Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral blood and bone marrow findings are presented for six homosexual males with Kaposi's sarcoma. Cytopenia in one or more cell lines was common in this group of patients, including two individuals with pancytopenia. Bone marrow findings in all patients, while not specific, were similar in that adequate numbers of normal appearing erythroid, myeloid, and megakaryocytic elements were present. Mild plasmacytosis as well as reticulin fiber increase were common findings. No patient, at time of study, demonstrated marrow involvement with Kaposi's sarcoma. We conclude that depression of peripheral blood counts in these patients was not due to marrow underproduction, and discuss possible mechanisms for increased blood cell destruction.
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PMID:Hematologic manifestations in homosexual men with Kaposi's sarcoma. 670 5

A 7-week-old infant with methylmalonic acidemia had pancytopenia and hypoplastic bone marrow. The patient responded to large doses of vitamin B12 treatment, and within 3 wk, the blood counts and bone marrow cellularity returned to normal. To understand the mechanism of marrow depression in this infant, we examined the effect of the patient's plasma and methylmalonic acid itself on the in vitro growth of bone marrow-committed stem cells. The patient's plasma obtained before B12 treatment completely inhibited the marrow cell growth, whereas the posttreatment plasma showed no inhibition. Methylmalonic acid when added to the culture dishes in concentrations comparable to those reported in plasma of methylmalonic acidemia patients, inhibited growth of marrow stem cells in a concentration-dependent fashion. On the other hand, 16 to 18 hr incubation of cells in the same concentration of methylmalonic acid did not affect the recovery of viability of the cells. The observations suggest that methylmalonic acid is inhibitory to the proliferation of marrow stem cells. The mechanism of inhibition is yet to be elucidated.
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PMID:Inhibition of bone marrow stem cell growth in vitro by methylmalonic acid: a mechanism for pancytopenia in a patient with methylmalonic acidemia. 725 44

Pancytopenia was observed in two 3-year-old geldings and one 11-year-old mare. All horses had a brief history (2 days to 4 weeks) of fever, anorexia, and depression. One of the three horses had blast cells present on a peripheral blood smear. Examination of the bone marrow showed substantial infiltration with neoplastic lymphoid cells. At necropsy, neoplastic cells were restricted to the bone marrow in one horse, present in bone marrow, liver, and spleen in the second horse, and reported in multiple tissues in the third horse, including bone marrow, kidneys, lung, myocardium and lymph nodes. The value of a bone marrow aspirate and core biopsy in the investigation of pancytopenia is highlighted.
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PMID:Pancytopenia secondary to lymphoid leukemia in three horses. 811 32

A 4-year old girl who received prophylactic therapy with oral cephalexin for 1 year because of a history of urinary tract infections, was referred for evaluation of short stature. On physical examination mildly dysmorphic features were observed. Blood counts disclosed pancytopenia, and bone marrow examination showed hypoplasia of all 3 cell lines. Chromosome analysis after exposure to a DNA cross-linking agent (diepoxybutane) showed a chromosomal breakage pattern consistent with Fanconi anemia. Discontinuation of cephalexin was followed by improvement in hematological values. This course of events supports the hypothesis that acquired bone marrow depression may be a manifestation of Fanconi anemia, warranting the appropriate diagnostic work up in every case of acquired bone marrow aplasia.
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PMID:[Fanconi anemia syndrome as a predisposing factor for acquired bone marrow aplasia]. 834 6

Bone marrow toxicity, mainly neutropenia, has been described as an uncommon secondary effect of most beta-lactams, and it is usually related to large cumulative doses. Although previously described for piperacillin, no cases of marrow depression caused by piperacillin/tazobactam have been reported to date. We report a case of reversible pancytopenia, with evidence of bone marrow depression, which occurred after a 17 d course of piperacillin/tazobactam. The drug was given to an underweight 18-year-old woman, at the usual dosage of 4/0.5 g three times a day. We stress the need for reducing the recommended dosage when treating underweight adult patients, and also of monitoring haematological parameters during prolonged treatments.
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PMID:Reversible bone marrow depression by high-dose piperacillin/tazobactam. 898 34

