Feline platynosomiasis: analysis of the association of infection levels with pathological and biochemical findings.

Platynosomiasis is a common feline hepatic disease caused by Platynosomum fastosum (Trematoda - Dicrocoelidae), which is also known as 'lizard poisoning'. Most reports of feline platynosomiasis show that this disease is sporadic and manifests with uncommon lesions; its pathogenicity is still not well understood. This study aimed to describe liver injuries and enzymatic changes associated with natural P. fastosum infection in 47 stray cats in an endemic area. Overall, 38.3% (18/47) of cats were parasitized, and 2,358 flukes (P. fastosum) were collected (131 - mean intensity of parasitism; 50.2 - mean abundance). The alanine transaminase (ALT) measure was significantly higher in parasitized animals, while alkaline phosphatase (ALP) showed no statistical difference between parasitized and non-parasitized animals. In infected animals, gross pathological lesions and microscopic liver injuries ranged from mild to severe, and were similar to those in previous descriptions of feline platynosomiasis. Nonetheless, the intensity of parasitism was not related to the severity of macroscopic or microscopic hepatic injuries. However, feline platynosomiasis should be considered in the differential diagnosis of feline liver disorders, as well as, in any program of helminth control, even if no clinical abnormalities are present.

Feline platynosomiasis: analysis of the association of infection levels with pathological and biochemical findings / Platinossomiase felina: análise da associação dos níveis de infecção com achados patológicos e bioquímicos

Abstract Platynosomiasis is a common feline hepatic disease caused by Platynosomum fastosum (Trematoda - Dicrocoelidae), which is also known as ‘lizard poisoning’. Most reports of feline platynosomiasis show that this disease is sporadic and manifests with uncommon lesions; its pathogenicity is still not well understood. This study aimed to describe liver injuries and enzymatic changes associated with natural P. fastosum infection in 47 stray cats in an endemic area. Overall, 38.3% (18/47) of cats were parasitized, and 2,358 flukes (P. fastosum) were collected (131 – mean intensity of parasitism; 50.2 – mean abundance). The alanine transaminase (ALT) measure was significantly higher in parasitized animals, while alkaline phosphatase (ALP) showed no statistical difference between parasitized and non-parasitized animals. In infected animals, gross pathological lesions and microscopic liver injuries ranged from mild to severe, and were similar to those in previous descriptions of feline platynosomiasis. Nonetheless, the intensity of parasitism was not related to the severity of macroscopic or microscopic hepatic injuries. However, feline platynosomiasis should be considered in the differential diagnosis of feline liver disorders, as well as, in any program of helminth control, even if no clinical abnormalities are present.

Resumo Platinossomiase é uma doença hepática felina comum causada por Platynosomum fastosum (Trematoda - Dicrocoelidae), também é conhecida como “envenenamento por lagartixa”. A maioria dos relatos de platinossomiase felina mostra que esta doença é esporádica e se manifesta com lesões incomuns; sua patogenicidade ainda não é bem compreendida. Este estudo objetivou descrever as lesões no fígado e alterações enzimáticas associadas à infecção natural por P. fastosum em 47 gatos errantes em uma área endêmica. No total, 38,3% (18/47) dos gatos estavam parasitados, e 2.358 trematódeos (P. fastosum) foram coletados (131 – intensidade média de parasitismo; 50,2 – abundância média). A quantidade de alanina transaminase (ALT) foi significativamente maior nos animais parasitados, enquanto a fosfatase alcalina (ALP) não apresentou diferença estatística entre os animais parasitados e não parasitados. Nos animais infectados, lesões patológicas macroscópicas e microscópicas hepáticas variaram de leve a grave, e foram semelhantes a descrições anteriores de platinossomiase felina. No entanto, a intensidade do parasitismo não foi relacionada à gravidade das lesões hepáticas macroscópicas ou microscópicas. Contudo, a platinossomiase felina deve ser considerada no diagnóstico diferencial de distúrbios hepáticos em felinos, assim como, em qualquer programa de controle de helmintos, mesmo que nenhuma anormalidade clínica esteja presente.

