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*For reference only for medical professionals who cover up the eyes of the blooming girl Neurology Many diseases are related to ophthalmology, such as cerebral hemorrhage, cerebral infarction, multiple sclerosis, myasthenia gravis, hepatolenticular degeneration,e.
For example, the involvement of the visual pathway can lead to decreased vision or visual field defec.
What is the first thing that comes to your mind when the following symptoms appear in the eye? Let's have a look! Medical records The patient is a 15-year-old female who was admitted to the hospital mainly because of "blurred vision in the left eye for 4 day.
History of present illness: blurred vision in the left eye after catching a cold 4 days ago, still able to read the fonts in books, no attention was paid, blurred vision in the left eye has gradually worsened in the past 4 days, and now he can see the manual clearly, accompanied by pain in the left eye area, MRI of the head showed no obvious abnormali.
The patient has had nasal congestion in the past two weeks and is now asymptomat.
He has no symptoms such as fever, sore throat, cough, diarrhea, and decreased sense of smell (taste), and has not used antipyretic dru.
Past history: 4 years ago, due to blurred vision in the right eye, he visited Hebei Children's Hospital and was diagnosed with "neuromyelitis optic.
He was given shock therapy with hormones, followed by oral administration of hormones, and the treatment was reduced in the second half of 201Found "hypothyroidism" for 4 years, oral treatment with Euthyrox, currently disabl.
Personal history and family history are unremarkab.
Vital signs: blood pressure 123/76mmHg, respiration 18/min, heart rate 75/m.
Nervous system physical examination: clear and eloquent, double pupils are large and round, sensitive to light reflex, both eyeballs can move in all directions, no diplopia and nystagmus, normal visual acuity in the right eye, decreased visual acuity in the left eye, about 30cm manual , no visual field defect, normal limb muscle strength, muscle tension, symmetrical tendon reflex, negative pathological sig.
Auxiliary examination: head MRI: no obvious abnormali.
▌ Further improvement of related examinations, no obvious abnormality was found in the enhanced brain MRI sc.
Cervical and thoracic spine MR plain scan + enhancement showed no obvious abnormali.
Optic nerve evoked potentials: prolonged P100 latency in the left e.
On the 28th, the lumbar puncture was completed: cerebrospinal fluid analysis: white blood cells: 13 × 106/L; no abnormality in cerebrospinal fluid biochemist.
Acid fastness and ink staining showed no abnormali.
Antiphospholipid antibodies were norm.
Results of cerebrospinal fluid delivery: cerebrospinal fluid MOG antibody IgG positive: 1:1+; serum MOG antibody IgG positive, 1:100++, AQP4, OB, MBP negati.
Immune-related examinations: antinuclear antibody: antinuclear antibody: positive 1:100 abnormal; CRP, immunoglobulin no abnormali.
Three items of rheumatism: complement C3: 880g/L; C-reactive protein: 70mg/L; ESR: 26mm/h; ACCP+anti-AKA, no abnormality in double-stranded DNA, lupus anticoagulant, antinuclear antibody, vasculitis screen Check negati.
▌ Localization and qualitative diagnosis According to the patient's performance of blurred vision in the left eye, decreased visual acuity in the left eye and abnormal visual evoked potentials in the nervous system, the localization diagnosis: left optic ner.
History of 3 previous clinical episodes, all with decreased vision in the left e.
Information provided by the other hospital: cervical MRI in June 2017 showed long-segment lesions of the spinal cord, head MRI in December 2017 showed multiple intracranial lesions, and AQP4 was negative for multiple examinations , an OB positi.
Combined with the cerebrospinal fluid MOG antibody IgG positive: 1:
To sum up the diagnosis: MOG antibody-positive neuromyelitis optica spectrum disea.
In terms of treatment, 800 mg of methylprednisolone pulse therapy was given, which was halved every 3 days and reduced to 52 mg of oral methylprednisolone table.
At the same time, potassium chloride sustained-release tablets, calcium tablets, and omeprazole capsules were given to reduce side effec.
