Randomized, double blind placebo-controlled pilot study of the antihypertensive effects of Grana Padano D.O.P. cheese consumption in mild - moderate hypertensive subjects.

OBJECTIVE: Grana Padano, an Italian protected designation of origin (PDO) semi-fat cheese, undergoes a long ripening period during which the proteolysis carried out by natural starter lactic acid bacteria releases peptides having sustained angiotensin-converting enzyme (ACE)-inhibitory activity. The length (generally 3-8 amino acid residues) and the sequence of these peptides are responsible for their ability to elicit ACE-inhibitory activity. The aim of this study has been the evaluation of the effect of a daily dietary supplement consisting in a small amount (30 g/day) of Grana Padano cheese, in terms of the lowering of the blood pressure (BP) of mild-moderate hypertensive subjects. PATIENTS AND METHODS: Thirty mild-moderate hypertensive patients, with BP values not on target (> 140 and/or > 90 mmHg) after at least 3 months of stable treatment were considered in this randomized, double-blind placebo-controlled cross-over study. All patients randomly received a dietary integration (30 g/day) of Grana Padano cheese or a placebo (made from flavored grated bread mixed with fats and salts in concentrations equal to those of the cheese). BP was evaluated at baseline and at the end of the active and placebo treatments (2 months each) by: - Office BP (OBP); - Automated Office BP (AOBP) using the BpTRU®, an automated oscillometric device that provides the average of multiple (n=6) blood pressure measurements; - Ambulatory Blood Pressure (ABP) 24 hour monitoring. RESULTS: Dietary integration with Grana Padano cheese resulted in a significant decrease in Office, Automated Office and Ambulatory BP. The mean decrease (vs. placebo) for 24-hour ABP was -3.5 mmHg for systolic and -2.4 mmHg for diastolic BP (p = 0.0063 and p = 0.0065, respectively). CONCLUSIONS: Daily dietary integration with 30 g of Grana Padano DOP cheese effectively reduces BP and may help mild-to-moderate hypertensive patients to reach a target BP.

Effect of bedtime dosing of barnidipine hydrochloride in non-dipper hypertensive patients with obstructive sleep apnoea not treated with continuous positive airway pressure.

OBJECTIVE: Obstructive sleep apnoea (OSA) is considered a cause of secondary hypertension. About 50% of patients with OSA show elevated blood pressure levels. Non-dipper pattern (blunted or absent nocturnal decrease of blood pressure) is frequently observed in patients with OSA and is associated with increased cerebral, cardiovascular and renal events. The aim of this study was to observe the effect of barnidipine calcium channel blocker on these patients. PATIENTS AND METHODS: Forty-one patients (mean age 69 ± 17 years, 18 females) with previously diagnosed OSA (by reduced channel home-based polysomnography) who were not being treated with continuous positive airway pressure (CPAP) because of contraindications or because of patient intolerance or rejection were evaluated. Non-dipper status was defined as the presence of a nighttime fall in systolic blood pressure (BP) which was < 10% that of daytime systolic BP as observed in a previous ambulatory blood pressure (ABP) monitoring. OSA was defined according to the presence of 5 or more episodes per hour of apnoea, hypopnoea or arousal due to respiratory effort. The reproducibility of non-dipping status was confirmed through a second 24-h ABP monitoring performed at baseline. On top of the previous stable treatment regimen (which excluded calcium-channel blockers), a 10 mg dosing of barnidipine hydrochloride at bedtime was added to all subjects during a 12-week period. RESULTS: Among the 41 non-dipper patients, 32 (78%) showed complete normalization of circadian rhythm. Add-on treatment with barnidipine was generally well tolerated. CONCLUSIONS: Bedtime dosing of the calcium-channel blocker (CCB) barnidipine significantly reduced mean nighttime systolic and diastolic ABP in hypertensive patients presenting with non-dipper pattern and OSA--not on CPAP treatment. Moreover, it restored the previously altered circadian rhythm in the majority of them.

