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Article ; Online: Soluble mannose receptor: A potential biomarker in Gaucher disease.

Beaton, Brendan / Hughes, Derralynn A

2024 Volume 112, Issue 5, Page(s) 794–801

Abstract: Purpose: Soluble mannose receptor (sMR) relates to mannose receptor expression on macrophages, and is elevated in inflammatory disorders. Gaucher disease (GD) has altered macrophage function and utilises mannose receptors for enzyme replacement therapy ( ...

Abstract	Purpose: Soluble mannose receptor (sMR) relates to mannose receptor expression on macrophages, and is elevated in inflammatory disorders. Gaucher disease (GD) has altered macrophage function and utilises mannose receptors for enzyme replacement therapy (ERT) endocytosis. sMR has not previously been studied in GD. Methods: sMR was measured by ELISA and correlated with GD clinical features including spleen and liver volume, haemoglobin and platelet count, bone marrow burden (BMB) scores and immunoglobulin levels. sMR was compared with biomarkers of GD: chitotriosidase, lyso-GL1, PARC, CCL3, CCL4, osteoactivin, serum ACE and ferritin. Results: Median sMR in untreated GD patients was 303.0 ng/mL compared to post-treatment 190.9 ng/mL (p = .02) and healthy controls 202 ng/mL. Median sMR correlated with median spleen volume 455 mL (r = .70, p = .04), liver volume 2025 mL (r = .64, p = .04), BMB 7 (r = .8, p = .03), IgA 1.9 g/L (r = .54, p = .036), IgG 9.2 g/L (r = .57, p = .027), IgM 1.45 g/L (r = .86, p < .0001), with inverse correlation to median platelet count of 125 × 10 Conclusions: sMR correlates with clinical features and biomarkers of GD and reduces following therapy.
MeSH term(s)	Humans ; Mannose Receptor ; Gaucher Disease/diagnosis ; Gaucher Disease/drug therapy ; Biomarkers ; Hemoglobins/metabolism ; Ferritins
Chemical Substances	Mannose Receptor ; Biomarkers ; Hemoglobins ; Ferritins (9007-73-2)
Language	English
Publishing date	2024-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	392482-8
ISSN	1600-0609 ; 0902-4441
ISSN (online)	1600-0609
ISSN	0902-4441
DOI	10.1111/ejh.14171
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Article ; Online: Lysosomal Acid Lipase Deficiency: Therapeutic Options.

Pastores, Gregory M / Hughes, Derralynn A

Drug design, development and therapy

2020 Volume 14, Page(s) 591–601

Abstract: Lysosomal acid lipase (LAL) deficiency is a metabolic (storage) disorder, encompassing a severe (Wolman disease) and attenuated (Cholesterol ester storage disease) subtype; both inherited as autosomal recessive traits. Cardinal clinical features include ... ...

Abstract	Lysosomal acid lipase (LAL) deficiency is a metabolic (storage) disorder, encompassing a severe (Wolman disease) and attenuated (Cholesterol ester storage disease) subtype; both inherited as autosomal recessive traits. Cardinal clinical features include the combination of hepatic dysfunction and dyslipidemia, as a consequence of cholesteryl esters and triglyceride accumulation, predominately in the liver and vascular and reticuloendothelial system. Significant morbidity can arise, due to liver failure and/or atherosclerosis; in part related to the severity of the underlying gene defect and corresponding enzyme deficiency. Diagnosis is based on demonstration of decreased LAL enzyme activity, complemented by analysis of the cognate gene defects. Therapeutic options include dietary manipulation and the use of lipid-lowering drugs. Sebelipase alfa, a recombinant enzyme replacement therapy, has garnered regulatory approval, following demonstration of improvements in disease-relevant markers and clinical benefit in clinical trials, which included increased survival in the most severe cases.
MeSH term(s)	Animals ; Atherosclerosis/etiology ; Cholesterol Ester Storage Disease/physiopathology ; Cholesterol Ester Storage Disease/therapy ; Humans ; Hypolipidemic Agents/therapeutic use ; Liver Failure/etiology ; Severity of Illness Index ; Sterol Esterase/therapeutic use ; Wolman Disease/physiopathology ; Wolman Disease/therapy ; Wolman Disease
Chemical Substances	Hypolipidemic Agents ; Sterol Esterase (EC 3.1.1.13) ; Sebelipase alfa (K4YTU42T8G)
Language	English
Publishing date	2020-02-11
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S149264
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Article ; Online: New drugs for the treatment of Anderson-Fabry disease.

