We evaluated serum albumin at time of admission, within 72 hours, in 135 geriatric patients who were older than 70 years to establish its role as a predictor of death and clinical outcome at time of discharge. Serum albumin values were reduced significantly in patients who died compared with those who were discharged in unchanged/impaired and improved conditions (3.01 +/- 0.68 g/dL, 3.18 +/- 0.55 g/dL, and 3.65 +/- 0.52 g/dL respectively, P < 0.0001). A correlation between serum albumin concentration at admission and number of days elapsed from admission and death was found (r = 0.43, P < 0.05). Mortality rate was 38.6% in patients with serum albumin values < 3.3 g/dL compared with 14.1% in those with albumin values > or = 3.3 g/dL (P < 0.005). Similar results were obtained even when the main diagnostic conditions, such as cardiocerebrovascular disease and cancer, were considered. The results demonstrate that in geriatric patients the serum albumin level at admission may be a predictor of mortality and clinical outcome at discharge.

The purposes of this study were threefold: (1) to compare values obtained by three conventional radioimmunoassays for serum bone-gla-protein (BGP) in a population of normal women, (2) to study the relationship between serum BGP and bone mineral density (BMD) measured at four different skeletal sites (lumbar spine, proximal femur, proximal and ultradistal radius), and (3) to compare the results obtained by the three assays with conventional markers of bone turnover. Ninety-seven normal women (age range 25 to 75 years, mean ± SD = 54.3 ± 10.9 years) were studied. Three independent assays were used to measure serum osteocalcin levels: a heterologous radioimmunoassay (RIA) (A) (Incstar Co., Stillwater, Minn.), a homologous RIA (B) (Nichols Institute, San Juan Capistrano, Calif.), and a two-site immunoradiometric assay (C) (Cis Biointernational, Gif-sur-Yvette, France). Mean ± SD values of serum osteocalcin in the group as a whole were 4.05 ± 1.37 μg/L by assay A, 6.03 ± 2.90 μg/L by assay B, and 22.67 ± 7.52 μg/L by assay C. Serum osteocalcin levels increased linearly with age; however, no correlation between serum BGP (whatever the assay used) and age was observed when only postmenopausal women were taken into account. When the effect of age was held constant by means of partial correlation analysis, only serum BGP levels measured by assays B and C were still inversely related with lumbar spine and ultradistal radius BMD; the latter assay was also weakly correlated with Ward's triangle BMD. After all the biochemical and clinical variables taken into consideration were introduced in a multiple regression equation, serum BGP still represented an important predictor of ultradistal radius and lumbar spine BMD only. Regarding relationships with other markers of bone turnover, the assay C in general showed the highest r values. In conclusion, our results indicate that commercially available BGP assays differ analytically and clinically; furthermore for the first time they show the existence of an inverse correlation between serum osteocalcin levels (which reflects bone turnover at the time of examination) and bone mass (which at a given time represents the balance of all previous metabolic events), after the influence of aging is excluded.

We performed this study in order to verify the existence of a correlation between early platelet count reduction and initial neurological impairment, infarct extension and mortality or clinical outcome in an established ischemic cerebral infarction. The results demonstrate that the platelet consumption and/or accumulation in the infarct area, expressed by circulating platelet decrease, is related to the severity of neurological involvement, infarct size and poor clinical outcome.

Plasma fibrinogen levels and platelet counts were evaluated in 30 patients with acute ischemic cerebral infarction (CI) three and nine days after the onset of symptoms. Hyperfibrinogenemia (379.4 +/- 80.3 vs 327.3 +/- 48.3 mg/dL of controls, p < 0.005), a reduction of platelet count (207.133 +/- 48.388 vs 288.375 +/- 61.373 x 10(9)/L of controls, p < 0.001), and an inverse correlation (r = -0.41, p < 0.05) between the two parameters were observed on day three. On day nine, platelet counts normalized while plasma fibrinogen levels slightly increased; the inverse correlation no longer occurred. The results suggest that in the earliest phase of stroke plasma fibrinogen levels may condition the extent of platelet accumulation or consumption in the ischemic area. This confirms in vivo that the platelet aggregation process is strictly dependent on fibrinogen concentration.

Journal Article Relationship between Circulating Platelets and Serum Concentrations of Creatine Kinase in Stroke Get access E D'Erasmo, E D'Erasmo Search for other works by this author on: Oxford Academic Google Scholar M Acca, M Acca Search for other works by this author on: Oxford Academic Google Scholar F S Celi, F S Celi Search for other works by this author on: Oxford Academic Google Scholar F Medici, F Medici Search for other works by this author on: Oxford Academic Google Scholar G Aliberti G Aliberti Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 38, Issue 2, 1 February 1992, Pages 320–321, https://doi.org/10.1093/clinchem/38.2.320 Published: 01 February 1992