The influence of pore size on osteoblast phenotype expression in cultures grown on porous titanium.

This study investigated the effect of pore size on osteoblastic phenotype development in cultures grown on porous titanium (Ti). Porous Ti discs with three different pore sizes, 312 µm (Ti 312), 130 µm (Ti 130) and 62 µm (Ti 62) were fabricated using a powder metallurgy process. Osteoblastic cells obtained from human alveolar bone were cultured on porous Ti samples for periods of up to 14 days. Cell proliferation was affected by pore size at day 3 (p=0.0010), day 7 (p=0.0005) and day 10 (p=0.0090) in the following way: Ti 62

Response of human alveolar bone-derived cells to a novel poly(vinylidene fluoride-trifluoroethylene)/barium titanate membrane.

This study investigated the response of human alveolar bone-derived cells to a novel poly(vinylidene fluoride-trifluoroethylene)/barium titanate (P(VDF-TrFE)/BT) membrane. Osteoblastic cells were cultured in osteogenic conditions either on P(VDF-TrFE)/BT or polytetrafluoroethylene (PTFE) for up to 14 days. At 7 and 14 days, the mRNA expression of Runt-related transcription factor 2 (RUNX2), Type I collagen (COL I), Osteopontin (OPN), Alkaline phosphatase (ALP), Bone sialoprotein (BSP), and Osteocalcin (OC), key markers of the osteoblastic phenotype, and of Bcl2-associated X protein (Bax), B-cell CLL/lymphoma 2 (Bcl-2), and Survivin (SUR), associated with the control of the apoptotic cell death, was assayed by real-time PCR. In situ ALP activity was qualitatively evaluated by means of Fast red staining. Surface characterization was also qualitatively and quantitatively assayed in terms of topography, roughness, and wettability. Cells grown on P(VDF-TrFE)/BT exhibited a significantly higher mRNA expression for all markers compared to the ones on PTFE, except for Bcl-2, which was not detected for both groups. Additionally, Fast red staining was noticeably stronger in cultures on P(VDF-TrFE)/BT at 7 and 14 days. At micron- and submicron scale, SEM images and roughness analysis revealed that PTFE and P(VDF-TrFE)/BT exhibited a smooth topography and a similar roughness, respectively. PTFE membrane displayed higher contact angles compared with P(VDF-TrFE)/BT, as indicated by wettability assay. The novel P(VDF-TrFE)/BT membrane supports the acquisition of the osteoblastic phenotype in vitro, while up-regulating the expression of apoptotic markers. Further in vivo experiments should be carried out to confirm the capacity of P(VDF-TrFE)/BT membrane in promoting bone formation in guided bone regeneration.

In vitro biocompatibility of poly(vinylidene fluoride-trifluoroethylene)/barium titanate composite using cultures of human periodontal ligament fibroblasts and keratinocytes.

