Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visceral leishmaniasis is a vector-borne systemic infection, which affects half a million people each year in many areas of the world. Typical disease manifests with fever, hepatosplenomegaly, pancytopenia, and progressive deterioration of the host. Although molecular methods appear promising as a non-invasive diagnostic tool, definite diagnosis still relies on the demonstration of the parasite in tissue. Pentavalent antimonial compounds remain the mainstay of treatment worldwide, except in India. During the past decade, short courses of lipid formulations of amphotericin B were assessed and proved effective; however, their cost precludes their wide use in developing countries. Miltefosine, an oral active agent, was recently identified, and might fulfil our expectations for an effective, safe, easily administered and affordable antileishmanial treatment.
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PMID:Visceral leishmaniasis in paediatrics. 1201 64

Hemophagocytosis in visceral leishmaniasis is rare and usually mild. However, presentation as hemophagocytic syndrome is exceptionally rare. We report the case of a 28 years man who presented with fever, hepatosplenomegaly, pancytopenia, reactive histiocytes and severe hemophagocytosis. Subsequent investigations revealed he had Leishmania donovani infection.
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PMID:Hemophagocytic syndrome as the presenting manifestation of visceral leishmaniasis. 1224 Aug 58

Visceral leishmaniasis (VL), which is transmitted by sandflies, is always present in at least 62 countries and is spreading to areas where it had not existed in the past. VL/HIV co-infections are becoming more and more common. In southern Europe, 25-70% of adult VL cases also have HIV infection. 1.5-9% of AIDS cases have newly acquired or reactivated VL. In the Mediterranean area, VL is the most common opportunistic parasitic infection among AIDS cases (i.e., 100 CD4/mcl). AIDS patients with VL have a much shorter survival period than other AIDS patients. VL can lie dormant for years but emerge clinically if an infected person has immunosuppression. Most VL/HIV co-infections in the western hemisphere are in Brazil. East African countries reporting VL/HIV co-infections include Ethiopia, Kenya, Malawi, and Sudan. Only one VL/HIV co-infected case has been found in Cameroon and in Guinea Bissau. VL/HIV co-infection cases tend to not have the usual VL clinical signs and symptoms (fever, weight loss, hepatosplenomegaly, polyadenopathies), making clinical diagnosis difficult. Since VL test sensitivity in HIV positive patients is reduced 20-40%, it is also difficult to make a serological diagnosis. In the first VL episode of HIV-infected patients, clinicians should use BMA, the safest and most sensitive test. Drug options for VL treatment include pentavalent antimonials, pentamidine, amphotericin B, and amphotericin B encapsulated in liposomes. Treatment failure is rather common in VL/HIV co-infected patients. Researchers from different centers need to conduct trials of various multi-therapy schedules. 70% of VL/HIV co-infected cases in southern Europe use intravenous drugs, suggesting that sharing of needles may account for the co-infection. The World Health Organization has mobilized against VL/HIV co-infections, including setting up a minimal surveillance system.
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PMID:Leishmania / HIV co-infections. 1229 May 65

Visceral leishmaniasis is a worldwide, disseminated intracellular protozoal infection that usually manifests by fever, hepatosplenomegaly, anemia, thrombocytopenia, leukopenia and hypergammaglobulinemia. Although anemia is a usual finding, Coombs' positive hemolytic anemia has rarely been reported in association with this disease. Pentavalent antimonials have been the preferred treatment for this disease for decades, but increasing numbers of treatment failure with antimony are being reported. Liposomal amphotericin B is a new drug which is highly efficacious in the treatment of visceral leishmaniasis and produces minimal toxicity. Here we report an infant with visceral leishmaniasis associated with Coombs' positive hemolytic anemia who was successfully treated with liposomal amphotericin B.
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PMID:Visceral leishmaniasis and Coombs' positive hemolytic anemia: a rare association in an infant treated with liposomal amphotericin B. 1469 14

Visceral leishmaniasis in Brazil is caused by Leishmania (Leishmania) chagasi and the dog is its most important reservoir. The clinical features in dogs include loss of weight, lymphadenopathy, renal failure, skin lesions, fever, hypergammaglobulinemia, hepatosplenomegaly, anemia, and, rarely, neurological symptoms. Most infected animals develop active disease, characterized by high anti-leishmania antibody titers and depressed lymphoproliferative ability. Antibody production is not primarily important for protection but might be involved in the pathogenesis of tissue lesions. An ELISA test was used to determine if there is an association between neurological symptoms and the presence of anti-L. chagasi antibodies in cerebrospinal fluid (CSF). Thirty serum and CSF samples from symptomatic mixed breed dogs (three with neurological symptoms) from a region of high incidence of visceral leishmaniasis in Brazil were examined for antibody using total parasite antigen and anti-dog IgG peroxidase conjugate. A high level of L. chagasi antibodies was observed in sera (mean absorbance SD, 1.939 0.405; negative control, N = 20, 0.154 0.074) and CSF (1.571 0.532; negative control, N = 10, 0.0195 0.040) from all animals studied. This observation suggests that L. chagasi can cause breakdown of filtration barriers and the transfer of antibodies and antigens from the blood to the CSF compartment. No correlation was observed between antibody titer in CSF and neurological symptoms.
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PMID:Anti-leishmania antibodies in cerebrospinal fluid from dogs with visceral leishmaniasis. 1270 Aug 26

