Periprosthetic fractures after hip prosthesis represent a constantly increasing clinical problem and a challenging complication to treat surgically. Among these, type B proximal femur fractures should be diagnosed correctly to be treated surgically. The aim of this study was to re-evaluate the type of surgical treatment of periprosthetic fractures. We examined the cases treated between January 2012 and February 2018, classifying them according to the U.C.S. AO/OTA. We evaluated the radiographic outcome according to the Beals and Tower criteria. Patients still alive were also re-evaluated according to the H.H.S. and the WOMAC score. We treated 48 patients (12 men, 35 women, average age 81 years), divided into 24 type B1, 14 type B2 and 10 type B3 fractures. The overall consolidation rate was 95.4%, while the major complication (implant dislocation, pseudoarthrosis and deep infection) rate was 12.5%. Clinically, it was possible to reassess 34 patients with a mean follow-up of 38.4 months, an average HHS of 75.89 and a mean WOMAC score of 79.93. Periprosthetic type B fractures are difficult to manage and require careful preoperative planning and appropriate intraoperative management. However, the overall clinical and radiographic result was satisfactory, although patients should still be aware of the risk of complications associated with this type of fracture.

Candida parapsilosis may be responsible for bloodstream infections (BSI) and it is characterised by an increased incidence of fluconazole resistance. A 75-year old woman with severe comorbidities received the insertion of a peripherally inserted central venous catheter. Fluconazole did not prevent a C. parapsilosis BSI hence caspofungin was started after a nephrotoxic first-line treatment with amphotericin B. The ratio of peak plasma concentration over the minimum inhibitory concentration (Cmax/MIC) was adopted to maximise efficacy of caspofungin. MIC and plasma Cmax values were obtained by broth microdilution and LC-MS, respectively. Interestingly, daily doses of 1 mg/kg (total daily dose, 50 mg) allowed the achievement of Cmax/MIC values > 10. The optimised regimen was safe and effective, leading to negative blood culture at day 8. The patient was discharged home at day 21. Therefore, individualised dosing regimens of caspofungin may be effective and safe even in the case of C. parapsilosis BSI.

BACKGROUND:An increasing number of candidemia episodes has been reported in patients cared for in internal medicine wards. These usually older and frail patients may not be suspected as having candidemia because they lack fever at the onset of the episode. To identify the risk factors associated with the lack of fever at the onset of candidemia (ie, the collection of the first positive blood culture for Candida spp.) in patients cared for in internal medicine wards, we compared 2 group of patients with or without fever. METHODS:We retrospectively review data charts from 3 tertiary care, university hospitals in Italy, comparing patients with or without fever at onset of candidemia. Consecutive candidemic episodes in afebrile patients and matched febrile controls were identified during the 3-year study period. Patient baseline characteristics and several infection-related variables were examined. Random forest analysis was used, given the number of predictors to be considered and the potential complexity of their relations with the onset of fever. RESULTS:We identified 147 candidemic episodes without fever at onset and 147 febrile candidemia episodes. Factors associated with the lack of fever at onset of candidemia were diabetes, Clostridium difficile infection, and a shorter delta time from internal medicine wards admission to the onset of candidemia. The only variable associated with fever was the use of intravascular devices. Quite unexpectedly, antifungal therapy was administered more frequently to patients without fever, and no differences on 30-day mortality rate were documented in the 2 study groups. CONCLUSIONS:Clinicians should be aware that an increasing number of patients with invasive candidiasis cared for in internal medicine wards may lack fever at onset, especially those with diabetes and C. difficile infection. Candidemia should be suspected in patients with afebrile systemic inflammatory response syndrome or in worsening clinical condition: blood cultures should be taken, and a timely and appropriate antifungal therapy should be considered.

A 73-year-old man was admitted to the Emergency Room (ER) for dyspnea and cough from several months. In ER were performed blood sampling, chest X-ray, electrocardiogram, echocardiogram and arterial blood gas. A thoracic ultrasound (US) revealed in the left side an abundant pleural effusion and a lung consolidation area of about 5 cm without air bronchogram. A thoracentesis showed the presence of hemorrhagic effusion. Chest computed tomography (CT) revealed micro-pulmonary embolism, abundant left pleural effusion with atelectasis of the lower ipsilateral lobe. Meanwhile the chest CT revised by the pulmonologist appeared suspicious for the presence of cancer, the cytological examination of pleural fluid revealed the presence of an adenocarcinoma. While the patient was waiting for the bronchoscopy he had a stroke and died in a few days. In conclusion, we believe that thoracic US has to be considered an extension of the physical examination, it is a bedside tool and it represents a valid diagnostic and therapeutic method. Therefore thoracic US, if closely linked to the physician’s activity, can directly affect the decision-making process and management of the patient with dyspnea.

