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PubMed1983

Antibodies reactive with surface membranes of cellular elements in the blood.

Autoreactive antibodies or immune complexes may accelerate clearance of mature erythrocytes, leukocytes, and platelets from the circulation in patients with rheumatologic and immunologic disorders. The most compelling evidence for immune injury to hematopoietic cells exists in patients with systemic lupus erythematosus and patients with Felty's syndrome and its variants. These disorders may also cause tissue inflammation, which in turn commonly results in underproduction of erythrocytes and development of thrombocytosis. However, recent evidence indicates that underproduction of hematopoietic cells may also result from immune injury to cellular elements in the bone marrow. In many laboratories, sensitive techniques are now clinically available for the detection of cell-associated immunoglobulin and complement. These assays have helped confirm the role of antibody in the pathogenesis of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura. However, recent data indicate that there is probably a continuum between the amount of immunoglobulin and complement found on normal cells and that found in a variety of disease states. In several of these disorders, additional evidence will be required to establish that the increase in cell-bound immunoglobulin leads to a decrease in the life-span of the cell. In order to provide significant help to the clinician managing an individual patient, these serologic tests must be capable of identifying the portion of the cell-associated protein actually involved in the destructive process. The availability of monoclonal reagents capable of identifying restricted regions on cell-bound immunoglobulin may help identify molecules bound specifically as antibody and may help identify the antigens involved in autoimmune disorders.

Anemia, Hemolytic, Autoimmune↗
PubMed1977

Splenectomy and subsequent mortality in veterans of the 1939-45 war.

A long-term follow-up of 740 American servicemen splenectomised because of trauma during the 1939-45 war showed a significant excess mortality from pneumonia and ischaemic heart-disease. Mortality from cirrhosis was also increased, but not significantly. The findings confirm that the risk of fatal infections is increased by asplenia; however, the risk of cancer was not increased, as it is in some other immunodeficiency states. Post-splenectomy thrombocytosis and hypercoagulability may account for the increased risk of fatal myocardial ischaemia in this group.

Cardiovascular Diseases↗
PubMed1987

White centered retinal hemorrhages in diabetic retinopathy.

Two hundred fifteen diabetic patients (430 eyes) with early proliferative retinopathy, moderate-to-severe nonproliferative retinopathy, and/or diabetic macular edema in each eye were examined for the presence of white centered retinal hemorrhages (WCRHs). Of the eyes examined, 15.6% demonstrated at least one WCRH and 4.9% showed five or more WCRHs. The prevalence of WCRHs was not significantly related to hypertension, anemia, leukocytosis, thrombocytopenia, thrombocytosis, abnormalities of coagulation, increased serum creatinine, or ingestion of oral contraceptives. Local factors associated with microvascular damage and repair are likely responsible for WCRHs in diabetics. Microaneurysms are at the center of many diabetic WCRHs, and the pale centers of many WCRHs in diabetic retinopathy may be platelet-fibrin aggregates.

Adult↗
PubMed1991

The platelet count as a simple measure to distinguish inflammatory bowel disease from infective diarrhoea.

A total of 212 adult patients with infective diarrhoea and 27 with inflammatory bowel disease (IBD), admitted consecutively to an infectious disease unit, were studied in order to determine whether clinical features and laboratory measurements performed on admission identified cases of IBD. Long-standing diarrhoea, blood in the faeces, anaemia, leucocytosis, thrombocytosis, raised ESR and a reduced concentration of serum albumin were more common in patients with IBD (P less than 0.05). The most striking difference was in the platelet count with 59% patients with IBD and 1.6% patients with infective diarrhoea having platelet counts greater than 450 x 10(9)/l. A raised platelet count in a patient admitted to hospital with 'acute gastro-enteritis' suggests IBD.

Adult↗
PubMed2002

Central diabetes insipidus and inv(3)(q21q26) and monosomy 7 in acute myeloid leukemia.

