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Background: Hereditary hemochromatosis is the most frequent cause of primary iron overload that is associated with HFE gene's mutation especially the C282Y mutation. The interaction between hemoglobin chain synthesis' disorders and the C282Y mutation may worsen the clinical picture of betathalassemia major (β-TM). Aim: To establish the prevalence of the C282Y mutations in Egyptian β-TM patients and to address its adverse effects. Methods: Two-hundred and five β-TM patients were recruited and divided into two groups based on their serum ferritin (SF); group I (N = 125) (SF ≤ 2500 ng/dl) and group II (N = 80) (SF > 2500 ng/dl). All patients were subjected to clinical and laboratory assessment with special emphasis on iron overload complications. Genotyping was assessed by polymerase chain reaction for detection of C282Y mutation in HFE gene. Results: The C282Y mutation was not detected in the studied β-TM neither in homozygous nor heterozygous state. There were several iron overload complications including cardiac complication (9.1%), liver disease (36.6%), delayed puberty (56.6%), primary (35.71%) and secondary amenorrhea (21.42%), short stature (27.3%), diabetes (3.4%), neutropenia (9.7%), arthralgia (10.2%), gastrointestinal (21.1%), depression (2.9%) and others (12.05%). Group I showed a statistically significant lower rate of taking iron-rich diet when compared to group II. Group II showed significant longer mean duration of disease, higher total transfusion rate per life, lower mean HbF% level, higher mean HbA% level, and higher rate of elevated liver enzymes than patients with SF ≤ 2500 ng/dl. Conclusion: The C282Y mutation was not detected in the studied cohort of Egyptian β-TM patients neither in homozygous nor heterozygous state in spite of manifestations of iron overload complications. [ABSTRACT FROM AUTHOR]

Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests.

Alopecia areata (AA) is an autoimmune disorder that manifests as nonscarring hair loss and imposes a substantial disease burden. The current study, using an e-claims database, assesses the disease burden, comorbidities, treatment patterns, specialties involved in the diagnosis of AA, healthcare resource utilization (HCRU), and associated costs in privately insured patients with AA in Dubai, United Arab Emirates. The retrospective longitudinal secondary study was conducted using Dubai Real-World Database e-claims data during 01 January 2014 to 30 June 2022. Patients with at least one diagnosis claim of AA during the index period (01 January 2015-30 June 2021) with continuous enrollment (one or more AA/non-AA claim in the post-index period) were included in the analysis. The patients were stratified into subcohorts based on diagnosis code and treatment patterns, as mild, moderate-to-severe, and others. Demographics, comorbidities, treatment patterns, specialists visited, and HCRU were assessed. The study included 11 851 patients with AA (mean age: mild: 37 years; moderate-to-severe: 36 years), with a male predominance (mild: 77.6%; moderate-to-severe: 60.8%). The most prevalent comorbidities in the moderate-to-severe AA subcohort were autoimmune and T-helper 2-mediated immune disorders, including contact dermatitis and eczema (62.1%), atopic dermatitis (36.1%), and asthma (36.1%). Most patients consulted dermatologists for treatment advice (mild AA: 87.4%; moderate-to-severe AA: 47.7%) and, notably, within 1 day of AA diagnosis. Topical steroids were frequently prescribed across cohorts, regardless of disease severity. Analysis of comorbidities among patients with AA indicated an additional HCRU burden among these subsets of patients. The median disease-specific HCRU cost was higher for psychological comorbidities versus autoimmune and T-helper 2-mediated immune disorders (US $224.99 vs US $103.70). There is a substantial disease and economic burden in patients with AA and associated comorbid conditions; therefore, investing in novel therapies that target the underlying autoimmune pathway may address the gap in effective management of AA., (© 2024 The Author(s). The Journal of Dermatology published by John Wiley & Sons Australia, Ltd on behalf of Japanese Dermatological Association.)

