Peripheral vascular disease and hypertension: a forgotten association?

Peripheral vascular disease (PVD) is associated with a high cardiovascular morbidity and mortality. Intermittent claudication is the most common symptomatic manifestation of PVD, but is also an important predictor of cardiovascular death, increasing it by three-fold, and increasing all-cause mortality by two to five-fold. Hypertension is a common and important risk factor for vascular disorders, including PVD. Of hypertensives at presentation, about 2-5% have intermittent claudication, with this prevalence increasing with age. Similarly, 35-55% of patients with PVD at presentation also have hypertension. Patients who suffer from hypertension with PVD have a greatly increased risk of myocardial infarction and stroke. Apart from the epidemiological associations, hypertension contributes to the pathogenesis of atherosclerosis, the basic underlying pathological process underlying PVD. Hypertension, in common with PVD, is associated with abnormalities of haemostasis and lipids, leading to an increased atherothrombotic state. Nevertheless, none of the large antihypertensive treatment trials have adequately addressed whether a reduction in blood pressure causes a decrease in PVD incidence. There is therefore an obvious need for such outcome studies, especially since the two conditions are commonly encountered together.     

Hypotension: a forgotten illness?

Low blood pressure is a frequently encountered phenomenon in clinical practice. Few practitioners in the Western world however regard chronic low blood pressure as a genuinely pathological disease state. Evidence is emerging that chronic hypotension is associated with considerable morbidity in the community. It has recently been implicated as the causative mechanism in patients with the chronic fatigue syndrome. Identification of low blood pressure can prove probjlematic, so ambulatory blood pressure monitoring may prove a more reliable method both for determining mean blood pressure levels and for identifying episodes of marked hypotension. Low blood pressure is broadly divided into two categories, chronic constitutional hypotension and hypotension associated with abnormal postural control. The causes are examined and the clinical presentations are discussed. An approach to investigation and diagnosis is outlined, and current options regarding treatment and management are described. The clinical spectrum of low blood pressure is wide. From young patients with vagally mediated syncope or patients with iatrogenic hypotension to elderly patients with autonomic degenerative conditions, there exists a substantial body of patients with potentially avoidable or treatable morbidity. Such a group requires more rigorous scientific investigation and a more sympathetic clinical approach.     

The vascular manifestations of Behçet's disease: a case report

Behçet’s disease is an inflammatory vasculitis which affects the arteries and veins. The vascular pathologies are the rare complications of this disease. We present here a patient with Behçet’s disease who has been hospitalized several times because of plurifocal vascular manifestations.     

Behçet disease: evolution of clinical manifestations

Clinical phenotypes of Beh?et disease (BD) vary among ethnic groups. We chronologically analyzed the clinical manifestations of BD in 412 patients meeting the Japanese criteria for BD seen at 2 Yokohama City University hospitals from July 1991 to December 2007. We examined the onset of individual symptoms in each patient. A single initial symptom appeared earlier than any other manifestation in 78% of the patients. Time from the initial symptom to diagnosis was 8.6 ± 10.1 years. Oral ulcer, the most common initial manifestation, preceded the diagnosis by 7.5 ± 10.2 years. Genital ulcer and eye and skin involvement appeared 1 or 2 years before diagnosis, whereas gastrointestinal, central nervous system, or vascular involvement developed later. The frequency of eye involvement was significantly higher in patients with neurologic lesions, but significantly lower in those with gastrointestinal or vascular involvement. However, no particular combination of major symptoms predicted the development of organ involvement. There has been a recent decrease in the rate of "complete" BD (patients having all 4 of the major symptoms of oral ulcers, genital ulcers, and eye and skin lesions), whereas the frequencies of arthritis, gastrointestinal, and vascular involvement have been increasing. Further assessment may allow the detection of early predictors of the more aggressive disease, which requires more intensive treatment.     

Short report: Melioidosis in Myanmar: forgotten but not gone?

A serologic survey of adults resident in Myanmar was conducted to define the presence of antibodies to Burkholderia pseudomallei, the cause of melioidosis. Antibodies were detectable by indirect hemagglutination assay (IHA) in 757 (78%) of 968 adults, of whom 69 (7%) had an IHA titer > or =1:160.     

Anderson–Fabry disease: Clinical manifestations of disease in female heterozygotes

Anderson–Fabry disease is a rare, X-chromosomal lipid storage disorder caused by a deficiency of lysosomal -galactosidase A. Clinical manifestations of Anderson–Fabry disease include excruciating pain in the extremities (acroparaesthesia), skin vessel ectasia (angiokeratoma), corneal and lenticular opacity, cardiovascular disease, stroke and renal failure, only renal failure being a frequent cause of death. Heterozygote female carriers have often been reported as being asymptomatic or having an attenuated form of the disease. To evaluate the spectrum of clinical signs in heterozygotes, a comprehensive clinical examination was performed on 20 carriers of Anderson–Fabry disease. This revealed that, in addition to the skin manifestation, various other clinical manifestations of the disease are present, including acroparaesthesia, kidney dysfunction, cerebrovascular disease, and gastrointestinal and heart problems. It therefore appears that Anderson–Fabry disease affects both hemizygotes and heterozyotes and therefore should be considered to be an X-linked dominant disease.     

The diabetic hand: a forgotten complication?

The manifestations of diabetes in the hand were much discussed in the 1970s and 1980s. The present review aims to revisit the diabetic hand and to discuss the pathology of the hand that may be clinically important in diabetic patients. In the strict sense of the term, the “diabetic hand” encompasses the three most widely studied conditions which have traditionally been associated with diabetes, namely limited joint mobility, Dupuytren's contracture and trigger finger. There is evidence that these entities are significantly more frequent in patients with diabetes and also that they may be associated with diabetes duration, poor metabolic control and presence of microvascular complications. In a more general sense, though, there are other conditions affecting the hands, which also occur more frequently in diabetes. From a practical point of view, increased alertness both for neuropathic hand ulcers in patients with profound neuropathy and for diabetic hand infections is absolutely necessary. Recently, reduced hand strength is beginning to be recognized as a further complication of diabetes. Thus, the hand may reveal substantial pathology in diabetes, and ideally, clinical examination should not ignore it.     

Osteoarthritis: a problem of growth not decay?

The traditional view of OA is that it is primarily a disease of articular cartilage that results, by altering the biomechanics of the joint, in secondary changes to the subchondral bone and, through secondary inflammation, other joint tissues. This focus on cartilage tends to ignore other musculoskeletal changes reported, especially those remote from affected joints. It has been proposed instead that generalized OA is a systemic musculoskeletal disorder with a metabolic component. Evidence for this position will be presented by summarizing changes identified in all the major musculoskeletal tissues. This will endeavour to show the links between these tissues, most of which have a common mesenchymal origin. Dysregulated tissue turnover, with the balance in favour of growth, will be seen to be a common thread underlying many of the changes described. It is proposed that the production of new tissue in the midst of existing tissue, in the wrong place and at the wrong time, could result in the changes observed and that reversion of cellular behaviour to an earlier, developmental-like, phenotype may provide a mechanism that could drive the disease process. New therapies may arise both from recognizing this whole musculoskeletal disease phenotype and by exploring what might be the factors underlying this cellular reversion.     

Cutaneous manifestations of adult-onset Still’s disease: a case report and review of literature

Clinical Rheumatology - Adult onset Still’s disease (AOSD) is a systemic inflammatory disorder of unknown etiology and pathogenesis characterized by high spiking fever, arthralgia or...