The Influence of SARS-CoV-2 on Minimally Invasive Therapeutic Approach for Benign Prostatic Hyperplasia.

Introduction: The COVID-19 pandemic definitely changed the management of patients with benign prostatic hyperplasia (BPH). This study followed the modalities of treatments in patients with BPH associated with SARS-CoV-2 attending the Urology Clinic of "Sf. Ioan" Emergency Clinical Hospital, Bucharest, Romania. Material and methods:The present study included 81 patients (mean age 63.2 years, age range 55-87 years) with SARS-CoV-2 and BPH who were admitted to our Urology Department between January 2021 and January 2022. The diagnosis of SARS-CoV-2 was based on the PCR test and that of BPH by using the diagnostic triad consisting of digital rectal examination, PSA, free PSA and ultrasound examination. It should be noted that some of the hospitalized patients were following treatment with alpha blockers and/or 5-alpha-reductase inhibitors at the time of admission. Results:Out of the 81 hospitalized cases, 13 required emergency endoscopic intervention under spinal anaesthesia (TURP or TURisP) for haemostasis because those patients presented with persistent haematuria which did not respond to conservative treatment. A number of 17 cases showed acute urinary retention during hospitalization and a urethrovesical catheter was fitted and will be re-evaluated urologically after the COVID episode. Of the remaining 51 subjects with BPH, 17 already had chronic urinary retention on admission, with urethrovesical probe present, 13 cases began during hospitalization with alpha-blocker treatment associated with 5-alpha-reductase inhibitors; meanwhile, there were no urological interventions to modify the treatment regimen in the remaining 21 patients, who were strictly managed on the side of COVID-19 infection. Conclusion:There was no clear influence of the evolution of patients with BPH due to SARS-CoV-2 pathology, and the general management trend was to delay chronic cases until the time of viral infection remission.

Guidelines for pre-clinical animal and cellular models of MuSK-myasthenia gravis.

Muscle-specific tyrosine kinase (MuSK) autoantibodies are the hallmark of a form of myasthenia gravis (MG) that can challenge the neurologist and the experimentalist. The clinical disease can be difficult to treat effectively. MuSK autoantibodies affect the neuromuscular junction in several ways. When added to muscle cells in culture, MuSK antibodies disperse acetylcholine receptor clusters. Experimental animals actively immunized with MuSK develop MuSK autoantibodies and muscle weakness. Weakness is associated with reduced postsynaptic acetylcholine receptor numbers, reduced amplitudes of miniature endplate potentials and endplate potentials, and failure of neuromuscular transmission. Similar impairments have been found in mice injected with IgG from MG patients positive for MuSK autoantibody (MuSK-MG). The active and passive models have begun to reveal the mechanisms by which MuSK antibodies disrupt synaptic function at the neuromuscular junction, and should be valuable in developing therapies for MuSK-MG. However, translation into new and improved treatments for patients requires procedures that are not too cumbersome but suitable for examining different aspects of MuSK function and the effects of potential therapies. Study design, conduct and analysis should be carefully considered and transparently reported. Here we review what has been learnt from animal and culture models of MuSK-MG, and offer guidelines for experimental design and conduct of studies, including sample size determination, randomization, outcome parameters and precautions for objective data analysis. These principles may also be relevant to the increasing number of other antibody-mediated diseases that are now recognized.

ß-glucans reduce LDL cholesterol in patients with myasthenia gravis.

We aimed at evaluating whether ß-glucans could improve low-density lipoprotein (LDL) cholesterol levels and/or glycemic control in patients with myasthenia gravis (MG), in whom statins usually have muscle-related side effects. Fifty-nine MG patients participated in the study and received a daily dietary supplement of 3 g of ß-glucans during 8 weeks. Body mass index (BMI) and blood sample analysis of lipid and glucose status were performed before and after 8 weeks intake of ß-glucans. In the 52 patients who completed the study, there was a significant reduction in total cholesterol, LDL, ApoA1 and ApoB (all P<0.003). However, glycemic control and BMI were unaltered. The present study indicates that 8 weeks daily intake of 3 g of ß-glucans significantly reduces total cholesterol, LDL, ApoA1 and ApoB in MG patients. ß-glucans may therefore be of value in improving lipid status in MG patients, without the muscle-related side effects accompanied by statins.

Vitamin D deficiency in patients with myasthenia gravis and improvement of fatigue after supplementation of vitamin D3: a pilot study.

