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Hepcidin, Interleukin-6 Levels and Iron Metabolism Parameters in Patients with Hepatic Glycogen Storage Diseases: A Cross-Sectional Study Hepcidin Interleukin6 Interleukin 6 Interleukin- Diseases CrossSectional Cross Sectional
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Nalin, Tatiéle

; Sperb-Ludwig, Fernanda

; Siebert, Marina

; Rizowy, Gustavo Mottin

; Weinstein, David A.

; Derks, Terry G. J.

; Souza, Carolina F. M. de

; Schwartz, Ida V. D.

Journal of Inborn Errors of Metabolism and Screening

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2024, Volume 12 elocation e20230015

Abstract: En | Text: En | PDF: En

Abstract Hepatic glycogen storage diseases (GSD) are characterized by recurrent episodes of hypoglycemia, and anemia has been recognized as a frequent complication of these disorders.This was a convenience cross-sectional study to evaluate hepcidin and IL-6 concentrations in patients with hepatic GSD and their association with anemia and other parameters of iron metabolism.Levels of hepcidin, IL-6, and markers of iron metabolism were measured in 32 patients receiving uncooked cornstarch therapy for GSD (GSD Ia= 18; Ib= 7; III= 3; IXa= 3; IXb= 1; median age 9.5 years). IL-6 concentrations were compared to those of 8 individuals heterozygous for GSD. Nine patients were anemic and five patients had hepatic adenomas. IL-6 levels were higher in patients than in heterozygotes. Eight patients had hyperferritinemia, and one had elevated transferrin saturation as well. Hepcidin correlated positively with ferritin levels. IL-6 correlated with hemoglobin, iron, transferrin, and transferrin saturation. There was no correlation between hepcidin and IL-6 levels. Patients with GSD Ib had the highest IL-6 levels.Anemia is a common finding in hepatic GSD, especially in GSD Ib, the type of GSD associated with the highest IL-6 levels. These findings suggest that inflammation is strongly associated with development of anemia in GSD Ib. hypoglycemia disordersThis disorders This crosssectional cross sectional IL6 IL 6 IL- metabolismLevels Levels IL6, 6, 3 Ia 18 7 III IXa IXb 1 95 9 5 9. years. years . years) adenomas heterozygotes hyperferritinemia well hemoglobin levelsAnemia Anemia

https://doi.org/10.1590/2326-4594-jiems-2023-0015

In vitro substrate reduction, chaperone and immunomodulation treatments reduce heparan sulfate in mucolipidosis III human fibroblasts reduction
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Sperb-Ludwig, Fernanda

; Ludwig, Nataniel Floriano

; Rizowy, Gustavo Mottin

; Velho, Renata Voltolini

; Schwartz, Ida Vanessa Doederlein

Genetics and Molecular Biology

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2023, Volume 46 N. 3 elocation e20230117

Abstract: En | Text: En | PDF: En

Abstract Mucolipidosis II and III (MLII and MLIII) are autosomal recessive diseases caused by pathogenic variants in GNPTAB and GNPTG genes that lead to defects in GlcNAc-1-phosphotransferase. This enzyme adds mannose 6-phosphate residues to lysosomal hydrolases, which allows enzymes to enter lysosomes. Defective GlcNAc-1-phosphotransferase causes substrate accumulation and inflammation. These diseases have no treatment, and we hypothesized that the use of substrate reduction therapy and immunomodulation may be beneficial at the cell level and as a future therapeutic approach. Fibroblasts from two patients with MLIII alpha/beta and 2 patients with MLIII gamma as well as from one healthy control were treated with 10 µM miglustat, 20 µM genistein, and 20 µM thalidomide independently. ELISA assay and confocal immunofluorescence microscopy were used to evaluate the presence of heparan sulfate (HS) and the impact on substrate accumulation. ELISA assay showed HS reduction in all patients with the different treatments used (p=0.05). HS reduction was also observed by immunofluorescence microscopy. Our study produced encouraging results, since the reduction in substrate accumulation, even partial, may offer benefits to the phenotype of patients with inborn errors of metabolism. MLII GlcNAc1phosphotransferase. GlcNAc1phosphotransferase GlcNAcphosphotransferase GlcNAc 1 phosphotransferase. phosphotransferase 6phosphate phosphate 6 hydrolases lysosomes inflammation treatment approach alphabeta alpha beta miglustat genistein independently (HS p=0.05. p005 p p=0.05 . 0 05 (p=0.05) results partial metabolism p00 p=0.0 (p=0.05 p0 p=0. (p=0.0 p=0 (p=0. p= (p=0 (p= (p