Chronic hepatitis C (HCV) in women of childbearing age is a major public health concern with ∼15 million women aged 15-49 years living with HCV globally in 2019. Evidence suggests HCV in pregnancy is associated with adverse pregnancy and infant outcomes. This includes ∼6% risk of infants acquiring HCV vertically, and this is the leading cause of HCV in children globally. However, few countries offer routine universal antenatal HCV screening, and direct-acting antivirals (DAAs) are not approved for pregnant or breastfeeding women although small clinical trials are ongoing. We conducted a survey of pregnant and postpartum women in 3 high HCV burden lower-middle-income countries to assess the acceptability of universal antenatal HCV screening and DAA treatment in the scenario that DAAs are approved for use in pregnancy. Pregnant and postpartum women attending antenatal clinics in Egypt, Pakistan, and Ukraine were invited to complete a survey and provide demographic and clinical data on their HCV status. Among the 630 women included (n=210 per country), 73% were pregnant and 27% postpartum, 27% were ever HCV antibody or PCR positive. Overall, 586 (93%) reported acceptability of universal antenatal HCV screening and 544 (88%) would take DAAs in pregnancy (92%, 98%, and 73% in Egypt, Pakistan, and Ukraine, respectively). Most said they would take DAAs in pregnancy to prevent vertical acquisition and other risks for the baby, and a smaller proportion would take DAAs for maternal cure. Our findings suggest that should DAAs be approved for use in pregnancy, the uptake of both HCV screening and DAA treatment may be high in women living in lower-middle-income countries., Competing Interests: Sarah Pett received institutional grants from Gilead, ViiV Healthcare, Janssen-Cilag, MRC, NIHR, and EDCTP. Manal H. El-Sayed received grants from Gilead. Ali Judd received institutional grants from Gilead. Intira Jeannie Collins received institutional grants from Gilead and ViiV Healthcare. The remaining authors have no conflicts to report., (Copyright © 2024 American Association for the Study of Liver Diseases.)

Background: Outcome of childhood acute lymphoblastic leukemia (ALL) in low- and middle-income countries is lagging in many aspects including diagnosis, risk stratification, access to treatment and supportive care., Objective: to report the outcome of childhood ALL at Ain Shams University Children's Hospitals with the use of risk-based protocols before the implementation of minimal residual disease technology and to evaluate the use of double delayed intensification (DDI) in standard risk patients., Methods: Two hundred and twenty patients with ALL diagnosed between January 2005 and December 2014 were included in the study. Patients were treated according to a modified CCG 1991 and 1961 for standard and high risk respectively. Patients were stratified into three risk groups: standard risk (SR), high-risk standard arm (HR-SA), and high-risk augmented arm (HR-AA)., Results: Among the whole cohort, the 10-year event-free survival (EFS) and overall survival (OS) were 78.1% and 84.3% respectively. Patients with Pre-B immunophenotype (IPT) had significantly better outcome than T-cell IPT (EFS 82.0% versus 58.6%, p < 0.001; OS 86.9% versus 69%, p = 0.003 for Pre-B and T-cell respectively). Among the SR group, patients treated with single delayed intensification (SDI) had comparable EFS and OS rates when compared to patients treated with DDI with EFS 82.4% versus 87.5%, p = 0.825 and OS 88.2% versus 93.5%, p = 0.638 for SDI and DDI groups, respectively., Conclusion: The use of risk-based protocol with simple laboratory techniques resulted in acceptable survival outcome in resource limited settings. The use of double delayed intensification showed no survival advantage in patients with standard risk., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

1. This study investigates the potential antifibrotic effect of losartan, AT-1 receptor antagonist, and/or praziquantel (PZQ) on acute and chronic hepatic fibrosis induced by Schistosoma mansoni (S. mansoni). 2. Schistosoma mansoni-infected mice were in two batches (I & II), each in four groups: (i) Infected untreated; (ii) treated with losartan, starting from the 4th or 12th weeks post-infection (PI); (iii) treated with PZQ in the 7th week PI; and (iv) treated with losartan, as group (ii) plus PZQ as group (iii). Comparable groups of uninfected mice were run in parallel with infected groups. Mice of batches I and II were killed 10 and 18 weeks PI, respectively. Hepatic content of hydroxyproline (HYP), serum levels and tissue expression of matrix metalloproteinase-2 (MMP-2), and transforming growth factor-β1 (TGF-β1) were determined. Parasitological, biochemical and histological parameters, which reflect disease severity and morbidity, were examined. 3. Losartan alone caused a considerable decrease in worm burden, hepatic tissue egg load with an increase in percentage of dead eggs, modulation of granuloma size and regression of inflammatory reactions, which was less obvious in the chronic stage. The best results were obtained when losartan was co-administered with PZQ, especially in the acute stage. This was revealed by a remarkable reduction in serum levels and tissue expression of MMP-2, TGF-β1 and HYP content, accompanied by conservation of hepatic reduced glutathione (GSH) versus the PZQ-treated group. 4. In conclusion, losartan has a promising antifibrotic action and could be introduced as a therapeutic tool with PZQ especially in acute schistosomal hepatic fibrosis., (© 2011 The Authors. Clinical and Experimental Pharmacology and Physiology © 2011 Blackwell Publishing Asia Pty Ltd.)