IFN-γ-induced macrophage antileishmanial mechanisms in mice: A role for immunity-related GTPases, Irgm1 and Irgm3, in Leishmania donovani infection in the liver.

In C57BL/6 mice, Leishmania donovani infection in the liver provoked IFN-γ-induced expression of the immunity-related GTPases (IRG), Irgm1 and Irgm3. To gauge the antileishmanial effects of these macrophage factors in the liver, intracellular infection was analyzed in IRG-deficient mice. In early- (but not late-) stage infection, Irgm3(-/-) mice failed to properly control parasite replication, generated little tissue inflammation and were hyporesponsive to pentavalent antimony (Sb) chemotherapy. Observations limited to early-stage infection in Irgm1(-/-) mice demonstrated increased susceptibility and virtually no inflammatory cell recruitment to heavily-parasitized parenchymal foci but an intact response to chemotherapy. In L. donovani infection in the liver, the absence of either Irgm1 or Irgm3 impairs early inflammation and initial resistance; the absence of Irgm3, but not Irgm1, also appears to impair the intracellular efficacy of Sb chemotherapy.

Relationship between butyrylcholinesterase activity and liver injury in mice acute infected with Toxoplasma gondii.

This study aimed to investigate the butyrylcholinesterase (BChE) activity in mice experimentally infected with Toxoplasma gondii during the acute phase. Twenty mice were divided in two groups with 10 animals each: group A was composed of uninfected mice while group B was formed by rodents infected with T. gondii. Five days after infection, blood was collected and serum separated, and fragments of liver and brain were obtained. In serum and liver homogenate was noted a significant reduction (P<0.05) in BChE activity in infected mice when compared with uninfected ones. In serum was observed an increase in the activity of alanine aminotransferase and urea, associated with reduction in alkaline phosphatase activity and in the levels of total protein and albumin. Histologically, there were foci of necrosis and parasites in the forms of tachyzoites and cysts, with bradyzoites in liver samples of infected animals. Based on these results, we conclude that toxoplasmosis reduces BChE activity in mice, and this alteration is probably related to the liver damage caused by the parasitism. Therefore, this enzymatic alteration can directly contribute to the pathogenesis of the disease.

Gastrointestinal nematode infection exacerbates malaria-induced liver pathology.

Mixed parasite infections are common in many parts of the world, but little is known of the effects of concomitant parasite infections on the immune response or severity of clinical disease. We have used the nonlethal malaria infection model of Plasmodium chabaudi AS in combination with the gastrointestinal nematode Heligmosomoides bakeri polygyrus to investigate the impact of nematode infections on malarial morbidity and antimalarial immunity. The data demonstrate that wild-type C57BL/6 mice coinfected with both parasites simultaneously exhibit a striking increase in mortality, while mice deficient in IFN-gamma or IL-23 survive coinfection. The increase in mortality in wild-type mice was associated with severe liver pathology characterized by extensive coagulative necrosis and an increase in hepatic IFN-gamma, IL-17, and IL-22 mRNA expression. This is the first demonstration of increased malaria-associated pathology associated with a switch toward a proinflammatory environment, involving not only IFN-gamma but also the IL-17/IL-23 axis, as a result of coinfection with a gastrointestinal helminth.

Activity of liver microsomal enzymes during the chronic phase of murine schistosomiasis