HomeStrokeVol. 22, No. 8Correlation between plasma fibrinogen levels and white blood cell count after cerebral infarction. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBCorrelation between plasma fibrinogen levels and white blood cell count after cerebral infarction. E D'Erasmo, M Acca, F S Celi and G Mazzuoli E D'ErasmoE D'Erasmo Search for more papers by this author , M AccaM Acca Search for more papers by this author , F S CeliF S Celi Search for more papers by this author and G MazzuoliG Mazzuoli Search for more papers by this author Originally published5 Apr 2018https://doi.org/10.1161/str.22.8.1089aStroke. 1991;22:1089"Correlation between plasma fibrinogen levels and white blood cell count after cerebral infarction.." Stroke, 22(8), p. 1089 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Stuller K, Jarrett B and DeVries A (2012) Stress and social isolation increase vulnerability to stroke, Experimental Neurology, 10.1016/j.expneurol.2011.01.016, 233:1, (33-39), Online publication date: 1-Jan-2012. Deb P, Sharma S and Hassan K (2010) Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis, Pathophysiology, 10.1016/j.pathophys.2009.12.001, 17:3, (197-218), Online publication date: 1-Jun-2010. Emsley H, Smith C, Tyrrell P and Hopkins S (2007) Inflammation in Acute Ischemic Stroke and its Relevance to Stroke Critical Care, Neurocritical Care, 10.1007/s12028-007-9035-x, 9:1, (125-138), Online publication date: 1-Aug-2008. Iturbe Hernández T, Moreno Chulilla J, Romero Colás M and Gutiérrez Martín M (2002) Fibrinógeno y recuento monocitario en la fase inicial del ictus isquémico, Medicina Clínica, 10.1016/S0025-7753(02)72319-1, 118:4, (159), Online publication date: 1-Jan-2002. Emsley H and Tyrrell P (2016) Inflammation and Infection in Clinical Stroke, Journal of Cerebral Blood Flow & Metabolism, 10.1097/01.WCB.0000037880.62590.28, 22:12, (1399-1419), Online publication date: 1-Dec-2002. Emsley H and Tyrrell P (2002) Inflammation and Infection in Clinical Stroke, Journal of Cerebral Blood Flow & Metabolism, 10.1097/00004647-200212000-00001, (1399-1419), Online publication date: 1-Dec-2002. August 1991Vol 22, Issue 8 Advertisement Article InformationMetrics Copyright © 1991 by American Heart Associationhttps://doi.org/10.1161/str.22.8.1089aPMID: 1866761 Originally publishedApril 5, 2018 PDF download Advertisement

Platelet parameters (number, platelet hematocrit, mean platelet volume, platelet distribution width) have been studied in 196 Type II elderly diabetics as well as in 90 sex- and age-matched controls. The diabetics were divided in two groups on the basis of the presence or absence of macroangiopathy diagnosed clinically and/or by Doppler flowmetry. The mean platelet volume proved to be larger in the macroangiopathic diabetics than in controls, whereas no differences were found between diabetics without established macroangiopathy and the controls. The results can be explained by supposing an enhanced peripheral platelet consumption in the vasculopathic diabetics, inducing an increase of the portion of circulating young large platelets.