Unlabelled: This study investigates the possible use of pentoxifylline (PTX), with antifibrotic and anti-inflammatory properties, as adjuvant in treatment of schistosomal liver fibrosis through determination of some profibrogenic cytokines, oxidative stress and collagen deposition. Animals were classified into seven groups: normal control (i), Schistosoma mansoni-infected untreated (ii), infected treated with praziquantel (PZQ) curative, 1000mg/kg (iii) or sub curative, 200mg/kg dose (iv), infected treated with PTX alone (10mg/kg/day; 5days/wk) for 8weeks starting from the 2nd to the 10th week post infection (v), or in addition to curative (vi) or sub curative dose of PZQ (vii). Serum transforming growth factor-β1 (TGF-β1), tumor necrosis factor-α (TNF-α), matrix metalloproteinases-2 (MMP-2) and hepatic hydroxyproline (Hyp) content, glutathione related antioxidant enzymes and malondialdehyde (MDA) were determined. Results showed that S. mansoni infection produced remarkable elevations in the serum levels of TGF-β1, TNF-α, MMP-2 and the hepatic contents of Hyp, glutathione reductase (GR), MDA with significant reduction in reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and superoxide dismutase (SOD) when compared with their corresponding normal controls. Treatment of infected mice with PTX in addition to PZQ curative rather than its sub curative dose produced the best results evidenced by complete normalization in the previously mentioned serum and hepatic parameters., Conclusion: PTX could attenuate liver fibrosis in early stages of S. mansoni infection through downregulation of profibrogenic cytokines, oxidative stress and collagen deposition., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Artemether is an efficacious antimalarial drug that also displays antischistosomal properties. Grapefruit juice increases the oral availability of a variety of the CYP3A4 substrates. This study was designed to evaluate the effect of repeated administration of grapefruit juice with artemether on the hepatic activities of cytochrome P-450 (CYP450) and cytochrome b5 (cyt b5), on the serum levels of some biochemical enzymes and antischistosome efficacy. Results showed that administration of grapefruit juice alone induced more inhibition in the hepatic activities of CYP450 and cyt b5 than that produced by Schistosoma mansoni infection. Moreover, it enhanced degeneration of eggs and accelerated healing of the pathological granulomatous lesions. Treatment of S. mansoni-infected mice with artemether at a total dose of 300 mg/kg resulted in total and female worm burden reductions of 66.7 and 90.1%, respectively, hence protecting the host from damage induced by schistosome eggs. Treatment of S. mansoni-infected mice with artemether at 150 mg/kg reduced the total and female worm numbers by 43.3 and 54.4%, respectively, thus somewhat ameliorating hepatic granulomatous lesions compared with the infected untreated group. This was associated with no change in the hepatic activities of CYP450 and cyt b5 and in the serum levels of total protein, albumin, globulin and alanine aminotransferase compared with the uninfected control group. Coadministration of grapefruit juice with the lower dose (150 mg/kg) of artemether eliminated eggs and granulomatous reactions. In this group, the inhibitory effects of grapefruit juice on CYP450 and cyt b5 were apparent but serum liver enzymes were unchanged compared with the uninfected control group. Coadministration of grapefruit juice with artemether achieved complete protection of the host from damage induced by schistosomal infection.

In a multicenter investigation of the potential antischistosomal activity of myrrh, a resin obtained from an African plant, different derivatives of the resin, including the commercial preparation Mirazid, were tested at different doses in mice and hamsters infected with Schistosoma mansoni. In mice infected with the Egyptian (CD) strain of S. mansoni, four of six groups treated with Mirazid did not show significant worm reduction, while the remaining groups showed significant but trivial reductions. In mice infected with the Puerto Rican (Mill Hill) strain of S. mansoni, a Mirazid solution was toxic for mice at high doses and produced modest or no worm reduction at lower doses. In hamsters and mice infected with Puerto Rican (NMRI) and Brazilian (LE) strains of S. mansoni and treated with the crude extract of myrrh in doses ranging from 180 to 10,000 mg/kg, no signs of antibilharzial activity were observed. Total tissue egg load and egg developmental stages were not affected by any of the treatment regimens. These results were in contrast to those obtained in praziquantel-treated animals in which 94% worm reduction and 100% egg reduction was observed. Based on the findings of this work, we cannot recommend the use of Mirazid in human cases of schistosomiasis.

