C. Lenzi

Prevalence of Helicobacter pylori infection in male patients with osteoporosis and controls.

Cytokines that regulate bone turnover (tumor necrosis factor-α, interleukin-6, etc.) may influence the pathogenesis of skeleton disorders, such as osteoporosis. Since Helicobacter pylori infection increases the systemic levels of inflammatory cytokines, we investigated the possibility that this infection increases the risk of developing osteoporosis and affects the bone metabolism in a group of male patients with osteoporosis. We examined 80 osteoporotic male patients and 160 controls for serum antibodies to H. pylori and the CagA protein and determined, in patients alone, the most important biochemical and instrumental parameters of the disease. Fifty-one patients (63.7%) and 107 controls (66.8%) were seropositive for H. pylori infection (nonsignificant); 30 infected patients (58.8%) and 43 infected controls (40.1%) were positive for anti-CagA antibodies (P = 0.028; OR = 2.13). Levels of estradiol in infected CagA-positive patients were significantly lower than in infected CagA-negative patients (28.5 [SD = 10.18] vs. 39.5 [SD = 14.50] pg/ml; P = 0.002) and uninfected patients (35.2 [SD = 12.7] pg/ml; P = 0.028). Levels of urinary cross-laps(a marker of bone resorption) were increased in patients infected by CagA-positive strains compared to patients infected by CagA-negative strains (282.9 [SD = 103.8] vs. 210.5 [SD = 150.1] μ g/mmol; P = 0.048) and uninfected patients (204.3 [SD = 130.1] μ g/mmol; P = 0.016). Differences among uninfected and infected patients, independent of CagA status, were observed for other markers of bone turnover, but they did not reach statistical significance. Infection by CagA-positive H. pylori strains is more prevalent in men with osteoporosis, who show reduced systemic levels of estrogens and increased bone turnover. H. pylori infection by strains expressing CagA may therefore be considered a risk factor for osteoporisis in men.

Association of anti-GM1 antibodies but not of anti-cytomegalovirus, Campylobacter jejuni and Helicobacter pylori IgG, with a poor outcome in Guillain–Barré syndrome

Few reports exist on the influence of humoral immune responses, against microorganisms involved in infections preceding Guillain-Barré syndrome (GBS) and GM1, on clinical outcome. Nor is there any data on the relation between anti-Helicobacter pylori antibodies and prognosis in patients with GBS. To address these questions, we assayed and correlated serum anti-GM1 IgG and IgM and anti-H. pylori, anti-Campylobacter jejuni and anti-cytomegalovirus (CMV) IgG with duration of hospitalization of GBS patients and prognosis at discharge. Patients with anti-GM1 alone or associated with anti-H. pylori antibodies had significant longer hospitalization to reach a low clinical score at discharge than those without (P=0.004). A significant difference was also found for the association of anti-GM1 with anti-CMV antibodies (P=0.019). A weak but significant association of anti-GM1 and anti-C. jejuni antibodies with long hospitalization and worse prognosis at discharge was also found (P=0.02). The statistical significance increased when patients with anti-GM1 and anti-microorganism antibodies were compared with those displaying anti-H. pylori or anti-CMV only. These findings provide further evidence that the level of circulating anti-GM1 IgG plays a role in determining recovery from disability in GBS patients irrespective of other IgG against microorganisms causing infections preceding GBS.

Infection by CagA-positive Helicobacter pylori strains in patients with ischemic heart disease: prevalence and association with exercise-induced electrocardiographic abnormalities.

The role of H. pylori infection in increasing the risk of ischemic heart diseases (IHD) is still debated. We determined serologically the prevalence of overall H. pylori and CagA-positive H. pylori infection in 63 consecutive patients with IHD and 189 gender- and age-matched controls. We also determined in patients the influence of the infection and the CagA serological status on the results of an exercise ECG test and other parameters considered possible variables that may enhance the risk of IHD. The prevalence of H. pylori infection in patients and controls was 79.3% and 73.0%, respectively (P = 0.403) and that of CagA-positive H. pylori infection was 69.8% and 42.3%, respectively (P = 0.0002). The scores of the ECG S-T segment and T-wave abnormalities in the course of an exercise ECG in uninfected patients and in patients infected by CagA-negative and CagA-positive H. pylori strains were (mean ± sd): 1.59 ± 0.67, 1.92 ± 0.64, and 2.19 ± 0.70, respectively; (P = 0.011, 95% confidence limits of difference 0.15–1.07, CagA-positive infected vs uninfected patients). There was no intergroup difference in the levels of peripheral whiteblood cells, glucose, cholesterol, triglycerides, creatinine, and systolic and diastolic pressure. In conclusion, genetic heterogeneity of H. pylori could possibly explain some conflicting results concerning the association of H. pylori infection with IHD. Coronary vessels of IHD patients infected by CagA-positive H. pylori strains may be damaged more severely than those of uninfected patients.

A case of acute heart failure associated with Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is a disease of the peripheral nervous system, which is caused by aberrant immune responses directed against some components of peripheral nerves. GBS is rarely accompanied by cardiovascular involvement. We describe a case of acute neuropathy complicated by sudden heart failure and left ventricular dysfunction which had a presumably neurogenic origin. Pathogenesis of acute heart failure is probably due to transitorial stunned myocardium and neurogenic cardiac injury. We show a rare case of transitorial and acute cardiac dysfunction by echocardiography and laboratory markers of heart failure.