The aim of this work was to evaluate the biocompatibility of poly(vinylidene fluoride-trifluoroethylene)/barium titanate (P(VDF-TrFE)/BT) membrane to be used in guided tissue regeneration (GTR). Fibroblasts from human periodontal ligament (hPDLF) and keratinocytes (SCC9) were plated on P(VDF-TrFE)/BT and polytetrafluorethylene membranes at a cell density of 20,000 cells well(-1) and cultured for up to 21 days. Cell morphology, adhesion and proliferation were evaluated in hPDLF and keratinocytes, while total protein content and alkaline phosphatase (ALP) activity were assayed only for hPDLF. Using a higher cell density, real-time polymerase chain reaction (PCR) was performed to assess the expression of typical genes of hPDLF, such as periostin, PDLs17, S100A4 and fibromodulin, and key phenotypic markers of keratinocytes, including involucrin, keratins 1, 10 and 14. Expression of the apoptotic genes bax, bcl-2 and survivin was evaluated for both cultures. hPDLF adhered and spread more on P(VDF-TrFE)/BT, whereas keratinocytes showed a round shape on both membranes. hPDLF adhesion was greater on P(VDF-TrFE)/BT at 2 and 4h, while keratinocyte adhesion was similar for both membranes. Whereas proliferation was significantly higher for hPDLF on P(VDF-TrFE)/BT at days 1 and 7, no signs of keratinocyte proliferation could be noticed for both membranes. Total protein content was greater on P(VDF-TrFE)/BT at 7, 14 and 21 days, and higher levels of ALP activity were observed on P(VDF-TrFE)/BT at 21 days. Real-time PCR revealed higher expression of phenotypic markers of hPDLF and keratinocytes as well as greater expression of apoptotic genes in cultures grown on P(VDF-TrFE)/BT. These results indicate that, by favoring hPDLF adhesion, spreading, proliferation and typical mRNA expression, P(VDF-TrFE)/BT membrane should be considered an advantageous alternative for GTR.

Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease.

INTRODUCTION: Periodontal disease is a chronic inflammation of the attachment structures of the teeth, triggered by potentially hazardous microorganisms and the consequent immune-inflammatory responses. In humans, the T helper type 17 (Th17) lineage, characterized by interleukin-17 (IL-17) production, develops under transforming growth factor-beta (TGF-beta), IL-1beta, and IL-6 signaling, while its pool is maintained by IL-23. Although this subset of cells has been implicated in various autoimmune, inflammatory, and bone-destructive conditions, the exact role of T lymphocytes in chronic periodontitis is still controversial. Therefore, in this study we investigated the presence of Th17 cells in human periodontal disease. METHODS: Gingival and alveolar bone samples from healthy patients and patients with chronic periodontitis were collected and used for the subsequent assays. The messenger RNA expression for the cytokines IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 in gingiva or IL-17 and receptor activator for nuclear factor-kappaB ligand in alveolar bone was evaluated by real-time polymerase chain reaction. The production of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 proteins was evaluated by immunohistochemistry and the presence of Th17 cells in the inflamed gingiva was confirmed by immunofluorescence confocal microscopy for CD4 and IL-17 colocalization. RESULTS: Our data demonstrated elevated levels of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 messenger RNA and protein in diseased tissues as well as the presence of Th17 cells in gingiva from patients with periodontitis. Moreover, IL-17 and the bone resorption factor RANKL were abundantly expressed in the alveolar bone of diseased patients, in contrast to low detection in controls. CONCLUSION: These results provided strong evidence for the presence of Th17 cells in the sites of chronic inflammation in human periodontal disease.

Mechanisms involved in the pressor response to noradrenaline injection into the cingulate cortex of unanesthetized rats.

The cingulate cortex (CC) is involved in cardiovascular modulation. CC electrical or chemical stimulation may evoke either pressor or depressor responses, depending on the stimulated site and experimental conditions such as anesthesia. Noradrenaline (NA) is involved in cardiovascular regulation and it is present throughout the cortex. However, there is no report on the cardiovascular effects of intracortical injections of NA. We attempted to verify the effect of NA injection into the CC and to identify possible receptor and peripheral mechanisms involved. NA injection caused pressor responses accompanied by bradycardia, in unanesthetized rats. These responses were markedly reduced under urethane anesthesia. The pressor response was blocked by intracortical pretreatment with phenoxybenzamine or the selective alpha(1)-antagonist WB4101, and it was not affected by pretreatment with the selective alpha(2)-antagonist RX821002, suggesting that alpha(1)-adrenoceptors mediate the response. The pressor response was potentiated by pretreatment with the ganglion blocker mecamylamine and it was abolished by pretreatment with the vasopressin antagonist, dTyr(CH(2)) (5)(Me)AVP or by hypophysectomy. Circulating vasopressin levels were increased after NA injection into the CC. The present results indicate that the pressor response to local injection of NA within the CC is independent of sympathetic nerve activation and is mediated by vasopressin release.