The effects of schistosomiasis on microsomal enzymes were studied on post-infection day 90 when accumulated damage and fibrosis are most intense but granulomatous reaction around the eggs harbored in the liver is smaller than during the earlier phases. Swiss Webster (SW) and DBA/2 mice of either sex (N = 12 per sex per group) were infected with 100 Schistosoma mansoni cercariae on postnatal day 10 and killed on post-infection day 90. Cytochrome P-450 (CYP) concentration and alkoxyresorufin-O-dealkylases (EROD, MROD, BROD, and PROD), p-nitrophenol-hydroxylase (PNPH), coumarin-7-hydroxylase (COH), and UDP-glucuronosyltransferase (UGT) activities were measured in hepatic microsomes. Age-matched mice of the same sex and strain were used as controls. In S. mansoni-infected mice, CYP1A- and 2B-mediated activities (control = 100 percent) were reduced in SW (EROD: male (M) 36 percent, female (F) 38 percent; MROD: M 38 percent, F 39 percent; BROD: M 46 percent, F 19 percent; PROD: M 50 percent, F 28 percent) and DBA/2 mice (EROD: M 64 percent, F 58 percent; MROD: M 60 percent; BROD: F 49 percent; PROD: M 73 percent) while PNPH (CYP2E1) was decreased in SW (M 31 percent, F 38 percent) but not in DBA/2 mice. COH did not differ between infected and control DBA/2 and UGT, a phase-2 enzyme, was not altered by infection. In conclusion, chronic S. mansoni infection reduced total CYP content and all CYP-mediated activities evaluated in SW mice, including those catalyzed by CYP2E1 (PNPH), CYP1A (EROD, MROD) and 2B (BROD, PROD). In DBA/2 mice, however, CYP2A5- and 2E1-mediated activities remained unchanged while total CYP content and activities mediated by other CYP isoforms were depressed during chronic schistosomiasis.

Activity of liver microsomal enzymes during the chronic phase of murine schistosomiasis.

The effects of schistosomiasis on microsomal enzymes were studied on post-infection day 90 when accumulated damage and fibrosis are most intense but granulomatous reaction around the eggs harbored in the liver is smaller than during the earlier phases. Swiss Webster (SW) and DBA/2 mice of either sex (N = 12 per sex per group) were infected with 100 Schistosoma mansoni cercariae on postnatal day 10 and killed on post-infection day 90. Cytochrome P-450 (CYP) concentration and alkoxyresorufin-O-dealkylases (EROD, MROD, BROD, and PROD), p-nitrophenol-hydroxylase (PNPH), coumarin-7-hydroxylase (COH), and UDP-glucuronosyltransferase (UGT) activities were measured in hepatic microsomes. Age-matched mice of the same sex and strain were used as controls. In S. mansoni-infected mice, CYP1A- and 2B-mediated activities (control = 100%) were reduced in SW (EROD: male (M) 36%, female (F) 38%; MROD: M 38%, F 39%; BROD: M 46%, F 19%; PROD: M 50%, F 28%) and DBA/2 mice (EROD: M 64%, F 58%; MROD: M 60%; BROD: F 49%; PROD: M 73%) while PNPH (CYP2E1) was decreased in SW (M 31%, F 38%) but not in DBA/2 mice. COH did not differ between infected and control DBA/2 and UGT, a phase-2 enzyme, was not altered by infection. In conclusion, chronic S. mansoni infection reduced total CYP content and all CYP-mediated activities evaluated in SW mice, including those catalyzed by CYP2E1 (PNPH), CYP1A (EROD, MROD) and 2B (BROD, PROD). In DBA/2 mice, however, CYP2A5- and 2E1-mediated activities remained unchanged while total CYP content and activities mediated by other CYP isoforms were depressed during chronic schistosomiasis.

In vitro effect of schistosomicidal drugs on hepatic arylsulfatase B from the schistosoma-infected mouse.

Arylsulfatase B (ASB) hydrolyzes the desulfation of N-acetylgalactosamine-4-sulfate at the non-reducing terminal of glycosaminoglycans. This enzyme activity was found to be elevated in mice schistosomiasis. In the present study, the catalytic and immunological properties of purified ASB from the liver of Schistosoma-infected mouse was investigated in the presence and absence of the schistosomicidal drugs praziquantel and Commiphora extract. The in vitro effect of praziquantel was found to be inhibitory with a Ki value of 5.5 x 10(-4) M while that of commiphora extract was as an activator. Furthermore, these drugs did not have an observed effect on the immunological properties of ASB with regard to its binding to its polyclonal rabbit antibody. These results indicate that some schistosomicidal drugs may reverse the alteration of the catalytic properties of the enzyme in schistosomiasis.