The hematologic consequences of infection with the noncytopathic lymphocytic choriomeningitis virus (LCMV) were studied in wild-type mice with inherent variations in their interferon (IFN)-alpha/beta responder ability and in mutant mice lacking alpha/beta (IFN-alpha/beta R0/0) or gamma IFN (IFN-gamma R0/0) receptors. During the first week of infection, wild type mice demonstrated a transient pancytopenia. Within a given genetic background, the extent of the blood cell abnormalities did not correlate with the virulence of the LCMV isolate but variations were detected between different mouse strains: they were found to depend on their IFN-alpha/beta responder phenotype. Whereas IFN-gamma R0/0 mice were comparable to wild-type mice, IFN-alpha/beta R0/0 mice exhibited unchanged peripheral blood values during acute LCMV infection. In parallel, the bone marrow (BM) cellularity, the pluripotential and committed progenitor compartments were up to 30-fold reduced in wild type and IFN-gamma R0/0, but remained unchanged in IFN-alpha/beta R0/0 mice. Viral titers in BM 3 d after LCMV infection were similar in these mice, but antigen localization was different. Viral antigen was predominantly confined to stromal BM in normal mice and IFN-gamma R0/0 knockouts, whereas, in IFN-alpha/beta R0/0 mice, LCMV was detected in > 90% of megakaryocytes and 10-15% of myeloid precursors, but not in erythroblasts Although IFN-alpha/beta efficiently prevented viral replication in potentially susceptible hematopoietic cells, even in overwhelming LCMV infection, unlimited virus multiplication in platelet and myeloid precursors in IFN-alpha/beta R0/0 mice did not interfere with the number of circulating blood cells. Natural killer (NK) cell expansion and activity in the BM was comparable on day 3 after infection in mutant and control mice. Adaptive immune responses did not play a major role because comparable kinetics of LCMV-induced pancytopenia and transient depletion of the pluripotential and committed progenitor compartments were observed in CD8(0/0) and CD4(0/0) mice, in mice depleted of NK cells, in lpr mice, and in perforin-deficient (P0/0) mice lacking lytic NK cells. Thus, the reversible depression of hematopoiesis during early LCMV infection was not mediated by LCMV-WE-specific cytotoxic T lymphocyte, cytolysis, or secreted IFN-gamma from virally induced NK cells but was a direct effect of IFN-alpha/beta.
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PMID:Virus-induced transient bone marrow aplasia: major role of interferon-alpha/beta during acute infection with the noncytopathic lymphocytic choriomeningitis virus. 905 52

One hundred cases of monocytic ehrlichiosis diagnosed in Israeli dogs were confirmed by the presence of anti-Ehrlichia canis indirect immunofluorescent antibody titres greater than 1:40. The disease occurred in all age groups and there was no sex predilection. German shepherd dogs were significantly over-represented whereas crossbreed dogs were significantly under-represented (P > 0.0005). The most common clinical signs were depression, lethargy, lymphadenomegaly, fever, anorexia, panting, pale mucous membranes and bleeding, of which epistaxis was most common. Thrombocytopenia, anaemia (mainly normocytic normochromic) and lymphopenia were the predominant haematological findings. Forty-nine of the 100 cases were followed up for a year. Thirty-two dogs survived and 17 died. A Cox proportional hazards regression model was used to examine the effect of host, environmental, and haematological prognostic factors on survival. It was concluded that severe anaemia, severe leucopenia, pancytopenia, a tendency to bleed (especially epistaxis) and being a German shepherd dog were important indicators of poor survival in cases of monocytic ehrlichiosis in dogs.
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PMID:Canine monocytic ehrlichiosis: a retrospective study of 100 cases, and an epidemiological investigation of prognostic indicators for the disease. 935 Nov 83

Clinical signs and haematological abnormalities of haemophagocytic syndrome of unknown origin are described for a male, nine-year-old rottweiler referred because of weakness, depression, mild weight loss and relapsing fever. Mucous membranes were pale and the spleen was enlarged. Ultrasonography revealed diffuse irregular structures in the enlarged spleen, and cytological examination of multiple fine needle aspirates of the spleen demonstrated extramedullary haematopoiesis. Haematological examination revealed pancytopenia and disseminated intravascular coagulation. A bone marrow smear contained numerous marrow macrophages with a cytologically benign appearance, containing phagocytosed haematopoietic cells. The dog died one week after referral. The differential diagnosis is discussed.
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PMID:Haemophagocytic syndrome with disseminated intravascular coagulation in a dog. 957 64

