Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.
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PMID:Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys. 632 13

In a prospective Swedish study started in 1977 and still in progress 10 328 newborn infants in an urban district were investigated for cytomegalovirus (CMV) excretion in the urine by the virus isolation test. Congenital infection was found in 50 cases (0.5%). Of 47 infected infants with known clinical status at birth 9 (19%) had hepatomegaly, splenomegaly, jaundice and/or petechiae. The symptoms were moderate or mild. Of the infants followed up, 2 (25%) of 8 neonatally symptomatic ones and 3 (9%) of 35 asymptomatic ones developed neurologic sequelae. Altogether 5 (12%) of 43 had permanent neurologic symptoms corresponding to 0.06% in the general population. The children ranged in age from 6 months to 4 yr at the last examination. 21 mothers of the 47 infants with known status at birth had a confirmed or presumed primary infection, 15 a confirmed or presumed secondary infection and 11 an undetermined type of infection. Of the 5 infants with neurologic sequelae, 1 with a grave psychomotor retardation and deafness was born to a mother with a primary infection in the 1st trimester; 1 infant with a moderate retardation and 3 deaf infants were all exposed to confirmed or presumed secondary maternal infections. Prospective serological studies of maternal sera in early pregnancy would have suspected only the gravely retarded infant to be at risk.
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PMID:Congenital cytomegalovirus infection and disease in Sweden and the relative importance of primary and secondary maternal infections. Preliminary findings from a prospective study. 633 Aug 80

A syndrome of acquired immunodeficiency within a group of outdoor-housed rhesus macaques (Macaca mulatta) with unusually high mortality has been identified at the California Primate Research Center. The cause of death for most of the affected animals included septicemia and/or chronic diarrhea with wasting, often complicated by other problems. In many cases, multiple or unusual infectious agents were isolated or recognized, including cytomegalovirus, Cryptosporidium spp., and Candida albicans. Septicemias due to usually innocuous agents such as Staphylococcus epidermidis and Alcaligenes faecalis were seen. Two animals developed cutaneous fibrosarcomas. Affected animals had generalized lymphadenopathy and splenomegaly, with depletion of T-cell populations, initially follicular hyperplasia followed by depletion, and absence of plasma cells. This spontaneous disease syndrome in nonhuman primates has similarities to acquired immune deficiency syndrome (AIDS) in humans, providing an animal model for the study of the complex factors modulating the immune system.
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PMID:The pathology of an epizootic of acquired immunodeficiency in rhesus macaques. 669 18

The original TORCH complex described clinically similar congenital infections caused by Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus, types 1 and 2. Cutaneous manifestations, including petechiae, purpura, jaundice, and dermal erythropoiesis, are commonly seen in toxoplasmosis, rubella, and cytomegalovirus infections. In herpes simplex virus infections, 80% of symptomatic infants show single or grouped cutaneous vesicles, oral ulcers, or conjunctivitis. Extracutaneous signs and symptoms are variable and can be severe. Significant clinical signs in congenital toxoplasmosis include diffuse intracerebral calcification, chorioretinitis, and microcephaly; congenital rubella can result in deafness, congenital heart disease, retinopathy, and brain calcification. Cytomegalic inclusion disease can include hepatomegaly, splenomegaly, paraventricular calcification, and intrauterine growth retardation. Localized or disseminated congenital herpes virus infection often involves the central nervous system and the eye. Diagnosis is confirmed by culture and identification of species-specific immunoglobulin M within the first 2 weeks of life. Histological examination contributes to the diagnosis in herpes simplex virus infection. Treatment for toxoplasmosis includes pyrimethamine with sulfadiazine or trisulfapyrimidine; congenital herpes simplex virus infection is treated with acyclovir. No specific therapy for congenital rubella or cytomegalovirus infections has been established, and so treatment is primarily supportive.
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PMID:TORCH syndrome. 764 Feb

A 4-month-old girl who was examined because of splenomegaly had portal vein thrombosis, which apparently resulted from a combination of cytomegalovirus infection and deficiency of both protein S and protein C. The cytomegalovirus infection, by damaging endothelial cells, may have triggered a cascade of events that was ultimately expressed as portal vein thrombosis resulting from deficiency of proteins S and C.
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PMID:Portal vein thrombosis caused by protein C and protein S deficiency associated with cytomegalovirus infection. 769 38

A national surveillance program for congenital cytomegalovirus (CMV) disease was initiated in 1990. In 4 years 285 cases were reported without seasonal patterns. Mean birth statistics were as follows: gestational age, 36 weeks; weight, 2,224 g; length, 45 cm; and head circumference, 30 cm. Of the infants 68% had CNS involvement, which was significantly (P < .005) associated with a direct bilirubin level of > or = 3 mg/dL, petechiae, an alanine aminotransferase level of > 100 U/L, a platelet count of < or = 75,000/mm3, hepatomegaly, and splenomegaly (P < .05). Maternal demographics revealed that the mean age was 23 years (range, 13-38 years), 59% were white, 33% were black, 47% had low incomes (receiving Medicaid), and 45% were primiparous. Compared with 1990 birth statistics in the United States, mothers of infants with congenital CMV disease were younger, and a greater percentage of these mothers were black. Two distinct maternal groups were identified on the basis of age, socioeconomic status, and parity. This finding may reflect different modes of transmission and suggest target populations for future CMV vaccine initiatives.
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PMID:Surveillance for congenital cytomegalovirus disease: a report from the National Congenital Cytomegalovirus Disease Registry. 775 93