Introduction. To evaluate the prevalence of cognitive impairment in patients older than 70 years at admission in an emergency department (not ICU) and its variation at the discharge. To assess the correlation between cognitive status and clinical outcome.Materials and methods. Observational and prospective study. Determination of common biochemical parameters and thyroid function at admission and multifunctional assessment with MMSE (repeated at the discharge), Barthel and Charlson indexes.Results. 149/ 205 consecutive patients (72.5%; age 81.5 +/- 6.0 years) had cognitive impairment (MMSE < 24). MMSE showed a significant correlation with age (p < 0.0001), Barthel Index (p < 0.0001), serum albumin (p = 0.0004), VES (p = 0.01) and FT3 (p = 0.03). Intra-hospital mortality showed a significant correlation with the presence of delirium (p = 0.0004), cognitive impairment (p = 0.0003), Barthel (p = 0.001) and Charlson (p = 0.03) indexes, age (p = 0.0004), glycaemia (p = 0.02), serum albumin (p = 0.02), LDH (p = 0.02), CRP (p = 0.03), creatinine (p = 0.04) and potassium (p = 0.03) levels. By multiple logistic analysis, cognitive impairment (p = 0.003) followed by hyperglycaemia (p = 0.01) emerged as the most important predictive factor of mortality. At discharge MMSE score resulted significantly higher than at admission (p < 0.0001), independently from the presence of delirium, functional impairment, comorbility and length of hospitalization.Conclusion. The present study documents a high prevalence of cognitive impairment in acutely-ill hospitalized elderly patients. Cognitive impairment appears to be the most important predictive factor of short-term mortality. Acute illness seem to induce a transient worsening of cognitive status, as suggested by the improvement of MMSE score at discharge, independently from the length of hospital stay and cognitive impairment at admission.

Results. 149/205 consecutive patients (72.5%; age 81.5 ± 6.0 years) had cognitive impairment (MMSE < 24). MMSE showed a significant correlation with age (p < 0.0001), Barthel Index (p < 0.0001), serum albumin (p = 0.0004), VES (p = 0.01) and FT3 (p = 0.03). Intra-hospital mortality showed a significant correlation with the presence of delirium (p = 0.0004), cognitive impairment (p = 0.0003), Barthel (p = 0.001) and Charlson (p = 0.03) indexes, age (p = 0.0004), glycaemia (p = 0.02), serum albumin (p = 0.02), LDH (p = 0.02), CRP (p = 0.03), creatinine (p = 0.04) and potassium (p = 0.03) levels. By multiple logistic analysis, cognitive impairment (p = 0.003) followed by hyperglycaemia (p = 0.01) emerged as the most important predictive factor of mortality. At discharge MMSE score resulted significantly higher than at admission (p < 0.0001), independently from the presence of delirium, functional impairment, comorbility and length of hospitalization.

We report a case of decompensated porto-pulmonary hypertension closely associated with the development of intra-portocaval shunt thrombosis. A woman with Laennec's cirrhosis was hospitalized because of severe dyspnea and edema. She underwent surgical portocaval anastomosis ten years ago. Imaging studies showed massive intra-shunt thrombosis, portal hypertension, ascites, pleuro-pericardial effusions and enlargement of right cardiac cavities. Cardiac catheterization allowed to rule out coronary and left-sided heart abnormalities and led to the diagnosis of pre-capillary pulmonary hypertension. Antithrombotic treatment with low molecular weight heparin was instituted. The management also included ACE inhibitors, spironolactone, low-salt diet and lactulose. The patient was discharged and three months later we observed the disappearance of edema, ascites and pleuro-pericardial effusions, a marked body weight reduction and improved dyspnea and liver function tests. A possible link between the development of intra-shunt thrombosis and clinical decompensation in our patient was hypothesized. In fact, it has been demonstrated that the increased portal pressure, caused by occlusion of portosystemic shunt, reduces renal plasma flow and increases systemic endothelin-1 concentration. In our patient the disappearance of edematous state and improved dyspnea observed after recanalization of the shunt strongly support this hypothesis.

A rare case of a patient with Sjogren syndrome and spontaneously acquired inhibitors of both factor VIII and factor IX is reported. Complete remission was obtained by means of immunosuppressive drugs.