One of the most commonly used drugs for clinical management of schistosomiasis is praziquantel (PZQ, CAS 55268-74-1). Now, PZQ is recognized, world wide, as a powerful therapeutic agent for the control of schistosomiasis. Previous studies have shown decreased activities of some of the microsomal drug-metabolizing enzymes in the livers of S. mansoni-infected mice. Consequently, this work was initiated in order to investigate the effect of PZQ treatment (in a total dose of 1000 mg/kg given on two consecutive days each of 500 mg/kg body weight) administered to mice with or without previous S. mansoni infection on selected liver microsomal drug-metabolizing enzymes. The effect of these factors on liver function was also studied. The drug was given orally seven weeks after infection with 80 Egyptian strains of S. mansoni cercariae/mouse. The activities of aminopyrine-N-demethylase, aniline hydroxylase and the hepatic glutathione content as well as the concentrations of gamma-glutamyl transferase were measured after different time intervals following the second dose of PZQ treatment. The results indicated a meaningful decrease in the activities of aminopyrine-N-demethylase and aniline hydroxylase and a high elevation in the concentrations of gamma-glutamyl transferase and the contents of hepatocellular glutathione in mice infected with S. mansoni compared with their corresponding control groups. After two weeks following the praziquantel treatment, there was an improvement in the activities of these enzymes towards the control values. Collectively, the present findings point to the importance of initiating more studies in this discipline and careful deliberation of results in order to fully understand the possible interactions of antibilharzial drugs with the liver microsomal drug-metabolizing enzymes.

The effect of Schistosoma mansoni infection on drug-metabolizing enzymes was investigated before and after treatment of S. mansoni-infected male albino mice with the antibilharzial drug praziquantel (CAS 55268-74-1). The drug was given in a total dose of 1000 mg/kg, and was administered at 500 mg/kg of body weight for two consecutive days each of 500 mg/kg of body weight. The drug was given 49 days after infection with 80 Egyptian strains of S. mansoni cercariae/mouse. The hepatic content of cytochrome P-450, cytochrome b-5 and NADPH cytochrome P-450 reductase were determined at 4, 8, 24, 72 h, one and two weeks after the second dose of treatment. The enzymes were determined in the microsomal fraction after homogenization and ultracentrifugation at 105,000 x g. The results indicate a marked decrease of most enzymes in the infected groups compared to normal controls. Two weeks after treatment there was an improvement of the level of most enzymes towards the normal values. The levels of liver function tests were also improved. Concerning the oogram pattern, there was a rapid change even after 8 h after the second dose of treatment. It was concluded that the antibilharzial drug could be considered as a safe drug with a rapid onset of action.

Colchicine in a dose of 200 micrograms kg body weight/day (5 days/week) was administered to groups of Schistosoma mansoni infected mice 12 weeks post infection, either alone or following previous praziquantel therapy at the 8th week of infection. Certain groups received colchicine for 6 weeks and others received it for 10 weeks. Colchicine alone did not significantly change the light microscopic appearance of schistosomal liver fibrosis, or hepatic collagen content estimated histomorphometrically, and did not reduce the elevated IL-2 serum level. Colchicine induced hepatic injury consisted of intense inflammatory reaction in granuloma and portal tracts, hepatocytic degeneration, and elevation of serum AST and ALT levels. Colchicine seemed to postpone granulomatous reaction healing and collagen deposition rather than inhibiting collagen formation or degrading it. Colchicine inhibited proliferation of hepatocytes of infected mice by expanding G2-M phases of cell cycle, thus reduced Ag NOR count and raised cell ploidy and cyclic AMP serum level. Subsidence of schistosomal infection by praziquantel prior to colchicine therapy greatly reduced inflammatory cellular reaction, significantly diminished hepatic collagen deposition and serum IL-2 level, minimized the elevated nuclear ploidy and cyclic AMP serum level that followed colchicine therapy when administered alone.