Review: NMOSD Neuromyelitis optica spectrum disorders (NMOSD) are a group of autoimmune-mediated inflammatory demyelinating diseases of the central nervous system that mainly involve the optic nerve and spinal co.
The pathogenesis of NMOSD is mainly related to the aquaporin 4 (AQP4) antibody, which is more common in young adults, mostly women, and is clinically characterized by severe optic neuritis (ON) and longitudinally extending long-stage transverse myelitis (LET.
The main clinical features, recurrence rate and high disability ra.
▌ Clinical manifestations Unilateral or bilateral optic neuritis and acute myelitis are the main manifestations of this disea.
The initial stage can be simple optic neuritis or myelitis, or bo.
NMOSD has 6 core clinical symptoms: optic neuritis, acute myelitis, extreme posterior zone syndrome, acute brainstem syndrome, acute diencephalic syndrome and cerebral syndrome [
▌ Auxiliary examinationAQP4-IgG is a highly specific diagnostic marker with a specificity of up to 90% and a sensitivity of about 7
NMO serum AQP4 antibody is mostly positive, while MS is mostly negative, which can be used as one of the identification criteria for NMO and .
Most of the cerebrospinal fluid pressures are normal, the leukocytes in the acute phase are more than 10×106/L, about 1/3 of the patients are more than 50×106/L, and a few cases can reach 500×106/L; neutrophils and eosinophils can be seen increa.
Acute phase biochemistry: protein is more than 1g/L, and sugar and chloride are mostly normal; about 20% of patients are CSF-specific oligoclonal band (OCB) positive, and IgG is significantly increas.
MOG-IgG is a biomarker for MOGAD, and it is almost not positive at the same time as AQP4-IgG, which has important differential diagnosis val.
The latency of visual evoked potential P100 was significantly prolonged, and the waveform could not be evoked in severe cas.
Serum other autoimmune antibodies: NMO patients may have positive serum ANAs, including ANA, anti-dsDNA, anti-SSA antibodies, and anti-SSB antibodi.
▌ Diagnosis principle of NMOSD: based on "medical history + core clinical symptoms + imaging features + biomarkers", with AQP4-IgG as the stratification, and referring to other subclinical and immunological evidence to make a diagnosis, in addition to Other diseases are exclud.
NMOSD diagnostic criteria [2]:NMOSD diagnostic criteria for AQP4-IgG positive (1) at least 1 core clinical feature (2) AQP4-IgG positive detection with a reliable method (3) exclusion of other diagnosesAQP4-IgG negative or NMOSD diagnostic criteria of unknown AQP4-IgG status (1) In 1 or more clinical episodes, at least 2 core clinical features and all of the following conditions are met: ① At least 1 core clinical feature is optic neuritis, acute long segment Transverse myelitis or medullary zone retal syndro.
② Spatial multiple (two or more different clinical core feature.
③Meet the additional conditions of M.
(2) AQP4-IgG detected by a reliable method is negative or not detect.
(3) exclude other diagnos.
Core clinical features (1) Optic neurit.
(2) Acute myelit.
(3) Posterior zone syndrome, episodic hiccups, nausea, and vomiting unexplained by other causes
(4) acute brainstem syndro.
(5) Symptomatic narcolepsy, diencephalic syndrome, and brain MRI with characteristic diencephalic lesions of NMO.
(6) Cerebral syndrome with characteristic cerebral lesions of NMO.
Additional conditions for NMOSD MRI in AQP4-IgG negative or unknown state (1) Acute optic neuritis: One of the following manifestations on brain MRI is requir.
① normal brain MRI or only non-specific white matter lesio.
②The optic nerve has long T2 signal or T1 enhanced signal ≥ 1/2 of the optic nerve length, or the lesion involves the optic chia.
(2) Acute myelitis: Long spinal cord lesions ≥3 consecutive vertebral segments, or corresponding spinal cord atrophy ≥3 consecutive vertebral segments in patients with a history of myelit.
(3) The last zone syndrome: lesions of the dorsal medulla oblongata / the last zo.