We report a case of a 22 years old type 1 diabetic man with a history of weight loss, weakness, anorexia, fever and recurrent urinary tract infection since February 2001. In April 2001, he presented anuria due to obstructive acute renal failure. Hepatosplenomegaly and lymphadenopathy were absent at physical examination. Laboratory tests revealed a high level of gamma globulin (53.4 g/l) and anaemia (haemoglobin 7.7 g/100 ml) without leukopenia and thrombocytopenia. CT scan showed multiple retroperitoneal lymphadenopathies causing compression of the two ureters, hydro-ureter associated with hydronephrosis, hepatosplenomegaly and multiple pulmonary nodes. Lymphadenopathies, anaemia, high level of gamma globulin, high titres of anti-leishmanial antibodies and the excellent outcome after treatment with meglumine antimoniate (Glucantime) confirmed visceral leishmaniasis. This report documented an unusual clinical presentation of Visceral leishmaniasis in a diabetic patient.
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PMID:[Obstructive acute renal failure revealing visceral leishmaniasis in a diabetic patient]. 1272 15

Leishmanioses are widespread in 88 countries of the tropical and subtropical zone, including regions of the Mediterranean Sea basin of Southern Europe. Actually, approximately 350 million of people live in Leishmania endemic areas and about 12 million of individuals are infected. Visceral leishmaniosis (kala-azar disease, tropical splenomegaly) is caused by at least 3 species of Leishmania protozoa: L. donovani, L. infantum and L. chagasi. The incidence of the disease is estimated at 500,000 new cases annually. The infection is transmitted by Phlebotomus or Lutzomyia mosquitos bites, in which intestines forms invasive to humans are developed. Leishmania spp. have a predilection to the reticulo-histiocytary system cells, leading to their proliferation and disruption, and after spreading to the circulation they invade spleen, liver and bone marrow. Visceral leishmaniosis should be suspected in travelers returning from tropical and subtropical areas with signs of splenomegaly and twice temperature spikes in a day. We reported a case of the kala-azar disease in the 22 year-old Polish patient seasonally working in Italy. The clinical picture was expressed by two daily pikes of fever proceeded by chills, excessive sweat, hepatosplenomegaly, lymphadenopathy, general weakness, abdominal pain and nausea. The Leishmania infection was complicated by candidiosis. Laboratory tests showed anaemia, thrombocytopenia, leucopenia, hypergammaglobulinaemia and a suppression of immunological cellular response. The diagnosis was confirmed by a presence of amastigota forms in macrophages of the bone marrow aspirate and a detection of specific antibodies to L. infantum by Westernblotting. The patient was successfully treated with Glucantime.
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PMID:[Visceral leishmaniasis]. 1291 Jun 4

Currently there are no effective orally administered drugs or visceral leishmaniasis or kala-azar, a parasitic disease affecting about 0.5 million people a year, majority of whom are in India and adjacent areas of Nepal. Symptoms of affected patients are fever, cachexia, hepatosplenomegaly and pancytopenia. The disease is usually fatal, if left untreated. Traditionally kala-azar is treated with four weeks of injections of sodium stibogluconate, a pentavalent antimonial. However, this treatment has not only shown resistance in 37-64% patients of the current Indian epidemic in Bihar (the epicentrre) but also life-threatening cardiotoxicity in 7-10% and treatment-related deaths in 5-10% cases, besides being unsuccessful at times. Parenteral amphotericin B is used as a secondary agent that shows 95% effectiveness but its toxicity and high cost of even the well tolerated liposomal complex precludes its wide use in the developing countries, where the disease is present in epidemic proportions. Recently, miltefosine (hexadecylphosphocholine), a compound originally developed as an antitumour agent has been shown to be an orally effective drugs against kala-azar. All clinical trials with this drug are conducted in India in patients of visceral leishmaniasis. A regimen of 100 mg per day or 50 mg twice daily for 3-4 weeks was observed to produce a cure rate of 100%. Gastrointestinal side effects were frequent (62%) but no patient discontinued the therapy. A phase III trial involving 300 HIV-negative adults and adolescents is underway in India and the drug is hoped to be licensed in the next 2-3 years. Few studies of phase II clinical trials mainly conducted in Kenya with another drug, sitamaquine or kalazaquine (WR 6026), an 8-aminoquinoline has also shown promise as an orally effective agent (in a dose of 1 mg/kg/day for two weeks) for visceral leishmaniasis. These Studies with two orally effective compounds, it appears, will open new vistas for orally effective, affordable and acceptable drugs in the armamentarium for the treatment of kala-azar. It is expected that in future we would have effective ways to prevent and treat all forms of leishmaniasis without discomforting the patient.
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PMID:Orally effective drugs for kala-azar (visceral leishmaniasis): focus on miltefosine and sitamaquine. 1462 Oct 30

