Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, histologic, and immunohistochemical features of six cases of hemorrhagic adrenal pseudocysts are reported together, with a review of the English literature on this topic since 1950. The mean age at presentation was 57 years (range, 30-72 yr). There were four men and 2 women. The average cyst size was 9.2 cm (range, 6-16 cm). In four patients, the hemorrhagic adrenal pseudocysts were incidental findings. The remaining two patients presented with an abdominal mass and hypertension, respectively. The hemorrhagic pseudocysts were unilocular cystic masses surrounded by a fibrous capsule and containing abundant amorphous material, blood, and fibrin. Numerous dilated, thin-walled, vascular channels that stained strongly for Factor VIII-related antigen, collagen IV, laminin, Ulex europaeus agglutinin I lectin, and CD34 were present within the fibrous capsule, cyst contents, and surrounding residual adrenal gland. These findings support a vascular origin for these lesions, and they are thought, therefore, to be related to endothelial adrenal cysts. The literature review of 111 vascular adrenal cysts (85 hemorrhagic pseudocystic type and 26 endothelial type) showed similar clinical features. The mean age at presentation was 44.5 years (range, 5 d-95 yr), with a female predominance (62%). The most common clinical presentation was abdominal pain (35%), followed by incidental findings (32%). There were no significant clinical differences between hemorrhagic and endothelial type cysts. In some cases, the presence of intracystic islands of cortical cells can cause diagnostic confusion with adrenal cortical tumors. The presence, however, of a rich intracystic and capsular vascular network, normal-appearing islands of cortical cells, and abundant thrombotic fibrinous material, rather than necrotic tumor cells, should rule out the possibility of a degenerating adrenal cortical neoplasm.
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PMID:Vascular adrenal cysts: a clinicopathologic and immunohistochemical study of six cases and a review of the literature. 919 68

A lipoma with a spindled proliferation within it, resembling known (myo)fibroblastic lesions such as fibrous histiocytoma or dermatofibrosarcoma protuberans, (ie, fibrohistiocytic lipoma), has not been previously reported. This tumor varies from other classic lipoma variants, including spindle cell lipoma, myolipoma, angiolipoma, and fibrolipoma. We examine the clinicopathologic findings of this new lipoma variant. The Soft Tissue Pathology Registry of the Armed Forces Institute of Pathology was searched for patients with "lipoma with fibrohistiocytic proliferation." Lesions that were better classified as other entities were excluded. Patient slides and clinical history, including associated lesions, family history, duration of symptoms, history of trauma, natural progression, and treatments, were reviewed. Immunohistochemistry was performed on cases with available material (n = 6). Twelve patients with fibrohistiocytic lipoma were included. All tumors revealed a well-distributed quilt-like proliferation or solid focus of slightly plump to relatively bland spindled cells with collagenous stroma in short fascicular and storiform growth patterns. These spindled cells resembled those seen in either fibrous histiocytoma or dermatofibrosarcoma protuberans. However, the spindled proliferation was all within a well-circumscribed lipoma. The lesions lack the dermal involvement or plump pleomorphism of fibrous histiocytoma and the dermal involvement or infiltrative growth pattern of dermatofibrosarcoma protuberans. The fatty component demonstrated heterogeneously sized adipocytes, as those seen in other lipomas. Inflammation and hemosiderin were minimal. Mast cells were not identified. The tumors were typically found in the subcutis of the trunk of men (10 of 12; one each on the wrist and leg; mean age, 31 years). The average size of the lesions was 3.0 cm, and they were present for a mean duration of 10 months prior to surgical excision. One patient had two concurrent lesions; all others had solitary tumors. Another patient had a intracranial dermoid cyst removed during childhood. Four patients had a personal or family history of hypercholesterolemia, hypertension, or myocardial infarction. There was no history of antecedent trauma. Cases studied were positive for vimentin, calponin (5 of 5), CD34 (3 of 5), and occasionally KP-1 or lysozyme in the spindled component, and all cases studied were negative for the actins, caldesmon, S-100 protein, desmin, cytokeratins, and epithelial membrane antigen. Although the actins were negative in our laboratory, the more sensitive calponin positivity suggests myofibroblastic phenotype of the spindled component of this lesion. CD34-positive fibroblasts were present in three of five cases. Of eight patients with follow-up, there were no recurrences; all patients were alive and free of disease over a mean of 10 years (range, 2 months to 31 years). We have identified a lipoma variant, fibrohistiocytic lipoma, that has not been previously described. In our experience the morphology and calponin positivity suggest myofibroblastic phenotype for the spindled cells, within a lipoma. This entity can be distinguished from fibrous histiocytoma, fibromatosis, dermatofibrosarcoma protuberans, spindle cell lipoma and other lipoma, and liposarcoma variants.
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PMID:Fibrohistiocytic lipoma: twelve cases of a previously undescribed benign fatty tumor. 1114 65