(4) acute brainstem syndrome: brainstem periependymal lesio.
▌ TreatmentTreatment during acute attack: (1) Glucocorticoids: high-dose methylprednisolone pulse therapy is the first choice, which can reduce the inflammatory response and promote the remission of NMO.
(2) Intravenous infusion of immune globulin: 4g/(.
d) intravenous infusion, usually for 5 consecutive days as a course of treatme.
(3) Plasma exchange: It is generally recommended to perform 3-5 times with 2-3L of plasma each time, and most replacements are effective after 1-2 tim.
Treatment during remission: (1) Azathioprine: 2-3 mg/kg/d alone or in combination with low-dose prednisone 75 mg/kg/d, usually after azathioprine takes effect (4-5 months), tape prednisone to low doses for long-term maintenance
(2) Rituximab: single 500-600 mg intravenous infusion, or 100 mg intravenous infusion, once a week, for 4 weeks, repeated after 6-12 mont.
(3) Methotrexate: good tolerance and compliance, suitable for patients who cannot tolerate the side effects of azathiopri.
(4) Cyclophosphamide: It may be effective in reducing the one-year recurrence ra.
It is intravenously infused at 7-25 mg/kg, once a month, for a total of 6 mont.
Conclusion The clinical manifestations of NMOSD are severe, and most of them have a high annual recurrence rate in the early stage, resulting in severe disability such as total blindness or parapleg.
One-third of patients die of respiratory failure, so early diagnosis and treatment are very importa.
References: [1] Wingerchuk DM, Banwell B, Bennett JL, et .
International consensus diagnostic criteria for neuromyelitis optical spectrum disorders [.
Neurology, 2015, 85(2): 177-18 [2] Huang Dehui, Wu Weiping , Hu Xueqia.
Guidelines for the diagnosis and treatment of neuromyelitis optica spectrum disorders in China (2021 edition) [.
Chinese Journal of Neuroimmunology and Neurology, 2021, 28(06): 423-43 Link: https://pubm.
ncb.
n.
n.
gov/26092914/https://k.
cn.
net/kcms/detail/deta.
aspx?dbcode=CJFQ&dbname=CJFDLAST2022&filename=ZSMB202106002&v=Mjc3NzlQUHo3R2JMRzRITkRNcVk5RlpvUjhlWDFMdXhZUzdEaDFUM3FUcldNMUZyQ1VSN2lmWXVkdkZpamhVcjc=
For example, the involvement of the visual pathway can lead to decreased vision or visual field defec.
What is the first thing that comes to your mind when the following symptoms appear in the eye? Let's have a look! Medical records The patient is a 15-year-old female who was admitted to the hospital mainly because of "blurred vision in the left eye for 4 day.
History of present illness: blurred vision in the left eye after catching a cold 4 days ago, still able to read the fonts in books, no attention was paid, blurred vision in the left eye has gradually worsened in the past 4 days, and now he can see the manual clearly, accompanied by pain in the left eye area, MRI of the head showed no obvious abnormali.
The patient has had nasal congestion in the past two weeks and is now asymptomat.
He has no symptoms such as fever, sore throat, cough, diarrhea, and decreased sense of smell (taste), and has not used antipyretic dru.
Past history: 4 years ago, due to blurred vision in the right eye, he visited Hebei Children's Hospital and was diagnosed with "neuromyelitis optic.
He was given shock therapy with hormones, followed by oral administration of hormones, and the treatment was reduced in the second half of 201Found "hypothyroidism" for 4 years, oral treatment with Euthyrox, currently disabl.
Personal history and family history are unremarkab.
Vital signs: blood pressure 123/76mmHg, respiration 18/min, heart rate 75/m.
Nervous system physical examination: clear and eloquent, double pupils are large and round, sensitive to light reflex, both eyeballs can move in all directions, no diplopia and nystagmus, normal visual acuity in the right eye, decreased visual acuity in the left eye, about 30cm manual , no visual field defect, normal limb muscle strength, muscle tension, symmetrical tendon reflex, negative pathological sig.