Feriozzi, Sandro / Hughes, Derralynn A

Journal of nephrology

2020 Volume 34, Issue 1, Page(s) 221–230

Abstract: Enzyme replacement therapy (ERT) of the Anderson-Fabry disease (AFD) has changed the outcome of patients. However, ERT has some limitations: a restricted volume of distribution, requirement for intravenous access, and stimulation of the production of ... ...

Abstract	Enzyme replacement therapy (ERT) of the Anderson-Fabry disease (AFD) has changed the outcome of patients. However, ERT has some limitations: a restricted volume of distribution, requirement for intravenous access, and stimulation of the production of anti-drug antibodies. Studies of new drugs aiming to improve the clinical effectiveness and convenience of therapy have been reported. Migalastat, a pharmacological chaperone, increases available enzymate activity in patients with mutations amenable to the therapy, is now available for clinical practice. It is orally administered, and while clinical trial results are promising, long term real world follow up is awaited. PEGylated enzyme has a longer half-life and potentially reduced antigenicity, compared with standard preparations; investigation of whether a longer dosing interval is viable is under way. Moss-derived enzyme has a higher affinity for mannose receptors, and appears to have access to renal tissue. Substrate reduction therapy is based on reducing the catabolism processes of the glycosphingolipids, and is currently under investigation as monotherapy. Gene therapy has now been initiated in clinical trail of in vivo and ex vivo technologies with early results are emerging. ERT represents a certain milestone of therapy for AFD with Migalastat now a newly available option. Other agents in clinical trial prevent further potential opportunities to improve outcomes in AFD.
MeSH term(s)	Enzyme Replacement Therapy ; Fabry Disease/diagnosis ; Fabry Disease/drug therapy ; Humans ; Mutation ; Pharmaceutical Preparations ; alpha-Galactosidase/therapeutic use
Chemical Substances	Pharmaceutical Preparations ; alpha-Galactosidase (EC 3.2.1.22)
Language	English
Publishing date	2020-03-20
Publishing country	Italy
Document type	Journal Article ; Review
ZDB-ID	1093991-x
ISSN	1724-6059 ; 1120-3625 ; 1121-8428
ISSN (online)	1724-6059
ISSN	1120-3625 ; 1121-8428
DOI	10.1007/s40620-020-00721-4
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Article ; Online: Fabry disease: will markers of early disease enable early treatment and better outcomes?

Hughes, Derralynn A

Current opinion in cardiology

2016 Volume 31, Issue 4, Page(s) 434–439

Abstract: Purpose of review: This review explores the clinical and pathological features of Fabry disease. New modalities of imaging, biomarkers and long-term treatment effects are discussed.: Recent findings: Fabry disease is clinically heterogeneous, and in ... ...

