Causes of hospitalisation before and after the 2009 L'Aquila earthquake.

On 6 April 2009, an earthquake struck L'Aquila. The San Salvatore Hospital was evacuated, and a field hospital was built. The study aimed to assess the epidemiologic impact of the earthquake through the analysis of patient population admitted to the field hospital during a 2-month period following the disaster. We retrospectively evaluated causes of hospitalisation and demographic data of patients admitted to (i) the Division of Internal Medicine and (ii) the Division of Emergency Medicine of the field hospital from 6 April, 2009 to 29 May, 2009. All data were compared with the admissions made at the same divisions of the San Salvatore Hospital during the same period of previous year. (i) Patient group (n = 102) and comparison group (n = 108). Mean patient age was higher, patients living in L'Aquila were more numerous, while mean length of stay was lower after than before the earthquake. Infectious diseases increased, while 'other' diseases decreased after the disaster both in admission and in discharge diagnoses. Gastroenterological diseases decreased with the earthquake but only in admission diagnoses. (ii) Patient group (n = 5255) and comparison group (n = 6564). Triage codes changed with the earthquake. Cardiovascular, psychiatric, gynaecological, infectious and chronic diseases increased, while pneumologic, gastroenterological, traumatic and 'other' diseases decreased after the quake. The number of hospitalised patients decreased with the tremor, while those discharged transferred to other hospitals and those who rejected hospitalisation increased. A natural disaster completely changes causes of hospitalisation in the Divisions of Internal and Emergency Medicine. These findings can be useful for the design of specific intervention programmes and for softening the detrimental effects of quakes.

Platelet activation in patients with the Raynaud phenomenon.

BACKGROUND: The Raynaud phenomenon (RP) is an exaggerated and reversible vasospasm of small arteries triggered by cold or emotional stress. Primary RP (PRP) term is used when the underlying condition is unknown. An altered regulation in vascular tone and/or release of soluble mediators from activated platelets plays a role in PRP through an increased oxidative stress. We assessed platelet activation and oxidative stress in patients with PRP by measuring platelet PAC-1, an index of glycoprotein (Gp) IIb/IIIa receptor activation, thromboxane A(2) (TXA(2)), an index of platelet activation and 8-epi-prostaglandin F(2α) (8-epi-PGF(2α)), a marker of endogenous in vivo peroxidation. METHODS: Eighteen asymptomatic patients with PRP (age 41.37 ± 16.94 years; 17 women, 1 man) and 18 healthy subjects (age of 35.11 ± 13.16 years; 16 women, 2 men) were studied. PAC-1 was analysed by flow cytometry while circulating TXB(2) , a stable metabolite of TXA(2) and 8-epi-PGF(2α) levels were assessed by ELISA kit. RESULTS: Our results show a significant platelet activation in PRP patients as indicated by increased PAC-1 expression (65.29 ± 15.24%; P < 0.001), TXB(2) (1477.83 ± 454.04 pg/mL; P= 0.003) and 8-epi-PGF(2α) circulating levels (42.50 ± 14.14 ng/mL; P < 0.001). An inverse correlation between the degree of PAC-1 expression and TXB(2) levels (r=-0.527; P= 0.02) was also found in PRP patients, suggesting that downregulation of GpIIb/IIIa receptor expression may occur during thrombocytopoiesis, as a consequence of the chronic exposure to increased TXB(2) concentration. CONCLUSIONS: Our study for the first time shows a marked activation of GpIIb/IIIa receptor in asymptomatic patients with PRP and supports antiplatelet therapy in PRP patients.