Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2745_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
29 Мб
Скачать
Positive Western blot: considered evidence of tick encounter, patient positive for Lyme disease
61
CSF Analysis
Patients with the disseminating Lyme disease can develop neurologic manifestations, or neuroborreliosis, of the disease, such as meningitis, facial nerve palsy, radiculoneuritis, and focal encephalitis. Lumbar puncture to analyze CSF is useful in determining a definitive diagnosis of Lyme disease as the source of those symptoms and what antibiotic would be the most useful for treatment. For example, oral amoxicillin is appropriate for treating arthritic manifestations of Lyme disease, but not neurologic; however, oral doxycycline could treat both. 61 It should be noted that CSF analysis for patients with neuroborreliosis and MS would yield OCBs, but the OCB antibodies found in the patient with suspected neuroborreliosis binds specifically to a protein from Borrelia, and the patient can be differentiated from a patient with MS.
23,64
Imaging
Persisting Lyme disease often affects the central nervous system with demyelinating lesions, which can be misdiagnosed as MS.
65
MRI may reveal white matter hyperintensities suggestive of inflammation or areas of demyelination. However, antibiotic treatment results in a decrease or disappearance of these hyperintensities. Clinical presentation and blood serology should rule out these regions of hyperintensities in patients with neuroborreliosis.
61,62
Gout
Pain from gout is often confused with that of MS, when another inflammatory source is gouty arthropathy presenting in a patient with MS. Gout is characterized by acute, intermittent episodes of synovitis caused by the accumulation of monosodium urate crystals in joint fluids, cartilage, bones, tendons, bursae, or other sites.
66,67
Pain from gout is often described as a sharp or burning
sensation and commonly presents with considerable erythema, swelling, and increased temperature. It most commonly affects
https://t.me/medicina_free
the great toe joint, although it can manifest in any synovial joint. Neuropathic, ongoing extremity pain can overlap with symptoms of gout manifesting in the great toe, ankle, or knee joints. Acute swelling, erythema, or increased temperature, particularly when manifesting in intermittent episodes, enforces gout as a probable differential diagnosis. Additionally, gout interacts with nociceptive pain secondary to musculoskeletal stress in MS and will likely lead to compensational pain as a result of the patient shifting gait to avoid putting weight on the affected joint. The characteristic findings of gout noted earlier can be used to differentiate a manifestation of gout from another source of synovitis in patients with MS.
67
References
Marrie RA, Reider N, Cohen J, et al. A systematic review of the incidence and
prevalence of autoimmune disease in multiple sclerosis. Mult Scler. 2015;21(3):282-
293. doi:10.1177/1352458514564490. Epub 2014/12/24.
Marrie RA, Horwitz R, Cutter G, Tyry T, Vollmer T. Association between comorbidity
and clinical characteristics of MS. Acta Neurol Scand. 2011;124(2):135-141. doi:10.1111/j.1600-0404.2010.01436.
Langer-Gould A, Albers K, Van Den Eeden S, Nelson L. Autoimmune diseases prior to
the diagnosis of multiple sclerosis: a population-based case-control study. Mult Scler. 2010;16(7):855-861.
Marrie RA, Horwitz RI, Cutter G, et al. Smokers with multiple sclerosis are more likely
to report comorbid autoimmune diseases. Neuroepidemiology. 2011;36:85-90.
Fanouriakis A, Mastorodemos V, Pamfil C, et al. Coexistence of systemic lupus
erythematosus and multiple sclerosis: prevalence, clinical characteristics, and natural history. Semin Arthritis Rheum. 2014;43:751-758.
Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-
1108.
Wallin M, Kurtzke J. Multiple sclerosis; epidemiology. Encycl Neurol Sci. 2014;3:153-
160.
Lisnevskaia L, Murphy G, Isenberg D. Systemic lupus erythematosus. Lancet.
2014;384(9957):1878-1888.
