A 40-year-old man presented with drooping of both eyelids and generalized weakness of two weeks duration. The symptoms were worse during the evening. He had been diagnosed with chronic myeloid leukaemia (CML) in chronic phase, four months previously, and was receiving regular imatinib, 400 mg/day. After three weeks of therapy, he had achieved a complete haematological response, and his constitutional symptoms had subsided. After three months of therapy, he showed a two-log reduction of BCR-ABL1 transcript. On presentation, he had bilateral ptosis (left). Physical examination was otherwise normal. A provisional diagnosis of ocular myasthenia gravis was made. He showed improvement in ptosis after administration of neostigmine. Repetitive nerve stimulation and anti-acetylcholine receptor antibody serology were positive, confirming the diagnosis of myasthenia gravis. He was started on pyridostigmine and prednisolone. Computed tomography of his chest showed a 2Á7 9 1Á7 cm mass in the anterior mediastinum, for which he underwent thymectomy. Histopathological examination showed thymic hyperplasia. He is currently asymptomatic with marked improvement in ptosis (right) and has achieved a partial molecular response (BCR-ABL1 transcript level, 1Á113%).Many cases of drug-induced myasthenia gravis have been reported. Drugs implicated include ribavirin, statins, fluoroquinolones, interferon, fludarabine, chloroquine, penicillamine, busulfan and carbamazepine. Development of myasthenia gravis during treatment with nilotinib has also been reported in a patient with CML. In the current case, myasthenia gravis was unmasked when the patient was treated with imatinib. Triggering of myasthenia by tyrosine kinase inhibitors and certain other drugs may be related to a disturbance of immune function. However, other possibilities, including a paraneoplastic manifestation of CML or co-incidental occurrence of myasthenia gravis and CML, cannot be ruled out.

Minimally invasive parathyroidectomy (MIP) is the standard of care for primary hyperparathyroidism (PHPT). Four dimensional computed tomography(4DCT) and F-18 Fluorocholine positron emission tomography/computed tomography (FCH PET/CT) localize adenomas accurately to perform MIP. We aimed to conduct a systematic review and metanalysis to evaluate the diagnostic performance of 4DCT and FCH PET/CT scan for quadrant wise localisation in PHPT patients and to do head-to-head comparison between these two modalities.Design, Patients and Measurement : After searching through PubMed and EMBASE databases, 46 studies (using histology as a gold standard) of 4DCT and FCH PET/CT were included.Results: Total number of patients included were 1651 and 952 for 4DCT scan (studies n = 26) and FCH PET/CT scan (studies n = 24) respectively. In per patient analysis, FCH PET/CT and 4DCT had pooled sensitivities of 92% (88−94) and 85% (73−92) respectively and in per lesion analysis, 90% (86−93) and 79% (71−84), respectively. In the subgroup with negative conventional imaging/persistent PHPT, FCH PET/CT had comparable sensitivity to 4DCT (84% [74−90] vs. 72% [46−88]). As per patient wise analysis, FCH PET/CT had better detection rates than 4DCT ([92.4 vs. 76.85], odds ratio −3.89 [1.6−9.36] p = .0024) in the subpopulation where both FCH PET/CT and 4DCT were reported. Conclusion:Both 4DCT and FCH PET/CT scan performed well in newly diagnosed patients, patients with persistent disease and in those with inconclusive conventional imaging results. FCH PET/CT scan had a higher pooled sensitivity than 4DCT in detecting patients with PHPT in head to head comparison.

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Background Leucovorin (folinic acid) is a commonly used antidote for severe toxicity with low-dose methotrexate, but its optimum dose is unclear, varying from 15 to 25 mg every 6-h. Methods Open-label RCT included patients with severe low-dose (≤ 50 mg/week) methotrexate toxicity defined as WBC ≤ 2 × 10^9/L or platelet ≤ 50 × 10^9/L and randomized them to receive either usual (15 mg) or high-dose (25 mg) intravenous leucovorin given every 6-h. Primary outcome was mortality at 30-days and secondary outcomes were hematological recovery and mucositis recovery. Trial Registration number: CTRI/2019/09/021152. Results Thirty-eight patients were included, most with underlying RA who had inadvertently overdosed MTX (taken daily instead of weekly). At randomization, the median white blood and platelet count were 0.8 × 10^9/L and 23.5 × 10^9/L. 19 patients each were randomized to receive either usual or high-dose leucovorin. Number (%) of deaths over 30-days was 8 (42) and 9 (47) in usual and high-dose leucovorin groups (Odds ratio 1.2, 95% CI 0.3 to 4.5, p = 0.74). On Kaplan–Meier, there was no significant difference in survival between the groups (hazard ratio 1.1, 95% CI 0.4 to 2.9, p = 0.84). On multivariable cox-regression, serum albumin was the only predictor of survival (hazard ratio 0.3, 95% CI 0.1 to 0.9, p = 0.02). There was no significant difference in hematological or mucositis recovery between the two groups. Conclusion There was no significant difference in survival or time-to hematological recovery between the two doses of leucovorin. Severe low-dose methotrexate toxicity carried a significant mortality.