Host differences in response to trickle infection with Fasciola gigantica in buffalo, Ongole and Bali calves.

Progressive weight gain, faecal egg counts, packed cell volume, percent eosinophils in blood, serum antibody and serum levels of glutamate dehydrogenase and gamma-glutamyl transpeptidase were recorded in seven swamp buffalo (Bubalis bubalis), 7 Ongole (Bos indicus) and four Bali calves (Bos sundiacus) which were infected orally with 15 metacercariae of Fasciola gigantica twice weekly for 32 weeks. Similar observations were made on four buffalo, 4 Ongole calves and 3 Bali calves maintained fluke-free as controls. Flukes were counted at slaughter 36 weeks after initial infection. Mean daily weight gains of infected Bali (228 +/- 100 (SD) g/day) and infected Ongole calves (328 +/- 57 (SD) g/day) were lower (p = 0.026 and 0.067, respectively) than those of control calves (405 +/- 107 (SD) g/day), but infected buffalo calves (379 +/- 78 (SD) g/day) had similar weight gains to those of the controls (p = 0.57). Throughout the trial, faecal Fasciola egg counts in buffaloes were about one-fifth of counts of Ongole calves, and counts in Bali calves were intermediate. Ongole calves had three times the number of flukes at slaughter in their liver compared to buffalo and Bali calves, which had similar numbers. However, there was evidence that Bali calves had acquired a degree of resistance about 24 weeks after infection commenced and may have lost adult flukes as a consequence.

Activity of some hepatic enzymes in schistosomiasis and concomitant alteration of arylsulfatase B.

The levels of arylsulfatases A and B, alpha-amylase, aspartate transcarbamylase, and gamma-glutamyl transpeptidase were investigated during the infection of mice with schistosoma mansoni. This infection caused a significant (p < 0.001) increase in the activity of hepatic arylsulfatase B (ASB), aspartate transcarbamylases and gamma-glutamyl transpeptidase. A non-significant difference occurred for alpha-amylase (p < 0.3) and arylsulfatase A (p > 0.5) when compared to the control. The specific activity of hepatic ASB was progressively increased with the progression of the Schistosoma-infection. Moreover, the kinetic studies of hepatic ASB in Schistosoma-infection showed that a slight decrease in the value of K(m) and about a 40% increase in V(max) when compared to the control. In addition, the pH optimum of hepatic ASB was altered from 6 to 7 as a result of schistosomiasis. These observations suggest that there are schistosomiasis-associated changes of the catalytic and kinetic properties of hepatic ASB.

[Serum gamma-glutamyltransferase alteration in hepatic schistosomiasis doesn't correlate with parasitic load and precedes ultrasound alterations]. / Elevação da gamma-glutamiltransferase sérica na hepatopatia esquistossomótica não se correlaciona com a carga parasitária e precede alterações ultra-sonográficas.

BACKGROUND: Liver disorders are the major manifestations of schistosomiasis mansoni. Factors that account for increased concentrations of cholestasis-indicating enzymes in the hepatosplenic form of the disease are unknown. OBJECTIVE: To assess the correlation between increased gamma-glutamyltransferase serum levels and both the parasitic load and ultrasound alterations in patients with schistosomiasis. PATIENTS AND METHODS: Twenty-five patients with the chronic form of schistosomiasis were assessed for the presence or absence of increased enzymatic levels, for the parasitic load (low x medium/high) and for ultrasound parameters. Furthermore, analysis of prothrombin time and a platelet count were performed. RESULTS: Of the 25 patients, 13 showed increased gamma-glutamyltransferase plasma levels. No significant correlation was found between increased gamma-glutamyltransferase levels and the parasitic load, or between increased enzyme levels and ultrasound alterations. Nor did the prothrombin index or the platelet count differ between the two groups (normal gamma-glutamyltransferase levels and increased gamma-glutamyltransferase levels). CONCLUSION: The parasitic load explains no rise in gamma-glutamyltransferase plasma levels in patients with the chronic form of schistosomiasis, and conventional ultrasound is not a sensitive method to detect the alteration suggested by the increased enzyme level in those patients.