This study aimed to test the therapeutic effect of two antischistosomal drugs metrifonate (CAS 52-68-6) and praziquantel (CAS 55268-74-1), either alone or in combination, on mice infected with schistosoma mansoni. Both drugs were given in half of their therapeutic doses 8 weeks post infection. Animals were sacrificed two weeks after the last dose. The efficacy of the drugs was evaluated using the number of ova/g tissue, the distribution and the number of Schistosoma worms. Praziquantel and metrifonate alone produced about 91% and 22% reduction in total worm burden. The reduction in ova count in intestine and liver was 96% and 85%, respectively, using praziquantel alone while it was only 6 and 12%, respectively, after metrifonate treatment. After treatment with both drugs given in combination the number of ova count was not changed as compared with praziquantel alone; also there was no change in the worm load as compared with praziquantel. It is concluded that a combination of a low dose of praziquantel with metrifonate failed to produce any significantly better effect.

The effects of cimetidine, bicarbonate and glucose on the bioavailability of the two brands of praziquantel (CAS 55268-74-1) available in Egypt were studied in normal healthy volunteers. Brand 1 when coadministered with cimetidine showed elevated concentration of the drug at all time intervals. The difference was statistically significant at 3, 4, 6 and 8 h following treatment. On the other hand coadministration of cimetidine with brand 2 (Distocide) showed elevated concentration of the drug 1 h post treatment. Analysis of the pharmacokinetic parameters revealed insignificant difference comparing brand 1 versus brand 1 plus cimetidine. Significant differences were observed between the elimination rate constant Ke (h-1) for brand 2 (0.017 +/- 0.004) alone versus brand 2 plus cimetidine (0.006 +/- 0.001). Coadministration of bicarbonate or glucose with either brand 2 or brand 1 tended to depress the serum concentration of praziquantel. Possible explanations of these findings are discussed.

The efficacy of two brands (brand 1 = Biltricide; Bayer AG, Leverkusen, Germany; brand 2 = Distocide; EPICO pharmaceuticals, Cairo, Egypt) of praziquantel (PZQ) in full and half doses (40 and 20 mg kg-1) monitored as percentage egg reduction and cure rate was investigated in S. mansoni infected school-children. A total of 506 school-children (8-16 years of age) were classified into three groups according to their intensity of infection, heavy [> 500 eggs per grams (epg)], moderate (100-500 epg) and light (< 100 epg), after examination three stool samples (three slides per sample) on three consecutive days. Percentage egg reduction and cure rate were monitored 4 and 10 weeks post-treatment for each dose regimen in the different test groups. Before testing the efficacy of either bran in patients, the pharmacokinetic parameters of the two brands were studied in non-infected normal volunteers. Statistical analysis of the pharmacokinetic parameters of brand 1 vs brand 2 (in a dose of 20 or 40 mg kg-1) revealed no significant difference in elimination (ke), absorption rate constant (ka), elimination half life (t1/2e), area under the time-concentration curve (Auc), serum maximum concentration (Cpmax) and time to maximum concentration (Tmax). As regards the efficacy of test drugs, statistical analysis revealed that up to 10 weeks post-treatment the two brands of PZQ in full dose were equally effective in reducing egg count as their half doses except in heavily infected cases treated with brand 2 of PZQ.(ABSTRACT TRUNCATED AT 250 WORDS)

In this work, praziquantel (EMBAY 8440, CAS 55268-74-1), an oral antihelminthic drug effective against the three species of schistosomes pathogenic to man, was tested alone and in combination with cimetidine (CAS 51481-61-9), aH2-receptor antagonist having a known potentiative power when combined with other drugs. Both drugs were tested in different doses and regimen either alone or in combination by giving them to S. mansoni infected Swiss albino mice (100 cercariae/mouse) 7 weeks post infection. Cimetidine was tested in doses of 50, 100 and 200 mg/kg for 2 consecutive days; praziquantel was given in doses of 100 and 500 mg/kg for 2 consecutive days. It was found that the best regimen was that of cimetidine and praziquantel when given simultaneously. Both drugs when given in a dose of 100 mg/kg for 2 consecutive days reduced the total worm load by 84.61%, while a percent reduction of 75.1% and 88.9% was recorded in hepatic and intestinal tissue egg load, respectively. Maximum efficacy was recorded when both drugs were given simultaneously at 200 mg/kg for 2 consecutive days. This regimen completely eradicated all schistosome worms and resulted in the maximum reduction in total tissue egg load (92%). The efficacy of this regimen was nearly the same as that of the full dose of praziquantel (500 mg/kg for 2 consecutive days), gave 100% worm eradication and 95% reduction in total tissue egg load.

