A Guyon's canal ganglion presenting as occupational overuse syndrome: A case report

<p>Abstract</p> <p>Background</p> <p>Occupational overuse syndrome (OOS) can present as Guyon's canal syndrome in computer keyboard users. We report a case of Guyon's canal syndrome caused by a ganglion in a computer user that was misdiagnosed as OOS.</p> <p>Case presentation</p> <p>A 54-year-old female secretary was referred with a six-month history of right little finger weakness and difficulty with adduction. Prior to her referral, she was diagnosed by her general practitioner and physiotherapist with a right ulnar nerve neuropraxia at the level of the Guyon's canal. This was thought to be secondary to computer keyboard use and direct pressure exerted on a wrist support. There was obvious atrophy of the hypothenar eminence and the first dorsal interosseous muscle. Both Froment's and Wartenberg's signs were positive. A nerve conduction study revealed that both the abductor digiti minimi and the first dorsal interosseus muscles showed prolonged motor latency. Ulnar conduction across the right elbow was normal. Ulnar sensory amplitude across the right wrist to the fifth digit was reduced while the dorsal cutaneous nerve response was normal. Magnetic resonance imaging of the right wrist showed a ganglion in Guyon's canal. Decompression of the Guyon's canal was performed and histological examination confirmed a ganglion. The patient's symptoms and signs resolved completely at four-month follow-up.</p> <p>Conclusion</p> <p>Clinical history, occupational history and examination alone could potentially lead to misdiagnosis of OOS when a computer user presents with these symptoms and we recommend that nerve conduction or imaging studies be performed.</p

Incidence of acute cerebrovascular events in patients with rheumatic or calcific mitral stenosis: a systematic review and meta-analysis

Background Patients with mitral stenosis (MS) may be predisposed to acute cerebrovascular events (ACE) and peripheral thromboembolic events (TEE). Concomitant atrial fibrillation (AF), mitral annular calcification (MAC) and rheumatic heart disease (RHD) are independent risk factors. Our aim was to evaluate the incidence of ACEs in MS patients and the implications of AF, MAC, and RHD on thromboembolic risks. Methods This systematic review was registered on PROSPERO (CRD42021291316). Six databases were searched from inception to 19th December 2021. The clinical outcomes were composite ACE, ischaemic stroke/transient ischaemic attack (TIA), and peripheral TEE. Results We included 16 and 9 papers, respectively, in our qualitative and quantitative analyses. The MS cohort with AF had the highest incidence of composite ACE (31.55%; 95%CI 3.60-85.03; I 2 =99%), followed by the MAC (14.85%; 95%CI 7.21-28.11; I 2 =98%), overall MS (8.30%; 95%CI 3.45-18.63; I 2 =96%) and rheumatic MS population (4.92%; 95%CI 3.53-6.83; I 2 =38%). Stroke/TIA were reported in 29.62% of the concomitant AF subgroup (95%CI 2.91-85.51; I 2 =99%) and in 7.11% of the overall MS patients (95%CI 1.91-23.16; I 2 =97%). However, the heterogeneity of the pooled incidence of clinical outcomes in all groups, except the rheumatic MS group, were substantial and significant. The logit-transformed proportion of composite ACE increased by 0.0141 (95% CI 0.0111-0.0171; p<0.01) per year of follow-up. Conclusion In the MS population, MAC and concomitant AF are risk factors for the development of ACE. The scarcity of data in our systematic review reflects the need for further studies to explore thromboembolic risks in all MS subtypes

Venetoclax induces rapid elimination of NPM1 mutant measurable residual disease in combination with low-intensity chemotherapy in acute myeloid leukaemia

Based on promising results in older adults with acute myeloid leukaemia (AML), we treated patients with NPM1mut measurable residual disease (MRD) using off-label venetoclax in combination with low-dose cytarabine or azacitidine. Twelve consecutive patients were retrospectively identified, including five with molecular persistence and seven with molecular relapse/progression. All patients with molecular persistence achieved durable molecular complete remission (CRMRD- ) without transplantation. Six of seven patients with molecular relapse/progression achieved CRMRD- after 1-2 cycles of venetoclax. This paper highlights the promising efficacy of venetoclax-based therapy to reduce the relapse risk in patients with persistent or rising NPM1mut MRD

Venetoclax induces rapid elimination of NPM1 mutant measurable residual disease in combination with low-intensity chemotherapy in acute myeloid leukaemia.

Based on promising results in older adults with acute myeloid leukaemia (AML), we treated patients with NPM1mut measurable residual disease (MRD) using off-label venetoclax in combination with low-dose cytarabine or azacitidine. Twelve consecutive patients were retrospectively identified, including five with molecular persistence and seven with molecular relapse/progression. All patients with molecular persistence achieved durable molecular complete remission (CRMRD- ) without transplantation. Six of seven patients with molecular relapse/progression achieved CRMRD- after 1-2 cycles of venetoclax. This paper highlights the promising efficacy of venetoclax-based therapy to reduce the relapse risk in patients with persistent or rising NPM1mut MRD

Incidence of acute cerebrovascular events in patients with rheumatic or calcific mitral stenosis: A systematic review and meta-analysis

Background: Patients with mitral stenosis (MS) may be predisposed to acute cerebrovascular events (ACE) and peripheral thromboembolic events (TEE). Concomitant atrial fibrillation (AF), mitral annular calcification (MAC) and rheumatic heart disease (RHD) are independent risk factors. Our aim was to evaluate the incidence of ACEs in MS patients and the implications of AF, MAC and RHD on thromboembolic risks. Methods: This systematic review was registered on PROSPERO (CRD42021291316). Six databases were searched from inception to 19th December 2021. The clinical outcomes were composite ACE, ischaemic stroke/transient ischaemic attack (TIA) and peripheral TEE. Results: We included 16 and 9 papers, respectively, in our qualitative and quantitative analyses. The MS cohort with AF had the highest incidence of composite ACE (31.55%; 95% CI 3.60–85.03; I2 = 99%), followed by the MAC (14.85%; 95% CI 7.21–28.11; I2 = 98%), overall MS (8.30%; 95% CI 3.45–18.63; I2 = 96%) and rheumatic MS population (4.92%; 95% CI 3.53–6.83; I2 = 38%). Stroke/TIA were reported in 29.62% of the concomitant AF subgroup (95% CI 2.91–85.51; I2 = 99%) and in 7.11% of the overall MS patients (95% CI 1.91–23.16; I2 = 97%). However, the heterogeneity of the pooled incidence of clinical outcomes in all groups, except the rheumatic MS group, was substantial and significant. The logit-transformed proportion of composite ACE increased by 0.0141 (95% CI 0.0111–0.0171; p < 0.01) per year of follow-up. Conclusion: In the MS population, MAC and concomitant AF are risk factors for the development of ACE. The scarcity of data in our systematic review reflects the need for further studies to explore thromboembolic risks in all MS subtypes