Summary.A retrospective study was conducted in 1216 cases to investigate the possible association between tobacco smoking and the risk of haematological malignancies. A small, but not significant, increase in malignancy was observed in smokers. Significant association was demonstrated between tobacco smoking and acute nonlymphoblastic leukaemia, and myelodysplastic syndromes. The duration and amount smoked increased the risk; heavy smokers presented significant positive associations with overall malignancies, acute nonlymphoblastic leukaemia, myelodysplastic syndromes, and monoclonal gammopathy of undetermined significance, whereas light smokers did not present any significant association. These data support a causal relationship between certain haematological malignancies and tobacco smoking. Further research is needed to examine the risk according to dose-response effect, and the variation in risk according to the histological subtype of the malignancy.

Patients with monoclonal gammopathy of undetermined significance (MGUS) have a serum monoclonal component (M-component), but no evidence of multiple myeloma, macroglobulinaemia, amyloidosis or other plasma cell proliferative disease. A long-term follow-up study (median 11.5 years) has been carried out in 263 cases of MGUS, 159 males (60.5%) and 104 females (39.5%), aged 40-89 years (median 66.5 years). The actuarial probability for malignant transformation was 6.1, 15.4 and 31.3% at 5, 10 and 20 years, respectively. At the final evaluation, 157 patients (59.7%), 119 (45.3%) of whom with no increase and 38 (14.4%) with an increase in serum M-component, died of causes unrelated to MGUS and without development of any plasma cell proliferative disease; 47 patients (17.9%) were still alive without increase in M-component; 11 patients (4.1 %) were still alive and at follow-up presented values of serum M-component > 30 g/l without any evidence of plasma cell proliferative or lymphoproliferative disease; 48 patients (18.3%) developed multiple myeloma (35 cases, 13.1%), solitary plasmacytoma of the bone (2 cases, 0.8%), macroglobulinaemia (4 cases, 1.6%), malignant lymphoma (3 cases, 1.2%), amyloidosis (2 cases, 0.8%), chronic lymphocytic leukaemia (1 case, 0.4%), and plasma cell leukaemia (1 case, 0.4%). The patients developing multiple myeloma, solitary plasmacytoma, macroglobulinaemia and plasma cell leukaemia had an increase in serum M-component, whereas no increase was found in malignant lymphoma, amyloidosis and chronic lymphocytic leukaemia. These findings and the data in the literature suggest that MGUS could be considered a preneoplastic condition; since no clinical and laboratory features are able to identify in advance the patients at high risk of disease progression, each patient must be followed up indefinitely.

The aim of the study was to verify the role of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic gamma-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid gamma-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symptoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy. The mean plasma and cerebrospinal fluid gamma-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the gamma-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy.

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.

The etiology of hepatorenal syndrome is still incompletely understood, but the nonosmotic release of arginine vasopressin (AVP) seems to have an important role. Since AVP presents a well-defined daily periodicity in its production and secretion, the aim of the study was to investigate the circadian rhythm in its circulating plasma concentrations in patients with hepatorenal syndrome, compared with healthy controls. Venous blood samples were drawn during a 24 hour period at 2 hourly intervals from a peripheral vein in 10 healthy subjects and in 10 patients with hepatorenal syndrome for the determination of the circulating plasma levels of AVP by radioimmunoassay. Statistical analysis was carried out by the ‘cosinor’ method. The controls presented a significant (p < 0.002) circadian rhythm in the AVP circulating levels, whereas no rhythm (p > 0.05) was found in patients. The circadian rhythms were significantly (p < 0.005) different between the two groups, patients having higher mean daily concentration and lower circadian variation of AVP. These results confirm the existence of a well-defined circadian rhythm of AVP in healthy subjects, whereas the hepatorenal syndrome patients present a complete loss of the circadian rhythm. It could be hypothesized that primitive damage in circadian time-keeping regulates the circadian rhythm of vasopressinergic neurons, or has a secondary effect on the peripheral vasodilatation in the course of advanced liver disease. This great upset in the temporal and functional organization, together with that of the renin-angiotensin-aldosterone system, could play an important role in promoting and/or in the maintenance of the hydroelectrolyte imbalance that characterizes the hepatorenal syndrome.