Microalbuminuria in essential hypertension.

Microalbuminuria (urinary albumin excretion equal to 30-300 mg/24 h) is a reliable indicator of premature cardiovascular mortality in diabetic patients and in the general population. In insulin-dependent and non-insulin-dependent diabetes mellitus microalbuminuria is a marker of initial diabetic nephropathy and predicts the evolution toward renal insufficiency. In essential hypertension the clinical and prognostic role of microalbuminuria is more controversial. While it is a recognised marker of cardiovascular complications and a reliable predictor of ischaemic heart disease, its prognostic value on the risk of progressive renal alterations is still uncertain because no prospective studies, taking microalbuminuria as a selection criterion and renal insufficiency as an end point, are available. Blood pressure control with antihypertensive drugs is accompanied by a reduction in urinary albumin excretion. The favourable effects of antihypertensive agents on microalbuminuria appear to be proportional to blood pressure reduction, but angiotensin-converting enzyme inhibitors and angiotensin-II-receptor antagonists show an additional beneficial effect on urinary albumin excretion. Whether the reduction of microalbuminuria obtained through pharmacological intervention has favourable prognostic implications remain to be demonstrated. However, screening for microalbuminuria is a relatively easy and inexpensive procedure and reveals a potentially treatable abnormality. Thus, considering that microalbuminuria identifies hypertensive subjects at higher risk than standard, urinary albumin excretion should be routinely measured in hypertensive patients and, in the presence of microalbuminuria, antihypertensive treatment should be intensified in order to obtain an optimal blood pressure control.

The lateral hypothalamus is involved in the pathway mediating the hypotensive response to cingulate cortex-cholinergic stimulation.

1. The injection of acetylcholine (ACh) into the medial prefrontal cortex (MPFC) caused marked hypotensive response in either unanesthetized or anesthetized rats. 2. The present experiment was designed to investigate anatomical connections of the ACh injection site in the MPFC with putative autonomic-related brain nuclei, as well as their possible involvement in the mediation of the hypotensive response to ACh. 3. For the above purpose, the bidirectional neuronal tracer biotinylated dextran amine (BDA) was injected into Cg1 and Cg3 areas, within the MPFC of male Wistar rats. Five days later the animals were sacrificed and brain slices were processed and analyzed to determine neuronal projections efferent from as well afferent to the MPFC. 4. Neuronal staining was more prominent in regions ipsilateral to the BDA injection site. Prominent efferent projections of the MPFC were observed in the contralateral MPFC: ipsi- and contralateral amygdala and hypothalamus; ipsilateral septal area, diagonal band, and zona incerta. 5. Similar but not equal patterns of neuronal labeling were observed when BDA injections were performed within the two adjacent MPFC areas. BDA injections centered in the ACh injection site in the Cg3 area caused strong labeling in the septal area and diagonal band as well as an overall hypothalamic labeling. Within the hypothalamus an intense cortical projection was observed in the lateral hypothalamus (LH). BDA injections into the Cg1 area caused a more evident labeling of the amygdaloid complex. 6. Neuronal cell bodies were evident throughout the MPFC as well as in the sensory-motor cortex when BDA was injected into the LH, thus indicating a massive ipsilateral cortical projection from the Cg3 to the LH. 7. Bilateral NMDA-induced lesions within the LH caused a significant attenuation of the depressor responses to ACh injection in the MPFC, whereas unilateral lesions were marginally effective. These results indicate the involvement of the LH in the mediation of the hypotensive response to ACh injection into the MPFC as well as the bilateral distribution of the hypotensive pathway.

[The usefulness and limits of the ambulatory monitoring of arterial pressure]. / Utilità e limiti del monitoraggio ambulatoriale della pressione arteriosa.

