This ‘Molybdenum Cofactor Deficiency Type A (MoCoD-A) - Epidemiology Forecast-2032' report delivers an in-depth understanding of the Molybdenum Cofactor Deficiency Type A (MoCoD-A), historical and forecasted epidemiology as well as the Molybdenum Cofactor Deficiency Type A (MoCoD-A) epidemiology trends in the United States, EU5 (Germany, France, Italy, Spain, and the United Kingdom) and Japan.
Molybdenum cofactor deficiency (MoCoD-A) is a severe autosomal recessive inborn error of metabolism characterized by neonatal presentation of intractable seizures, feeding difficulties, developmental delays, microcephaly with brain atrophy and coarse facial features.
MoCoD-A is caused by homozygous or compound heterozygous mutation in the MOCS1 gene on chromosome 6p21 due to which patients cannot produce a substance known as cyclic pyranopterin monophosphate (cPMP). This results in deficiency of the molybdenum cofactor dependent enzymes sulfite oxidase, xanthine dehydrogenase, aldehyde oxidase and mitochondrial amidoxime reducing component.
The resultant accumulation of sulfite, taurine, S-sulfocysteine and thiosulfate contributes to the severe neurological impairment. Most patients die in early childhood from infections. The resultant accumulation of sulfite, taurine, S-sulfocysteine and thiosulfate contributes to the severe neurological impairment. Most patients die in early childhood from infections.
The diagnosis of molybdenum cofactor deficiency is established by identification of biallelic mutation in MOCS1 by detecting elevated sulfites (in urine test), elevated S-sulfocysteine (in urine test), low uric acid (in blood or urine test) and high levels of xanthine and hypoxanthine (in blood test). Finally, genetic testing confirms the diagnosis and type of MoCoD.
The disease epidemiology covered in the report provides historical as well as forecasted epidemiology segmented by total prevalent population of MoCoD, total diagnosed prevalent population of MoCoD and type-specific diagnosed prevalence of MoCoD covering the United States, EU-5 countries (Germany, France, Italy, Spain, and the United Kingdom) and Japan from 2019 to 2032.
The Molybdenum Cofactor Deficiency Type A (MoCoD-A) report will allow the user to -
Study Period: 2019-2032
Molybdenum Cofactor Deficiency Type A (MoCoD-A) Disease Understanding
Molybdenum cofactor deficiency (MoCoD-A) is a severe autosomal recessive inborn error of metabolism characterized by neonatal presentation of intractable seizures, feeding difficulties, developmental delays, microcephaly with brain atrophy and coarse facial features.
MoCoD-A is caused by homozygous or compound heterozygous mutation in the MOCS1 gene on chromosome 6p21 due to which patients cannot produce a substance known as cyclic pyranopterin monophosphate (cPMP). This results in deficiency of the molybdenum cofactor dependent enzymes sulfite oxidase, xanthine dehydrogenase, aldehyde oxidase and mitochondrial amidoxime reducing component.
The resultant accumulation of sulfite, taurine, S-sulfocysteine and thiosulfate contributes to the severe neurological impairment. Most patients die in early childhood from infections. The resultant accumulation of sulfite, taurine, S-sulfocysteine and thiosulfate contributes to the severe neurological impairment. Most patients die in early childhood from infections.
Molybdenum Cofactor Deficiency Type A (MoCoD-A) Diagnosis
The diagnosis of molybdenum cofactor deficiency is established by identification of biallelic mutation in MOCS1 by detecting elevated sulfites (in urine test), elevated S-sulfocysteine (in urine test), low uric acid (in blood or urine test) and high levels of xanthine and hypoxanthine (in blood test). Finally, genetic testing confirms the diagnosis and type of MoCoD.
Molybdenum Cofactor Deficiency Type A (MoCoD-A) Epidemiology Perspective
The disease epidemiology covered in the report provides historical as well as forecasted epidemiology segmented by total prevalent population of MoCoD, total diagnosed prevalent population of MoCoD and type-specific diagnosed prevalence of MoCoD covering the United States, EU-5 countries (Germany, France, Italy, Spain, and the United Kingdom) and Japan from 2019 to 2032.
Molybdenum Cofactor Deficiency Type A (MoCoD-A) Detailed Epidemiology Segmentation
- As per the assessment of the publisher, the total prevalent population of Molybdenum Cofactor Deficiency (MoCoD) in the 7MM was found to be 242 in 2021, which are expected to increase at a Compound Annual Growth Rate (CAGR) of 0.22% during the study period.