Abstract	Purpose of review: This review explores the clinical and pathological features of Fabry disease. New modalities of imaging, biomarkers and long-term treatment effects are discussed. Recent findings: Fabry disease is clinically heterogeneous, and in women the clinical severity has recently been linked to skewing of X-inactivation. Two phenotypes have been described, one with early onset manifestations is including pain and one with later onset single organ manifestations; however, the cardiac outcomes in these two groups appear similar. Fibrosis is found in renal and cardiac tissues on biopsy and appears to be a critical point in the pathology of Fabry disease after which response to enzyme replacement therapy is more limited. In-vitro studies have suggested that lyso-globotriaosylceramide may have an important role in the generation of fibrosis. Imaging, including cardiac magnetic resonance imaging, may have a role in detection of early stages of the disease. Long-term outcomes for patients treated with enzyme replacement therapy are now being described with some suggestion that patients treated at earlier points in the disease course may have better outcomes. Summary: Recent advances in understanding pathology, disease processes and treatment effects may enable future rational targeting of treatment with improved outcomes.
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	645186-x
ISSN	1531-7080 ; 0268-4705
ISSN (online)	1531-7080
ISSN	0268-4705
DOI	10.1097/HCO.0000000000000308
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Article: Lysosomal Storage Disorders and Malignancy.

Pastores, Gregory M / Hughes, Derralynn A

Diseases (Basel, Switzerland)

2017 Volume 5, Issue 1

Abstract: Lysosomal storage disorders (LSDs) are infrequent to rare conditions caused by mutations that lead to a disruption in the usual sequential degradation of macromolecules or their transit within the cell. Gaucher disease (GD), a lipidosis, is among the ... ...

Abstract	Lysosomal storage disorders (LSDs) are infrequent to rare conditions caused by mutations that lead to a disruption in the usual sequential degradation of macromolecules or their transit within the cell. Gaucher disease (GD), a lipidosis, is among the most common LSD, with an estimated incidence of 1 in 40,000 among the Caucasian, non-Jewish population. Studies have indicated an increased frequency of polyclonal and monoclonal gammopathy among patients with GD. It has been shown that two major sphingolipids that accumulate in GD, namely, β-glucosylceramide 22:0 (βGL1-22) and glucosylsphingosine (LGL1), can be recognized by a distinct subset of CD1d-restricted human and murine type II natural killer T (NKT) cells. Investigations undertaken in an affected mouse model revealed βGL1-22- and LGL1-specific NKT cells were present and constitutively promoted the expression of a T-follicular helper (TFH) phenotype; injection of these lipids led to downstream induction of germinal center B cells, hypergammaglobulinemia, and the production of antilipid antibodies. Subsequent studies have found clonal immunoglobulin in 33% of sporadic human monoclonal gammopathies is also specific for the lysolipids LGL1 and lysophosphatidylcholine (LPC). Furthermore, substrate reduction ameliorated GD-associated gammopathy in mice. It had been hypothesized that chronic antigenic stimulation by the abnormal lipid storage and associated immune dysregulation may be the underlying mechanism for the increased incidence of monoclonal and polyclonal gammopathies, as well as an increased incidence of multiple myeloma in patients with GD. Current observations support this proposition and illustrate the value of investigations into rare diseases, which as 'experiments of nature' may provide insights into conditions found in the general population that continue to remain incompletely understood.
Language	English
Publishing date	2017-02-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720869-2
ISSN	2079-9721
ISSN	2079-9721
DOI	10.3390/diseases5010008
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Article ; Online: Eliglustat for Gaucher's disease: trippingly on the tongue.

Hughes, Derralynn A / Pastores, Gregory M

Lancet (London, England)

2015 Volume 385, Issue 9985, Page(s) 2328–2330

MeSH term(s)	Enzyme Inhibitors/therapeutic use ; Enzyme Replacement Therapy ; Female ; Gaucher Disease/drug therapy ; Glucosylceramidase/therapeutic use ; Humans ; Male ; Pyrrolidines/therapeutic use
Chemical Substances	Enzyme Inhibitors ; Pyrrolidines ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2015-06-13
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/S0140-6736(15)60206-9
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Article ; Online: Non-neuronopathic lysosomal storage disorders: Disease spectrum and treatments.

Pastores, Gregory M / Hughes, Derralynn A

Best practice & research. Clinical endocrinology & metabolism

2015 Volume 29, Issue 2, Page(s) 173–182

Abstract: Distinctive facial features, hepatosplenomegaly or cardiomyopathy with or without associated skeletal dysplasia are clinical manifestations that may be suggestive of an underlying lysosomal storage disorder (LSD), However, these features may not be ... ...