Auxiliary examination: head MRI: no obvious abnormali.
▌ Further improvement of related examinations, no obvious abnormality was found in the enhanced brain MRI sc.
Cervical and thoracic spine MR plain scan + enhancement showed no obvious abnormali.
Optic nerve evoked potentials: prolonged P100 latency in the left e.
On the 28th, the lumbar puncture was completed: cerebrospinal fluid analysis: white blood cells: 13 × 106/L; no abnormality in cerebrospinal fluid biochemist.
Acid fastness and ink staining showed no abnormali.
Antiphospholipid antibodies were norm.
Results of cerebrospinal fluid delivery: cerebrospinal fluid MOG antibody IgG positive: 1:1+; serum MOG antibody IgG positive, 1:100++, AQP4, OB, MBP negati.
Immune-related examinations: antinuclear antibody: antinuclear antibody: positive 1:100 abnormal; CRP, immunoglobulin no abnormali.
Three items of rheumatism: complement C3: 880g/L; C-reactive protein: 70mg/L; ESR: 26mm/h; ACCP+anti-AKA, no abnormality in double-stranded DNA, lupus anticoagulant, antinuclear antibody, vasculitis screen Check negati.
▌ Localization and qualitative diagnosis According to the patient's performance of blurred vision in the left eye, decreased visual acuity in the left eye and abnormal visual evoked potentials in the nervous system, the localization diagnosis: left optic ner.
History of 3 previous clinical episodes, all with decreased vision in the left e.
Information provided by the other hospital: cervical MRI in June 2017 showed long-segment lesions of the spinal cord, head MRI in December 2017 showed multiple intracranial lesions, and AQP4 was negative for multiple examinations , an OB positi.
Combined with the cerebrospinal fluid MOG antibody IgG positive: 1:
To sum up the diagnosis: MOG antibody-positive neuromyelitis optica spectrum disea.
In terms of treatment, 800 mg of methylprednisolone pulse therapy was given, which was halved every 3 days and reduced to 52 mg of oral methylprednisolone table.
At the same time, potassium chloride sustained-release tablets, calcium tablets, and omeprazole capsules were given to reduce side effec.
Review: NMOSD Neuromyelitis optica spectrum disorders (NMOSD) are a group of autoimmune-mediated inflammatory demyelinating diseases of the central nervous system that mainly involve the optic nerve and spinal co.
The pathogenesis of NMOSD is mainly related to the aquaporin 4 (AQP4) antibody, which is more common in young adults, mostly women, and is clinically characterized by severe optic neuritis (ON) and longitudinally extending long-stage transverse myelitis (LET.
The main clinical features, recurrence rate and high disability ra.
▌ Clinical manifestations Unilateral or bilateral optic neuritis and acute myelitis are the main manifestations of this disea.
The initial stage can be simple optic neuritis or myelitis, or bo.
NMOSD has 6 core clinical symptoms: optic neuritis, acute myelitis, extreme posterior zone syndrome, acute brainstem syndrome, acute diencephalic syndrome and cerebral syndrome [
▌ Auxiliary examinationAQP4-IgG is a highly specific diagnostic marker with a specificity of up to 90% and a sensitivity of about 7
NMO serum AQP4 antibody is mostly positive, while MS is mostly negative, which can be used as one of the identification criteria for NMO and .
Most of the cerebrospinal fluid pressures are normal, the leukocytes in the acute phase are more than 10×106/L, about 1/3 of the patients are more than 50×106/L, and a few cases can reach 500×106/L; neutrophils and eosinophils can be seen increa.
Acute phase biochemistry: protein is more than 1g/L, and sugar and chloride are mostly normal; about 20% of patients are CSF-specific oligoclonal band (OCB) positive, and IgG is significantly increas.
MOG-IgG is a biomarker for MOGAD, and it is almost not positive at the same time as AQP4-IgG, which has important differential diagnosis val.
The latency of visual evoked potential P100 was significantly prolonged, and the waveform could not be evoked in severe cas.