Leishmaniasis is a zoonosis caused by an intracellular parasite belonging to the genus Leishmania. In Europe, Africa, South America and China, visceral leishmaniasis is caused by L. infantum. The vectors of leishmaniasis are phlebotomine sandflies belonging to the genera Phlebotomus. According to the World Health Organization there are 2 million new cases each year and 1/10 of the world's population is at risk of infection. Leishmaniasis is considered a zoonosis and human are generally accidental hosts. The animal reservoir includes rodents, dog and other mammals. Several studies have indicate that half of the dogs with antileishmanial antibodies have no signs of disease although, animal with subclinical infections are potentially infectious to sand flies. The factors determining susceptibility or resistence to visceral leishmaniasis remain unclear, but the genetics of the host may play a major role. Clinical signs are: intermittent fever, hepatosplenomegaly, skin lesions and ulcers, alopecia, onychogryphosis, anemia, thrombocytopenia and hypergammaglobulinemia. In mice, the outcome of infection depends on the polarized activation of one of two subsets of CD4+ T cells, Th1 or Th2, the subdivision into Th1 and Th2 cells is based on the pattern of cytokines that they produce. Th1 cells produce gamma interferon (IFN-gamma) and interleukin -2 (IL-2), whereas Th2 cells produce IL-4, IL-5, and IL-10. An important difference between susceptible and resistant mice is that the resistant mice are able to switch to a Th1 profile and control the disease. An important factor in the "decision" to form a Th1 or Th2 phenotype is the early cytokine environment, and IL-12 is one of the cytokines that contributes significantly to the establishment of the Th1 phenotype. Canine leishmaniosis is endemic in the Mediterranean basin and, in most cases is caused by the parasite Leishmania infantum. The main clinical findings are skin lesions, local or generalized lymphoadenopathy, loss of body weight, glomerulopathy, ocular lesions, epistaxis and lameness. Non pruritic skin lesions are the usual manifestation and several forms have been described, such as exfoliative dermatitis and alopecia, and ulcerative, nodular and pustular dermatitis. Seroepidemiological studies of canine leishmaniasis have revealed a large number of asymptomatic seropositive animals. Moreover in areas where leishmaniasis is highly endemic, high proportion of apparently healthy animals show low levels of anti-Leishmania antibodies. Others have regressive forms of the desease, and their antibody levels will decrease in the following months or years; still others maintain low levels of antibodies without developing the desease for many years. However, the total number of infected animals is unknown. Canine leishmaniasis is a major zoonosic parasitic disease, enzootic in the Mediterranean area, caused by the intracellular protozoan Leishmania infantum. The dog is the main reservoir host of the parasite. However, most infected dogs do not present any clinical signs, and there is evidence that Leishmania infection prevalence rates in areas of endemicity are higher than those ascertained by serological studies. Visceral leishmaniasis is becoming a real problem of public health because it is an opportunistic infection in immunocompromised patients and in human immunodeficiency virus-positive subjects. The detection of the extent of the infection, particularly among asymptomatic dogs, is of great importance for the control of leishmaniasis. PCR has been applied successfully in recent years to detect Leishmania spp. even in the cases with any of the clinical manifestation of leishmaniasis. Very recently, real-time PCR for Leishmania has been applied to evaluate the parasitic load of dog tissues both at the time of the diagnosis and during follow-up of the therapy and to measure cytokine mRNA levels in different clinical samples of infected and uninfected dogs.
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PMID:[Interpretation of laboratory data during cryptic leishmaniasis in dog]. 1530 23

The authors describe an unusual case of a disseminated bacille Calmette-Guerin (BCG) infection in a 3-month-old girl who presented with a huge hepatosplenomegaly, fever, and pancytopenia. Clinically, an infantile kala-azar or lymphoma/leukemia was suspected. However, after thorough clinical and paraclinical investigations, the case was diagnosed as a disseminated BCG infection. The child died 2 weeks after starting antituberculosis treatment. Autopsy revealed diffuse histiocytic infiltration in the liver, spleen, and mesenteric lymph nodes, which were loaded with acid-fast bacilli. Three interesting findings were noticed in this case: circulating monocytes in the peripheral blood were loaded with ghost acid-fast bacilli; bone marrow smears revealed numerous Gaucher cell-like macrophages loaded with negative images of Mycobacterium tuberculi; and there was extensive marrow necrosis. These findings have not been previously reported in the literature.
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PMID:Peripheral blood and marrow findings in disseminated bacille Calmette-Guerin infection. 1570 85


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