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Hematologic Abnormalities (hematologic + abnormality)

Distribution by Scientific Domains

Medical Sciences	85%

Selected Abstracts

Hematologic abnormalities in children and young adults receiving tacrolimus-based immunosuppression following cardiothoracic transplantation

PEDIATRIC TRANSPLANTATION, Issue 2 2001
Nancy C. Dobrolet
Abstract: To define the incidence, course, and etiology of hematologic abnormalities in children on tacrolimus-based immunosuppression, we reviewed records of 106 transplant patients (70 heart, 16 heart and lung, 20 double lung), 0,21 yr of age, who were transplanted at the Children's Hospital of Pittsburgh from 1989 to 1997. Fifty-four of the 106 patients (51%) developed 65 abnormal hematologic episodes (32 anemia, nine neutropenia, nine thrombocytopenia, 15 simultaneous anemia and neutropenia with or without thrombocytopenia). Common etiologies included: infections, post-transplant lymphoproliferative disease, and medications. Eleven episodes (seven anemia, one neutropenia, and three simultaneous anemia and neutropenia) had unclear etiologies and process of elimination suggested an association with tacrolimus. Interventions included filgrastim (effective in 15 of 15 patients, with resolution of neutropenia in a median of 5 days) and epoetin alfa (effective in five of 16 patients, including four of four patients with anemia possibly related to tacrolimus). Five patients (two with neutropenia and three with simultaneous neutropenia and anemia) were switched to cyclosporin A (CsA); rapid resolution occured in four of the five patients, suggesting a possible association of the hematologic abnormalities with tacrolimus. In summary, hematologic abnormalities are common in children on tacrolimus-based immunosuppression. Most of these hematologic abnormalities are caused by common etiologies; however, a sub-population exists where tacrolimus may be the etiologic agent. Anemia and neutropenia respond to treatment with epoetin alfa and filgrastim. After thorough investigation, a trial switch to CsA may be warranted. [source]

Recommendation for a definition of acute symptomatic seizure

EPILEPSIA, Issue 4 2010
Ettore Beghi
Summary Purpose:, To consider the definition of acute symptomatic seizures for epidemiological studies, and to refine the criteria used to distinguish these seizures from unprovoked seizures for specific etiologies. Methods:, Systematic review of the literature and of epidemiologic studies. Results:, An acute symptomatic seizure is defined as a clinical seizure occurring at the time of a systemic insult or in close temporal association with a documented brain insult. Suggestions are made to define acute symptomatic seizures as those events occurring within 1 week of stroke, traumatic brain injury, anoxic encephalopathy, or intracranial surgery; at first identification of subdural hematoma; at the presence of an active central nervous system (CNS) infection; or during an active phase of multiple sclerosis or other autoimmune diseases. In addition, a diagnosis of acute symptomatic seizure should be made in the presence of severe metabolic derangements (documented within 24 h by specific biochemical or hematologic abnormalities), drug or alcohol intoxication and withdrawal, or exposure to well-defined epileptogenic drugs. Discussion:, Acute symptomatic seizures must be distinguished from unprovoked seizures and separately categorized for epidemiologic purposes. These recommendations are based upon the best available data at the time of this report. Systematic studies should be undertaken to better define the associations in question, with special reference to metabolic and toxic insults, for which the time window for the occurrence of an acute symptomatic seizure and the absolute values for toxic and metabolic dysfunction still require a clear identification. [source]

Tuberculosis Caused by Mycobacterium microti in South American Camelids

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2009
P. Zanolari
Background: Infection with Mycobacterium microti can cause chronic disease in animals and threaten human health through its zoonotic potential. Objective: To describe clinical findings, diagnostic investigations, necropsy, and epidemiology results in South American camelids (SAC) infected with M. microti, member of the Mycobacterium tuberculosis complex. Animals: Eleven SAC with tuberculous lesions. Methods: Description of 10 llamas and 1 alpaca, aged 4,18 years, from 6 herds with a history of wasting and weakness admitted to the Vetsuisse-Faculty of Berne over 8 years. Results: Clinical signs included weight loss, recumbency, and anorexia in late stages of the disease. Respiratory problems were seen in 6 animals of 11. No consistent hematologic abnormalities were identified. Suspect animals were examined in detail by abdominal ultrasonography and thoracic radiology. Abnormal findings such as enlarged mediastinal, mesenteric, or hepatic lymph nodes were seen only in animals with advanced disease. Single comparative intradermal tuberculin test with bovine protein purified derivate (PPD) and avian PPD was negative in all animals. At necropsy, typical tuberculous lesions were found, and confirmed by bacteriological smear and culture, molecular methods, or both. Conclusions and Clinical Importance: Infection caused by M. microti should be considered a differential diagnosis in chronic debilitating disease with or without respiratory signs in SAC. Antemortem confirmation of the diagnosis remains challenging at any stage of infection. Because cases of M. microti infection have been reported in immunocompromized human patients, the zoonotic potential of the organism should be kept in mind when dealing with this disease in SAC. [source]