https://doi.org/10.1590/1678-4685-gmb-2023-0117

Homocysteine and methylmalonic acid in Phenylketonuria patients
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Hoss, Giovana Regina Weber

; Sperb-Ludwig, Fernanda

; Tonon, Tássia

; Poloni, Soraia

; Behringer, Sidney

; Blom, Henk J.

; Maillot, François

; Schwartz, Ida Vanessa Doederlein

Genetics and Molecular Biology

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2023, Volume 46 N. 3 elocation e20230103

Abstract: En | Text: En | PDF: En

Abstract Hyperhomocysteinemia and vitamin B12 deficiency have been reported in patients with phenylketonuria. In this study, total homocysteine (tHcy) and methylmalonic acid (MMA) levels were analyzed in samples from 25 phenylketonuria (PKU) patients. Comparisons were made between pre- and post-treatment values (n= 3); on treatment values, between periods with high and normal/low phenylalanine (Phe) levels (n= 20); and in women before, during and after pregnancy (n= 3). THcy levels decreased after treating PKU with metabolic formula (p=0.014). Except for a pregnant woman before pregnancy, none of the patients had tHcy values above the normal range. In fact, tHcy was < 5 μmol/L in 34% of the samples. We observed a decrease in Phe, tHcy, and tyrosine levels during pregnancy. MMA levels did not differ significantly, with values remaining in the normal range. These data indicate that there was no B12 deficiency in patients who adhere to the diet. In conclusion, in PKU patients treated with metabolic formula, tHcy is frequently not elevated, remaining even in the lower normal range in some patients. Thus, clinical follow-up and adherence to dietary treatment are crucial to prevent B12 deficiency. B B1 study (tHcy (MMA 2 (PKU pre posttreatment post n= n (n 3 3) normallow low Phe (Phe 20 20) 3. . p=0.014. p0014 p p=0.014 0 014 (p=0.014) fact μmolL μmol L 34 significantly diet conclusion elevated Thus followup follow up p001 p=0.01 01 (p=0.014 p00 p=0.0 (p=0.01 p0 p=0. (p=0.0 p=0 (p=0. p= (p=0 (p= (p

https://doi.org/10.1590/1678-4685-gmb-2023-0103

Characterization of the 3'UTR of the BTD gene and identification of regulatory elements and microRNAs
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Silva, Gerda Cristal Villalba

; Borsatto, Taciane

; Schwartz, Ida Vanessa Doederlein

; Sperb-Ludwig, Fernanda

Genetics and Molecular Biology

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2022, Volume 45 N. 1 elocation e20200432

Abstract: En | Text: En | PDF: En

Abstract Reduced biotinidase activity is associated with a spectrum of deficiency ranging from total deficiency to heterozygous levels, a finding that is not always explained by the pathogenic variants observed in the BTD gene. The investigation of miRNAs, regulatory elements and variants in the 3’UTR region may present relevance in understanding the genotype-phenotype association. The aims of the study were to characterize the regulatory elements of the 3’UTR of the BTD gene and identify variants and miRNAs which may explain the discrepancies observed between genotype and biochemical phenotype. We evaluated 92 individuals with reduced biotinidase activity (level of heterozygotes = 33, borderline = 35, partial DB = 20 or total DB= 4) with previously determined BTD genotype. The 3’UTR of the BTD gene was Sanger sequenced. In silico analysis was performed to identify miRNAs and regulatory elements. No variants were found in the 3’UTR. We found 97 possible miRNAs associated with the BTD gene, 49 predicted miRNAs involved in the alanine, biotin, citrate and pyruvate metabolic pathways and 5 genes involved in biotin metabolism. Six AU-rich elements were found. Our data suggest variants in the 3'UTR of BTD do not explain the genotype-phenotype discrepancies found in Brazilian individuals with reduced biotinidase.