Chromosomal anomalies involving region 3q21q26 have been reported associated with thrombocytosis in various hematological malignancies, such as chronic myeloid leukemia, myelodysplastic syndrome, and acute myeloid leukemia (AML). Recent reports described the association of central diabetes insipidus with AML and chromosomal anomalies involving region 3q21q26. We review the database in our institution and report five cases of inv(3)(q21q26) in consecutive cytogenetic studies of AML and myelodysplastic syndromes from 1992 to 2000, two cases presented as sole abnormalities and three cases were associated with monosomy 7. Only one case was associated with central diabetes insipidus. The literature of 3q21q26 syndrome and central diabetes insipidus in myeloid leukemia is reviewed.

Adult↗
PubMed2002

Establishment of a large cell lung cancer cell line (Y-ML-1B) producing granulocyte colony-stimulating factor.

We established a new lung cancer cell line, designated Y-ML-1B, from a lung cancer of a 70-year-old Japanese man with leukocytosis and thrombocytosis. Before surgical resection, the white blood cell and platelet counts were elevated to 34,400/mm3 and 668,000/mm3, respectively, and the granulocyte colony-stimulating factor (G-CSF) level in the serum was increased at 141 pg/mL. The primary tumor showed an undifferentiated morphology with large cells and induced extensive thickening of the pleura in the right hemithorax. The Y-ML-1B cells grow as a monolayer, with a doubling time of 19 hours, and are tumorigenic in nude mice, which showed a morphology similar to the primary tumor in xenografts. Analysis of the supernatant of cell culture medium of Y-ML-1B showed elevated levels of G-CSF and other cytokines such as interleukin (IL)-6, IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF), consistent with the high levels detected in the patient's serum. Cytogenetic analysis revealed aneuploidy of greater than 56 in metaphases with many structural abnormalities. Mutation analysis of the tumor suppressor genes showed that Y-ML-1B is inactivated in TP53 and RASSF1A, but not in p14(ARF), p16(INK4A), or RB. Neither activating mutations of KRAS or NRAS nor amplification of MYC or MDM2 were detected. Y-ML-1B expressed N-cadherin but not E-cadherin. This newly established cell line might serve as a useful model for studying the molecular pathogenesis for large cell cancers of the lung which express high levels of cytokines.

Aged↗
PubMed2002

[Massive bilateral adrenal hemorrhage after conservative tumor surgery in the isthmus of a horseshoe kidney].

OBJECTIVE: To present a fatal case of massive bilateral suprarrenal haemorrhage (MBSH) after partial nephrectomy. CLINICAL CASE: An 82 year old male treated with oral anticoagulants was diagnosed by means of CT scan and arteriography of having an avascular tumor located at the isthmus of a horseshoe kidney. A tumorectomy with safety surgical margins was performed; It was diagnosed of having a renal adenocarcinoma, which was almost completely necrotic. During the postoperative period, the patient presented abdominal pain, nausea, fever, hypotension and severe respiratory distress. Biochemical studies showed mild hyponatremia and azotemia, accompanied by anemia, leucocytosis and thrombocytosis. An abdominal CT scan demonstrated a MBSH, which produced the patients death soon afterwards. DISCUSSION: Tumoral pathology of horseshoe kidneys presents important topographic and anatomopathologic differences with respect to non-fused kidneys. MBSH is a rare complication of many stress processes especially if an anticoagulant treatment coexists. The treatment has to be initiated as soon as we suspect MBSH, which should be confirmed by hormonal determinations and/or the presence of hyperdense suprarenal lesions at the CT scan.

Adenocarcinoma↗
PubMed2003

[Adult Kawasaki disease].