Induction of cytochrome P450 2A6 expression in humans by the carcinogenic parasite infection, opisthorchiasis viverrini.

The purpose of this study was to examine in vivo the activity of cytochrome P450 (CYP) 2A6, an enzyme capable of activating carcinogens, including N-nitrosodimethylamine, in humans with the carcinogenic liver fluke infection, opisthorchiasis viverrini, before and after treatment with the antiparasitic agent, praziquantel. Coumarin hydroxylase activity of CYP 2A6 was assessed by administering a probe drug, coumarin, and measuring its metabolite, 7-hydroxycoumarin, in urines collected between 0-2 h and 2-4 h of 106 people with varying intensities of Opisthorchis viverrini infection. Five individuals who did not excrete any detectable 7-hydroxy coumarin (and have a genetic defect probably leading to an absence of catalytic activity of the CYP 2A6 protein) were excluded from analysis. Infected people excreted an average of 22.7 mumol of 7-hydroxycoumarin in the first 2 h after taking the drug, whereas the mean of the uninfected group was 19.4 mumol; this difference did not reach statistical significance (P = 0.10). However, a highly significant increase in CYP 2A6-related activity was observed in infected individuals who also had radiological evidence of biliary fibrosis (28.1 mumol) compared to those without (19.4 mumol; P = 0.01). Reassessments of coumarin hydroxylase activity of CYP 2A6 made 2 months after praziquantel treatment showed highly significant reductions in the amount of 7-hydroxycoumarin excreted among the infected groups but no difference in the uninfected group. These results suggest that expression of CYP 2A6 is induced among chronically infected people who also have fibrosis of the intrahepatic bile duct. As already demonstrated in an animal model and now observed in humans for the first time, this increase in CYP 2A6-related enzyme activity may represent an important mechanistic link between inflammatory products of chronic liver fluke infection (e.g., DNA alkylation damage from endogenously formed N-nitrosamines) and the high risk of cholangiocarcinoma faced by infected individuals.

Circulating enzyme activities of collagen turnover and undulin in patients with various degrees of schistosomiasis and alcoholic liver cirrhosis.

In contrast to alcoholic liver disease, schistosomiasis leads to presinusoidal hepatic fibrosis, which determines the prognosis of the disease. Since conventional liver function tests and liver biopsy provide little information about the dynamics of the fibrotic process, we measured the activities of two circulating enzymes of collagen turnover, namely serum galactosylhydroxylysyl-glucosyl-transferase and plasma prolidase activity, together with undulin, a novel extracellular matrix glycoprotein. The study encompassed 15 healthy control subjects. 69 patients with various stages of Schistosoma mansoni/hematobium infection [28 with early active infection and no organ involvement, 27 with hepatosplenic involvement, and 14 with complications of portal hypertension] and 16 patients with alcoholic liver cirrhosis. Liver biopsies were obtained from 30 schistosomal patients for histopathological grading. Serum galactosylhydroxylysyl-glucosyl-transferase was significantly increased in all clinical stages of schistosomiasis (p < 0.05), but normal in alcoholic cirrhosis. In contrast, plasma prolidase activity showed a significant increase only in early schistosomiasis (p < 0.01), but dropped to subnormal levels in advanced stages (p < 0.001). Undulin was highly elevated both in alcoholic patients and in all schistosomal groups (p < 0.001), and was capable of distinguishing between early and advanced schistosomal stages. We conclude that serum undulin may be a valuable non-invasive parameter for monitoring the course of schistosomal and alcoholic liver disease.

Pharmacokinetic profile of methotrexate and 5-fluorouracil in normal and bilharzial-infested mice.

