[Extranodal lymphomas. A rare clinical entity or a protean disease? A case report]. / I linfomi extranodali. Entità clinica rara o affezione proteiforme? Descrizione di un caso.

Aim of the present study is to describe a case of extranodal lymphoma localized in paravertebral site, near to thoracic spine. The clinical onset of the affection was as a radicular sciatalgic pain, resistant to long-term current therapy by NSAIDs, and determined by neuroradicular involvement by the neoplastic bulk. The interest of the present case is determined by: 1) the presence of a pain which, for a long while, mimicked one of the most trivial painful syndromes; 2) the fact that extranodal lymphomas are not so rare ones. An extensive research of such entities is therefore mandatory; 3) the diagnosis was made by means of non-invasive examination, and needle biopsy was performed only to confirm a picture which was already patent.

[Acute reversible degenerative myopathy complicating Lyme disease: description of a case] / Miopatia acuta degenerativa reversibile in corso di malattia di Lyme: descrizione di un caso clinico.

Lyme's disease is a commonly found disorder whose etiological agent is a spirochete named Borrelia burgdorferi. Its clinical presentation is usually well known, and three stages are described. However it may present symptoms which may resemble many infectious or autoimmune diseases as well. The aim of the present study is to describe a case of first stage Lyme's disease whose main clinical picture is muscoloskeletal involvement, which may mimic dermatomyositis. Many subtle characteristics (age of onset, atypical cutaneous rash) together with the involvement of muscular masses other than scapular or pelvic ones, and the bio-humoral positivity for anti-Borrelia antibodies allowed correct diagnosis to be made. We emphasize that instrumental and invasive examinations, such as electromyography and muscular biopsy, were not diagnostic in such cases.

[Spontaneous staphylococcal abscess of psoas muscle]. / Ascesso stafilococcico spontaneo del muscolo psoas.

An abscess of the psoas muscle is a rare occurrence and pathogenetic interpretation usually proves difficult. Abscessing of the psoas may be due either to direct diffusion of infections of adjacent structure or to hematogenous spread. However, not uncommonly, a "spontaneous" abscess occurs, which cannot be correlated to other sites of infections or sepsis. The Authors describe two cases of abscesses of the psoas muscle following Staphylococcus aureus sepsis of unknown origin.

[Dissection of the epiaortic vessels: an emergency pathology as the cause of focal cerebral ischemia. The evaluation of a case load of 7 patients]. / Dissezione dei vasi epiaortici: una patologia emergente come causa di ischemia cerebrale focale. Valutazione di una casistica di 7 pazienti.

Dissection of the epiaortic vessels is an emerging cause of focal cerebral ischemia, especially in young patients. Non-invasive diagnostic devices (ultrasound, nuclear magnetic resonance) have greatly improved the ability to suspect and identify it. We report our clinical experience with 5 patients affected by carotid artery dissection and 2 patients affected by vertebral artery dissection. Vessel dissection generally occurred spontaneously; it was preceded by head or cervical trauma in 2 cases. Arterial hypertension was commonly associated, and headache was always present together with other focal neurological signs. Clinical suspicion was confirmed by ultrasound duplex scanning: although never conclusive, it always showed typical Doppler patterns. Nuclear magnetic resonance has become an acknowledged means of definitive diagnosis although angiography remains the gold standard. In any case, diagnosis requires clinical suspicion and the accurate correlation of clinical data and instrumental results. Therapy consisted in anticoagulant and antiplatelet drugs. The clinical course of our patients was favorable in all cases, and no recurrences were recorded.

Repeated sympathetic stimuli elicit the decline and disappearance of prostaglandin modulation and an increase of vascular resistance in humans.

To investigate the role of prostaglandins I2 and E2 in modulating the vasoconstrictor response to sympathetic stimulation, repeated and proximate cold pressor tests were performed in 23 healthy young volunteers. Limb vascular resistance (blood flow measured by venous occlusion plethysmography), prostaglandin I2 (as 6-ketoprostaglandin F1 alpha) and prostaglandin E2 plasma levels (detected by radioimmunoassay), and plasma catecholamines (detected by high-performance liquid chromatography and electrochemical detection) were measured. A progressive increase in the duration of the vasoconstrictor response was observed with repetition of cold applications (p less than 0.001, by analysis of variance for trends). This increase was associated with a progressive decrease in cold-induced elevation of 6-ketoprostaglandin F1 alpha and prostaglandin E2 plasma levels until, after five stimulations, neither prostaglandin was detectable. The maximum detected concentration of norepinephrine did not significantly change, but its area under the curve in time showed a trend toward an increase. Epinephrine levels did not significantly change. The increase of vascular resistance was significantly correlated with the decrease of both prostaglandins (r = 0.93, p less than 0.05 for prostaglandin E2 and r = 0.89, p less than 0.05 for 6-ketoprostaglandin F1 alpha), whereas no significant correlations were found between variations of vascular resistance and catecholamines. Prostaglandin blockade induced by diclofenac sodium administration caused, from the first cold application, a pattern of the vasoconstrictor response and plasma prostaglandin and norepinephrine changes similar to that observed at the fifth cold application in untreated subjects, when prostaglandins are no longer detectable in plasma. We conclude that an increased vasoconstrictor response to sympathetic stimulation in humans may result from a diminished inhibitory influence of prostaglandins on adrenergic transmission.

