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 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

A 39-year-old man presented with sudden loss of visual acuity caused by two retinal hemorrhages with no choroidal neovascularization (confirmed by fluorescein angiography). The patient was hospitalized for malaise, progressive pancytopenia, hepatosplenomegaly, progressive anemia, and perianal inflammation. Positive serologies were obtained for toxoplasmosis (IgG) and Leishmania (1/160). A diagnosis of visceral leishmaniasis was made, and the patient was treated with pentavalent antimonials. Two months later, best-corrected visual acuity was 20/25, with no residual scotoma. Indirect ophthalmoscopy showed complete resolution of the hemorrhages. This patient was an otherwise healthy immunocompetent adult who presented frank visceral leishmaniasis and retinal hemorrhages as the only ocular or systemic hemorrhagic findings, with spontaneous resolution after improvement of platelet levels. This rare cause of macular hemorrhage should be considered in areas where Leishmania is endemic.
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PMID:Intraretinal hemorrhage associated with leishmaniasis. 1275 96

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

In this study, we have developed a vaccine with Leishmania donovani promastigote membrane antigens (leishmanial antigens (LAg)) encapsulated in a liposome carrier formulated with distearyol (DSPC, transition temperature (Tc) = 54 degrees C) derivative of l-alpha-phosphatidyl choline, for immunizing BALB/c mice against progressive visceral leishmaniasis. This formulation could limit hepatosplenomegaly to almost normal levels and conferred strong levels of protection in both liver and spleen against challenge infection. Immunization with liposomal LAg activated peritoneal macrophages for enhanced leishmanicidal activity in association with NO production, and induced antibody as well as T-cell mediated immune responses. Production of both IFN-gamma and IL-4 by splenic T cells, and serum IgG1 and IgG2a, suggest induction of a mixed Th1/Th2 response following immunization. Experimental challenge corresponded with elevated DTH, and mitogen and antigen specific cellular responses. Increased production of NO and IFN-gamma by spleen cells, and down regulation of IL-4, demonstrate that an initial stimulation of a mixed Th1/Th2 response by vaccination instructs Th1 responses and resistance against a progressive infection by L. donovani.
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PMID:A mixed Th1/Th2 response elicited by a liposomal formulation of Leishmania vaccine instructs Th1 responses and resistance to Leishmania donovani in susceptible BALB/c mice. 1500 44

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

In order to investigate epidemiological and clinical characteristics of visceral leishmaniasis in children up to 15 years old, a prospective study was carried out in Alagoas, Brasil from 1981 to 1995. Of the 530 diagnosed cases, predominantly from the rural area of Alagoas State, 58% were male and 42% female, being 55.3% children under 5 years old. The most frequently observed clinical manifestations were: hepatosplenomegaly, fever and parlor. The average size of the liver and the spleen of patients with shorter time of disease (<30 days) were smaller than those presenting sickness for a extended time (>or= 360 days). No matter the length of disease there was reduction of the liver and the spleen after treatment. However, the reduction of the spleen was higher in those patients with less time of sickness. With relation to liver that difference was not observed.
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PMID:[Clinical and epidemiological aspects of visceral leishmaniasis in children up to 15 years of age in Alagoas, Brasil]. 1533 62

In the present study, we aimed to carry out an epidemiological and entomological survey on a visceral leishmaniasis (VL) focus located on the northern central part of Anatolia, Turkey. Five villages of Corum province, where five confirmed cases of human visceral leishmaniasis (HVL) (one patient/village) were reported between June 1998 and August 2001 were included in the study. A total of 625 children and 131 dogs were sampled and the physical examination was carried out by authorized physicians and veterinarians. An indirect fluorescent antibody test (IFAT) was performed by standard procedures for human and dog sera, while the direct agglutination test (DAT) was only performed for dog sera. Sand fly collection was performed in three villages by CDC miniature light traps. Hepatosplenomegaly and hepatomegaly were detected in two and eight children, respectively. The seropositivity rate among children was found to be 0.16% (1/625) in the region. The seroprevalence of canine infection in these five villages ranged between 0.0% and 28.26%. In two villages, named Ahlatcik and Asagifindikli, no seropositive dogs were found. A total of 1218 sand flies were collected throughout the study. Six species of Phlebotomus were identified: P. transcaucasicus, P. neglectus, P. halepensis, P. tobbi, P. papatasi, and P. jacusieli. P. transcaucasicus was found to be the predominant species in Cevizli (47.44%; 343/723) and Ucoluk (79.95%; 351/439) villages, while P. tobbi was abundant in Kucukerikli (42.85%; 24/56).
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PMID:Serological and entomological survey in a zoonotic visceral leishmaniasis focus of North Central Anatolia, Turkey: Corum province. 1571 53

Leishmania amazonensis is widely recognised as a cause of cutaneous leishmaniasis in Latin America, but it can also disseminate to produce atypical visceral leishmaniasis with hepatitis and lymphadenopathy. The patient, an 8-year-old Brazilian boy, presented with a febrile illness and hepatosplenomegaly, elevated liver enzymes and generalised adenopathy. Serological tests using antigens of L. chagasi, the typical cause of visceral leishmaniasis in Latin America, were inconclusive. Leishmania amazonensis was eventually isolated in a culture of a lymph node. The patient recovered fully after treatment with meglumine antimoniate. As this case illustrates, L. amazonensis produces a spectrum of disease that includes atypical American visceral leishmaniasis with evidence of hepatocellular injury and generalised lymphadenopathy.
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PMID:Atypical American visceral leishmaniasis caused by disseminated Leishmania amazonensis infection presenting with hepatitis and adenopathy. 1619 85

The present paper reports a case of 6-year-old male child, suffering from pallor, fever and hepatosplenomegaly. A clinical diagnosis of enteric fever with a second possibility of malaria was considered. Laboratory findings included bicytopenia, hyperbilirubinemia and raised liver enzymes. Bone marrow examination revealed active hemophagocytosis. On extensive search few amastigote forms of Leishmania donovani were seen. Patient was negative for other viral, bacterial and malaria infections. The final diagnosis of hemophagocytic syndrome associated with visceral leishmaniasis was made. There was response of anti-Leishmanial treatment with improvement in clinical condition.
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PMID:Hemophagocytic syndrome associated with visceral leishmaniasis. 1674 36


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