Introduction: Insulin resistance, a novel cardiovascular risk factor, is often associated with increased plasminogen activator inhibitor-1 levels and impaired vasodilation. Insulin infusion in the forearm induces plasminogen activator inhibitor-1 and tissue plasminogen activator expression and endothelium-dependent vasodilation in normal subjects. The present study explores the relationship between insulin-induced vasodilatory and fibrinolytic properties of the endothelium in women with polycystic ovary syndrome, frequently affected by insulin resistance and early atherosclerosis.Materials and methods: Metabolic, hormonal and fibrinolytic parameters were evaluated in 64 patients with polycystic ovary syndrome (19 insulin-resistant and 45 insulin-sensitive) and in 25 controls. In 16 women with polycystic ovary syndrome, 8 insulin-resistant and 8 insulin-sensitive, blood flow, plasminogen activator inhibitor-1 and tissue plasminogen activator expression were evaluated during insulin infusion into the forearm.Results: Elevated basal plasminogen activator inhibitor-1 levels were found in women with polycystic ovary syndrome, correlating directly with insulin levels. Plasminogen activator inhibitor-1 expression increased during insulin infusion in at( women with polycystic ovary syndrome, but was delayed and sustained in insulin-resistant patients (p < 0.01). Vasodilatory response to insulin was blunted (p < 0.01) and tissue plasminogen activator expression abolished in insulin-resistant patients (p < 0.01).Conclusion: Our study demonstrates that women with polycystic ovary syndrome and insulin resistance show a blunted endothelial-dependent vasoditation. The impaired endothelial release of tissue-plasminogen activator and the sustained plasminogen activator inhibitor-1 release during insulin infusion suggest a hypofibrinolytic state in PCOS patients with insulin resistance. This hemodynamic and fibrinolytic derangement may contribute to the pathogenesis of early atherosclerosis in insulin resistance. (c) 2005 Elsevier Ltd. Ali rights reserved.

A relationship may exist between endothelial-mediated vasodilation and tissue-type plasminogen activator (t-PA) release. However, the existing evidence is mainly based upon exogenous agonist administration, and needs testing under more physiological conditions. We evaluated the link between t-PA, the key fibrinolytic factor in man, and forearm reactive hyperemia, a model of endogenous endothelial-mediated vasodilation, in 13 uncomplicated hypertensive subjects and six elderly hypertensive patients with atherosclerotic peripheral vascular disease and hypercholesterolemia (i.e a group in whom post-ischemic hyperemia was probably defective because of dysfunctional endothelium). To characterize further the phenomenon, 29 additional uncomplicated hypertensive patients underwent intra-arterial drug infusions. Study variables were forearm blood flow (strain-gauge plethysmography), arterial and venous concentrations of t-PA mass concentrations, and calculated net release (forearm plasma flow × veno-arterial differences). Reactive hyperemia was induced by inflating a cuff midway between systolic and diastolic pressure for 10 min; blood and forearm blood flow were sampled before and after cuff release. Post-ischemic t-PA release increased in uncomplicated hypertensives, and did not change in hypercholesterolemic atherosclerotic patients in whom post-ischemic vasodilation was negligible. Local adenosine (n = 9), acetylcholine (n = 12) and bradykinin (n = 8) vasodilated similarly, but only bradykinin increased t-PA release. Thus, reactive hyperemia stimulates t-PA release, and that relationship is altered when endothelium is dysfunctional. Release of t-PA is independent of forearm vasodilatation per se, adenosine or biological products of muscarinic stimulation and may, perhaps, be related to the activity of the endogenous kininogen/kinin system.