Thrombolytic versus fibrinogenolytic activity of rt-PA and streptokinase in patients with acute myocardial infarction.

In this study the concentration of plasma breakdown products of cross-linked fibrin (XDP), serum fibrinogen-fibrin degradation products (FDP), and plasma fibrinogen were measured before and at the end of the administration of single-chain recombinant tissue-type plasminogen activator (rt-PA, 100 mg IV over three hours) or streptokinase (1.5 million units over one hour), respectively, in two groups, each composed of 22 patients with acute myocardial infarction. The XDP concentration was not statistically different between the two groups at the end of thrombolytic treatment, whereas FDP and fibrinogen concentrations were significantly different (FDP: streptokinase 396 +/- 287 vs rt-PA 177 +/- 222 micrograms/mL, p less than 0.01; fibrinogen: streptokinase 71 +/- 43 vs rt-PA 181 +/- 49 mg/dL, p less than 0.001). These results indicate that the two drugs have equipotent thrombolytic activity at this administration regimen but that rt-PA causes a markedly more selective lysis of fibrin in comparison with streptokinase.

The antihypertensive and renal activities of potassium canrenoate are associated with increased renal prostaglandin excretion.

1. In a double-blind, randomized, cross-over study the effects of potassium canrenoate administration (100 mg twice daily for 10 days orally) on renal prostaglandin synthesis (prostaglandin E2 and prostaglandin F2 alpha) were evaluated in 10 normotensive females and in 10 females with essential hypertension. 2. When compared with normotensive subjects, hypertensive patients in baseline conditions showed a reduced excretion of urinary prostaglandin E2 associated with an excessive prostaglandin F2 alpha production. 3. Potassium canrenoate significantly reduced mean blood pressure in hypertensive patients [from 118.9 +/- 8.7 mmHg (1.62 +/- 0.12 kPa) to a peak minimum value of 104.7 +/- 9.8 mmHg (1.42 +/- 0.13 kPa) on the seventh day of treatment; P less than 0.01 for the whole period] but not in control subjects [from 88 +/- 9.4 mmHg (1.20 +/- 0.13 kPa) to 84.3 +/- 8.3 mmHg (1.15 +/- 0.11 kPa) on the eighth day, NS] even though potassium canrenoate significantly increased sodium excretion in both groups. Renal prostaglandin excretion was affected differently in the two groups: in control subjects excretion of both prostaglandin E2 and prostaglandin F2 alpha was increased after drug administration, whereas in hypertensive patients only prostaglandin E2 excretion was enhanced.

Bartter's syndrome and chondrocalcinosis: a possible role for hypomagnesemia in the deposition of calcium pyrophosphate dihydrate (CPPD) crystals.

A new case of association between Bartter's syndrome and chondrocalcinosis is reported. The patient was shown to have marked hypomagnesemia. Indomethacin and magnesium therapy was started and resulted in increased magnesemia, even if it did not reach normal levels. There was complete remission of articular symptoms and no progression on the radiological picture after 2 years of continuous magnesium and indomethacin therapy. The 7 available family members were studied to assess the possible presence of a familial form of chondrocalcinosis and/or hypomagnesemia. The literature is reviewed and reports of previously described associations between Bartter's syndrome and chondrocalcinosis are summarized. The possible role of hypomagnesemia in predisposing to deposition of calcium pyrophosphate dihydrate crystal in cartilagine is also discussed.

Efficacy of mexiletine in chronic ventricular arrhythmias: a multicentre double-blind medium-term trial.

In a multicentre double-blind, inpatient, placebo-controlled trial the effects on premature ventricular beats (PVBs) of mexiletine in a standard, submaximal dose were studied by Holter monitoring in 144 outpatients. After wash-out, mexiletine was administered for 14 days. The effects were re-tested, after one week of a placebo, in a second 14-day period of mexiletine administration. Of the patients 73% in the first period and 82.5% in the second period responded to mexiletine (a reduction of 75% or more of PVBs/24 h--p less than 0.001 compared with the placebo for both periods). Mexiletine also significantly reduced the Lown class of PVBs and the frequence of paired PBVs, ventricular tachycardia, multiform beats and R on T wave phenomenon. Mexiletine showed an equivalent effectiveness in the four main aetiological groups of arrhythmias. Fifty nine patients complained of adverse effects (gastrointestinal or neurological) the intensity of which led to the stopping of the treatment in 16 of them. These results show that mexiletine is highly effective, even in submaximal doses, in preventing ventricular arrhythmias of whatever origin.

Treatment of hypertensive emergencies: classic and newer approaches.