The interpretation of blood pressure values, measured by the physician in the medical environment, has some limitations. Blood pressure fluctuates considerably due to circadian rhythm and various environmental stimuli and thus casual readings may not be representative of the true blood pressure status of the patient. Non-invasive ambulatory blood pressure monitoring has greatly increased our knowledge regarding the diagnosis, treatment efficacy, natural history and even prognosis of hypertension. This technique allows the evaluation of repeated blood pressure measurements at given times (daytime, nighttime, early-morning) and in different conditions (awake, asleep, at rest, during physical or mental activity etc.). Many studies have shown that the whole-day values obtained with such devices correlate better with the morbidity and mortality associated with hypertension than does casual office blood pressure. The 24-hour blood pressure recording is useful in the diagnosis of hypertension, particularly to discriminate so called white coat hypertension (for which the term isolated clinic hypertension has recently been proposed). Ambulatory blood pressure monitoring provides reliable and detailed information on the efficacy of pharmacological treatment and its ability to cover the whole day. These considerations notwithstanding, the application of this technique is still far from routine in the clinical management of arterial hypertension. Its major limit is that the normalcy of ambulatory blood pressure values still remains to be calculated, and only hypothetical normal reference values, derived from studies of selected normotensive populations, are presently available.

Medial prefrontal cortex acetylcholine injection-induced hypotension: the role of hindlimb vasodilation.

The injection of acetylcholine (ACh) into the cingulate region of the medial prefrontal cortex (MPFC) causes a marked fall in arterial blood pressure which is not accompanied by changes in heart rate. The purpose of the present study was to investigate the hemodynamic basis for this stimulus-induced hypotension in Sprague-Dawley rats. The study was designed to determine whether a change in the vascular resistance of hindlimb, renal or mesenteric vascular beds contributes to the fall in arterial pressure in response to ACh injection into the cingulate cortex. Miniature pulsed-Doppler flow probes were used to measure changes in regional blood flow and vascular resistance. The results indicated that the hypotensive response was largely due to a consistent and marked vasodilation in the hindlimb vascular bed. On this basis, an additional experiment was then undertaken to determine the mechanisms that contribute to hindlimb vasodilation. The effect of interrupting the autonomic innervation of one leg on the hindlimb vasodilator response was tested. Unilateral transection of the lumbar sympathetic chain attenuated the cingulate ACh-induced vasodilation in the ipsilateral, but not in the contralateral hindlimb. These results suggest that the hypotensive response to cingulate cortex-ACh injection is caused by skeletal muscle vasodilation mediated by a sympathetic chain-related vasodilator system.

Psychological constructs associated with emotional blood pressure response and white coat phenomenon.

Some hypertensive and non-hypertensive subjects have a striking blood pressure response to a medical environment (white coat phenomenon), although it is unlikely that its presence, degree, and duration can be routinely predicted. Despite the common observation that "anxious" patients may present with this reaction when a physician measures their blood pressure, no psychological variables have thus far been linked to white coat phenomenon in formal analyses. Ambulatory blood pressure monitoring is a useful tool to disclose the phenomenon since it allows precise evaluation of repeated blood pressure measurements outside the medical environment. To investigate the possible relationship between psychological profile and white coat phenomenon, we have planned to administer a series of psychometric tests to 120 subjects undergoing ambulatory blood pressure monitoring. The present data are derived from an analysis of the first set of 70 patients. Thirty-four subjects who presented with white coat phenomenon (defined as office blood pressure elevated by at least 15% over the mean 24-hour ambulatory blood pressure value) and 36 comparable subjects who did not have this reaction underwent a series of psychometric tests evaluating cognitive behavior, hostility, cynicism, anger, anxiety state, coping ability and strategies, and quality of life. Of the various psychometric tests, the scores of three relevant scales (healthcare-related fears, mental efficiency and behavioral disengagement) were significantly higher in the group of patients with white coat phenomenon, while in both groups, emotional instability was higher than the clinical cut-off point. There were no significant differences between the two groups regarding signs and repression of anger (anger-out and anger-in), cynicism, hostility, or anxiety state. Our data seem to indicate that the subjects most likely to show an overt blood pressure increase in the medical environment are those who evidence healthcare-related fears and emotional instability but are not necessarily anxious. They exhibit high coping skills in cognitive resolution of stressing situations (such as blood pressure measurement) but do not combine these strategies with an adequate behavioral response and do not feel that behavioral involvement is necessary for the management of their clinical condition.