Reactive hyperemia (RH) is a physiological vasodilator response mediated by endothelial-dependent and independent factors triggered by ischemia. Aim of the study was to evaluate whether RH releases tissue plaminogen activator (t-PA), the key fibrinolytic mechanism in man. We also tried to identify the underlying mechanisms by infusing adenosine (ADE), an endothelial-independent vasodilator, acetylcholine (ACH), a nitric oxide (NO)-releasing substance, and bradykinin (BK), an agonist acting also through release of an endothelium-derived hyperpolarizing factor (EDHF). A total of 39 uncomplicated essential hypertensive men (EH, age: 48±7yrs, 148±7/92±10 mmHg) were recruited. Forearm blood flow (FBF, venous plethysmography), arterial (A) and venous (V) t-Pa antigen concentrations (ELISA) to derive REL (V-AxFBF) were measured before and after RH induced by a 10-min inflation of a pressure cuff at mid systo-diastolic values (n=13). The same procedure was carried out before and after 10-min intraarterial infusions of ADE (5mg/dl tissuexmin-1, n=10), ACH (15μg/ dl tissuexmin-1, n=12) and BK (500 ng/ dl tissuexmin-1, n=4). Results (means±SD or medians[interquartile range]): 1 min after cuff release, FBF increased from 3.2±1.6 to 18±3 ml/minxdl-1 (p<.001), and t-PA REL from 1.4 [1] to 49 [9] ng/mlxmin-1 (p<.01) respectively. ADE, ACH and BK increased (p<0.001) FBF to a similar extent (ADE: from 3.5±0.8 to 17.6±4, ACH: from 3.2±0.8 to 14.8±3.2: BK: from 3.1±0.8 to 16.3±2.1 ml/dlxmin-1) but only BK increased t-PA REL (ADE: from -0.4[1] to 0. [10]; ACH: from 0.2 [1] to -0.5[18], BK: from -0.4[0.9] to 19[38] ng/mlxmin-1] (p<0.04). RH, a physiological vasodilator response to ischemia, releases t-PA in EH, showing a relationship between endothelial-mediated vasomotion and local fibrinolysis, and possibly implying that a reduced endothelial mediated vasomotion leads to defective fibrinolysis.Enhanced local t-PA REL by RH could not be explained by vasodilatation per se or direct effects of either ADE or NO produced in response to ACH stimulation. Rather, the selective t-PA releasing effect of BK may suggest a preferential involvement of EDHF.

The effects of a 24-day regimen containing 15 μg ethinyl estradiol (EE) plus 60 μg gestodene on cycle control and on hemostasis, were evaluated in 58 healthy women (age 19–47 years). All women received the pill for 12 months. Withdrawal bleeding at every cycle during the tablet-free interval was experienced by 84.5% of the women. The overall incidence of irregular bleedings was 19.3%. Hemostasis was evaluated in 20 women. No changes in plasma fibrinogen concentrations, nor in prothrombin fragment F1+2 were observed. A slight increase in thrombin-antithrombin III complexes was observed after 6 and 12 months of oral contraceptive use. Antithrombin III activity significantly increased after one-year of pill intake. The concentrations of tissue plasminogen activator and plasminogen activator inhibitor, both antigen and activity, did not change. These results show that very low doses of EE, such as 15 μg, do not impair hemostasis in healthy females. However, the reduction for the EE dose is responsible of some of the effects on cycle control.

To the Editor: It is known that methylxanthines, especially theophylline, increase production of urine and enhance excretion of water and electrolytes with a pattern similar to that produced by thiazides. The underlying mechanisms, which remain controversial, appear to be mainly mediated by antagonism of adenosine receptors 1 and by other effects on adenylate cyclase, phosphodiesterase and intracellular calcium. 2 A 29-year-old man was admitted to the hospital in January 2000 for an evaluation of his renal function. The patient had consumed large quantities of black Chinese and Nepalese tea and complained of heart throbbing and blood pressure. On admission he had abnormally creatinine and urea clearance and enhanced urinary excretion of creatinine, urea, sodium, and potassium (Table 1). He underwent abdomen ultrasonography, doppler imaging of renal arteries, and a kidney scan; no alterations were found. The glomerular filtration rate (GFR), as calculated by the method described by Gates, 3 appeared to be normal. Blood pressure was in the high range. An eye examination showed stage 1-hypertensive retinopathy. The patient's thyroid function, plasma renln activity, blood and urine aldosterone, and cathecolamines concentrations were in the normai range. The finding of decreased serum iron levels suggested impaired iron absorption due to the tannates contained in tea.4 We speculated that the increases of creatinine and urea clearance and of sodium and potassium urine excretion could be due to the effect of the large quantities of ingested tea; the estimated daily dose of methylxanthines during the last year was 250 to 300 nag caffeine and 5 to 6 mg theophylline (apart from tea, the patient's diet was poor in xanthine-containing foods). 5 Methylxanthines in normal subjects appear to inhibit solute reabsorption in both the proximal nephron and the diluting segments without changing either GFR or renal blood flow appreciably. 5 Accordingly, such a discrepancy between GFR and creatinine clearance in our patient could be reasonably ascribed to the increase of creatinine excretion. During his stay in the hospital, the patient was kept on a normal salt intake (6 to 8 g/day), xanthine-poor diet. This was followed by a decrease in urine volume, solute excretion, and free water clearance (Table 1). His palpitations ceased. The patient was discharged with the diagnosis of arterial hypertension (stage 1) and advised to decrease sodium intake and limit tea drinking.