Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

[Q]: Context: Despite advances in the diagnosis and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive. Insight may be gained from study of early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may account for disease. We performed exome sequencing of eight subjects from six kindreds with onset of portal hypertension of indeterminate etiology during infancy or childhood. Three subjects from two consanguineous families shared the identical rare homozygous p.N46S mutation in DGUOK, a deoxyguanosine kinase required for mitochondrial DNA replication; haplotype sharing demonstrated that the mutation in the two families was inherited from a remote common ancestor. All three affected subjects had stable portal hypertension with noncirrhotic liver disease for 6-16 years of follow-up. This mutation impairs adenosine triphosphate binding and reduces catalytic activity. Loss-of-function mutations in DGUOK have previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension. Interestingly, treatment of patients with human immunodeficiency viral infection with the nucleoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers deoxyguanosine kinase levels in vitro; the current findings implicate these effects on deoxyguanosine kinase in the causal mechanism.
Answer: Our findings provide new insight into the mechanisms mediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of DGUOK deficiency, and provide a new genetic test for a specific cause of idiopathic noncirrhotic portal hypertension. (Hepatology 2016;63:1977-1986).
[A]: Does recurrent recessive mutation in deoxyguanosine kinase cause idiopathic noncirrhotic portal hypertension?


[Q]: Context: The aim of this study was to visualize early stage prostate cancer (Cap) in a clinical setting. In previous studies, the results of magnetic resonance imaging (MRI) for screening Cap have rarely been confirmed by well-designed multisite prostate biopsy.', 'The prostate glands of 90 men with elevated prostate-specific antigen (PSA) were imaged by dynamic contrast-enhanced MRI (DCE-MRI) before transrectal ultrasound-guided 14-cores prostate biopsy. Each core was divided into three subcore fractions (total of 42 fractions) to generate a histological localization diagram, which was compared with localization-visualized DCE-MRI.', "The detection rate of Cap in 57 patients with PSA < 10.0 ng/ml was 36.8% as determined by the initial biopsy. DCE-MRI uncovered 92.9% of the clinically significant Caps and its specificity was 96.2% for the first biopsy session. One case with positive DCE-MRI and a negative primary biopsy was positive with additional biopsies. All of 26 DCE-MRI positive cases had significant Cap, and two of eight patients with histological Cap and negative or equivocal imaging had significant cancer. In total, 9 of 20 cases with DCE-MRI stage T2 underwent radical prostatectomy. All of them had organ-confined disease, although 33-77% (mean 63%) of them were expected to be rated T3 or higher by Partin's table.
Answer: DCE-MRI can identify early stage Cap with high sensitivity and specificity, and can predict the histological grade to some extent. DCE-MRI prior to biopsy should be applied to younger patients with surgical indications. Otherwise, we recommend the definitive diagnosis of Cap by utilizing DCE-MRI alone.
[A]: Is dynamic contrast-enhanced magnetic resonance imaging ( DCE-MRI ) a useful modality for the precise detection and staging of early prostate cancer?


[Q]: Context: Mild hyperhomocysteinaemia (HHC) is associated with an increased risk of premature atherothrombotic cerebrovascular disease. We investigated the clinical efficacy with regard to the incidence of cardiovascular events of treatment of mild HHC with vitamin B(6) plus folic acid.', 'We studied 224 consecutive patients with clinically manifest atherothrombotic cerebrovascular disease with onset before the age of 56. Follow-up was obtained in 203 (90.6%) patients. At baseline, 52 (25.6%) were hyperhomocysteinaemic after methionine loading and started treatment with vitamin B(6) (250 mg) plus folic acid (5 mg); 151 (74.4%) were normohomocysteinaemic (reference group).', 'During follow-up (median 57 months), 31 (20.5%) of the normo- and 11 (21.2%) of the hyperhomocysteinaemic patients had a new cardiovascular event. The crude incidence rate per person-year for any cardiovascular event was similar in both groups (0.043 [CI, 0.029-0.057] in the normo- vs. 0.045 [CI, 0.021-0. 069] in the hyperhomocysteinaemic group). Multivariate Cox-regression analyses showed that hypertension and cholesterol levels were associated with an increased risk of new cardiovascular events in the total group [relative risk [RR] (yes vs. no), 7.4 (3. 4-16.0) and RR (per 1 mmol/l), 1.9 (CI, 1.4-2.7)]. The adjusted RR for new cardiovascular events in the hyper- as compared to the normohomocysteinaemic patients was 0.96 (CI, 0.48-1.92).
Answer: These data are consistent with a protective effect of treatment with vitamin B(6) plus folic acid in patients with premature atherothrombotic cerebrovascular disease and post-methionine HHC.
[A]:
Are normohomocysteinaemia and vitamin-treated hyperhomocysteinaemia associated with similar risks of cardiovascular events in patients with premature atherothrombotic cerebrovascular disease . A prospective cohort study?