Eastern Equine Encephalitis in 9 South American Camelids

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2007
Rose Nolen-Walston
Background: Eastern equine encephalitis (EEE) virus is a mosquito-borne togavirus (alphavirus) that causes severe (often fatal) encephalitis in many mammalian species, but it has not been reported previously in South American camelids. Hypothesis: South American camelids can become naturally infected with EEE virus and show encephalitic signs similar to those observed in other affected species. Animals: Nine cases (8 alpacas and 1 llama, aged 3.5 weeks to 12 years) were identified; 4 of 9 were ,10 weeks old. All cases were from the East Coast of the United States and presented in late summer and fall. Methods: A retrospective study was performed to include confirmed cases of EEE in camelids in North America before 2006. Results: Eight of nine (89%) camelids died or were euthanized in extremis, with the mean time to death of 2 days. Clinical signs were consistent with encephalitis and included fever, lethargy, ataxia, seizures, recumbency, torticollis, opisthotonus, and vestibular signs. No consistent hematologic abnormalities were identified, and cerebrospinal fluid contained an increased protein concentration in the single camelid analyzed. No successful therapy was identified. EEE was confirmed by alphavirus detection by using immunohistochemistry (IHC) and polymerase chain reaction (PCR) in the central nervous system (CNS) and by serology. Findings included polioencephalitis with lymphocytic perivascular cuffing; neutrophil infiltration; gliosis; neuron satellitosis; necrosis; and edema, with intracytoplasmic alphavirus within neurons and glial cells. No virus was detected in extraneural tissues. Conclusions and Clinical Importance: In endemic areas, EEE should be considered a differential diagnosis for young and adult camelids with CNS disease. Brain histopathology with indirect IHC or PCR is diagnostic. [source]

Hematologic abnormalities in children and young adults receiving tacrolimus-based immunosuppression following cardiothoracic transplantation

FasL/Fas pathway is involved in dengue virus induced apoptosis of the vascular endothelial cells,,

JOURNAL OF MEDICAL VIROLOGY, Issue 8 2010
Hongwu Liao
Abstract The hallmark of the dengue hemorrhagic fever/dengue shock syndrome is hematologic abnormality. The pathogenesis of dengue hemorrhagic fever/dengue shock syndrome remains unknown. Our work showed that the dengue virus serotype-2 induced apoptosis in human umbilical vein endothelial cells. Fas (CD95), Tumor Necrosis Factor receptors, and Tumor Necrosis Factor-related apoptosis-inducing ligand receptors are the most common death receptors, which can induce apoptosis. Compared with the untreated human umbilical vein endothelial cells, Fas expression was increased both in the mRNA level and on the surface of infected human umbilical vein endothelial cells. FasL was expressed at similar levels on human umbilical vein endothelial cells over a course of dengue virus serotype-2 infection, but the expression in mRNA level was increased in infected human umbilical vein endothelial cells. It is possible that there is soluble FasL secreted from human umbilical vein endothelial cells in the supernatant. Tumor Necrosis Factor-related apoptosis-inducing ligand receptor 1 and Tumor Necrosis Factor receptors 1,2 were constantly very low, whereas Tumor Necrosis Factor-related apoptosis-inducing ligand receptors 2,4 decreased after dengue virus serotype-2 infection. This result suggested that dengue virus serotype-2 may inhibit Tumor Necrosis Factor-related apoptosis-inducing ligand receptors-induced apoptosis. The apoptotic rates in human umbilical vein endothelial cells were decreased upon the addition of caspase family inhibitors. In addition, activated caspase 8 and caspase 3 were also observed by Western blot following dengue virus serotype-2 infection. Thus, it is shown that the Fas/FasL pathway may participate in dengue virus-induced apoptosis of vascular endothelial cells in vitro. J. Med. Virol. 82:1392,1399, 2010. © 2010 Wiley-Liss, Inc. [source]

Gastric Neoplasia in Horses

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2009
S.D. Taylor
Background: Gastric neoplasia of horses is incompletely described. Objective: Provide history, clinical signs, and clinicopathological and pathological findings associated with gastric neoplasia in horses. Animals: Twenty-four horses with gastric neoplasia. Methods: Retrospective study. History, clinical signs, and clinicopathological and pathologic findings in horses diagnosed histologically with gastric neoplasia were reviewed. Results: Horses ranged in age from 9 to 25 years (median 18 years at presentation). There was no apparent breed or sex predisposition. The most common presenting complaints were inappetance (17/24), weight loss (14/24), lethargy (7/24), hypersalivation (7/24), colic (5/24), and fever (5/24). The most consistent clinical signs were tachypnea (10/19), decreased borborygmi (8/19), and low body weight (7/17). Useful diagnostic tests included rectal examination, routine blood analysis, gastroscopy, abdominocentesis, and transabdominal ultrasound examination. Anemia was the most common hematologic abnormality encountered (7/19), and hypercalcemia of malignancy was seen in 4/16 horses. Squamous cell carcinoma was the most common tumor identified (19/24), and was most often (14/19) found as a single ulcerated, necrotic mass in the nonglandular portion of the stomach. Other gastric neoplasms encountered were leiomyoma (n=2), mesothelioma (n=1), adenocarcinoma (n=1), and lymphoma (n=1). Metastatic neoplasia was found in 18/23 horses. The median time from onset of clinical signs to death was 4 weeks, and all horses died or were euthanized because of gastric neoplasia. Conclusions: Squamous cell carcinoma is the most common primary gastric neoplasia in horses. The survival time after diagnosis of gastric neoplasia in horses is short. [source]