- In the 7MM, the diagnosed prevalent cases of Molybdenum Cofactor Deficiency (MoCoD) were 49 in 2021. Out of these cases, the United States accounted for about 51% (25 cases) of the total diagnosed prevalent cases among the 7MM, in 2021.
- There are three forms of MoCoD named types A, B, and C. Molybdenum cofactor deficiency type-A (MoCoD-A) is the most common form and the only one for which there is definitive therapy that improves outcome. In 2021, the total diagnosed prevalent cases of MoCoD-A in the US was 16.
- Among the European countries, Germany, France, and the UK had the highest diagnosed prevalent population of MoCoD-A with three cases each, in 2021. On the other hand, Spain had only one reported case in 2021.
- In 2021, Japan accounted for three cases of MoCoD-A. These cases are have decreased from previous years and is expected to increase during forecast period (2022-2032) as the decreasing crude birth rate is compensated by the expected increase in the diagnosis rate.
Scope of the Report
- The report covers the descriptive overview of Molybdenum Cofactor Deficiency Type A (MoCoD-A), explaining its symptoms, etiology, pathogenesis, and various diagnostic approaches.
- The report provides insight into the 7MM historical and forecasted patient pool covering the United States, EU5 countries (Germany, France, Italy, Spain, and the United Kingdom), and Japan.
- The report assesses the disease risk and burden of Molybdenum Cofactor Deficiency Type A (MoCoD-A).
- The report helps to recognize the growth opportunities in the 7MM with respect to the patient population.
- The report provides the segmentation of the disease epidemiology for 7MM as the prevalent population of MoCoD, diagnosed prevalent population of MoCoD, and type-specific diagnosed prevalent population of MoCoD).
Report Highlights
- 11-Year Forecast of Molybdenum Cofactor Deficiency Type A (MoCoD-A)
- 7MM Coverage
- Total Prevalent Population of MoCoD
- Total Diagnosed Prevalent Population of MoCoD
- Type-specific Diagnosed Prevalence of MoCoD
Key Questions Answered
- What are the disease risk and burdens of Molybdenum Cofactor Deficiency Type A (MoCoD-A)?
- What is the historical Molybdenum Cofactor Deficiency Type A (MoCoD-A) patient pool in the United States, EU5 (Germany, France, Italy, Spain, and the UK), and Japan?
- What would be the forecasted patient pool of Molybdenum Cofactor Deficiency Type A (MoCoD-A) at the 7MM level?
- What will be the growth opportunities across the 7MM with respect to the patient population pertaining to Molybdenum Cofactor Deficiency Type A (MoCoD-A)?
- Out of the above-mentioned countries, which country would have the highest patient population of Molybdenum Cofactor Deficiency Type A (MoCoD-A) during the forecast period (2022-2032)?
- At what CAGR the population is expected to grow across the 7MM during the forecast period (2022-2032)?
Reasons to Buy
The Molybdenum Cofactor Deficiency Type A (MoCoD-A) report will allow the user to -
- Develop business strategies by understanding the trends shaping and driving the 7MM Molybdenum Cofactor Deficiency Type A (MoCoD-A) epidemiology forecast.
- The Molybdenum Cofactor Deficiency Type A (MoCoD-A) epidemiology report and model were written and developed by Masters and Ph.D. level epidemiologists.
- The Molybdenum Cofactor Deficiency Type A (MoCoD-A) epidemiology model developed by the publisher is easy to navigate, interactive with dashboards, and epidemiology based on transparent and consistent methodologies. Moreover, the model supports data presented in the report and showcases disease trends over the 11-year forecast period using reputable sources.
Key Assessments
- Patient Segmentation
- Disease Risk and Burden
- Risk of disease by the segmentation
- Factors driving growth in a specific patient population
Geographies Covered
- The United States
- EU5 (Germany, France, Italy, Spain, and the United Kingdom)
- Japan
Study Period: 2019-2032
Table of Contents
1 Key Insights2 Report Introduction4 Executive Summary of Molybdenum Cofactor Deficiency Type-A7 Key Opinion Leaders' Views9 Publisher Capabilities10 Disclaimer11 About the Publisher
3 Molybdenum Cofactor Deficiency Type-A Epidemiology Overview at a Glance
5 Disease Background and Overview
6 Epidemiology and Patient Population
8 Appendix
List of Tables
List of Figures