BACKGROUND: Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder. Vitamin D has important roles both in the autoimmune response and in skeletal muscles. We determined the levels of 25-hydroxy vitamin D [25(OH)D] in patients with MG and in healthy subjects to determine whether vitamin D deficiency is present in MG and whether vitamin D supplementation has beneficial effects on fatigue. METHODS: Plasma levels of 25(OH)D were analyzed in 33 patients with MG (22 males; mean age, 58 years) and in 50 healthy age- and sex-matched blood donors, without vitamin D3 medication. MG composite (MGC) score assessed fatigue. Thirteen patients with MG without previous vitamin D3 supplementation were started on vitamin D3 supplementation (cholecalciferol) 800 IU/day, with a follow-up examination after 2.5-10 months (mean, 6 months). RESULTS: Patients with MG without pre-existing vitamin D3 supplementation (N = 16) had a mean MGC of 4.5 and lower plasma 25(OH)D levels (mean, 51 ± 19 nM) than healthy controls (69 ± 21 nM) (P = 0.017). Seventeen patients had pre-existing vitamin D3 supplementation, because of corticosteroid treatment, and their mean 25(OH)D was 79 ± 22 nM and mean MGC was 5.5. In the 13 patients who received cholecalciferol, 25(OH)D was overall increased at follow-up with 22% (P = 0.033) and MGC score improved by 38% (P = 0.05). CONCLUSIONS: Plasma 25(OH)D levels are significantly lower in patients with MG compared with healthy controls. As vitamin D has beneficial effects on the autoimmune response and on fatigue score in patients with MG, we suggest monitoring this parameter in patients with MG and supplementation with vitamin D3 when 25(OH)D levels are low.

Monozygous twins with neuromuscular transmission defects at opposite sides of the motor endplate.

Disorders affecting the postsynaptic side of the neuromuscular junction include autoimmune myasthenia gravis (MG) as well as some of the congenital myasthenic syndromes (CMS). Lambert-Eaton myasthenic syndrome (LEMS) is an acquired autoimmune neuromuscular disorder in which autoantibodies are directed against the presynaptic calcium channels. Here we describe two monozygous twin brothers: case 1 was diagnosed with an indeterminate form of acquired postsynaptic neuromuscular junction defect at age 32 and case 2 with LEMS at age 47. Case 1 presented clinically with mild generalized myasthenic weakness, neurophysiological examination revealed disturbed neuromuscular transmission along with probable myositis and serum analysis regarding antibodies against the acetylcholine receptor and muscle-specific tyrosine kinase was negative. Case 2 presented with proximal muscle fatigue accompanied by areflexia at rest and antibodies against the P/Q-type voltage-gated calcium channels were present. Neurophysiologically, case 2 had reduced baseline compound motor action potential amplitudes on neurography, decrement on low-frequency repetitive nerve stimulation (RNS) and pathological increment on high frequency RNS. To our knowledge this is the first case report of its kind and adds an intriguing contrast to the more common diagnosis of CMS in monozygous twins.

Neurophysiological and mitochondrial abnormalities in MuSK antibody seropositive myasthenia gravis compared to other immunological subtypes.

OBJECTIVE: To compare the electrophysiological and histopathological features of immunological myasthenia gravis (MG) subtypes. METHODS: Fifty MG patients underwent clinical examination, MuSK-Ab and AChR-Ab analysis. The majority underwent quantitative and single-fiber electromyography (QEMG, SFEMG), repetitive nerve stimulation and deltoid muscle biopsy. From muscle specimens with histological mitochondrial dysfunction, we amplified mitochondrial DNA (mtDNA). In specimens with mtDNA deletions, the nuclear gene POLG1 was sequenced. RESULTS: Five AChR-Ab seropositive [AChR(+)] and 5 seronegative [AChR(-)] patients were MuSK-Ab seropositive [MuSK(+)]. Five of 7 neurophysiologically examined MuSK(+) patients (71%) had proximal myopathic pattern, compared to 7 of 31 MuSK(-)/AChR(+) patients (23%) (P=0.012). SFEMG was abnormal in all examined MuSK(+) patients. All 7 biopsied MuSK(+) and 32 MuSK(-) patients (89%) had cytochrome c oxidase (COX) negative fibers. Three of five MuSK(+) and 13 of 20 MuSK(-) patients analyzed had multiple mtDNA deletions but no POLG1 mutations. CONCLUSIONS: Similar degree of SFEMG abnormalities was present in proximal muscles among MuSK(+) and AChR(+) patients. Proximal myopathy was over-represented in MuSK(+) patients; however, both MuSK(+) and MuSK(-) patients had mild myopathy with frequent mitochondrial abnormalities. SIGNIFICANCE: The weakness in MuSK(+) patients is most likely due to disturbed neuromuscular transmission. The frequently encountered mitochondrial dysfunction in MG warrants further study.

[Complete urinary retention secondary to lumbosacral zona]. / Rétention vésicale complète secondaire à un zona lombo-sacré.

A case of complete urinary retention related to a HZV neurogenic bladder is reported. Different findings of the disease are discussed, e.g., urodynamics and physiopathology.