HomeStrokeVol. 22, No. 2Relationship between platelet and white blood cell counts during the early phase of cerebral infarction. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBRelationship between platelet and white blood cell counts during the early phase of cerebral infarction. E D'Erasmo, F S Celi, M Acca and G Mazzuoli E D'ErasmoE D'Erasmo , F S CeliF S Celi , M AccaM Acca and G MazzuoliG Mazzuoli Originally published5 Apr 2018https://doi.org/10.1161/str.22.2.283aStroke. 1991;22:283"Relationship between platelet and white blood cell counts during the early phase of cerebral infarction.." Stroke, 22(2), p. 283 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Sadeghi F, Kovács S, Zsóri K, Csiki Z, Bereczky Z and Shemirani A (2019) Platelet count and mean volume in acute stroke: a systematic review and meta-analysis, Platelets, 10.1080/09537104.2019.1680826, 31:6, (731-739), Online publication date: 17-Aug-2020. Thornton P, McColl B, Greenhalgh A, Denes A, Allan S and Rothwell N (2010) Platelet interleukin-1α drives cerebrovascular inflammation, Blood, 10.1182/blood-2009-11-252643, 115:17, (3632-3639), Online publication date: 29-Apr-2010. Hadidi E, Mojtahedzadeh M, Paknejad M, Nikfar S, Zamani M, Sahraian M, Eftekhar B, Khajavi M, Najafi A, Ghaffarzadeh M, Eftekhari R, Soleimani V, Esmaily H, Rouini M and Abdollahi M (2006) Alterations of blood IL-8, TGF-β1 and nitric oxide levels in relation to blood cells in patients with acute brain injury, Therapy, 10.2217/14750708.3.3.399, 3:3, (399-405), Online publication date: 1-May-2006. Hadidi E, Mojtahedzadeh M, Paknejad M, Nikfar S, Zamani M, Sahraian M, Eftekhar B, Khajavi M, Najafi A, Ghaffarzadeh M, Eftekhari R, Soleimani V, Esmaily H, Rouini M and Abdollahi M (2006) Alterations of blood IL-8, TGF-beta1 and nitric oxide levels in relation to blood cells in patients with acute brain injury, Therapy, 10.1586/14750708.3.3.399, 3:3, (399-405), Online publication date: 1-May-2006. Alexandrova M, Bochev P, Markova V, Bechev B, Popova M, Danovska M and Simeonova V (2004) Dynamics of free radical processes in acute ischemic stroke: influence on neurological status and outcome, Journal of Clinical Neuroscience, 10.1016/j.jocn.2003.10.015, 11:5, (501-506), Online publication date: 1-Jun-2004. Gunsilius E, Petzer A, Stockhammer G, Kähler C and Gastl G (2001) Serial Measurement of Vascular Endothelial Growth Factor and Transforming Growth Factor-β1 in Serum of Patients With Acute Ischemic Stroke, Stroke, 10.1161/01.STR.32.1.275-b, 32:1, (275-278), Online publication date: 1-Jan-2001. Choi-Kwon S, Yang Y, Kim E, Jeon M and Kim J (1998) Nutritional status in acute stroke: undernutrition versus overnutrition in different stroke subtypes, Acta Neurologica Scandinavica, 10.1111/j.1600-0404.1998.tb07292.x, 98:3, (187-192), Online publication date: 1-Sep-1998. Kim J, Chopp M, Chen H, Levine S, Carey J and Welch K (1995) Adhesive glycoproteins CD11a and CD18 are upregulated in the leukocytes from patients with ischemic stroke and transient ischemic attacks, Journal of the Neurological Sciences, 10.1016/0022-510X(94)00203-Z, 128:1, (45-50), Online publication date: 1-Jan-1995. Boisseau M (1994) The role of anti-myeloid series treatment in ischemic vascular disorders Anticoagulation, 10.1007/978-1-4612-2668-0_9, (177-219), . February 1991Vol 22, Issue 2 Advertisement Article InformationMetrics Copyright © 1991 by American Heart Associationhttps://doi.org/10.1161/str.22.2.283aPMID: 2003297 Originally publishedApril 5, 2018 PDF download Advertisement

We evaluated the incidence of hypo- versus hypercalcemia and hypo- versus hyperphosphatemia in a survey of 158 patients with malignancy; 55/158 had bone metastases. When serum calcium levels were corrected for albuminemia, the incidence of hypo- and hypercalcemia was respectively 10.8% and 10.1%. Hypophosphatemia was found in 29.7% patients, hyperphosphatemia in 2.5%. The incidence was slightly different in presence of bone metastases. Hypocalcemia and hypophosphatemia prevailed in osteoblastic metastases and hypercalcemia in osteolytic metastases. The incidence of hypocalcemia and hypophosphatemia in malignancy was therefore surprisingly high, even apart from the presence of bone metastases. Both hypo- and hypercalcemia were associated with elevated serum alkaline phosphatase levels. Moreover, a calcium-phosphorus product reduction was observed in osteoblastic metastases, suggesting a condition of secondary hyperparathyroidism.

The aim of this study was to evaluate the incidence of hypocalcemia and hypomagnesemia and the relationship between calcium and magnesium serum levels in 82 hospitalized cancer patients, 61 of whom were in the terminal phase of the disease. The frequency of hypocalcemia and hypomagnesemia was 13.4% and 17.1% respectively. The incidence of hypocalcemia in patients with hypomagnesemia was 28.6%, while in those with normal or high magnesium serum levels it was 10.3%. The lowest magnesium serum level was observed in hypocalcemic patients. It may thus be concluded that hypocalcemia and hypomagnesemia are a frequent complication of malignant tumors mostly in the terminal stage of the disease, and that even hypomagnesemia could contribute to the development of tumor-associated hypocalcemia.

The study was performed on patients with ischaemic cerebral infarction in order to obtain information on serial changes of some platelet parameters and to test their prognostic significance. Platelet count, obtained within 48 h after cerebral infarction, was significantly lower than in the control group (213,611 +/- 65,652 mm-3 vs. 299,525 +/- 60,611 mm-3, P less than 0.001), reaching the normal level on the ninth day and thereafter. The mean platelet volume was significantly greater than in the controls (11.26 +/- 1.29 fl vs. 8.93 +/- 0.93 fl, P less than 0.001), and normalization generally occurred on the forty-fifth day. The mean platelet count was significantly lower in the patients who died than in those who survived (P less than 0.025 and P less than 0.05 respectively on the first to second and fourth day after infarction). The reduction of platelet count and the increase of mean volume appear to be related to an increased platelet consumption in the infarction area, associated with an in vivo platelet activation, as larger platelets are more responsive to platelet activity and aggregability tests. The lower mean platelet count observed in the patients who died suggests that the platelet value might be considered as a prognostic index of cerebral infarction.