PURPOSE: Review of the literature on adult Kawasaki disease. CURRENT KNOWLEDGE AND KEY POINTS: Kawasaki disease is an acute multisystemic vasculitis affecting predominantly young children. Several studies have suggested that Kawasaki disease is mediated by bacterial superantigens. The diagnosis is established on clinical criteria since no specific laboratory test yet exists for this disorder. The severity of Kawasaki disease relates to the possible occurrence of coronary aneurysms in 20% of childhood cases. Treatment with intravenous immunoglobulins before day 10 is recommended to prevent aneurysm formation. The occurrence of Kawasaki disease is unusual in adults and 52 cases only have been reported in adult patients. Seventy-one per cent of cases occur between 18 and 30 years. The incidence of specific clinical features is quite similar between adults and children. However meningitis and thrombocytosis are more common in children than in adults, while conversely both arthralgias and liver function abnormalities are more common among adults. Coronary aneurysms are less common in the adults with Kawasaki disease. Other diseases with similar clinical presentation such as drug hypersensitivity reaction and the toxic shock syndrome must be ruled out. Kawasaki disease is often diagnosed after the acute phase at the step of desquamation, when it is too late to expect any beneficial effect from immunoglobulins. FUTURE PROSPECTS AND PROJECTS: Diagnostic criteria of Kawasaki disease have not been validated in an adult population. Criteria of exclusion are necessary to eliminate toxic shock syndrome and drug hypersensitivity syndrome. An international retrospective study to collect data on epidemiologic, clinical, laboratory, and cardiovascular features of adult Kawasaki disease is necessary to validate specific diagnostic criteria and to improve the knowledge on this disease.

Adolescent↗
PubMedDate not supplied

[Acquired idiopathic sideroblastic anemia. Apropos of 39 cases].

We report a series of 39 cases of acquired idiopathic sideroblastic anemia accounting for 12 p. 100 of the 330 cases of myelodysplastic syndrome diagnosed in our department in six years. Patients' mean age was high (70.8 years). Anemia was present in 92 p. 100 of the cases and was of the macrocytic type in 87 p. 100 of the patients. Only two patients (5 p. 100) had neutropenia and two (5 p. 100) had thrombocytopenia. Thrombocytosis was observed in 17 cases (43 p. 100); it was usually moderate. The mean proportion of medullary ring-sideroblasts was 35 +/- 14 p. 100. A clonal abnormality was found in 4 of the 11 karyotype examinations performed. The course of the disease was marked by recurrences of anemia which required regular blood transfusions in 82 p. 100 of the cases. In at least 30 p. 100 of the patients followed up for more than 30 months, these transfusions were responsible for secondary haemochromatosis. Conversely, in only three patients (7.5 p. 100) the disease progressed to acute leukemia. On the other hand, 4 patients (10 p. 100) developed thrombocythemia (greater than 1,000 x 10(9)/1). Median actuarial survival rate was 48 months. There were only two factors of poor prognosis: age over 70 and anemia with less than 8 g/dl haemoglobin at the time of diagnosis. Transfusion haemochromatosis is the principal risk in acquired idiopathic sideroblastic anemia: this risk can be prevented by iron chelating agents in patients with frequent blood perfusions.

Aged↗
PubMedDate not supplied

[Periarteritis nodosa with heart valve disease disclosed by occlusion of the central artery of the retina].

We report a case of periarteritis nodosa revealed by blindness due to occlusion of the central retinal artery. The disease appeared after a serous otitis and was accompanied by thrombocytosis. Its outcome was favourable under corticosteroid therapy, but it was complicated by aortic valve regurgitation. Lesions of fibrinoid necrosis were found on the aortic cusps removed during surgical replacement. It seems highly probable that the ocular and valvular lesions were specific, although this cannot be directly demonstrated. The case presented here is exceptional, and the relevant literature is reviewed.

Aortic Valve↗
PubMed1997

[POEMS syndrome].

POEMS syndrome is an acronym defined by Bardwick (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal component and Skin changes). Other various clinical and biological features are reported: edema, cachexia, microangiopathic glomerulopathy, most rarely pulmonary hypertension, cutaneous necrosis. Thrombocytosis or polycythemia may be a prominent feature. POEMS syndrome is sometimes associated with lymphoproliferative disorder. Castelman-like disease is frequently observed as pathologic findings on lymph nodes. Distinction between POEMS syndrome and osteosclerotic myeloma is delicate. The rate of the monoclonal protein is modest-always less than 30 g/L-and is almost of the lambda light chain class. In contrast to multiple myeloma this syndrome is rarely associated with hypercalcemia, skeletal fracture, renal involvement and increasing of M component during evolution. Bone marrow plasmocytosis is usually less than 15% and the kinetic phenotype and genetic characteristics of the plasma cell remain those found in monoclonal gammopathy of undetermined significance. The pathophysiology of this syndrome remains largely unknown but overproduction of pro-inflammatory cytokines are reported, especially TNF alpha, IL-6 and IL-1 beta. Some clinical manifestations seem to be cytokine related. Polyneuropathy and cachexia are the main cause of death. A part corticosteroid and cure of solitary bone lesion, treatment is disappointing and survival is 60% at five years.

