Clinical characteristics and course of plantar vein thrombosis: a series of 22 cases.

OBJECTIVES: To evaluate the clinical presentation and disease course of symptomatic plantar vein thrombosis. PATIENTS AND METHODS: Patients with a first diagnosis of symptomatic plantar vein thrombosis at our institution were retrospectively identified from a prospectively maintained database. All patients underwent complete venous compression sonography extended to the plantar veins because of local symptoms at the sole of the foot. Clinical characteristics were obtained from the medical records. RESULTS: Between 2005 and 2013, 22 patients were diagnosed with a first episode of plantar vein thrombosis (64% women, mean age at diagnosis 58.2 years, range 32-79 years). All patients reported moderate to heavy pain of the sole of the foot. The lateral plantar veins (96%) were more frequently affected than the medial plantar veins (41%) and extension into the deep calf veins was common (27%). Half of the episodes were idiopathic, with subsequent diagnosis of occult malignancy in two of these patients. In seven patients (32%), plantar vein thrombosis occurred in association to physical strain to the foot. All patients were treated with anticoagulation. Symptomatic pulmonary embolism was not observed and during a mean follow up of 21 months, the post-thrombotic syndrome did not occur. However, recurrences were common (27%) and frequently again affected the plantar veins. CONCLUSION: Plantar vein thrombosis should be considered as an important differential diagnosis of acute foot pain.

[Cerebrovascular diseases]. / Erkrankungen der hirnversorgenden Gefässe.

In the majority of the cases cerebrovascular disease is caused by atherosclerosis. Duplexsonography is the diagnostic tool of first choice. Management of cardiovascular risk factors is of paramount importance in secondary prevention of atherosclerotic vascular complications. Patients with a symptomatic internal carotid artery stenosis >70% have a clear indication for revascularization. Asymptomatic patients with >60% stenosis benefit from revascularisation if the perioperative risk for death or stroke is below 3%. The optimal revascularization strategy highly depends on the expertise of the local surgeon or endovascular specialist. In younger patients with cerebrovascular disease rare causes such as dissection, large vessel arteritis, fibromuscular dysplasia or vasospasms have to be considered.

HIV-associated renal diseases and highly active antiretroviral therapy-induced nephropathy.

Renal disease is becoming an increasingly prevalent entity in human immunodeficiency virus (HIV)-infected patients; it occurs in a variety of clinical settings and is associated with histopathological changes. HIV-related renal impairment can present as acute or chronic kidney disease; it can be caused directly or indirectly by HIV and/or by drug-related effects that are directly nephrotoxic or lead to changes in renal function by inducing metabolic vaculopathy and renal damage. Acute renal failure is frequently caused by the toxic effects of antiretroviral therapy or nephrotoxic antimicrobial substances used in the treatment of opportunistic infections. Chronic renal disease can be caused by multiple pathophysiological mechanisms, leading to HIV-associated nephropathy, a form of collapsing focal glomerulosclerosis, thrombotic microangiopathy, and various forms of immune complex glomerulonephritis. The increase in life expectancy and alteration of lipid metabolism due to receipt of highly active antiretroviral therapy are expected to result in an increased prevalence of diabetes and hypertension and, thus, to secondary diabetic and hypertensive renal damage. Antiretroviral agents, such as indinavir and tenofovir, have been associated with nephrotoxic drug effects that have been shown to be reversible in most cases. In this article, we review the current knowledge about acute and chronic HIV-associated renal disease, metabolic alterations and related nephropathies, and toxic drug effects of combination antiretroviral pharmacotherapy.

[Options in HIV therapy: present and future]. / Therapieoptionen bei HIV Realität und Zukunft.

Highly active antiretroviral therapy (HAART) has markedly decreased HIV-associated mortality. It consists of a combination of three antiretroviral drugs from four different classes: nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors and inhibitors of virus-cell fusion. Increasing resistance against antiretroviral drugs calls for the development of new compounds and drug classes. The growing understanding of molecular mechanisms in HIV-replication led to the identification of further steps which might serve as novel antiretroviral targets. Uninfected cells could be protected from HIV by inhibiting extracellular binding mechanisms. Improvement of existing antiretroviral drugs and further development of novel therapeutic targets will enrich antiretroviral treatment.

Insulin induces upregulation of vascular AT1 receptor gene expression by posttranscriptional mechanisms.