Abstract	Distinctive facial features, hepatosplenomegaly or cardiomyopathy with or without associated skeletal dysplasia are clinical manifestations that may be suggestive of an underlying lysosomal storage disorder (LSD), However, these features may not be evident in certain subtypes associated primarily with central nervous system involvement. Age at onset can be broad, ranging from infancy to adulthood. Diagnosis may be delayed, as manifestations may be slow to evolve (taking months to years), particularly in those with later (adult-)onset, and in isolated cases (i.e., those without a prior family history). Diagnosis of individual subtypes can be confirmed using a combination of biochemical and molecular assays. In a few LSDs, treatment with hematopoietic stem cell transplantation, enzyme replacement or substrate reduction therapy is available. Symptomatic and palliative measure may enhance quality of life for both treatable and currently untreatable cases. Genetic counseling is important, so patients and their families can be informed of reproductive risks, disease prognosis and therapeutic options. Investigations of underlying disease mechanisms are enhancing knowledge about rare diseases, but also other more common medical conditions, on account of potential convergent disease pathways.
MeSH term(s)	Cardiomyopathies/etiology ; Dysostoses/etiology ; Enzyme Replacement Therapy ; Genetic Counseling ; Genetic Therapy ; Hematopoietic Stem Cell Transplantation ; Hepatomegaly/etiology ; Humans ; Lysosomal Storage Diseases/complications ; Lysosomal Storage Diseases/therapy ; Physical Therapy Modalities ; Renal Insufficiency/etiology ; Splenomegaly/etiology
Language	English
Publishing date	2015-03
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2014.08.005
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Article ; Online: Enzyme, substrate, and myeloma in Gaucher disease.

Hughes, Derralynn A

American journal of hematology

2009 Volume 84, Issue 4, Page(s) 199–201

MeSH term(s)	Animals ; Cytokines/blood ; Disease Models, Animal ; Gaucher Disease/classification ; Gaucher Disease/complications ; Gaucher Disease/ethnology ; Gaucher Disease/genetics ; Gaucher Disease/immunology ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genotype ; Glucosylceramidase/deficiency ; Glucosylceramidase/genetics ; Glucosylceramidase/physiology ; Humans ; Hypergammaglobulinemia/etiology ; Incidence ; Jews/genetics ; Mice ; Multiple Myeloma/epidemiology ; Multiple Myeloma/genetics ; Neoplasms/epidemiology ; Neoplasms/genetics ; Organ Specificity ; Phenotype ; Point Mutation ; Risk
Chemical Substances	Cytokines ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2009-04
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.21375
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Article ; Online: Early therapeutic intervention in females with Fabry disease?

Hughes, Derralynn A

Acta paediatrica (Oslo, Norway : 1992)

2008 Volume 97, Issue 457, Page(s) 41–47

Abstract: Unlabelled: Anderson-Fabry disease is an X-linked lysosomal storage disorder resulting from deficiency of alpha-galactosidase A. The subsequent accumulation of globotriaosylceramide (Gb3) in cells and tissues of the body has multisystemic effects and ... ...

