Determination of pH turning point with pH mapping of the gastroesophageal junction: an alternative technique to orientate esophageal pH monitoring.

Manometric location of the lower esophageal sphincter (LES) has been mandatory before esophageal pH monitoring, despite costs and discomfort related with esophageal manometry. The aims of the study were: (i) to map the pH of the gastroesophageal junction (GEJ) to determine a pH turning point (PTP) and its relation with LES; and (ii) to test the feasibility of this technique to orientate esophageal pH monitoring. We studied 310 adult patients who underwent esophageal manometry and pH monitoring off acid-suppressive therapy. GEJ pH mapping was carried out by step-pulling the pH sensor from 5 cm below to 5 cm above LES, and a PTP was determined when pH changed from below to above 4, in centimeters from the nostril. Thirty-six patients referred only for pH monitoring were studied with pH sensor placed at 5 cm above the PTP. Out of 310 patients, a PTP was found in 293 (94.5%): inside LES in 86.3%, into the stomach in 8.2% and in the esophageal body in 5.5% of patients. The median distance between PTP and place where pH sensor monitored reflux was 8 cm. Among 36 patients who performed pH monitoring without LES manometry, there was no gastric monitoring during reflux testing. In adult patients investigated off acid suppressive therapy, GEJ pH mapping with reflux monitoring 5 cm above the PTP can be an alternative technique to perform esophageal pH monitoring when LES manometry is not available. Additional studies are needed before the widespread use of GEJ pH mapping in the clinical practice.

Renal metastasis from prostatic adenocarcinoma: a potential diagnostic pitfall.

We report a case of renal metastases from prostate cancer to show that the possibility of tumor metastasis, although rare, should always be considered in the differential diagnosis of renal mass.

Pulmonary tuberculosis revealed by lupus vulgaris in an immunocompetent patient.

A seventy-four-year-old patient had lupus vulgaris associated with the nodular, confluent ulcerated type of pulmonary tuberculosis. The diagnosis had been missed on several occasions. The presence of cutaneous tuberculosis in developed countries is emphasized again. It is also stressed that chronic dermatosis of unknown nature in an immunocompetent patient may have a tubercular origin. Complete resolution of the disease was achieved after almost two years of anti-tubercular therapy.

Detection of Chlamydia pneumoniae but not Helicobacter pylori in atherosclerotic plaques of aortic aneurysms.

Recent reports suggest an association between Chlamydia pneumoniae and Helicobacter pylori bacteria and atherosclerosis. We studied 51 patients (mean age, 68.3 years) who underwent abdominal aortic aneurysm surgery. For each patient we performed a microimmunofluorescence test for immunoglobulin G (IgG), IgA, and IgM antibodies to C. pneumoniae specific antigen (TW-183). Anti-H. pylori antibodies were determined by means of an EIA-G test. Each aortic aneurysm surgical specimen was sampled into multiple sections of 0.3 cm2 each and frozen at -20 degrees C. Two samples of each aneurysm were used for a nested PCR with two sets of C. pneumoniae and two sets of H. pylori specific primers. Specimens were treated with a solution containing 20 mM Tris-HCl, Tween 20-Nonidet P-40 (0.5% [vol/vol] each), and 100 micrograms of proteinase K per ml and incubated at 60 degrees C for 1 h and at 98 degrees C for 10 min. DNA was extracted twice with phenol-chloroform-isoamylic alcohol and precipitated with sodium acetate-ethanol by standard methods. Forty-one patients were seropositive for C. pneumoniae with past-infection patterns in 32 patients (16 < or = IgG < 512; 32 < or = IgA < 256) and high antibody titers in 9 patients (IgG > or = 512). In 26 of 51 patients, C. pneumoniae DNA was detected in aortic aneurysm plaque specimens. Of these patients, 23 had a serologic past-infection pattern, 2 had an acute reinfection pattern, and 1 was seronegative. Forty-seven of 51 patients were seropositive for H. pylori. In all cases PCR showed no evidence of H. pylori presence in plaque specimens. This study provides data on a possible C. pneumoniae involvement in the pathogenesis of aortic aneurysm and additional evidence for an association between this agent and atherosclerosis. Conversely, notwithstanding a high H. pylori seroprevalence observed, our results tend to rule out the possibility of a direct involvement of H. pylori in atherosclerosis.