The elevated levels of lipid peroxide product as malondialdehyde (MDA) in plasma, liver, spleen, intestine and kidney of Schistosome-infected mice were differently ameliorated by treatment with praziquantel (EMBAY 8440, CAS 55268-74-1) (2 x 500 mg/kg body wt.) being nearly normalized in plasma and intestine, moderately improved in liver and slightly affected in spleen and kidney. However, the drug failed to affect the MDA levels in the different organs of healthy mice. Moreover, the increased hepatic superoxide dismutase (SOD) activity in infected mice was normalized while the decreased activities in the other tissues were further decreased than normal values in response to praziquantel treatment. Interestingly, in healthy mice, the drug similarly inhibited SOD activities in blood, spleen and kidney. The specificity of this action remains to be clarified. Possible explanations of these findings are given.

The schistosomicidal efficacy of praziquantel (2 x 500 mg/kg), oxamniquine (1 x 100 mg/kg) and combined one-third the curative dose of each of them (333 mg/kg praziquantel + 33 mg/kg oxamniquine), were correlated to gonadal steroid hormonal changes and state of disease immunopathology, in mice infected with 100 Schistosoma mansoni (S. mansoni) cercariae. Maximum efficacy recorded with combination regimen particularly 4 weeks after treatment, was accompanied by maximum reduction in granuloma volume (65%), least fall in testosterone level (-56.2 and -60.2% in male and female mice respectively) and increased progesterone level (+33.9 and +81.5% in male and female mice respectively). These findings revealed a potentiated effect of combination therapy on mature infection and the possible involvement of gonadal steroid hormones in affecting the efficacy of schistosomicidal drugs and state of disease immunopathology.

The disposition phenazone (antipyrine) was used to study the effect of Schistosoma mansoni infection on the activity of drug metabolizing enzymes in mice. Plasma elimination rate constant (Ke), elimination half-life (t1/2e), clearance (CL) and apparent volume of distribution (Vd) were estimated 8 and 12 weeks after infection of mice with 80 S. mansoni cercariae. Liver and kidney function tests were performed simultaneously. Infection increased the levels of glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), lactic dehydrogenase (LDH), alkaline phosphatase (AP) and total proteins 8 and 12 weeks post infection. At the same time a decrease was recorded in the total cholesterol level. Moreover infection with S. mansoni produced a decrease in phenazone clearance with an increase in the area under the curve (AUC) of the drug 8 and 12 weeks post infection. Elimination half-lives were 57.92 +/- 14.10 and 72.72 +/- 4.14 min 8 and 12 weeks after infection, respectively, compared to 19.29 +/- 3.30 and 26.14 +/- 5.31 min in corresponding controls. No statistically significant change was recorded in the volume of distribution of phenazone in the groups studied. In addition no significant correlation was found between parameters of phenazone disposition and the enzyme levels studied 8 and 12 weeks after infection.

The activities of GOT and GPT in the hemolymph of B. alexandrina were significantly decreased by S. mansoni infection. However, the total protein concentration and AcP activity were increased. Although the snail starvation decreased AcP activity in the ovotestis, it increased GOT activity in the other organs of the snails. On the other hand, the snail feeding after starvation increased significantly AcP activity in ovotestis. Natural and synthetic molluscicides inhibited the activities of GOT and GPT, however, they increased the total protein concentrations and AcP activities in the examined organs.

Schistosoma mansoni infection in mice resulted in a marked decrease in blood glucose and liver glycogen accompanied by a significant increase in hepatic glucose-6-phosphatase (G-6-Pase) activity. Moreover, the results indicated that infection produced a significant increase in blood pyruvate and hepatic glucose-6-phosphate dehydrogenase (G-6-PD) activity with a significant decrease in blood lactate. Infected mice were treated with praziquantel which was given at two doses of 500 mg/kg body wt on two consecutive days. Seven and 14 days respectively after drug administration, such treatment caused a marked improvement in the previous aspects of carbohydrate metabolism. This is indicated by the tendency of the blood glucose of infected mice to be restored, the marked increase in their liver glycogen content, the normalization of their blood lactate and pyruvate as well as by the marked decrease of their hepatic G-6-Pase activity and the progressive increase in their hepatic G-6-PD activity. Praziquantel given to normal mice moderately affected the blood glucose and the previously mentioned hepatic enzymes. However, the drug markedly increased the liver glycogen content of normal mice and failed to elicit any change in their blood pyruvate and lactate. Possible explanations of these findings are discussed.