Abstract	Unlabelled: Anderson-Fabry disease is an X-linked lysosomal storage disorder resulting from deficiency of alpha-galactosidase A. The subsequent accumulation of globotriaosylceramide (Gb3) in cells and tissues of the body has multisystemic effects and significantly impacts upon quality of life and survival of individuals with this condition. In general, Anderson-Fabry disease is more severe in male patients; however, despite X-linkage, females may develop severe signs and symptoms of the disease, although there is considerable phenotypic heterogeneity, which correlates most closely with age. Histological analyses of biopsies have shown evidence of Gb3 storage in the kidney and heart in female patients. Gb3 levels are also elevated in the urine of females, although plasma Gb3 levels are not reliably elevated. The efficacy of enzyme replacement therapy (ERT) with recombinant human alpha-galactosidase A has been demonstrated in females in a clinical trial and in observational studies, including those using data from outcome surveys. Benefits include a reduction in left ventricular mass, stabilization of renal function and improvements in pain and quality of life. Conclusion: If early intervention with ERT in females is to be advocated, it is necessary to demonstrate not only that females with Anderson-Fabry disease have clinical and biochemical features of alpha-galactosidase A deficiency and respond to ERT, but also that early intervention prevents the onset of the later manifestations of the disorder. Any strategy for early therapy should also balance future advantages against any impact on quality of life.
MeSH term(s)	Age Factors ; Cardiomyopathies/enzymology ; Cardiomyopathies/etiology ; Cardiovascular Diseases/enzymology ; Cardiovascular Diseases/etiology ; Disease Progression ; Fabry Disease/complications ; Fabry Disease/diagnosis ; Fabry Disease/drug therapy ; Fabry Disease/genetics ; Fabry Disease/physiopathology ; Female ; Glomerular Filtration Rate ; Humans ; Hypertrophy, Left Ventricular/etiology ; Isoenzymes/therapeutic use ; Trihexosylceramides/analysis ; Trihexosylceramides/blood ; alpha-Galactosidase/therapeutic use
Chemical Substances	Isoenzymes ; Trihexosylceramides ; agalsidase alfa (2HLC17MX9G) ; globotriaosylceramide (71965-57-6) ; alpha-Galactosidase (EC 3.2.1.22)
Language	English
Publishing date	2008-04
Publishing country	Norway
Document type	Journal Article ; Review
ZDB-ID	203487-6
ISSN	1651-2227 ; 0365-1436 ; 0803-5253
ISSN (online)	1651-2227
ISSN	0365-1436 ; 0803-5253
DOI	10.1111/j.1651-2227.2008.00649.x
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Article: Fabry disease.

Thomas, Atison S / Hughes, Derralynn A

Pediatric endocrinology reviews : PER

2014 Volume 12 Suppl 1, Page(s) 88–101

Abstract: Fabry disease (FD) is an X-linked disorder caused by deficiency of the enzyme alpha-galactosidase A, required for the degradation of globotriaosylceramide. Accumulation of substrate occurs in multiple cell types resulting in a multi-system disorder, ... ...

Abstract	Fabry disease (FD) is an X-linked disorder caused by deficiency of the enzyme alpha-galactosidase A, required for the degradation of globotriaosylceramide. Accumulation of substrate occurs in multiple cell types resulting in a multi-system disorder, affecting both males and females. Clinical features include neuropathic pain and angiokeratoma, with subsequent development of proteinuria, renal failure, left ventricular hypertrophy, arrhythmias and stroke. Beyond palliative therapies for organ involvement and pain control, enzyme replacement therapy directed at the underlying metabolic defect became available in 2001-2003. Knowledge of the pathophysiology and clinical features of FD is vital for assessing the rationale and evidence of efficacy of therapies for FD and their limitations. Whilst ERT improves many of the symptoms of FD, its effect on the natural history of the disorder has yet to be fully demonstrated. Improved understanding of the appropriate use of adjunctive therapies and the development of new treatment strategies, including pharmacologic chaperone therapy and gene therapy, coupled with long term clinical outcome data on the effects of ERT are all key components of optimising treatment for FD.
MeSH term(s)	Enzyme Replacement Therapy ; Fabry Disease/drug therapy ; Fabry Disease/genetics ; Female ; Humans ; Isoenzymes/therapeutic use ; Male ; Treatment Outcome ; alpha-Galactosidase/therapeutic use
Chemical Substances	Isoenzymes ; agalsidase alfa (2HLC17MX9G) ; alpha-Galactosidase (EC 3.2.1.22) ; agalsidase beta (RZD65TSM9U)
Language	English
Publishing date	2014-09
Publishing country	Israel
Document type	Journal Article ; Review
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
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