Ulivieri C, Baldari CT. Regulation of T Cell activation and differentiation by
extracellular vesicles and their pathogenic role in systemic lupus erythematosus and multiple sclerosis. Molecules. 2017;22.
Buzas EI, György B, Nagy G, Falus A, Gay S. Emerging role of extracellular vesicles
in inflammatory diseases. Nat Rev Rheumatol. 2014;10(6):356-364.
Mantravadi S, Ogdie A, Kraft WK. Tumor necrosis factor inhibitors in psoriatic
arthritis. Expert Rev Clin Pharmacol. 2017;10(8):899-910. doi:10.1080/17512433.2017.1329009.
Smolen JS, Aletaha D, McInnes IB. Rheumatoid arthritis. Lancet.
2016;388(10055):2023-2038. doi:10.1016/s0140-6736(16)30173-8.
https://t.me/medicina_free
Ritchlin CT, Colbert RA, Gladman DD. Psoriatic arthritis. N Engl J Med.
2017;376:957-970.
Veale DJ, Ritchlin C, FitzGerald O. Immunopathology of psoriasis and psoriatic
arthritis. Ann Rheum Dis. 2005;64(suppl 2):ii26-ii29. doi:10.1136/ard.2004.031740. Epub 2005/02/15. PubMed PMID: 15708930; PubMed Central PMCID: PMCPMC1766860.
Marrie RA, Patten SB, Tremlett H, Wolfson C, Leung S, Fisk JD. Increased incidence
and prevalence of psoriasis in multiple sclerosis. Mult Scler Relat Disord. 2017;13:81-86. doi:10.1016/j.msard.2017.02.012.
Steere AC, Strle F, Wormser GP, et al. Lyme borreliosis. Nat Rev Dis Primers.
2016;2:16090. doi:10.1038/nrdp.2016.90. Epub 2016/12/16.
Gladman DD. Overview of the Clinical Manifestations of Systemic Lupus
Erythematosus in Adults. In: Curtis MR , ed. UpToDate; 2018. Available at
https://www.uptodate.com/contents/overview-of-the-clinical-manifestations-of­systemic-lupus-erythematosus-in-adults?
search=lupus%20rash&source=search_result&selectedTitle=2150&usage_type=d efault&display_rank=2#H11. Retrieved October 30, 2018.
Hirohata S. Epidemiology of neuropsychiatric systemic lupus erythematosus. In:
Hirohata S , ed. Neuropsychiatric Systemic Lupus Erythematosus. Cham: Springer;
2018.
Wallace DJ. Diagnosis and Differential Diagnosis of Systemic Lupus Erythematosus in
Adults. In: Curtis MR , ed. UpToDate; 2017. Available at
https://www.uptodate.com/contents/diagnosis-and-differential-diagnosis-of­systemic-lupus-erythematosus-in-adults? search=systemic%20lupus%20erythematosus&source=search_result&selectedTitle=
3150&usage_type=default&display_rank=3. Retrieved October 28, 2018.
Scherder RJ, Kant N, Wolf ET, Pijnenburg BCM, Scherder EJA. Sensory function and
chronic pain in multiple sclerosis. Pain Res Manag. 2018;2018:1-9.
Nick ST, Roberts C, Billiodeaux S, et al. Multiple sclerosis and pain. Neurol Res.
2012;34(9):829-841. doi:10.1179/1743132812Y.0000000082.
Olek MJ. Diagnosis of Multiple Sclerosis in Adults. In: Dashe JF , ed. UpToDate; 2018.
Available at https://www.uptodate.com/contents/diagnosis-of-multiple-sclerosis-in-
adults? search=multiple%20sclerosis&source=search_result&selectedTitle=2150&usage_
type=default&display_rank=2. Retrieved on October 10, 2018.
Farina G, Magliozzi R, Pitteri M, et al. Increased cortical lesion load and intrathecal
inflammation is associated with oligoclonal bands in multiple sclerosis patients: a combined CSF and MRI study. J Neuroinflammation. 2017;14(1):40. doi:10.1186/s12974-017-0812-y. Epub 2017/02/23.