Humans↗
PubMed1997

Diagnostic criteria of the myeloproliferative disorders (MPD): essential thrombocythaemia, polycythaemia vera and chronic megakaryocytic granulocytic metaplasia.

Philadelphia chromosome-positive essential thrombocythaemia (Ph(+)-ET) and chronic granulocytic leukaemia (Ph(+)-CGL) constitute a separate malignant disease entity, whereas essential thrombocythaemia (ET), polycythaemia vera (PV) and chronic megakaryocytic granulocytic metaplasia (CMGM) belong to the Philadelphia chromosome-negative (Ph-) myeloproliferative disorders. The megakaryocytes in Ph(+)-ET and Ph(+)-CGL are abnormal and small with round nuclei, showing little lobulation. Both the number and size of megakaryocytes in Ph-ET, -PV and -CMGM are typically increased. Enlarged megakaryocytes with mature cytoplasm and multilobulated nuclei and their tendency to cluster in a normal or slightly increased cellular bone marrow represent the hallmark of ET. In reactive thrombocytosis the size and morphology of increased megakaryocytes are normal. The characteristic increase and clustering of enlarged mature and pleomorphic megakaryocytes with multilobulated nuclei and proliferation of erythropoiesis in a moderate to marked hypercellular bone marrow with hyperplasia of dilated sinuses is the diagnostic hallmark of untreated PV. In secondary polycythaemia, in which increased cellularity of the erythroid cell line may be present, the number, size and morphology of megakaryocytes remain small and normal. CMGM, including early stages without myelofibrosis and advanced myelofibrotic stages of agnogenic myeloid metaplasia, appears to be a distinct neoplastic proliferation of neutrophilic granulopoiesis and megakaryopoiesis. The histopathology of the bone marrow in CMGM is dominated by atypical, enlarged and immature megakaryocytes with cloud-like nuclei which are not seen in ET and PV. Myelofibrosis in ET, PV and CMGM is graded in no reticulin fibrosis (MFO), early reticulin fibrosis (MF1), advanced reticulin sclerosis with minor collagen fibrosis (MF2) and advanced collagen fibrosis with or without osteosclerosis (MF3). Myelofibrosis is not a feature of ET, may occur in PV, and constitutes a prominent feature of CMGM during the natural history of the disease.

Bone Marrow↗
PubMed2000

Gelatinous bone marrow transformation in a case of idiopathic myelofibrosis: a morphological paradox.

A 74-year-old woman with severe, but asymptomatic weight loss was found to have splenomegaly, thrombocytosis, and neutrocytosis. A trephine biopsy showed a hypercellular bone marrow with a proliferation of abnormal megakaryocytes, mild reticulin fibrosis, and osteosclerosis, i.e., features of an early stage of idiopathic myelofibrosis. In contrast to this predominant pattern, the marrow also contained a distinct hypocellular focus of gelatinous transformation (GMT) in which hematopoietic and fat cells were replaced by gelatinous substances that were characterized as hyaluronic acid mucopolysaccharides histochemically. GMT is a rare disorder of unknown pathogenesis, and is an unspecific indicator of severe illness which most often occurs in patients with a background of weight loss. This is the first reported case of gelatinous changes in an otherwise fibrotic bone marrow, a constellation which a priori seemed to be incompatible.

Adipose Tissue↗
PubMedDate not supplied

Anorectal fistula: an unusual presentation in a Crohn's disease patient.