The pharmacokinetics of two commonly used anticancer drugs, methotrexate (MTX) and 5-fluorouracil (5-FU), were investigated in normal and bilharzial-infested mice. Liver glucose-6-phosphatase activity and antipyrine clearance were used as parameters of liver function. Liver glucose-6-phosphatase activity was significantly reduced in bilharzial-infested mice compared with the normal controls. Bilharzial infestation caused a significant reduction in the elimination (beta) and clearance rate (Cl) of antipyrine, whereas its elimination half-life (t1/2 beta) was increased in comparison with the normal controls. A similar pattern was also obtained after MTX and 5-FU administration in bilharzial mice, compared to controls. These results indicate that hepatic bilharziasis causes a significant reduction in the hepatic clearance and elimination of MTX and 5-FU, whereas their areas under the concentration-time curve were significantly increased. These findings may have to be considered in the treatment of bilharzial cancer patients.

Ethanol challenge in non-alcoholic patients with schistosomiasis.

AIMS: To evaluate serum gamma glutamyltransferase (GGT) activity in a group of non-alcoholic patients with the hepatointestinal form of schistosomiasis; and the response of both GGT and alkaline phosphatase to an ethanol challenge in two subgroups of patients with different baseline serum concentrations of GGT. METHODS: Seventy six non-alcoholic, non-smoking hepatitis B virus (HBV) negative men with normal body mass index, who denied blood product transfusion or use of medication, were studied (30 healthy volunteers (control group) and 46 patients with the hepatointestinal form of schistosomiasis). GGT activities were determined in all subjects and the ethanol test (measurement of GGT and alkaline phosphatase (ALP) before and 24 hours after the ingestion of 1 g/kg of ethanol) was performed in 14 patients (7 with GGT below 25 IU/l and seven with GGT above 25 IU/l). The ethanol serum concentrations were determined in the samples collected one hour after ingestion of the solution in four patients with schistosomiasis. RESULTS: The mean serum ethanol concentration one hour after the ingestion was 0.7 g/l and all patients were clinically intoxicated. GGT was below 25 IU/l in all 30 volunteers and in 33 of the patients with schistosomiasis. In 13 patients the GGT varied from 28 to 140 IU/l. The two enzymes GGT and ALP determined in the 14 patients submitted to the test were positively correlated in the baseline samples (r = 0.8130) as well as in the samples obtained 24 hours after stimulation (r = 0.7921). Neither the plasma activity of GGT nor the GGT:ALP ratio was affected by the ethanol challenge. CONCLUSIONS: These results suggest that the mechanisms for the increase of GGT serum activity in schistosomiasis and in alcoholism differ. In the latter, microsomal induction increases GGT serum activity, while alterations in the biliary tree may be responsible for the increase observed in patients with schistosomiasis.

Characterization of two dipeptidases purified from hepatic schistosome egg granulomas in mice. Leukotriene D4 hydrolases of granulomatous tissue.

Extracts prepared from tissue with granulomatous inflammation experimentally produced in liver of CBA-strain mice showed increased hydrolysis of leukotriene D4 (LTD4), Leu-Leu and Ala-Gly as compared with normal hepatic cells. Two dipeptidases, Leu-Leu dipeptidase and Ala-Gly dipeptidase, were purified from hepatic granulomas, and quantitative conversion of LTD4 into leukotriene E4 (LTE4) by both enzymes was demonstrated. M(r) values of the purified enzymes were 178,000 for Leu-Leu dipeptidase and 183,000 for Ala-Gly dipeptidase. The enzymes showed homogeneity, appearing as a single band on SDS/PAGE, and the M(r) values of the subunits were 56,000 and 57,000 for Leu-Leu and Ala-Gly dipeptidase respectively. The amino acid compositions of the two enzymes differed considerably from each other. The activity of Leu-Leu dipeptidase was inhibited by bestatin and captopril and stabilized with MnCl2. The Km for LTD4 was 25 microM with a V(max.) of 49.0 mumols/min per mg. In contrast, the activity of Ala-Gly dipeptidase was inhibited by cilastatin, cytinylglycine, EDTA and dithiothreitol, and also by captopril. The Km for LTD4 was 5.3 microM with a V(max.) of 50.4 mumols/min per mg. The findings indicate that the conversion of LTD4 into LTE4 by microsomal dipeptidases is elevated during granulomatous tissue reaction. This enzyme activity may become useful for biochemical quantification of the pathological tissue reaction that occurs in organized granulomas.