Venables PJW, Maini RN. Diagnosis and Differential Diagnosis of Rheumatoid
Arthritis. In: Romain PL , ed. UpToDate; 2014. Available at
https://www.uptodate.com/contents/diagnosis-and-differential-diagnosis-of­rheumatoid-arthritis?
search=rheumatoid%20arthritis&source=search_result&selectedTitle=1150&usag e_type=default&display_rank=1. Retrieved October 28, 2018.
Agmon-Levin N, Damoiseaux J, Kallenberg C, et al. International recommendations for
the assessment of autoantibodies to cellular antigens referred to as anti-nuclear antibodies. Ann Rheum Dis. 2014;73(1):17-23.
https://t.me/medicina_free
Ghajarzadeh M, Jalilian R, Sahraian MA, et al. Pain in multiple sclerosis.
Maedica(Buchar). 2018;13(2):125-130.
Walsh DA, McWilliams DF. Pain in rheumatoid arthritis. Curr Pain Headache Rep.
2012;16:509-517.
Walsh DA, McWilliams DF. Mechanisms, impact and management of pain in
rheumatoid arthritis. Nat Rev Rheumatol. 2014;10:581-592.
Di Franco M, Guzzo M, Spinelli F, et al. Pain and systemic lupus erythematosus.
Reumatismo. 2014;66(1):33-38.
Waldheim E, Ajeganova S, Bergman S, Frostegard J, Welin E. Variation in pain related
to systemic lupus erythematosus (SLE): a 7-year follow-up study. Clin Rheumatol. 2018;37:1825-1834.
Kalliolias GD, Ivashkiv LB. TNF biology, pathogenic mechanisms and emerging
therapeutic strategies. Nat Rev Rheumatol. 2016;12(1):49-62. doi:10.1038/nrrheum.2015.169. PubMed PMID: 26656660; PubMed Central PMCID: PMCPMC4809675.
Kemanetzoglou E, Andreadou E. CNS demyelination with TNF-α blockers. Curr
Neurol Neurosci Rep. 2017;17(4). doi:10.1007/s11910-017-0742-1. PubMed PMID: 28337644; PubMed Central PMCID: PMCPMC5364240.
Mohan N, Edwards ET, Cupps TR, et al. Demyelination occurring during anti–tumor
necrosis factor α therapy for inflammatory arthritides. Arthritis Rheum. 2001;44(12):2862-2869.
Haas TL, Emmerich CH, Gerlach B, et al. Recruitment of the linear ubiquitin chain
assembly complex stabilizes the TNF-R1 signaling complex and is required for TNF-mediated gene induction. Mol Cell. 2009;36(5):831-844. doi:10.1016/j.molcel.2009.10.013. Epub 2009/12/17. PubMed PMID: 20005846.
Monaco C, Nanchahal J, Taylor P, Feldmann M. Anti-TNF therapy: past, present and
future. Int Immunol. 2014;27(1):55-62.
Probert L. TNF and its receptors in the CNS: the essential, the desirable and the
deleterious effects. Neuroscience. 2015;302:2-22.
Locksley RM, Killeen N, Lenardo MJ. The TNF and TNF receptor superfamilies:
integrating mammalian biology. Cell. 2001;104(4):487-501. Epub 2001/03/10. PubMed PMID: 11239407.
Smolen JS, Landewé R, Bijlsma J, et al. EULAR recommendations for the management
of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update. Ann Rheum Dis. 2017;76(6). doi:10.1136/annrheumdis-2016-210715.
Bowen JD, Qian P. Oral rather than intravenous corticosteroids should be used to treat
MS relapses–No. Mult Scler. 2017;23(8):1058-1060.
Chataway J. Oral Versus Intravenous Steroids in Multiple Sclerosis Relapses–A
Perennial Question? London, England: Sage Publications; 2014.
van der Goes MC, Jacobs JW, Bijlsma JW. The value of glucocorticoid co-therapy in
different rheumatic diseases–positive and adverse effects. Arthritis Res Ther. 2014;16(suppl 2):S2. doi:10.1186/ar4686.