Recent studies provide increasing evidence that postnatal neovascularization involves bone marrow-derived circulating endothelial progenitor cells (EPCs). The regulation of EPCs in patients with coronary artery disease (CAD) is unclear at present. Therefore, we determined the number and functional activity of EPCs in 45 patients with CAD and 15 healthy volunteers. The numbers of isolated EPCs and circulating CD34/kinase insert domain receptor (KDR)-positive precursor cells were significantly reduced in patients with CAD by approximately 40% and 48%, respectively. To determine the influence of atherosclerotic risk factors, a risk factor score including age, sex, hypertension, diabetes, smoking, positive family history of CAD, and LDL cholesterol levels was used. The number of risk factors was significantly correlated with a reduction of EPC levels (R=-0.394, P=0.002) and CD34-/KDR-positive cells (R=-0.537, P<0.001). Analysis of the individual risk factors demonstrated that smokers had significantly reduced levels of EPCs (P<0.001) and CD34-/KDR-positive cells (P=0.003). Moreover, a positive family history of CAD was associated with reduced CD34-/KDR-positive cells (P=0.011). Most importantly, EPCs isolated from patients with CAD also revealed an impaired migratory response, which was inversely correlated with the number of risk factors (R=-0.484, P=0.002). By multivariate analysis, hypertension was identified as a major independent predictor for impaired EPC migration (P=0.043). The present study demonstrates that patients with CAD revealed reduced levels and functional impairment of EPCs, which correlated with risk factors for CAD. Given the important role of EPCs for neovascularization of ischemic tissue, the decrease of EPC numbers and activity may contribute to impaired vascularization in patients with CAD. The full text of this article is available at http://www.circresaha.org.
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PMID:Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease. 1144 Sep 84

We studied 4 new cases of juxtaglomerular cell tumor and compared their morphologic and immunohistochemicalfeatures with 2 renal hemangiopericytomas and 5 cutaneous glomus tumors. The juxtaglomerular tumors were resectedfrom 2 males and 2 females (mean age at diagnosis, 23 years). Three patients manifested with severe hypertension. Tumors ranged from 2.2 to 8.0 cm and were well circumscribed. The tumors consisted of solid sheets and nodules of variably sized tumor cells with round, oval, and spindled nuclei alternating with edematous microcystic foci. Nuclear atypia, present in all tumors, was a prominent feature in 2. Mitotic activity was not identified. All cases showed hemorrhage, numerous mast cells, and thick-walled blood vessels. Unusual features included coagulative tumor necrosis, a hemangiopericytoma-like vascular pattern, and hyalinized stroma. All tumors were immunoreactive for CD34 and actin. Ultrastructural analysis revealed the presence of rhomboid-shaped renin protogranules. Patients were treated by partial or radical nephrectomy and followed up for 14 to 48 months. There were no recurrences or metastases. The characteristic clinical and morphologic features of juxtaglomerular cell tumor permit distinction from renal hemangiopericytoma and other renal tumors.
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PMID:Juxtaglomerular cell tumor: a clinicopathologic study of four cases and review of the literature. 1204 49

