Suprarenal artery stenosis may be mistaken for renal artery stenosis in Doppler studies.

There are several limitations in using colour-flow-Doppler (CFD) to diagnose renal artery stenosis. This report describes a case of "false positive" stenosis of the renal artery diagnosed using CFD. A patient affected by arterial hypertension and with a suspected stenosis of the renal artery was examined using CFD. However, the patient was in fact suffering from suprarenal artery stenosis.

Cardiac troponin I in acute coronary ischemic syndromes. Epidemiological and clinical correlates.

UNLABELLED: The present study was aimed to investigate the variability of cardiac troponin I (cTnI) in the first week of acute myocardial infarction (AMI) course with regard to some epidemiological and clinical parameters and in patients with non-AMI acute coronary ischemic disease. Serum cTnI was assayed in 82 patients, 42 affected with AMI and 40 with non-AMI acute coronary ischemic disease, on admission in coronary care unit, within 6 h after the onset of symptoms, and, in AMI group, on 24 and 48 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th day. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died, >60 years old and with anterolateral necrosis are constantly higher than in survivors, <60 years old and with inferoposterior necrosis, respectively. (2) The cTnI concentration is already returned in normal range at 7th day of illness course in survivors and in patients with inferoposterior AMI. (3) The 24-h peak level of cTnI is significantly higher in fibrinolysed than in patients who didn't undergo fibrinolysis. (4) A direct correlation between the cTnI value and the Killip class is present either in the whole group or in any subset of patients and the progressive decrease of the cTnI concentration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is higher in unstable than in stable anginous patients and normal subjects but not in stable angina with respect to healthy controls. CONCLUSIONS: (1, 2) The less increase and the early return in normal range of cTnI serum levels which occur in AMI subgroups with a better prognosis could be regarded as favourable prognostic signs. (3) The persistent higher values of cTnI in fibrinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relase of cTnI from myocardium represents a reliable biochemical marker following the wash-out associated to a successful reperfusion. (4) The persistent increase of cTnI in AMI patients with advanced Killip class suggests that the high cTnI values are not only a strong index of myocardial necrosis but also of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (5) The hypothesis can be reasonably advanced that the higher values of cTnI in unstable angina are due to focal areas of myocardial necrosis undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission.

[Troponin I in acute ischemic cardiopathy]. / La troponina I nella cardiopatia ischemica acuta.

BACKGROUND: The present study was aimed at investigating cardiac troponin I values in the first week of acute myocardial infarction and in non-infarct acute coronary ischemic syndromes. METHODS: Eighty-two patients, 42 with acute myocardial infarction, 10 with stable angina and 30 with primary unstable angina, were enrolled in the study. Blood was collected within 6 hours of symptom onset and, in the group with acute myocardial infarction, after 24 and 48 hours, and on day 7. RESULTS: Serum troponin I increased within the first 6 hours of myocardial infarction, reached the peak after 24 hours, at 48 hours it decreased, and remained above the normal range until day 7. However, troponin I values 1) were constantly higher in patients who died, in those > 60 years old and in those with antero-lateral necrosis than in survivors, in those < 60 years old and in those with infero-posterior necrosis, respectively; 2) returned to normal range on day 7 in survivors and in patients with infero-posterior acute myocardial infarction; 3) were significantly higher in fibrinolysed patients than in those who did not undergo thrombolysis; 4) were higher in patients classified as Killip class > 2. Serum troponin I values were in the normal range in non-infarct acute coronary ischemic syndromes, but were higher in unstable than in stable angina. CONCLUSIONS: The lesser increase and the early return to the normal range of cardiac troponin I levels in the subgroups of patients with myocardial infarction having a better clinical course could be regarded as a favorable prognostic sign. Since the persistent higher values of cardiac troponin I in fibrinolysed subjects are associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent post-thrombolysis release of cardiac troponin I from the myocardium represents a biochemical marker of a successful reperfusion. The persistent high cardiac troponin I values in patients with advanced Killip class suggest that the neuropeptide is an index of ongoing myocyte injury and hemodynamic impairment as well. The higher values of cardiac troponin I in unstable angina are probably due to focal areas of myocardial necrosis undetectable by conventional enzymatic serum markers.

