Community acquired pneumonia in internal medicine: a one-year retrospective study based on pneumonia severity index.

Community acquired pneumonia (CAP) represents the sixth cause of death and the first cause of death for an infectious disease in the USA. The aim of the present study is to evaluate how CAP is managed in a hospital setting, with particular attention to the wards of internal medicine, compared to the recommendations based and validated PSI (Pneumonia Severity Index). 42 subjects were included in the study, 25 males and 17 females. According to the PSI, nine (21%) patients were classified in class I, two (5%) in class II, ten (24%) in class III, fifteen (36%) in class IV and six (14%) in class V. Three patients died during the stay in the hospital (2 males and 1 female), all in the highest PSI class (V). According to the criteria used to evaluate the adequacy of the admission to the hospital, twentyeight patients were classified in the HRG, with an appropriate admission, whilst fourteen (33%) were in the LRG, with an inappropriate admission to the hospital. The data of the study confirm the validity of a PSI based strategy for the management of CAP since admittance to the hospital. This approach is not yet widely implemented in Italy, and a better dialogue between hospital and health system representatives would be convenient, to reduce costs and ensure the safety of patients affected by CAP.

[Hyponatremia in cirrhosis with ascites]. / L'iponatremia nel cirrotico con ascite.

Hyponatremia complicates ascitic hepatic cirrhosis with frequency and gravity related to the gravity of the cirrhosis itself. When hyponatremia develops, it worsens the already present secondary hyperaldosteronism and makes therapy with spironolactone inefficacious. From a pathophysiologic viewpoint a pathogenetic role in determining hyponatremia is attributable to the reduced plasmatic renal perfusion; in several patients a syndrome of inappropriate ADH secretion develops. Other neurohormonal systems (catecholamines, prostaglandins, natriuretic hormones) are probably very important in modifying renal hemodynamics and renal tubular function. In some patients a causative role for hyponatremia is attributable to iatrogenic factors (e.g.: diuretics). From a therapeutic viewpoint, we examine some schedules, pharmacologic or not, that, however, are far from being useful for all patients. We discuss, mainly, water restriction, osmotic diuretics with or without loop diuretics, loop diuretics followed by sodium reintegration and concentration-reinfusion of ascites or application of peritoneovenous shunt.

[Castleman's disease with isolated renal location: clinical case]. / Malattia di Castleman con localizzazione renale isolata: caso clinico.

In a review of the literature the authors delineate the present nosographic and descriptive characteristics of Castleman's disease. They then report the case of an adult woman who came to their attention because of persistent, low-grade fever, sweating, malaise and polyarthralgia. Laboratory data evidenced increased acute-phase reactants, polyclonal hypergammaglobulinemia, and anemia due to "chronic disease". Diagnostic imaging documented a right renal mass. A nephrectomy was performed. Histopathological studies confirmed hyaline-vascular type Castleman's disease with monoclonal B-cell lymphoproliferation. The clinical and laboratory anomalies regressed after surgery and continue to be absent after 1 year of follow-up. The authors conclude their presentation by pointing out the peculiarities of this case that do not correspond with the traditional distinctive features of the disease.

[Ascites as preeminent manifestation of primary hypothyroidism. Clinical case]. / L'ascite come preminente manifestazione di ipotiroidismo primitivo. Caso clinico.

The case of an adult male who came to clinical evaluation because of an abundant ascites without any obvious cardiac or hepatic explanation is reported. The exudative characteristics of the ascitic fluid, the elevated serum-ascites albumin gradient, some electrocardiographic anomalies, hypercholesterolemia and a slight macrocytic anemia prompted a clinical diagnosis of probable hypothyroidism. This was also due to an anamnesis of remote antithyroid radiometabolic treatment. The serum hormone levels and the ultrasonogram of the gland confirmed the diagnosis. Hormonal substitutive therapy led to thyroid-stimulating hormone normalization and to a progressive decrease of the ascites, that eventually disappeared. This case, which involves a rare manifestation of hypothyroidism, underscores the need to consider thyroid diseases in the differential diagnosis of ascites and to include thyroid-stimulating hormone dosage among the laboratory tests to be ordered when suspicious clinical or biochemical data are present (mainly, the exudative aspect of the ascites).

Thromboxane and prostacyclin biosynthesis in heart failure of ischemic origin: effects of disease severity and aspirin treatment.

SUMMARY BACKGROUND: Thromboembolism is a relatively common complication of chronic heart failure (HF) and the place of antiplatelet therapy is uncertain. OBJECTIVES: We characterized the rate of thromboxane and prostacyclin biosynthesis in chronic HF of ischemic origin, with the aim of separating the influence of HF on platelet activation from that of the underlying ischemic heart disease (IHD). PATIENTS AND METHODS: We compared urinary 11-dehydro-thromboxane (TX)B(2), 2,3 dinor 6-keto-PGF(1alpha,) 8-iso-prostaglandin (PG)F(2alpha), and plasma N-terminal pro-brain natriuretic peptide (NT-pro-BNP), asymmetric dimethylarginine (ADMA), and soluble CD40 ligand (sCD40L), in 84 patients with HF secondary to IHD, 61 patients with IHD without HF and 42 healthy subjects. RESULTS: HF patients not on aspirin had significantly higher urinary 11-dehydro-TXB(2) as compared with healthy subjects (P < 0.0001) and IHD patients not on aspirin (P = 0.028). They also showed significantly higher 8-iso-PGF(2alpha) (P = 0.018), NT-pro-BNP (P = 0.021) and ADMA (P < 0.0001) than IHD patients not on aspirin. HF patients on low-dose aspirin had significantly lower 11-dehydro-TXB(2) (P < 0.0001), sCD40L (P = 0.007) and 2,3-dinor-6-keto-PGF(1alpha) (P = 0.005) than HF patients not treated with aspirin. HF patients in NYHA classes III and IV had significantly higher urinary 11-dehydro-TXB(2) than patients in classes I and II, independently of aspirin treatment (P < 0.05). On multiple linear regression analysis, higher NT-pro-BNP levels, lack of aspirin therapy and sCD40L, predicted 11-dehydro-TXB(2) excretion rate in HF patients (R(2) = 0.771). CONCLUSIONS: Persistent platelet activation characterizes HF patients. This phenomenon is related to disease severity and is largely suppressable by low-dose aspirin. The homeostatic increase in prostacyclin biosynthesis is impaired, possibly contributing to enhanced thrombotic risk in this setting.

Subclinical coeliac disease is a frequent cause of iron-deficiency anaemia.

BACKGROUND: Although it is known that anaemia may be the only presenting symptom in coeliac disease, prevalence figures of unsuspected coeliac disease in anaemic patients are not available. The aim of this study was to assess the clinical usefulness of antigliadin and antiendomysial antibody tests in the diagnostic algorithm of anaemic patients. METHODS: Two hundred consecutive anaemic patients were tested for antigliadin antibodies, and those positive were also tested for antiendomysial antibodies. All patients positive for antigliadin and antiendomysial antibodies underwent intestinal biopsy. RESULTS: Sixteen patients were antigliadin antibody-positive, and 10 were also antiendomysial antibody-positive. In all 10 a jejunal biopsy was consistent with coeliac disease (prevalence, 5%). This prevalence rose to 8.5% when patients with macrocytic anaemia or with microcytic anaemia due to previous bleeding or responsive to oral iron therapy were excluded from the calculation. CONCLUSIONS: Coeliac disease is a frequent cause of iron-deficiency anaemia, and antigliadin and antiendomysial antibody tests should be always performed in the diagnostic algorithm of anaemic patients.