Acute exacerbations of asthma in adults: role of Chlamydia pneumoniae infection.

Respiratory infections precipitate wheezing in many asthmatic patients and may be involved in the aetiopathogenesis of asthma. Several studies have demonstrated that viral infections may provoke asthma. Bacterial infections seem to play a minor role. However, Chlamydia pneumoniae has been recently reported as a possible cause of asthma. The aim of the present study was to evaluate the role of C. pneumoniae infection in acute exacerbations of asthma in adults. Seventy four adult out-patients with a diagnosis of acute exacerbation of asthma were studied. Acute and convalescent (> or = 3 weeks) serological determination of antibodies to cytomegalovirus, respiratory syncytial virus, adenovirus, influenza A and B, parainfluenza 1 and 3, Mycoplasma pneumoniae and Legionella pneumophila were performed by means of immunofluorescence tests. C. pneumoniae specific antibodies were detected by two microimmunofluorescence tests using a specific antigen (TW-183) and a kit with three chlamydial antigens. Pharyngeal swab specimens were also obtained for C. pneumoniae identification. Samples for bacterial culture were obtained in patients with productive cough (15 out of 74 patients). Fifteen patients (20%) presented seroconversion to at least one of the studied pathogens. Seven were found to be infected by virus, six by C. pneumoniae alone, and one by M. pneumoniae. One more patient showed seroconversion to C. pneumoniae and cytomegalovirus.(ABSTRACT TRUNCATED AT 250 WORDS)

Two family outbreaks of Chlamydia pneumoniae infection.

During autumn 1992, we observed two unrelated family outbreaks of Chlamydia pneumoniae infection. Family A consisted of grandmother (aged 77 yrs), father (aged 41 yrs), mother (aged 38 yrs), daughter (aged 10 yrs), and two sons (aged 6 yrs and 3 months, respectively). The grandmother and daughter suffered from pneumonia, father from pharyngitis and bronchitis and the older son from mild bronchitis. No symptoms were recorded in the mother and younger son. Symptomatic subjects showed a fourfold increase in immunoglobulin G (IgG) titre for Chlamydia pneumoniae, determined by a microimmunofluorescence test with specific antigen (TW-183). Other serological studies against Mycoplasma pneumonia, Legionella pneumophila, influenza virus type A and B, adenovirus and respiratory syncytial virus (RSV) were negative. Sputum culture gave a positive result for Haemophilus influenzae, colony forming units (cfu) = 10(4).ml-1 in the grandmother. No serum positivity was recorded in the mother and younger son, who remained asymptomatic. All symptomatic patients were successfully treated with macrolides. Family B consisted of mother (aged 63 yrs) and daughter (aged 36 yrs). Both suffered from Chlamydia pneumoniae pneumonia. Diagnosis was made by means of serological microimmunofluorescence test, and direct identification using an indirect immunofluorescence test on pharyngeal swab. Sputum culture and other serological tests remained negative. Both patients were successfully treated with macrolides. These observations emphasize the relevance of Chlamydia pneumoniae in family cluster respiratory infections.

Incidence of community-acquired pneumonia caused by Chlamydia pneumoniae in Italian patients.

The incidence of Chlamydia pneumoniae as a cause of community-acquired pneumonia was evaluated in a one-year prospective study in 108 patients with community-acquired pneumonia. The bacteriological diagnosis was based on culture of sputum or bronchial aspirate and examination of acute and convalescent phase sera for Mycoplasma pneumoniae, Legionella pneumophila and Chlamydia pneumoniae. A definitive microbiological diagnosis was obtained in 58 (54%) patients. Chlamydia pneumoniae was the causative agent in 14 patients (13%) on the basis of positive serological tests; in 10 of the 14 patients Chlamydia pneumoniae was also detected by means of an indirect immunofluorescence test using pharyngeal swab specimens. In conclusion, Chlamydia pneumoniae seems to be a common etiological agent of community-acquired pneumonia, as increasingly reported in the last six to seven years.