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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied four patients with posterior brawny scleritis. Two underwent enucleation for suspected melanoma, and in the other two, the correct diagnosis was made and effective therapy begun. Of seven other eyes with brawny scleritis from other sources, five were enucleated after diagnosis of choroidal melanoma and one for suspected intraocular tumor. This experience and other previous reports indicate the high incidence of diagnostic confusion regarding brawny scleritis. We therefore emphasized clinical symptoms and signs of brawny scleritis: inflammation, tenderness or pain of the globe, history of collagen vascular disease, proptosis, bilaterality, and retinal and choroidal detachment. A preserved normal choroidal vascular pattern over an elevated subretinal mass may be indicative of posterior brawny scleritis. Scleral biopsy is useful for tissue diagnosis. Radioactive phosphorus uptake tests and ultrasonography may erroneously indicate choroidal melanoma and lead to enucleation of a potentially salvageable globe.
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PMID:Clinical manifestations of brawny scleritis. 67 4

Electron probe microanalysis demonstrates the presence of aluminium, magnesium, iron, calcium, phosphorus in and around blood vessels in the pallidum (vascular siderosis) and in the putaminal parenchyma in five out of six cases of striatonigral degeneration, associated with orthostatic hypotension in two of these cases. These results suggest that striatonigral degeneration could be the result of a vascular disease, the result of an elemental intoxication of unknown cause.
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PMID:[Presence of aluminum and magnesium in the cerebral arteries and parenchyma of patients with striatonigral syndrome: study by Castaing's microprobe]. 82 52

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

Individuals with diabetes mellitus may have increased in vivo platelet activity. Abnormal platelet function could contribute to the increased incidence of vascular disease in diabetes mellitus. The biochemical mechanism(s) for platelet hyperactivation is unknown. We examined the hypothesis that platelet phosphoinositide turnover, a key signal-transducing mechanism involved in platelet activation, was abnormal in diabetic subjects. Platelets were harvested from 16 subjects with insulin-dependent diabetes mellitus (IDDM) and 19 healthy, nondiabetic control subjects of comparable age. Plasma beta-thromboglobulin (beta-TBG), a specific marker of platelet activity in vivo, was increased in IDDM (67.1 +/- 7.3 ng/ml) compared with control (41.0 +/- 6.0 ng/ml) subjects (P less than .005). [32P]orthophosphate (32Pi) incorporation into the individual phosphoinositides and phosphatidic acid (PA) reached isotopic equilibrium by 120 min for IDDM and control subjects. Specific activity (dpm 32P/micrograms phosphorus) of phosphatidylinositol 4-phosphate (PIP) and phosphatidylinositol 4,5-bisphosphate (PIP2) was not different between IDDM and control subjects. Under these conditions, basal 32Pi incorporation into PIP2 and PIP but not phosphatidylinositol (PI) or PA was significantly lower in IDDM subjects. There was significantly decreased [32P]PIP2 and [32P]PIP hydrolysis and decreased [32P]PA formation in IDDM after platelet stimulation with 4 U/ml human thrombin. There were no differences in [32P]PI hydrolysis between the two groups. The mass of PIP2 was reduced (P less than .005) in the platelets from IDDM (0.71 +/- 0.23 nmol/10(9) platelets) compared with control (1.65 +/- 0.53 nmol/10(9) platelets) subjects. Similarly, PIP was lower (P less than .001) in IDDM (0.66 +/- 0.09 nmol/10(9) platelets) than in control (2.92 +/- 0.43 nmol/10(9) platelets) subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased platelet phosphoinositide turnover and enhanced platelet activation in IDDM. 254 8

Several hematologic abnormalities have been defined in patients with diabetes mellitus, despite the lack of classic hematologic pathologic findings in this condition. Studies of the erythrocyte and the formation of hemoglobin A1c have provided a means of documenting glycemia and a model reaction for diabetic sequelae through postsynthetic protein modification. Oxygen affinity has been noted to be abnormal in the diabetic erythrocyte, concomitant with a decreased concentration of inorganic phosphorus, glycosylation of the 2,3-diphosphoglycerate binding site or preexisting vascular disease. Red cell membrane viscosity has also been documented to be increased in the hyperglycemic subject. Abnormalities in the polymorphonuclear leukocyte have been described, involving the properties of adherence, random migration, chemotaxis, phagocytosis and killing. Certain metabolic abnormalities are also present in this cell type. The lymphocyte has been shown to have abnormal metabolic properties, mitogen responses and cell surface properties in diabetes both in animals and human subjects. Certain subpopulations of lymphocytes appear to be especially vulnerable to changes concomitant with diabetes mellitus. In vitro abnormalities of platelet behavior have been widely studied, although the in vivo significance of these findings remains controversial. Studies of the fluid phase of coagulation have suggested the existence of a hypercoagulable state in hyperglycemic subjects. The clinical significance of most of these findings remains to be defined. Nevertheless, the observation that many of the abnormalities described are reversible when hyperglycemia is corrected has given impetus to the development of improved systems of glucose "control" for diabetic patients.
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PMID:Hematologic alterations in diabetes mellitus. 700 87