Idiopathic nodular glomerulosclerosis (ING) is an enigmatic condition that resembles nodular diabetic glomerulosclerosis but occurs in nondiabetic patients. We reviewed clinicopathologic features, immunohistochemical profiles, and outcomes in 23 patients with ING diagnosed from among 5,073 native renal biopsy samples (0.45%) at Columbia University from January 1996 to March 2001. This cohort, in which diabetes mellitus was excluded, consisted predominantly of older (mean age, 68.2 years) white (73.9%) men (78.3%). Clinical findings at presentation included renal insufficiency in 82.6% (mean serum creatinine = 2.4 mg/dL), proteinuria (> 3 g/d in 69.6%; mean 24-hour urine protein = 4.7 g/d), and-less frequently-full nephrotic syndrome (21.7%). There was a high prevalence of hypertension (95.7%; mean = 15.1 +/- 3.4 years), smoking (91.3%; mean = 52.9 +/- 6.9 pack-years), hypercholesterolemia (90%), and extrarenal vascular disease (43.5%). All 23 patients had prominent diffuse and nodular mesangial sclerosis, glomerular basement membrane thickening, arteriosclerosis, and arteriolosclerosis. Immunohistochemical staining for CD34, a marker of endothelial cells, showed an increased number of vascular channels within ING glomeruli compared with normal controls. Follow-up data were available for 17 patients, 6 of whom reached end-stage renal disease (ESRD) (35.3%). By Kaplan-Meier estimates, the median time after biopsy to ESRD was 26 months. Predictors of progression to ESRD included continuation of smoking (P =.0165), lack of angiotensin II blockade (P =.0007), degree of tubular atrophy and interstitial fibrosis (P =.0517), and degree of arteriosclerosis (P =.0096). In conclusion, ING is a progressive vasculopathic lesion linked to hypertension and cigarette smoking.
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PMID:Idiopathic nodular glomerulosclerosis is a distinct clinicopathologic entity linked to hypertension and smoking. 1220 16

The association of membranous glomerulonephritis with benign tumors is rarely described. This report represents, to the best of our knowledge, the first documented account of the simultaneous occurrence of juxtaglomerular cell tumor of the kidney and membranous glomerulonephritis. A young Chinese woman presented with hypertension and proteinuria, whereupon investigations disclosed a renal tumor. She underwent surgical resection, and histologic examination of the tumor revealed CD34-positive uniform polygonal cells with accompanying mast cells, disposed in sheets with focal papillary pattern punctuated by cytokeratin-positive tubular structures. Characteristic rhomboid crystalline granules were identified ultrastructurally. The kidney adjacent to the tumor showed features of membranous glomerulonephritis and hypertensive arteriopathy. Proteinuria improved following tumor resection, but the patient had persistent hypertension attributable to renal hypertensive arteriopathy. This report also highlights the recently described observation of CD34 positivity in juxtaglomerular cell tumors.
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PMID:A case of juxtaglomerular cell tumor associated with membranous glomerulonephritis. 1457 36