https://doi.org/10.1590/1678-4685-gmb-2020-0432

A decade of molecular diagnosis of Mucolipidosis II and III in Brazil: a pooled analysis of 32 patients
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Ludwig, Nataniel F

; Sperb-Ludwig, Fernanda

; Randon, Dévora N

; Bernardi, Pricila

; Giuliani, Liane R

; Moreno, Carolina A

; Cavalcanti, Denise P

; Silva, Luiz CS da

; Schwartz, Ida V D

Journal of Inborn Errors of Metabolism and Screening

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2021, Volume 9 elocation e20200029

Abstract: En | Text: En | PDF: En

Abstract GlcNAc-1-phosphotransferase is a hexameric complex formed by subunits α, β, and γ, where the first two are encoded by the GNPTAB gene and the third by the GNPTG gene. Pathogenic variants identified in the GNPTAB gene cause the diseases Mucolipidosis II and III alpha/beta, which are severe and characterized by an overflow of lysosomal hydrolases into the extracellular environment, and their absence in lysosomal compartments causes an accumulation of non-degraded macromolecules. Methodology: a retrospective study that included 32 unrelated Brazilian patients with a clinical and genetic diagnosis of Mucolipidosis II/III alpha/beta. The regional frequency of the altered alleles was determined. Results: The patients were from all regions of Brazil. The most prevalent variants were c.3503_3504del, associated with the severe form of the disease, and c.1208T>C, associated with the milder form. Variant c.3503_3504del is the most frequently found in the Midwest, Northeast, and Southeast regions of Brazil. In the South, 42.8% of the alleles present the c.1196C>T variant. Conclusions: From the perspective of all patients diagnosed with Mucolipidosis II/III in Brazil, it is possible to conclude that different regions present allelic frequencies of specific pathogenic variants, which can be explained by the occurrence of a founding effect or high inbreeding rates.

https://doi.org/10.1590/2326-4594-jiems-2020-0029 225 downloads

The fructose-1,6-bisphosphatase deficiency and the p.(Lys204ArgfsTer72) variant
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Pinheiro, Franciele Cabral

; Ligabue-Braun, Rodrigo

; Siqueira, Ana Cecília Menezes de

; Matuella, Camila

; Souza, Carolina Fischinger Moura de

; Monteiro, Fabíola Paoli

; Kok, Fernando

; Schwartz, Ida Vanessa Doederlein

; Sperb-Ludwig, Fernanda

Genetics and Molecular Biology

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2021, Volume 44 N. 2 elocation e20200281

Abstract: En | Text: En | PDF: En

Abstract Fructose-1,6-bisphosphatase (FBPase) deficiency is a rare inborn error of fructose metabolism caused by pathogenic variants in the FBP1 gene. As gluconeogenesis is affected, catabolic episodes can induce ketotic hypoglycemia in patients. FBP1 analysis is the most commonly used approach for the diagnosis of this disorder. Herein, a Brazilian patient is reported. The proband, a girl born to a consanguineous couple, presented with severe hypoglycemia crisis in the neonatal period. At the age 17 months, presented a new crisis accompanied by metabolic acidosis associated with a feverish episode. Genetic analysis was performed by next-generation sequencing (NGS), identifying the NM_000507.3:c.611_614del variant in homozygosis in the FBP1 gene. In silico analysis and 3D modeling were performed, suggesting that this variant is associated with a loss of sites for substrate and Mg2+ binding and for posttranslational modifications of FBPase. The c.611_614del variant is located in a repetitive region of the FBP1 gene that appears to be a hotspot for mutational events. This frameshift creates a premature termination codon in the last coding exon which escapes the nonsense-mediated decay mechanism, according to in silico analysis. This variant results in an intrinsically disordered protein with loss of substrate recognition and post-translational modification sites.

https://doi.org/10.1590/1678-4685-gmb-2020-0281 308 downloads

Prevalence of the most common pathogenic variants in three genes for inborn errors of metabolism associated with sudden unexpected death in infancy: a population-based study in south Brazil
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Randon, Dévora N.