Severe postpartum hypertension and reversible cerebral angiopathy associated with ergot derivative (methergoline) administration.

A 36-year-old woman (gravida 2, para 2) delivered a healthy child by cesarean section at the 37th week of an unremarkable gestation. Blood pressure remained within normal range throughout the pregnancy, surgery, and for the 9 following days. On day 10, about 36 hours after the initiation of oral methergoline to suppress lactation, the patient complained of severe posterior headache, flashing scotomata, hypertension, tonico-clonic seizures and then homonymous left hemianopsia and hemiparesis. Blood pressure monitoring confirmed intermittent and severe hypertension. Angiography demonstrated diffuse narrowing of the small and medium cerebral arteries. Transcranial Doppler ultrasound examination disclosed a bilateral increase in mean flow velocity. Progressive normalization of blood pressure, obtained with labetalol and oral clonidine, was accompanied by amelioration of the neurological deficits until a complete recovery and normalization of transcranial Doppler flow velocity occurred. This case provides further evidences that hypertension might play a major pathogenetic role in reversible cerebral angiopathy. Some ergot derivatives (including methergoline) might trigger the initial rise in blood pressure.

Magnesium and cardiovascular drugs: interactions and therapeutic role.

Numerous experimental, epidemiological and clinical studies have pointed out a relevant role for magnesium deficiency in the development of many cardiovascular diseases. Some pharmacological treatments may interfere with magnesium turnover, and magnesium deficiency may alter the pharmacokinetics and pharmacodynamics of some cardiovascular drugs. Loop and thiazide-like diuretics increase magnesiuresis, and total bodily magnesium deficiency may appear during prolonged treatment with diuretically active doses of these drugs. The potassium retaining agents, such as amiloride, triamterene and spironolactone, tend to retain magnesium but they are not magnesium-retaining substances to the extent to which they are potassium-retaining diuretics. The interaction between magnesium and digitalis is complex. Magnesium, acting as an indirect antagonist of digoxin at the sarcolemma Na(+)-K(+)-ATPase pump, reduces cardiac arrhythmias due to digoxin poisoning. Recent controlled studies have shown that treatment with magnesium significantly reduces the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with congestive heart failure without digoxin toxicity. Magnesium improves the efficacy of digoxin in slowing the ventricular response in atrial fibrillation. Digoxin reduces tubular magnesium reabsorption, and in patients with congestive heart failure this interaction may be cumulative with other causes of magnesium deficiency (diuretics, diet, poor intestinal absorption). The complex and potentially life-threatening interactions between magnesium and some cardiovascular drugs suggest that magnesium status should be carefully monitored in patients receiving such drugs. Therapy with magnesium is rapidly acting, has a safe toxic-therapeutic ratio, is easy to administer and titrate. The correction of magnesium deficit should therefore always be considered for patients with cardiopathy.

Cardiovascular response to the injection of acetylcholine into the anterior cingulate region of the medial prefrontal cortex of unanesthetized rats.

