Search

Background: During Ramadan, the ninth month of the lunar Islamic calendar, adult Muslims are obliged to fast, which involves refraining from taking any food, beverages, or oral medications from dawn to sunset. Fasting's effect on seizure control is not fully understood, and a few observational studies have provided inconclusive results. This study aimed to investigate the effect of fasting during Ramadan on seizure control and quality of life in adult patients with epilepsy., Methods: This was a prospective observational study over a 3-month period (one month before fasting, the fasting month, and one month after fasting). We recruited adult patients with active epilepsy who were able to fast during the month of Ramadan. The primary outcome measures were as follows: 1) seizure control and 2) quality of life score using the Arabic version of the Ferrans and Powers Quality of Life Index (QLI). Changes in anticonvulsant medications were not allowed during the study period. We used a seizure log provided to participants to record the number of seizures during the 3-month period. Quality of life was scored at the end of each month of the study period., Results: Thirty-seven patients were studied (59% males). The mean age was 30 years (range, 14-51 years), and mean age at epilepsy onset was 13 years (range, 0.5-35 years). On average, patients were on three antiepileptic medications at baseline (range: 2-5). A total of 1576 seizures were reported during the 3-month follow-up, where seizures prior to fasting represented 35.5% of all seizures. Multilinear regression analysis revealed a significant decline of seizures by 21% during the fasting month compared with baseline (adjusted coefficient = 0.79, p < 0.01, 95% confidence interval (CI); 0.61-0.98, R2 = 0.81) and by 29% during post fasting compared with baseline (adjusted coefficient = 0.71, p < 0.01, 95% CI; 0.53-0.90, R2 = 0.79). No significant change was found in the QLI scores calculated during the three months of the study period., Conclusion: Fasting during Ramadan might have a positive impact on seizure control in patients with epilepsy, which continued during the month following fasting, whereas the quality of life scores were not affected by fasting., Competing Interests: Declaration of competing interest The authors declare that there is no conflict of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Key Clinical Message: Molybdenum cofactor deficiency is a rare and fatal genetic disorder. Due to recurrence in the family, the etiological diagnosis could have impacted family planning and alertness to future offspring. Molybdenum cofactor deficiency (MoCD) is a rare and fatal genetic disorder that impairs molybdenum‐dependent enzymes, resulting in conspicuous elevated urine sulfite levels and lowered serum uric acid levels. The disorder may be early‐onset, causing high fatality in neonates due to secondary complications, or late‐onset, manifesting in the first 2 years of life. Severe seizures, progressive neurological degeneration, motor abnormalities, and feeding difficulties are hallmarks of MoCD. Due to the similarity of clinical findings with those of sulfite oxidase deficiency and its neurological findings with hypoxic–ischemic encephalopathy, determining the true etiology remains challenging in MoCD patients. This case report presents a neonate in the first week of life with early onset refractory seizures, motor abnormalities, hypoactivity, and poor feeding behavior. Administering anti‐epileptic drugs did not improve the patient's condition, who started decompensating further. Nevertheless, a thorough screening for metabolic disorders revealed low serum uric acid and high sulfite levels in the urine, indicating potential MoCD. A whole exome sequencing (WES) was thus consulted for confirmatory diagnosis. Unfortunately, the patient's WES results were received after his demise, revealing MoCD caused by a novel variant of the MoCS2 gene that has not yet been reported to the best of our knowledge. This case emphasizes the need to disseminate crucial information regarding MoCD and its etiologies for prompt molecular diagnosis to reduce morbidity and mortality. [ABSTRACT FROM AUTHOR]