Seixas D, Foley P, Palace J, Lima D, Ramos I, Tracey I. Pain in multiple sclerosis: a
systematic review of neuroimaging studies. Neuroimage Clin. 2014;5:322-331. doi:10.1016/j.nicl.2014.06.014.
O’Connor AB, Schwid SR, Herrmann DN, Markman JD, Dworkin RH. Pain associated
with multiple sclerosis: systematic review and proposed classification. Pain.
https://t.me/medicina_free
2008;137(1):96-111. doi:10.1016/j.pain.2007.08.024. Epub 2007/10/12. PubMed PMID: 17928147.
He J, Li Z. An era of biological treatment in systemic lupus erythematosus. Clin
Rheumatol. 2018;37(1):1-3. doi:10.1007/s10067-017-3933-x. Epub 2017/12/14. PubMed PMID: 29234909; PubMed Central PMCID: PMCPMC5754454.
Reff ME, Carner K, Chambers KS, et al. Depletion of B cells in vivo by a chimeric
mouse human monoclonal antibody to CD20. Blood. 1994;83(2):435-445. Epub 1994/01/15. PubMed PMID: 7506951.
Feldman SR. Epidemiology, Clinical Manifestations, and Diagnosis of Psoriasis. In:
Ofori AO , ed. UpToDate; 2018. Available at
https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and­diagnosis-of-psoriasis?
search=risk%20factors%20psoriasis&source=search_result&selectedTitle=1150& usage_type=default&display_rank=1#H3. Retrieved October 28, 2018.
Singh JA, Saag KG, Bridges SL, et al. 2015 American College of Rheumatology
guideline for the treatment of rheumatoid arthritis. Arthritis Rheumatol. 2016;68(1):1-26.
Group TMSS. TNF neutralization in MS. Results of a randomized, placebo-controlled
multicenter study. Neurology. 1999;53(3):457. doi:10.1212/wnl.53.3.457.
van Oosten BW, Barkhof F, Truyen L, et al. Increased MRI activity and immune
activation in two multiple sclerosis patients treated with the monoclonal anti-tumor necrosis factor antibody cA2. Neurology. 1996;47(6):1531-1534. Epub 1996/12/01. PubMed PMID: 8960740.
Aguiar R, Araujo C, Martins-Coelho G, Isenberg D. Use of rituximab in systemic lupus
erythematosus: a single center experience over 14 years. Arthritis Care Res (Hoboken). 2017;69(2):257-262. doi:10.1002/acr.22921. Epub 2016/04/26. PubMed PMID: 27110698.
Castillo-Trivino T, Braithwaite D, Bacchetti P, Waubant E. Rituximab in relapsing and
progressive forms of multiple sclerosis: a systematic review. PLoS One. 2013;8(7):e66308. doi:10.1371/journal.pone.0066308. Epub 2013/07/12.
Owens GP, Bennett JL, Gilden DH, Burgoon MP. The B cell response in multiple
sclerosis. Neurol Res. 2006;28(3):236-244. doi:10.1179/016164106x98099. Epub 2006/05/12. PubMed PMID: 16687047.
Hauser SL, Waubant E, Arnold DL, et al. B-cell depletion with rituximab in relapsing–
remitting multiple sclerosis. N Engl J Med. 2008;358(7):676-688.
Firestein GS, Gabriel SE, McInnes IB, ODell JR. Kelley and Firesteins Textbook of
Rheumatology. Philadelphia, PA: Elsevier; 2017.
Setty AR, Curhan G, Choi HK. Obesity, waist circumference, weight change, and the
risk of psoriasis in women: Nurses’ Health Study II. Arch Intern Med. 2007;167(15):1670-1675.