The Philadelphia chromosome-negative chronic myeloproliferative disorders (CMPD), polycythemia vera (PV), essential thrombocythemia (ET) and chronic idiopathic myelofibrosis (IMF), have overlapping clinical features but exhibit different natural histories and different therapeutic requirements. Phenotypic mimicry amongst these disorders and between them and nonclonal hematopoietic disorders, lack of clonal diagnostic markers, lack of understanding of their molecular basis and paucity of controlled, prospective therapeutic trials have made the diagnosis and management of PV, ET and IMF difficult. In Section I, Dr. Jerry Spivak introduces current clinical controversies involving the CMPD, in particular the diagnostic challenges. Two new molecular assays may prove useful in the diagnosis and classification of CMPD. In 2000, the overexpression in PV granulocytes of the mRNA for the neutrophil antigen NBI/CD177, a member of the uPAR/Ly6/CD59 family of plasma membrane proteins, was documented. Overexpression of PRV-1 mRNA appeared to be specific for PV since it was not observed in secondary erythrocytosis. At this time, it appears that overexpression of granulocyte PRV-1 in the presence of an elevated red cell mass supports a diagnosis of PV; absence of PRV-1 expression, however, should not be grounds for excluding PV as a diagnostic possibility. Impaired expression of Mpl, the receptor for thrombopoietin, in platelets and megakaryocytes has been first described in PV, but it has also been observed in some patients with ET and IMF. The biologic basis appears to be either alternative splicing of Mpl mRNA or a single nucleotide polymorphism, both of which involve Mpl exon 2 and both of which lead to impaired posttranslational glycosylation and a dominant negative effect on normal Mpl expression. To date, no Mpl DNA structural abnormality or mutation has been identified in PV, ET or IMF. In Section II, Dr. Tiziano Barbui reviews the best clinical evidence for treatment strategy design in PV and ET. Current recommendations for cytoreductive therapy in PV are still largely similar to those at the end of the PVSG era. Phlebotomy to reduce the red cell mass and keep it at a safe level (hematocrit < 45%) remains the cornerstone of treatment. Venesection is an effective and safe therapy and previous concerns about potential side effects, including severe iron deficiency and an increased tendency to thrombosis or myelofibrosis, were erroneous. Many patients require no other therapy for many years. For others, however, poor compliance to phlebotomy or progressive myeloproliferation, as indicated by increasing splenomegaly or very high leukocyte or platelet counts, may call for the introduction of cytoreductive drugs. In ET, the therapeutic trade-off between reducing thrombotic events and increasing the risk of leukemia with the use of cytoreductive drugs should be approached by patient risk stratification. Thrombotic deaths seem very rare in low-risk ET subjects and there are no data indicating that fatalities can be prevented by starting cytoreductive drugs early. Therefore, withholding chemotherapy might be justifiable in young, asymptomatic ET patients with a platelet count below 1500000/mm(3) and with no additional risk factors for thrombosis. If cardiovascular risk factors together with ET are identified (smoking, obesity, hypertension, hyperlipidemia) it is wise to consider platelet-lowering agents on an individual basis. In Section III, Dr. Gianni Tognoni discusses the role of aspirin therapy in PV based on the recently completed European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Study, a multi-country, multicenter project aimed at describing the natural history of PV as well as the efficacy of low-dose aspirin. Aspirin treatment lowered the risk of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke (relative risk 0.41 [95% CI 0.15-1.15], P =.0912). Total and cardiovascular mortality were also reduced by 46% and 59%, respectively. Major bleedings were slightly increased nonsignificnsignificantly by aspirin (relative risk 1.62, 95% CI 0.27-9.71). In Section IV, Dr. Giovanni Barosi reviews our current understanding of the pathophysiology of IMF and, in particular, the contributions of anomalous megakaryocyte proliferation, neoangiogenesis and abnormal CD34(+) stem cell trafficking to disease pathogenesis. The role of newer therapies, such as low-conditioning stem cell transplantation and thalidomide, is discussed in the context of a general treatment strategy for IMF. The results of a Phase II trial of low-dose thalidomide as a single agent in 63 patients with myelofibrosis with meloid metaplasia (MMM) using a dose-escalation design and an overall low dose of the drug (The European Collaboration on MMM) will be presented. Considering only patients who completed 4 weeks of treatment, 31% had a response: this was mostly due to a beneficial effect of thalidomide on patients with transfusion dependent anemia, 39% of whom abolished transfusions, patients with moderate to severe thrombocytopenia, 28% of whom increased their platelet count by more than 50 x 10(9)/L, and patients with the largest splenomegalies, 42% of whom reduced spleen size of more than 2 cm.
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PMID:Chronic myeloproliferative disorders. 1463 83