; Sperb-Ludwig, Fernanda

; Vianna, Fernanda S. L.

; Becker, Ana P. P.

; Vargas, Carmen R.

; Sitta, Angela

; Sant’Ana, Alexia N.

; Schwartz, Ida V. D.

; Bitencourt, Fernanda H. de

Genetics and Molecular Biology

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2020, Volume 43 N. 3 elocation 20190298

Abstract: En | Text: En | PDF: En

Abstract Citrullinemia type 1 (CTLNI), long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency (LCHADD), and mut0 methylmalonic acidemia (mut0 MMA) are inborn errors of metabolism (IEMs) associated with sudden unexpected death in infancy (SUDI). Its most common pathogenic variants are: c.1168G>A (CTLNI, ASS1 gene), c.1528G>C (LCHADD, HADHA gene), c.655A>T and c.1106G>A (mut0 MMA, MUT gene). Considering the absence of estimates regarding the incidence of these diseases in Brazil, this study sought to investigate the prevalence of its main pathogenic variants in a healthy population in the southern region of the country. A total of 1,000 healthy subjects from Rio Grande do Sul were included. Genotyping was performed by real-time PCR. Individuals found to be heterozygous for c.1528G>C underwent further acylcarnitine profile analysis by tandem mass spectrophotometry. Allele and genotype frequencies were calculated considering Hardy-Weinberg equilibrium. The c.1528G>C variant was detected in heterozygosity in two subjects (carrier frequency = 1:500; allele frequency = 0.001; minimum prevalence of LCHADD = 1: 1,000,000), whose acylcarnitine profiles were normal. Variants c.1168G>A, c.655A>T, and c.1106G>A were not identified. These results denote the rarity of these IEMs in Southern Brazil, highlighting the need to expand the investigation of IEMs in relation to infant morbidity and mortality within the country.

https://doi.org/10.1590/1678-4685-gmb-2019-0298 803 downloads

Humoral immune response in adult Brazilian patients with Mucolipidosis III gamma
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Sperb-Ludwig, Fernanda

; Alegra, Taciane

; Velho, Renata Voltolini

; Ludwig, Nataniel

; Siebert, Marina

; Jobim, Mariana

; Vairo, Filippo

; Schwartz, Ida V. D.

Genetics and Molecular Biology

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sep 2019, Volume 42 N. 3 Pages 571 - 573

Abstract: En | Text: En | PDF: En

Abstract Mucolipidosis II and III (ML II and III) alpha/beta and ML III gamma are lysosomal diseases caused by GlcNAc-1-phosphotransferase deficiency. Previous data indicate that MLII patients have functionally impaired immune system that contributes to predisposition to infections.We evaluated the immunological phenotype of three Brazilian patients with ML III gamma. Our data suggest that the residual activity of GlcNAc-1-phosphotransferase in patients with ML III gamma is enough to allow the targeting of the lysosomal enzymes required for B-cell functions maintenance.

https://doi.org/10.1590/1678-4685-gmb-2018-0246 589 downloads

Diagnosis and Management of Classica Homocystinuria in Brazil: A Summary of 72 Late-Diagnosed Patients
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Poloni, Soraia

; Hoss, Giovana W.

; Sperb-Ludwig, Fernanda

; Borsatto, Taciane

; Doriqui, Maria Juliana R.

; Leão, Emília K.E.A

; Boa-Sorte, Ney

; Lourenço, Charles M.

; Kim, Chong A.