Gladman DD. Clinical Manifestations and Diagnosis of Psoriatic Arthritis. In: Romain
PL , ed. UpToDate; 2017. Available at https://www.uptodate.com/contents/clinical-
manifestations-and-diagnosis-of-psoriatic-arthritis? search=psoriatic%20arthritis&source=search_result&selectedTitle=1150&usage_
type=default&display_rank=1. Retreived October 20, 2018.
Gladman DD, Ritchlin C. Treatment of Psoriatic Arthritis. In: Romain PL , ed.
UpToDate; 2018. Available at https://www.uptodate.com/contents/treatment-of-
psoriatic-arthritis?
https://t.me/medicina_free
search=psoriatic%20arthritis%20treatment&source=search_result&selectedTitle=1 150&usage_type=default&display_rank=1#H20469265. Retrieved October 30,
2018.
Chang S, Chambers CJ, Liu F, Armstrong AW. Successful treatment of psoriasis with
ustekinumab in patients with multiple sclerosis. Dermatol Online J. 2015;21(7). Available at https://escholarship.org/uc/item/3bs971cr.
Nair JJ, Singh TP. Sjogren’s syndrome: review of the aetiology, pathophysiology &
potential therapeutic interventions. J Clin Exp Dent. 2017;9(4):e584.
Gabrielli A, Avvedimento EV, Krieg T. Scleroderma. N Engl J Med. 2009;
360(19):1989-2003.
Schur PH. Neuropsychiatric Manifestations of Systemic Lupus Erythematosus. In:
Wilterdink JL , ed. UpToDate; 2014. Available at
https://www.uptodate.com/contents/neuropsychiatric-manifestations-of-systemic­lupus-erythematosus?
search=lupus%20psychosis&source=search_result&selectedTitle=1150&usage_t ype=default&display_rank=1. Retrieved October 28, 2018.
Toledano M, Weinshenker BG, Solomon AJ. A clinical approach to the differential
diagnosis of multiple sclerosis. Curr Neurol Neurosci Rep. 2015;15(8):57. doi:10.1007/s11910-015-0576-7. Epub 2015/06/27.
Ross Russell AL, Dryden M, Pinto AA, Lovett J. Lyme disease: diagnosis and
management. Pract Neurol. 2018;18(6):455-464. doi:10.1136/practneurol-2018-
001998.
Brandle SM, Obermeier B, Senel M, et al. Distinct oligoclonal band antibodies in
multiple sclerosis recognize ubiquitous self-proteins. Proc Natl Acad Sci USA. 2016;113:7864-7869.
Santino I, Comite P, Gandolfo GM. Borrelia burgdorferi, a great chameleon: know it to
recognize it! Neurol Sci. 2010;31(2):193-196. doi:10.1007/s10072-009-0175-y. Epub 2009/11/07. PubMed PMID: 19894021.
Winter DA. Human balance and posture control during standing and walking. Gait
Posture. 1995;3(4):193-214.
Shekelle PG, Newberry SJ, FitzGerald JD, et al. Management of gout: a systematic
review in support of an American College of Physicians clinical practice guideline. Ann Intern Med. 2017;166(1):37-51. doi:10.7326/M16-0461.
https://t.me/medicina_free
C H A P T E R 1 3
Pulmonary Complications in Multiple Sclerosis
Priyank Trivedi Anthony J. Smith Joseph T. Cooke
Introduction
Pulmonary complications are a significant cause of morbidity and mortality in patients with multiple sclerosis (MS). Symptoms are insidious, and respiratory dysfunction may present as late as 9 years after the onset of neurologic symptoms. 1 The pattern, severity, and morbidity of respiratory failure is related to the size and location of the demyelinating plaques within the central nervous system. The respiratory dysfunction is related to the degree of neurologic involvement and related respiratory muscle weakness. This is manifested as loss of ventilation control, sleep apnea, difficulty swallowing, and an ineffective cough. Current and future treatments for MS may also result in a decreased immune response to infection. The respiratory failure treatment is often supportive, with both invasive and noninvasive mechanical ventilation.