An unusual case of an anorectal fistula presenting with hip pain and extensive lower limb muscle wasting in a patient with Crohn's disease is reported. This report emphasizes the important role of a thorough history, a complete physical examination, and a thorough search for evaluating such cases. Any progressive local irritation and pain in a Crohn's disease patient may indicate possible fistulous involvement. Nonspecific laboratory findings such as leukocytosis, anemia, decreased albumin level, and thrombocytosis may be considered as supportive indicators. Barium contrast studies and enhanced computed tomography scan may be helpful but can be falsely negative in the presence of a fistula, as in this case. These findings illustrate that the clinician must not be dissuaded from the diagnosis simply based on negative radiological findings because the presence of a fistula may be impossible to determine preoperatively.

Adult↗
PubMed1996

Platelet-associated bleeding disorders.

OBJECTIVE: To provide a review of platelet disorders, treatment, and nursing care. DATA SOURCES: Review articles and book chapters pertaining to quantitative and qualitative platelet disorders. CONCLUSIONS: Platelet-associated bleeding disorders are classified as quantitative (abnormal number), qualitative (abnormal function), or hypercoagulable states (errors in hemostasis). The resulting complications include thrombocytosis, thrombocytopenia, hypercoagulation, or bleeding dyscrasias. The administration of drugs, plasma, or platelet therapy may be beneficial to these patients. IMPLICATIONS FOR NURSING PRACTICE: Patients with platelet disorders are at great risk of life-threatening hemorrhage and require close monitoring to prevent unnecessary sequelae. Patient instruction to prevent trauma is required.

Blood Platelet Disorders↗
PubMed1991

[Platelet hyperaggregation induced by low molecular weight heparin in adult respiratory distress syndrome].

A case is reported of a 68-year-old woman admitted to the intensive care unit with an adult respiratory distress syndrome (ARDS) due to accidental poisoning with anhydrous phthalic acid. She was given prophylactic low molecular weight heparin (Fraxiparine). During the period of intensive care (mechanical ventilation with positive end-expiratory pressure), the patient experienced a stroke from which she recovered only partially. During pleurectomy for persistent pneumothorax, a lung biopsy was carried out. It confirmed the diagnosis of ARDS and recognized multiple pulmonary arterial thrombi. Because of these two thrombotic phenomena, a coagulation defect was searched for. Platelet aggregation tests were all positive with heparin and two low molecular weight fractions. The patient recovered remarkably once she was no longer given Fraxiparine, being extubated nine days afterwards. Six months after discharge, the patient's platelets still aggregated with heparin. The possible mechanism was a heparin-platelet-endothelium complex. It is noteworthy that, in this case, no thrombocytopaenia was found. It may have been countered by thrombocytosis, induced by cellular factors released during ARDS.

Aged↗
PubMed1986

[Pseudohypoxemia and a myeloproliferative syndrome].

In the interval between the sampling of blood and analysis of the blood gas composition, the partial pressure of oxygen falls. The rate of fall depends on the temperature, initial level of partial pressure of oxygen in arterial blood, white cell and platelet count. Pseudohypoxaemia secondary to leukaemia and thrombocytosis can be recognized if the arterial blood sample is kept in ice until analysis can be carried out.

Aged↗
PubMed2001

Moyamoya syndrome with spherocytosis: effect of splenectomy on strokes.

A 3-year-old male patient with hereditary spherocytosis who developed moyamoya syndrome, presenting hemiplegia, and slurred speech is reported. Transient ischemic attacks occurred repeatedly with hemolytic crises. Magnetic resonance imaging and angiography revealed bilateral occlusion of the internal carotid and middle cerebral arteries with the formation of moyamoya vessels and multiple infarctions in the basal ganglia. Although splenectomy can increase the risk of stroke, no stroke occurred after splenectomy. On aspirin and dipyridamole therapy the patient has been free of neurologic deficits and progression of the vasculopathy for 5 years. This rare observation suggests that anemic hypoxia more greatly contributes to the progression of moyamoya syndrome than postsplenectomy thrombocytosis or reduced deformability of spherocytes.

Aspirin↗