; Souza, Carolina F. M. de

; Rocha, Helio

; Ribeiro, Marcia

; Steiner, Carlos E.

; Moreno, Carolina A.

; Bernardi, Pricila

; Valadares, Eugenia

; Artigalas, Osvaldo

; Carvalho, Gerson

; Wanderley, Hector Y. C.

; D’Almeida, Vânia

; Santana-da-Silva, Luiz C.

; Blom, Henk J.

; Schwartz, Ida V. D.

Journal of Inborn Errors of Metabolism and Screening

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2018, Volume 6 elocation e180007

Abstract: En | Text: En | PDF: En

Abstract This study described a broad clinical characterization of classical homocystinuria (HCU) in Brazil. This was a cross-sectional, observational study including clinical and biochemical data from 72 patients (60 families) from Brazil (South, n = 13; Southeast, n = 37; Northeast, n = 8; North, n = 1; and Midwest, n = 1). Parental consanguinity was reported in 42% of families. Ocular manifestations were the earliest detected symptom (53% of cases), the main reason for diagnostic suspicion (63% of cases), and the most prevalent manifestation at diagnosis (67% of cases). Pyridoxine responsiveness was observed in 14% of patients. Only 22% of nonresponsive patients on treatment had total homocysteine levels <100 mmol/L. Most commonly used treatment strategies were pyridoxine (93% of patients), folic acid (90%), betaine (74%), vitamin B12 (27%), and low-methionine diet + metabolic formula (17%). Most patients diagnosed with HCU in Brazil are late diagnosed, express a severe phenotype, and poor metabolic control. Milder forms of HCU are likely underrepresented due to underdiagnosis.

https://doi.org/10.1177/2326409818788900 1352 downloads

10.

New approaches to the treatment of orphan genetic disorders: Mitigating molecular pathologies using chemicals
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VELHO, RENATA V.

; SPERB-LUDWIG, FERNANDA

; SCHWARTZ, IDA V.D.

Anais da Academia Brasileira de Ciências

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aug 2015, Volume 87 N. 2 Pages 1375 - 1388

Abstract: Pt En | Text: Pt En | PDF: Pt | PDF: En

Com o avanço e a popularização de técnicas moleculares, a identificação de mutações genéticas que causam doenças aumentou drasticamente. Deste modo, o número de laboratórios disponíveis para investigar uma determinada doença e, consequentemente, o número de diagnósticos, aumentou ao longo do tempo. Embora seja necessário identificar mutações e fornecer diagnósticos, é crucial também desenvolver abordagens terapêuticas específicas baseadas nestas informações. Esta revisão tem como objetivo destacar os avanços recentes em terapias mutação-alvo com produtos químicos que mitiguem a patologia mutacional ao nível molecular, para doenças que, para a maior parte, não têm tratamento eficaz. Atualmente, existem várias estratégias sendo utilizadas para corrigir diferentes tipos de mutações, incluindo as seguintes: a identificação e caracterização de compostos readthroughtraducionais; redirecionamento de splicingmediado por oligonucleotídeos de sentido contrário; reparo por mismatch; e salto de exon. Estas terapias e outras abordagens são revistas neste artigo.

With the advance and popularization of molecular techniques, the identification of genetic mutations that cause diseases has increased dramatically. Thus, the number of laboratories available to investigate a given disorder and the number of subsequent diagnosis have increased over time. Although it is necessary to identify mutations and provide diagnosis, it is also critical to develop specific therapeutic approaches based on this information. This review aims to highlight recent advances in mutation-targeted therapies with chemicals that mitigate mutational pathology at the molecular level, for disorders that, for the most part, have no effective treatment. Currently, there are several strategies being used to correct different types of mutations, including the following: the identification and characterization of translational readthrough compounds; antisense oligonucleotide-mediated splicing redirection; mismatch repair; and exon skipping. These therapies and other approaches are reviewed in this paper.

https://doi.org/10.1590/0001-3765201520140711 4124 downloads

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