Serious complications of treatment in hypertensive crises have been reported for nearly all drugs, so that testing of further antihypertensive drugs in the management of hypertensive emergencies is desirable. In the present study, the clinical efficacy and effects on cardiac function of intravenously infused clonidine were tested in 20 hypertensives with severely elevated blood pressure (diastolic blood pressure over 130 mm Hg). In all patients, the normalization of blood pressure was achieved together with a reduction in total and peripheral vascular resistance. Heart rate showed a slight and brief decrease. Cardiac performance (determined by radionuclide angiocardiography) was improved as indicated by the significant increase in ejection fraction and decrease in both end-diastolic and end-systolic volumes. The dosage of clonidine was progressively increased until a normal blood pressure (mean blood pressure less than or equal to 105 mm Hg) was obtained. The total mean dose required for control of blood pressure was 403 +/- 97.8 micrograms, administered over a mean period of 32 +/- 5.9 min. Side effects, represented by dry mouth and drowsiness, were well tolerated and of short duration. It is concluded that clonidine is an effective and safe alternative in the treatment of hypertensive emergencies.

Pentoxifylline treatment in patients with occlusive peripheral arterial disease. Circulatory changes and effects on prostaglandin synthesis.

Pentoxifylline has recently been reported to stimulate in vitro the synthesis of prostacyclin. However it is not known so far whether the drug is able to stimulate prostacyclin synthesis in man also in vivo. In the present study the effects of pentoxifylline on prostaglandin synthesis and several circulatory parameters were studied in 10 controls and 10 patients with occlusive arterial disease after acute i.v. and medium term oral treatment. Prostacyclin (as 6-keto-PGF1 alpha) and PGE2 plasma concentrations have been measured together with arterial blood flow, peripheral vascular resistance, platelet aggregation and red blood cell deformability. Pentoxifylline was found both in healthy subjects and patients to significantly increase prostacyclin plasma concentration after i.v. treatment. In medium term oral treatment prostacyclin concentration was found to increase only two hours after administration and not 8 hours after. No significant variations in PGE2 plasma concentration were found at any time in both groups. Pentoxifylline significantly enhanced resting and post-ischemic blood flow of the lower limbs and simultaneously decreased peripheral vascular resistance both in healthy subjects and patients. Different grades of delayed platelet aggregation and increased red blood cell deformability were also observed. In conclusion results of the present placebo controlled study show that pentoxifylline increases arterial blood flow in patients with occlusive arterial disease. Moreover pentoxifylline induces a temporary stimulation of prostacyclin synthesis which can be suggested to contribute to the clinical activity of the drug as far as an antithrombotic effect in terms of inhibition of platelet aggregation is concerned.

Changes in cardiac function after effective treatment of hypertensive emergencies with i.v. clonidine.

Clonidine administration by i.v. infusion in 12 patients with hypertension emergencies (diastolic blood pressure over 130 mmHg) resulted in the normalization of blood pressure (BP) in all patients. Lowering of BP was associated with a reduction in total and lower limb vascular resistance. Heart rate showed a slight and brief decrease. Cardiac performance (determined by radionuclide angiocardiography) was improved as indicated by the significant increase of ejection fraction and decrease of both end-diastolic and end-systolic volumes. The dosage of clonidine was progressively increased until a normal BP (mean BP less than or equal to 105 mmHg) was obtained. In all patients a normal BP was achieved and in none was an initial hypertension effect observed. The total mean dose required for control of BP was 382.5 +/- 98.3 micrograms, administered over a mean period of 26.5 +/- 4.6 min. Side-effects, represented by dry mouth and drowsiness, were well tolerated and of short duration. It is concluded that clonidine is an effective and safe alternative in the treatment of hypertensive emergencies.

A study of the antihypertensive effect and some pharmacodynamic aspects of nifedipine in medium-term treatment.

The antihypertensive activity of nifedipine in medium-term treatment has been studied in 30 patients affected by II and III WHO grade essential hypertension. After a 6-day period of placebo, patients were randomly allotted to group A (treated with single 10-mg doses of nifedipine) and group B (treated with single 20-mg doses). Treatment with nifedipine continued for 18 days. Patients in both groups were given one daily dose during the first 6 days, two daily doses in the following 6 days and three daily doses in the last 6 days. 1. Antihypertensive effect: In both groups, only three daily doses gave a satisfactory 24-hour antihypertensive activity. Nifedipine as monotherapy administered in single doses of both 10 mg (group A) and 20 mg (group B) normalized blood pressure (BP) and the measured antihypertensive effect was not statistically different in the two groups. The antihypertensive effect lasted between 7 and 8 hours after drug administration (both doses) and did not diminish with increasing duration of treatment or number of daily doses. 2. Change in heart rate: Nifedipine induced an increase in HR which diminished with shortening of the time interval between daily administrations. The effect on HR was unaltered throughout the whole experimental period. 3. Side-effects: Nifedipine did not induce orthostatic hypotension in any patient. Eleven of the 30 patients complained of side-effects, the most common being headache and palpitations. Incidence and severity of side-effects were not correlated with dose, whereas duration was longer with 20 mg. Side-effects never necessitated withdrawal of the drug.