Recent studies suggest that postnatal neovascularization relies not exclusively on sprouting of preexisting vessels ("angiogenesis"), but also involves the contribution of bone marrow-derived circulating endothelial progenitor cells (EPCs). EPCs can be isolated from peripheral blood or bone marrow mononuclear cells, CD34(+) or CD133(+) hematopoietic progenitors. Infusion of EPCs was shown to promote postnatal neovascularization of ischemic tissue after myocardial infarction in animal models and initial clinical trials. Moreover, circulating endothelial precursor cells can home to denuded arteries after balloon injury and contribute to endothelial regeneration, thereby limiting the development of restenosis. Thus, circulating endothelial cells may exert an important function as endogenous repair mechanism to maintain the integrity of the endothelial monolayer and to promote ischemia-induced neovascularization. However, risk factors for coronary artery disease, such as diabetes, hypercholesterolemia, and hypertension are associated with impaired number and function of EPC in patients with coronary artery disease. Therapeutically, the reduction of EPC number and the decreased functional activity in patients with coronary artery disease was counteracted by 3-hydroxy-3-methylglutaryl coenzymeA (HMG-CoA) reductase inhibitors (statins), vascular endothelial growth factor (VEGF), estrogen, or exercise. At the molecular level, these factors are well established to activate the phosphatidyl-inositol-3-kinase (PI3K)-Akt-dependent activation of the endothelial nitric oxide synthase (eNOS), suggesting that the PI3K-Akt-eNOS signaling pathway may be involved in the transduction of atheroprotective factors. Taken together, the balance of atheroprotective and proatherosclerotic factors may influence EPC levels and their functional capacity to improve neovascularization and endothelial regeneration.
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PMID:Risk factors for coronary artery disease, circulating endothelial progenitor cells, and the role of HMG-CoA reductase inhibitors. 1584 10

Obesity has been linked to cardiovascular disease, hypertension, diabetes and the metabolic syndrome, with elevated markers of systemic inflammation. Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane adhesion molecule involved in leukocyte migration to sites of inflammation. In human obesity, elevated expression of the soluble form of ICAM-1 (sICAM-1) is positively correlated with abdominal fat deposition. Increases in adiposity have also been correlated with macrophage infiltration into adipose tissue. Here we investigate adipose tissue production and transcriptional regulation of ICAM-1 in a mouse model of dietary obesity. After feeding mice a high-fat diet, ICAM-1 expression in serum and adipose tissue was analyzed by ELISA, Northern blotting, real-time quantitative PCR, and flow cytometry. After 6 mo on the high-fat diet, sICAM-1 levels significantly correlated with body weight and abdominal fat mass. ICAM-1 mRNA was expressed in adipose tissue of mice, with significantly higher levels in males than females. After only 3 wk, there were adipose tissue-specific increases in mRNAs for ICAM-1, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in male mice. Analysis of the stromal-vascular fraction of male adipose tissue revealed CD11b-negative cells with increased surface ICAM-1 and CD34. We also found two populations of F4/80+, CD11b+, ICAM-1+ cells, one of which also expressed CD14 and CD11c and was increased in response to a high-fat diet. These results indicate that within 3 wk on a high-fat diet, male mice exhibited significant increases in pro-inflammatory factors and immune cell infiltration in adipose tissue that may represent links between obesity and its associated inflammatory complications.
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PMID:ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice. 1680 3

Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord blood-derived CD34+ cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34- or CD34+ cells (1 x 10(5)-5 x 10(5)/mL/kg body weight) i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-alpha levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34- cell-treated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34+ cells significantly improved survival time (duration, 63-291 min). As compared with normothermic controls, all CD34- cell-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34+ cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34+ cell therapy during heatstroke. Our data indicate that CD34+ cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure.
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PMID:Human umbilical cord blood-derived CD34+ cells cause attenuation of multiorgan dysfunction during experimental heatstroke. 1750 7


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