme-linked immunosorbent assay (ELISA). RESULTS: There was a significant negative correlation between cord blood PAPP-A levels and birth weight (r=-0.23; P=0.023) and length (r=-0.24; P=0.016). Using the classification made according to their length, it was found that newborns with short lengths had significantly higher mean PAPP-A levels than neonates with normal and long lengths (P=0.022; P=0.002, respectively), whereas the difference between infants with normal lengths and infants with long lengths was not found to be statistically significant (P>0.05). On the other hand, there was a difference between the mean PAPP-A levels of the neonate groups classified according to weight; however, these differences were not statistically significant (P>0.05). CONCLUSION: We concluded that increased cord blood PAPP-A levels were associated with birth length and weight decreases; however, PAPP-A levels affected birth length more than birth weight.

Transient silent ischemia after percutaneous transluminal coronary angioplasty manifested with a bizarre electrocardiogram.

Silent myocardial ischemia is recognized as a common manifestation after percutaneous coronary interventions possibly due to induction of coronary artery spasm. A 54-year-old man was performed primary percutaneous transluminal coronary angioplasty with the diagnosis of acute myocardial infarction. His 18-hour control electrocardiogram showed big-notched inverted T waves in precordial, III, and aVF leads without any chest pain. These bizarre electrocardiographic findings were restored after a brief period indicating silent ischemia that is caused by coronary artery spasm.

HLA-DR B1 and DQ B1 polymorphisms in patients with coronary artery ectasia.

OBJECTIVES: The purpose of our study was to evaluate the significance of polymorphisms in HLA class II genes in coronary artery ectasia (CAE) patients. METHODS AND RESULTS: Twenty-six patients with CAE without associated cardiac defects were enrolled in the study. CAE was defined as luminal dilation of 1.5- to 2.0-fold of normal limits. Ninety-five healthy subjects who were donors for different organ transplantations, were chosen as control group. Physical examination, electrocardiography and chest X-ray were completely normal in these cases. Both the patients and the control group were screened and compared for their HLA class II genotypes. HLA-DR B1*13, DR16, DQ2 and DQ5 genotypes were significantly more frequent in the patient group. When the known risk factors of coronary heart disease were compared in the patients carrying these genotypes with the non-carrying group, no significant differences were encountered. CONCLUSIONS: HLA-DR B1*13, DR16, DQ2 and DQ5 may be associated with the pathogenesis and increase the risk of CAE.

In vivo effect of losartan on platelet aggregation in patients with hypertension.

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 +/- 12.8 and 149.2 +/- 17.3 mmHg, respectively. Mean DBP decreased from 93.7 +/- 8.2 to 87.7 +/- 10.3 mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% +/- 24.3% before and 58.3% +/- 18.1% after the treatment. The same variables with ristocetin were 66.8% +/- 21.6% and 60.8% +/- 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.