In experiments with three species of animals (mice, rabbits, monkeys) irradiated with sublethal and lethal doses of gamma-irradiation, it was observed, that leukinferon used in 4 hours or 10 days after provided antiradiation therapeutical effect. When lethal dose was used (mice) the survival of animals was significantly increased. The preparation decreased depression of the functional activity of leukocytes as it was observed with IFH-alpha and gamma-production. Pestoring this function was accelerated. Phenomena pancytopenia and thrombocytopenia induced by radiation were decreased. Therapeutical effect was explained with capacity of the preparation to defence the hemopoietic organs from the radiation and to stimulate hematopoiesis. So, spleen weights and quantity of cells into bone marrow were higher in experimental group in comparison with control at any observation. CFUs were also higher (with optimal dose of preparation). Stimulation of the restoring processes was confirmed also by more intensive increasing of the reticulocyte quantities in the circulation of experimental monkeys within 20 days. Then their level became more close in both groups. The preparation stimulated also differentiation of immune effectors: immature neutrophils were absent in the circulation of experimental monkeys. Production of IFN-gamma (which is function of T-lymphocytes) was restored more fast. As a result, immunoreactivity of monkeys in experimental group was more complete and restored faster: the growth of the automicroflora on the skin surface became to increase 7 days later and was restrained. Leukinferon hindered the development of acute radiation sickness symptoms.
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PMID:[Therapeutic antiradiation properties of leukinferon]. 960 7

Aplastic anemia is a rare complication of liver transplantation (<1%). However, an increasing number of cases of aplastic anemia have been recently reported when liver transplantation is performed for non-A, non-B, non-C fulminant hepatic failure. The aim of this study is to reevaluate the importance and the incidence of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure, and to propose preventive measures, diagnostic and management guidelines to try to reduce the incidence, morbidity and mortality associated with this complication. In this report a case of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure is described. In addition, the pertinent literature on aplastic anemia after liver transplantation, since the first description of that complication in 1987, is reviewed. A 20-year-old woman developed aplastic anemia 14 weeks after liver transplantation for fulminant non-A, non-B, non-C hepatitis. After failure of G-CSF treatment, she was treated with intensive immunosuppression (FK 506, ATG, high-dose steroids). She is well 1 year post-transplantation, with normal liver tests and with bone marrow recovery. Through a Medline literature search (1988-1999), we identified 30 additional cases of aplastic anemia following liver transplantation for non-A, non-B, non-C fulminant hepatic failure. Of all liver transplantations performed for that indication at five participating centers, the mean incidence of aplastic anemia was 23.2%. Mean age was 10 years (1.2-29) and the male/female ratio was 4.6. For treating aplastic anemia, different modalities were used: ATG ( n=12), ALG ( n=1), OKT 3 ( n=1), G-CSF ( n=6), a 6-HLA-compatible bone marrow transplantation ( n=3), and none ( n=12). The mortality rate remains high (39%), with infections and bleeding as the two most frequent causes of death. Based on this literature review, we conclude that aplastic anemia is a relatively common complication of liver transplantation for non-A, non-B, non-C fulminant hepatic failure in children and young adults. An unknown viral agent operating through immune-mediated mechanisms is probably responsible. The myelotoxic environment inherent to transplantation (e.g. azathioprine, trimethoprim) probably has a cumulative effect. Preventive measures (e.g. not using myelotoxic drugs) should be adopted in high-risk children and young adults transplanted for non-A, non-B, non-C fulminant hepatic failure. Early detection of bone marrow depression, a low threshold for performing a bone marrow biopsy, and prompt treatment are pivotal. Intensive standard supportive care with broad-spectrum antibiotics and anti-fungal agents is essential during phases of pancytopenia. Although spontaneous recovery has been described under maintenance immunosuppression, increased immunosuppression, in particular with ATG, may reverse the aplastic anemia and promote bone marrow recovery. In unresponsive patients, six-HLA-identical bone marrow transplantation has been successful.
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PMID:Aplastic anemia after transplantation for non-A, non-B, non-C fulminant hepatic failure: case report and review of the literature. 1193 68


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