BACKGROUND: An interaction of insulin with angiotensin II effects could be pathophysiologically important for the pathogenesis of atherosclerosis and hypertension. METHODS AND RESULTS: We examined the effect of insulin on AT1 receptor gene expression in cultured vascular smooth muscle cells (VSMCs). A 24-hour incubation with insulin (100 nmol/L) produced a 2-fold increase in AT1 receptor density on VSMCs, as assessed by radioligand binding assays. This enhanced AT1 receptor expression was caused by a time- and concentration-dependent upregulation of the AT1 receptor mRNA levels, as assessed by Northern analysis. The maximal effect was detected after a 24-hour incubation of cells with 100 nmol/L insulin (270+/-20%). AT1 receptor upregulation was caused by a stabilization of the AT1 receptor mRNA, because the AT1 receptor mRNA half-life was prolonged from 5 hours under basal conditions to 10 hours after insulin stimulation. In contrast, insulin had no influence on AT1 receptor gene transcription, as assessed by nuclear run-on assays. The insulin-induced AT1 receptor upregulation was followed by an increased functional response, because angiotensin II evoked a significantly elevated intracellular release of calcium in cells that were preincubated with 100 nmol/L insulin for 24 hours. The insulin-induced AT1 receptor upregulation was dependent on tyrosine kinases, as assessed by experiments with the tyrosine kinase inhibitor genistein. Furthermore, experiments using the intracellular calcium chelator bis(2-amino-5-methylphenoxy)ethane-N, N,N',N'-tetraacetic acid tetraacetoxymethyl ester suggest that intracellular calcium release may be involved in AT1 receptor regulation. CONCLUSIONS: Insulin-induced upregulation of the AT1 receptor by posttranscriptional mechanisms may explain the association of hyperinsulinemia with hypertension and arteriosclerosis, because activation of the AT1 receptor plays a key role in the regulation of blood pressure and fluid homeostasis.

Treatment of liver injuries at level I and level II centers in a multi-institutional metropolitan trauma system. The Midwest Trauma Society Liver Trauma Study Group.

OBJECTIVE: The development of trauma systems and trauma centers has had a major impact on the fate of the critically injured patient. However, some have suggested that care may be compromised if too many trauma centers are designated for a given area. As of 1987, the state of Missouri had designated six adult trauma centers, two Level I and four Level II, for the metropolitan Kansas City, Mo, area, serving a population of approximately 1 million people. To determine whether care was comparable between the Level I and II centers, we conducted a concurrent evaluation of the fate of patients with a sentinel injury, hepatic trauma, over a 6-year period (1987-1992) who were treated at these six trauma centers. METHODS: All patients during the 6-year study period who suffered liver trauma and who survived long enough to be evaluated by computerized tomography or celiotomy were entered into the study. Patients with central nervous system trauma were excluded from analysis. Information concerning mechanism of injury, RTS, Injury Severity Score (ISS), presence of shock, liver injury scoring, mode of treatment, mortality, and length of stay were recorded on abstract forms for analysis. Care was evaluated by mortality, time to the operating room (OR), and intensive care unit (ICU) and hospital length of stay. RESULTS: Over the 6-year period 300 patients with non-central nervous system liver trauma were seen. Level I centers cared for 195 patients and Level II centers cared for 105. There was no difference in mean ISS or ISS > 25 between Level I and II centers. Fifty-five (28%) patients arrived in shock at Level I centers and 24 (23%) at Level II centers. Forty-eight patients (16%) died. Thirty-two (16%) died at Level I centers, and 16 (15%) died at Level II centers. Twenty of 55 patients (36%) in shock died at Level I centers, and 11 of 24 (46%) died at Level II centers (p = 0.428). Forty-three patients (22%) had liver scaling scores of IV-VI at Level I centers, and 10 (10%) had similar scores at Level II centers (p < 0.01). With liver scores IV-VI, 22 of 43 (51%) died at Level I centers and 10 of 14 (71%) died at Level II centers (p = 0.184). There was no difference in mean time or in delays beyond 1 hour to the OR for those patients in shock between Level I and II centers. There was a longer ICU stay at Level II centers (5.0 +/- 8.3 vs. 2.8 +/- 8.4 days, p = 0.04). This difference was confined to penetrating injuries. There was no difference in hospital length of stay. CONCLUSIONS: In a metropolitan trauma system, when Level I and II centers were compared for their ability to care for victims of hepatic trauma, there was no discernible difference in care rendered with respect to severity of injury, mortality, delays to the OR, or hospital length of stay. It was observed that more severe liver injuries were seen at Level I centers, but this did not seem to significantly affect care at Level II centers. There was a longer ICU stay observed at Level II centers owing to penetrating injuries, possibly because there were fewer penetrating injuries treated at these facilities. Although the bulk of patients were seen at Level I centers, care throughout the system was equivalent.