Increased release of interleukin-6 by oesophageal mucosa in children with reflux oesophagitis.

OBJECTIVE: To evaluate the release of interleukin-6 (IL-6) by oesophageal mucosa and to establish the serum levels of IL-6 and C-reactive protein (CRP), and plasma fibrinogen in children with reflux oesophagitis. DESIGN: In a prospective study, IL-6 release by tissue fragments obtained from oesophageal biopsies was determined and serum IL-6 and CRP as well as plasma fibrinogen were analysed. METHODS: The study population comprised ten children with reflux oesophagitis, diagnosed on the basis of 24 h oesophageal pH monitoring and endoscopy with biopsies. Ten children with recurrent abdominal pain were studied for comparative purposes. Biopsy tissue fragments were processed to obtain a cell suspension and the release of IL-6 was determined in culture medium. Serum IL-6 levels were measured by ELISA, serum CRP by turbidimetry, and plasma fibrinogen by spectrophotometry. RESULTS: Oesophageal cells obtained from reflux oesophagitis patients synthesize and release in vitro a significantly higher amount of IL-6 than controls (71.26+/-19.5 versus 31.67+/-8.02 pg/10(6) cells; P<0.01). Serum IL-6, serum CRP and plasma fibrinogen levels were not statistically different between patients with reflux oesophagitis and controls. CONCLUSIONS: These results suggest a short-term action of IL-6 since its effects could be exerted only in the microenvironment of the oesophageal mucosa.

Adult height in girls with central precocious puberty treated with gonadotropin-releasing hormone analogues and growth hormone.

GnRH analogues (GnRHa) represent the treatment of choice in central precocious puberty (CPP), because arresting pubertal development and reducing either growth velocity (GV) or bone maturation (BA) should improve adult height. However, in some patients, GV decrease is so remarkable that it impairs predicted adult height (PAH); and therefore, the addition of GH is suggested. Out of twenty subjects with idiopathic CPP (treated with GnRHa depot-triptorelin, at a dose of 100 microg/kg im every 21 days, for at least 2-3 yr), whose GV fall below the 25th percentile for chronological age, 10 received, in addition to GnRHa, GH at a dose of 0.3 mg/kg x week s.c., 6 days weekly, for 2-4 yr; and 10 matched for BA, chronological age, and duration of GnRHa treatment, who showed the same growth pattern but refused GH treatment, served to evaluate the efficacy of GH addition. No patient showed classical GH deficiency. Both groups discontinued treatment at a comparable BA (mean +/- SEM): 13.2 +/- 0.2 in GnRHa plus GH vs. 13.0 +/- 0.1 yr in the control group. At the conclusion of the study, all the patients had achieved adult height. Adult height was considered to be attained when the growth during the preceding year was less than 1 cm, with a BA of over 15 yr. Patients of the group treated with GH plus GnRHa showed an adult height significantly higher (P < 0.001) than pretreatment PAH (160.6 +/- 1.3 vs. 152.7 +/- 1.7 cm). Target height (TH) was significantly exceeded. The group treated with GnRH alone reached an adult height not significantly higher than pretreatment PAH (157.1 +/- 2.5 vs. 155.5 +/- 1.9 cm). TH was just reached but not significantly exceeded. The gain in centimeters obtained, calculated between pretreatment PAH and final height, was 7.9 +/- 1.1 cm in patients treated with GH combined with GnRHa; whereas in patients treated with GnRHa alone, the gain was just 1.6 +/- 1.2 cm (P = 0.001). Furthermore, no side effects have been observed either on bone age progression or ovarian cyst appearance and the gynecological follow-up in the GH-treated patients (in comparison with those treated with GnRHa alone). In conclusion, a gain of 7.9 cm in adult height represents a significant improvement, which justifies the addition of GH for 2-3 yr during the conventional treatment with GnRHa, especially in patients with CPP, and a decrease in GV so marked as to impair PAH, not allowing it to reach even the third centile.