Schistosoma mansoni: angiotensin converting enzyme activity in mice under the influence of praziquantel and/or captopril.

Murine schistosomiasis is usually associated with hepatic granulomatous lesions together with high serum and granuloma angiotensin converting enzyme (ACE) activity. Praziquantel (PRZ) which is known to reduce granuloma size was studied to show whether this effect is related to changes in ACE activity. Furthermore, captopril was studied to show whether by inhibiting ACE activity, the drug could also affect granuloma size. PRZ, captopril, and their combination led to significant reduction in liver granuloma. However, in normal mice, captopril was shown to increase rather than decrease serum ACE. The decrease in ACE activity by PRZ was correlated with its curative effect in infected mice. However, in experimentally induced pulmonary granulomata, the drug reduced granuloma size without affecting ACE activity of either serum or granuloma. It may be concluded that reduction in ACE activity may be beneficial as far as diminution of granuloma size is concerned and irrespective of whether there is an active infection or not. The possible use of Captopril as an antihypertensive in bilharzial infections associated with hypertension would probably not adversely affect the granulomatous lesions.

Serum trypsin in hepatosplenic schistosomiasis in the Sudan.

Serum trypsin was measured by radioimmunoassay in 30 patients with hepatosplenic schistosomiasis and 30 healthy controls. Patients with hepatosplenic schistosomiasis had a significantly lower serum trypsin 164.3 +/- 43.3 ng/ml than controls 241.3 +/- 74.0 ng/ml (P less than 0.001). It is concluded that the exocrine pancreatic function is impaired with regard to serum trypsin in hepatosplenic schistosomiasis.

Enzyme activities and protein concentrations in serum of patients with hepatosplenic schistosomiasis.

The hepatosplenic form of Schistosoma mansoni infection contributes considerably to morbidity and mortality in endemic areas. The present study investigated serum protein concentrations and serum enzyme activities of 58 Sudanese patients with hepatosplenic schistosomiasis. All of them had a history of infection with S. mansoni and one or several episodes of oesophageal bleeding due to portal hypertension. Diagnosis was based on clinical (n = 24), ultrasonographical (n = 18) and histological (n = 16) grounds. The control group consisted of 40 Sudanese healthy blood donors. Serum albumin was found to be significantly lower in patients with hepatosplenic schistosomiasis (median = 37 g/l) than in controls (median = 47 g/l). Serum enzyme analysis revealed only minimal alterations of cellular enzyme activities, but a marked decrease of cholinesterase activity. Serum albumin concentration correlated significantly with cholinesterase activity. We conclude that liver function in patients with schistosomiasis and portal hypertension is partially disturbed. Low serum albumin and low cholinesterase activity reflected an impaired protein synthesis of the liver. Destruction of parenchymal liver cells was mild or absent.

Bioquímica da esquistossomose mansônica: envolvimento dos siderossomos nos processos inflamatórios hepáticos / Biochemistry of schistosomiasis mansoni: involvement of siderosomes in hepatic inflammatory processes

Os processos inflamatórios que se desenvolvem durante as etapas avançadas da esquistossomose mansônica foram relacionados, com o acúmulo de siderossomos, a capacidade dos ions ferrosos/férricos de desencadearem a formaçäo de radicais livres e a peroxidaçäo de lipídios membranáceos, assim como à diminuiçäo da estabilidade das membranas dos diversos componentes do comportamento lisossômico hepático. Os lisossomos isolados de figados de camundongos infectados por 100 cercárias, com 80 e 100 dias de infecçäo, foram respectivamente, 2,5 e quase 4 vezes mais frágeis que os controles, isolados de figados de camundongos näo infectados. A presença de siderossomos em grande quantidade foi demonstrada por espectrometria aos raios-X