Pulmonary Function Testing
Pulmonary function tests may not be the most sensitive marker of respiratory muscle dysfunction in MS. 2 Common measurements used to measure respiratory function in patients with MS include vital capacity (VC), maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), and maximal voluntary ventilation (MVV).
Reduction of the VC suggests significant diaphragmatic weakness. Patients often exhibit correlative signs such as
https://t.me/medicina_free
paradoxical abdominal breathing. The MIP, MEP, and MVV, in contrast, are more sensitive indicators of respiratory muscle weakness. 3 Similar to other neuromuscular diseases, the decline in MIPmax and MEPmax precede changes in lung volumes. Patients with moderately severe MS on average exhibit a 40% decline in MIP and a 60% decline in MEP.
8
MVV measures the respiratory muscle endurance. This decreases in parallel to the decrease in MEP.
4
Studies have demonstrated a larger decrease in expiratory muscle strength than in inspiratory muscle strength. Expiratory muscle weakness can occur without inspiratory muscle weakness in patients with mild disease. 5 This pattern can be explained by the progression of paresis in patients with MS. In MS, muscular impairment generally progresses from lower to upper extremities. The abdominal muscles become impaired earlier than the muscles of the diaphragm and intercostal muscles. This results in impaired expiration before inspiration.
6
This can be clinically manifested as an ineffective cough and
an inability to clear secretions. Respiratory muscle weakness occurs both in patients who are
ambulatory and wheelchair bound. However, patients who are ambulatory with minimal upper extremity involvement have a much smaller decline in MEP, VC, and MVV and essentially no decline in MIP when compared with patients who are wheelchair bound with significant upper extremity impairment
4
(Figure 13.1). Patients with a mild degree of neurologic
impairment rarely show any abnormalities in pulmonary function testing with normal (VC), forced expiratory volume in 1 s (FEV1), total lung capacity (TLC), and residual volume (RV). In contrast, patients with more advanced disease may show lung volume loss with a decreased VC and a preserved FEV1/FVC ratio. This pattern suggests restrictive lung disease; however, the TLC tends to be preserved in MS
5
(Figure 13.2). This is attributable to submaximal inspiratory and expiratory efforts that are expected in patients with whole body muscle weakness, which results in an increase of the residual volume (RV). The rise in the RV correlates with the decline in the MEP.
https://t.me/medicina_free
FIGURE 13.1 Measures of respiratory muscle function by
category of neurologic disability expressed as percent
predicted.
Reproduced with permission from Smeltzer SC, Skurnick JH,
Troiano R. Respiratory function in multiple sclerosis: utility of
clinical assessment of respiratory muscle function. Chest.
1992;101:479-484.
https://t.me/medicina_free
FIGURE 13.2 Pulmonary function test results by category of
neurologic disability expressed as percent predicted.
Reproduced with permission from Smeltzer SC, Skurnick JH,
Troiano R. Respiratory function in multiple sclerosis: utility of
clinical assessment of respiratory muscle function. Chest.
1992;101:479-484.
Although MIPs and MEPs provide for a more useful tool than usual pulmonary function tests, they can be difficult to administer in patients with facial and bulbar muscle weakness.
7
Clinical indices may be the best predictor of expiratory
muscle weakness. 5 Activities such as talking, coughing, and upper extremity strength serve as reliable markers of muscle strength. Talking requires complex coordination of upper and lower respiratory muscles, and coughing requires muscle contraction against a closed glottis. Smeltzer et al developed a pulmonary index score that appeared to be the best predictor of expiratory muscle weakness. The score comprised four parameters: patient’s report of his or her ability to handle secretions/mucus, patient’s report of a weakened cough, examiner’s evaluation of a patient’s cough when asked to voluntarily cough as forcefully as possible, and the patient’s ability to count on a single exhalation. Using stepwise regression analysis it was concluded that the index score, upper extremity weakness, and MVV accounted for 60% of the variance in maximal expiratory muscle strength.
5
https://t.me/medicina_free