Injection of acetylcholine (ACh) (2.5-60 nmol) into the anterior cingulate cortex caused dose-dependent hypotensive responses (Emax = -25.3 mmHg) and no change in the heart rate. The hypotensive response to 30 nmol of ACh was blocked by local pretreatment with atropine (3 nmol) or 4-DAMP (6.7 nmol), a non-tropine muscarinic antagonist. When the same dose of atropine was injected i.v., no changes were observed in the hypotensive response to intracortical ACh. This observation rules out the possible leakage of ACh into the peripheral circulation and favors the idea of a cortical site of action. The injection of the same dose of ACh into the corpus callosum or the occipital cortex did not cause changes in the cardiovascular system. The present results confirm earlier evidence that the cingulate cortex is involved in the control of the autonomic system and indicate that cholinergic muscarinic receptors in the cingulate cortex mediate a hypotensive response without a change in heart rate.

Prolonged treatment with ursodeoxycholic acid for primary biliary cirrhosis.

Eighteen patients affected with biopsy-proved primary biliary cirrhosis (PBC) (histological stage III and IV) received ursodeoxicholic acid (UDCA) 600 mg for 1 year. Signs and symptoms and biochemical tests (glutamic and oxalcetic transaminase, glutamic and pyruvic transaminase, bilirubine, gamma-glutamyl transpeptidase, alkaline phosphatase, leucine aminopeptidase, bile acids, plasma proteins electrophoresis, immunoglubulins A, G and M) and antimitochondrial antibodies were evaluated before the treatment and every four months during the treatment. The results were compared with those obtained in 8 untreated patients affected PBC. The control group of patients were comparable (as far as age, histological stage, biochemical tests are concerned) to the group who received UDCA. Bilirubine, ALP, gamma-GT and LAP decreased during the treatment with UDCA and remained lower than baseline values until the end of the observation (12 months), while no changes occurred in the untreated patients. Both in the treated and untreated group plasma protein electrophoresis, serum immunoglubulins A, G and M remained unchanged, as well as anti-mitochondrial antibody. A moderate reduction of transaminases and bile acids was observed in the group of patients receiving UDCA but it did not reach statistical significance. In 16 out of the 18 treated patients pruritus disappeared and resulted diminished in the remaining 2 patients. No significant amelioration of pruritus was observed in the patients who did not receive UDCA. In conclusion, our data show that prolonged treatment with UDCA drastically reduces pruritus and improves cholestasis biochemical tests in patients affected with symptomatic PBC.(ABSTRACT TRUNCATED AT 250 WORDS)

[Prolymphocytic B-cell leukemia with fatal acute liver failure. A case report]. / Leucemia a prolinfociti B con insufficienza epatica acuta fatale. Descrizione di un caso.

Prolymphocytic leukemia (LPL) is a well defined entity with a relatively low incidence in our country. This disease usually is seen in patients over 50 years of age, and there is a very definite male preponderance. This lymphoproliferative disorder is characterized by very high white cells counts, massive splenomegaly, poor response to therapy and short term survival. The neoplastic cell in prolymphocytic leukemia usually is of B-cell origin (80% of cases). In our patient, affected by B-lineage prolymphocytic leukemia, a acute hepatic failure occurred, leading him to death in a short time. Autoptic findings evidenced a massive leukemic infiltration of the liver with parenchymal necrosis that caused fatal hepatic failure. Autoptic findings did not show histological patterns of acute viral infections or of any other infectious or systemic disease which could have induced a so massive liver injury. In literature there are no evidences of such a massive and lethal involvement of the liver during prolymphocytic leukemia or chronic lymphocytic leukemia and patients affected by LPL generally come to death because of other causes.

[Zidovudine in the treatment of HIV-related thrombocytopenia. A study of 11 cases]. / La zidovudina nel trattamento della piastrinopenia HIV-correlata. Uno studio di 11 casi.

HIV-related thrombocytopenia sometimes requires a therapeutic choice: current therapies are similar to those applied in idiopathic thrombocytopenic purpura. Some Authors described a positive effect on platelets with Zidovudine (AZT) administration. We evaluated the efficacy of this drug in a group of 11 HIV-seropositive patients. Our results were not encouraging: increase in platelet count was obtained in a few patients only and it generally was of little importance.