Although most forms of glomerulonephritis in man are thought to have an immunopathogenesis, certain clinical and experimental observations support the role of other non-immunologic mechanisms in the progression of these diseases. 1. Intra-renal vascular disease thought to be secondary to hypertension, may be responsible for ischemic glomerular sclerosis. 2. Hypertension may damage the diseased glomerulus directly, as has been demonstrated in experimental glomerulonephritis, in the remnant kidney, and in experimental diabetes mellitus. 3. Alterations in glomerular structure and function in the remnant kidney suggest that adaptations to nephron loss may contribute to further renal damage. 4. Glomerular sclerosis occurs under circumstances where immunologic mechanisms are highly unlikely, such as aging, reflex nephropathy, chronic aminonucleoside administration, and protein loading. 5. Preservation of renal function can be achieved by phosphorus restriction in the remnant kidney and in nephrotoxic serum nephritis.
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PMID:Mechanisms of progression in glomerulonephritis. 703 41

Chronic renal insufficiency ultimately culminating in end-stage renal disease requiring dialysis or transplantation is a major health problem in the United States. The first task confronting the physician caring for a patient with renal disease is to decide whether the renal insufficiency is acute or chronic. The initial differential diagnostic approach to chronic renal insufficiency consists of determining whether the patient has glomerular disease or interstitial or vascular disease on the basis of a careful history taking, urinalysis, and measurement of 24-hour protein excretion. Further refinement of diagnostic considerations often requires serologic studies, renal biopsy, or imaging the urinary tract with ultrasonography or computed tomography. Management considerations begin with the identification and correction of any acute reversible causes of renal insufficiency in patients with chronic renal disease. Recent studies have shown that effective antihypertensive therapy, especially with angiotensin-converting enzyme inhibitors, restriction of dietary protein, and excellent glycemic control in patients with diabetes, can retard the progression of chronic renal disease. Once these therapeutic strategies are in place, it is important to anticipate and treat the multiple manifestations of chronic progressive renal insufficiency: fluid overload, hyperkalemia, metabolic acidosis, abnormalities of calcium, phosphorus, and vitamin D metabolism, and anemia.
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PMID:Chronic renal insufficiency: a diagnostic and therapeutic approach. 1021 59

Hyperphosphatemia is a predictable consequence of chronic renal failure and is present in most patients on dialysis. Traditionally, the risk associated with elevated serum phosphorus has focused on its impact on renal osteodystrophy. A growing body of evidence, however, suggests that abnormalities in serum phosphorus, calcium-phosphorus product (CaxP), and parathyroid hormone (PTH) levels are resulting in vascular and visceral calcification, thereby contributing to the substantially increased risk of cardiovascular death in this population. In this analysis, we review in detail the literature that describes these associations. We show that the current treatment paradigm for serum phosphorus and secondary hyperparathyroidism is ineffective for a large segment of dialysis patients. Currently, 60% of hemodialysis patients have phosphorus greater than 5.5 mg/dL, and 40% have CaxP greater than 60 mg(2)/dL(2). It is our belief that prevention of uremic calcification, cardiac death, and vascular disease should assume primary importance when evaluating the risks associated with elevated levels of phosphorus, CaxP, and PTH. We recommend that target levels should become 9.2 to 9.6 mg/dL for calcium, 2.5 to 5.5 mg/dL for phosphorus, less than 55 mg(2)/dL(2) for CaxP product, and 100 to 200 pg/mL for intact PTH.
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PMID:Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: recommendations for a change in management. 1138 11

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
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PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

Cardiovascular disease is extremely common in patients with end-stage renal disease (ESRD) and accounts for at least 50% of deaths among these patients. Vascular calcifications (VC) have been recently implicated as a possible cause of this excess cardiovascular mortality. Medial calcification is a striking feature of vascular disease in patients with ESRD. The traditional view that VC is a degenerative and passive process has been seriously challenged, based on strong evidence suggesting that VC is an active and highly regulated process similar to bone formation. Different data support the notion that elevated levels of phosphorus and/or other uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells, which can produce bone matrix proteins. This nidus can then mineralize if the balance of pro-mineralizing factors outweighs inhibitory factors. The advent of newer noninvasive screening tests have generated great interest for screening patients with ESRD for vascular calcifications. Control of serum phosphorus with sevelamer, a recently developed non-calcium, non-aluminum phosphate binder, have attenuated or arrested progression of coronary artery and aortic calcifications compared to treatment with calcium-based binders. Amino bisphosphonates, have shown to completely inhibit soft tissue calcifications, calciphylaxis and prevent death in animal models. The first generation bisphosphonate, etidronate, reduces the progression of coronary artery calcifications patients receiving long-term hemodialysis and intravenous pamidronate has produced a rapid improvement of calciphylaxis. In conclusion, VC is a widespread phenomenon in patients with ESRD with important cardiovascular consequences. A better understanding of the processes of VC is leading to therapies to retard or improve this phenomenon and will probably have an important impact on patient mortality.
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PMID:Vascular calcifications in chronic kidney disease: are there new treatments? 1585 37


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