A 58 year old woman developed systemic symptoms, interstitial lung disease, splenomegaly, leukopenia and anti-histone and anti-nuclear antibodies (ANA), while treated with hydralazine for hypertension. Five months after presentation she was admitted with high fever, skin rash and atypical lymphocytosis due to acute cytomegalovirus (CMV) infection. Worsening leukopenia and increased ANA were found, and high titres of anti-DNA antibodies, anti-cardiolipin antibodies and rheumatoid factors appeared. Hydralazine was stopped and the patient gradually became asymptomatic. All autoantibodies spontaneously disappeared (over 16 weeks), and the white cell count and spleen size became normal. The patient was found to be a slow acetylator and to have both HLA-DR4 and selective IgA deficiency. Thus, a multifactorial genetic susceptibility to develop drug-induced lupus was brought out in stages first by hydralazine and then by CMV, yet all manifestations and autoantibodies resolved spontaneously, demonstrating the complex interplay of varied environmental factors with a genetic predisposition in the pathogenesis of autoimmunity.
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PMID:Effect of acute cytomegalovirus infection on drug-induced SLE. 783 Nov 73

We reviewed the thirty cases of cytomegalovirus infections with occurred in previously healthy patients, hospitalised for fever from 1981 to 1992. Pregnant women, transplant recipients, HIV infected persons and all immunocompromised subjects were excluded. We observed 34 cases (18 women, 16 men) whose mean age was 34 years (17 to 79). Fever appeared progressively (73%), persisted more than 15 days (87%) and was well tolerated. The main functional symptoms were headaches, myalgia (53%), profuse sweat (50%), abdominal pain, diarrhea, recent loss of weight, dry cough (51%). Splenomegaly was present in 24% of the cases. Chest X ray was always normal. Differential blood count was always inverse and an authentic mononucleosis syndrome was present in 91%: it appeared mainly 13 days after onset of symptoms. Hepatic abnormalities were nearly constant, especially cytolytic (97%) (transaminases three or four times upper the normal limit) but also cholestatic (62%). Thrombopenia has been noticed once (48,000/mm3). Serological diagnosis was confirmed with Elisa test (anti CMV Ig M: 30 cases) or complement fixation test (seroconversion: one, significant increase of the titers: two). CMV viremia, studied in seven patients, was positive in three. Spontaneous or treated (NSAI in 30%) outcome was nearly always favourable (97%). Two patients presented severe complications: meningo encephalitis and spleen rupture. CMV infection in previously healthy patients has to be suspected, without waiting for the mononucleosis syndrome, in view of a prolonged, well tolerated febrile illness, without pharyngitis, associated with hyperlymphocytosis and mild cytolysis. A careful follow-up is needed to detect the rare but severe complications.
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PMID:[Clinical, biological and developmental aspects of cytomegalovirus infection in immunocompetent patients: apropos of 34 hospitalized patients]. 805 48

9-(2-Phosphonylmethoxyethyl)-2,6-diaminopurine (PMEDAP) is a broad-spectrum antiviral agent with potent activity against DNA viruses and retroviruses. We now demonstrate that PMEDAP is highly efficacious when given orally to mice infected with either Moloney murine sarcoma virus (MSV), Friend leukemia virus (FLV), or murine cytomegalovirus (MCMV). PMEDAP markedly delayed MSV-induced tumor initiation when administered orally at 50, 100, or 250 mg/kg/day during 5 subsequent days. At the highest dose (250 mg/kg/day), PMEDAP completely prevented tumor formation in the MSV-infected animals. PMEDAP also caused 84-96% inhibition of FLV-induced splenomegaly when given orally to FLV-infected mice at 50-250 mg/kg/day. These PMEDAP treatment regimens were also markedly effective in increasing the survival rate of MCMV-infected mice. Intraperitoneal PMEDAP achieved a comparable antiviral activity at 2- to 5-fold lower doses than oral PMEDAP. However, the therapeutic index (ratio of the toxic dose to the antivirally effective dose) of oral PMEDAP was substantially higher than that of intraperitoneal PMEDAP. Oral PMEDAP at doses of 100, 250, or 500 mg/kg resulted in plasma PMEDAP levels of 0.5-2.5 micrograms/ml, which were sustained for 3 or 6 hours after administration and may account for the high antiviral efficacy achieved.
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PMID:Efficacy of oral 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine (PMEDAP) in the treatment of retrovirus and cytomegalovirus infections in mice. 838 73

A follow-up study of 179 cases of human immunodeficiency virus (HIV) seropositive neonates born from HIV seropositive mothers is reported. At the time of the present study, HIV infection resulting from maternofetal transmission was found in 50 cases, while 108 infants were not infected; HIV infection remained uncertain in 16 cases; 5 infants were lost for follow-up. Out of the 50 infected cases, 20 were less than two-year old, 17 were 2-5 year old and 13 were older than 5 years. Very few remained asymptomatic after the age of 6 months, the most common symptoms being adenopathies and/or hepatomegaly and/or splenomegaly. Twenty-six had an acquired immunodeficiency syndrome (AIDS). Six died, from pneumocystosis (3), cytomegalovirus infection (1) and septicemia (2). Virus culture and polymerase chain reaction were the most efficient laboratory methods for early diagnosis of HIV infection, both being positive in more than 95% of the infected cases after the age of 3 months. A close clinical and biological supervision is recommended in these infants and children because of the permanent threat of infectious diseases in relation to their immunodeficiency. Treatment associates: 1) antiviral therapy with AZT as soon as the HIV infection is diagnosed; 2) primary prophylaxis against pneumocystosis with trimethoprim-sulfamethoxazol; 3) IV immunoglobulins in the case of repeated bacterial infection; 4) regular evaluation of the nutritional status and psychological assistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Management of HIV-seropositive newborn infants. Personal experience apropos of 179 cases]. 839 76


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