Serum other autoimmune antibodies: NMO patients may have positive serum ANAs, including ANA, anti-dsDNA, anti-SSA antibodies, and anti-SSB antibodi.
▌ Diagnosis principle of NMOSD: based on "medical history + core clinical symptoms + imaging features + biomarkers", with AQP4-IgG as the stratification, and referring to other subclinical and immunological evidence to make a diagnosis, in addition to Other diseases are exclud.
NMOSD diagnostic criteria [2]:NMOSD diagnostic criteria for AQP4-IgG positive (1) at least 1 core clinical feature (2) AQP4-IgG positive detection with a reliable method (3) exclusion of other diagnosesAQP4-IgG negative or NMOSD diagnostic criteria of unknown AQP4-IgG status (1) In 1 or more clinical episodes, at least 2 core clinical features and all of the following conditions are met: ① At least 1 core clinical feature is optic neuritis, acute long segment Transverse myelitis or medullary zone retal syndro.
② Spatial multiple (two or more different clinical core feature.
③Meet the additional conditions of M.
(2) AQP4-IgG detected by a reliable method is negative or not detect.
(3) exclude other diagnos.
Core clinical features (1) Optic neurit.
(2) Acute myelit.
(3) Posterior zone syndrome, episodic hiccups, nausea, and vomiting unexplained by other causes
(4) acute brainstem syndro.
(5) Symptomatic narcolepsy, diencephalic syndrome, and brain MRI with characteristic diencephalic lesions of NMO.
(6) Cerebral syndrome with characteristic cerebral lesions of NMO.
Additional conditions for NMOSD MRI in AQP4-IgG negative or unknown state (1) Acute optic neuritis: One of the following manifestations on brain MRI is requir.
① normal brain MRI or only non-specific white matter lesio.
②The optic nerve has long T2 signal or T1 enhanced signal ≥ 1/2 of the optic nerve length, or the lesion involves the optic chia.
(2) Acute myelitis: Long spinal cord lesions ≥3 consecutive vertebral segments, or corresponding spinal cord atrophy ≥3 consecutive vertebral segments in patients with a history of myelit.
(3) The last zone syndrome: lesions of the dorsal medulla oblongata / the last zo.
(4) acute brainstem syndrome: brainstem periependymal lesio.
▌ TreatmentTreatment during acute attack: (1) Glucocorticoids: high-dose methylprednisolone pulse therapy is the first choice, which can reduce the inflammatory response and promote the remission of NMO.
(2) Intravenous infusion of immune globulin: 4g/(.
d) intravenous infusion, usually for 5 consecutive days as a course of treatme.
(3) Plasma exchange: It is generally recommended to perform 3-5 times with 2-3L of plasma each time, and most replacements are effective after 1-2 tim.
Treatment during remission: (1) Azathioprine: 2-3 mg/kg/d alone or in combination with low-dose prednisone 75 mg/kg/d, usually after azathioprine takes effect (4-5 months), tape prednisone to low doses for long-term maintenance
(2) Rituximab: single 500-600 mg intravenous infusion, or 100 mg intravenous infusion, once a week, for 4 weeks, repeated after 6-12 mont.
(3) Methotrexate: good tolerance and compliance, suitable for patients who cannot tolerate the side effects of azathiopri.
(4) Cyclophosphamide: It may be effective in reducing the one-year recurrence ra.
It is intravenously infused at 7-25 mg/kg, once a month, for a total of 6 mont.
Conclusion The clinical manifestations of NMOSD are severe, and most of them have a high annual recurrence rate in the early stage, resulting in severe disability such as total blindness or parapleg.
One-third of patients die of respiratory failure, so early diagnosis and treatment are very importa.
References: [1] Wingerchuk DM, Banwell B, Bennett JL, et .
International consensus diagnostic criteria for neuromyelitis optical spectrum disorders [.
Neurology, 2015, 85(2): 177-18 [2] Huang Dehui, Wu Weiping , Hu Xueqia.
Guidelines for the diagnosis and treatment of neuromyelitis optica spectrum disorders in China (2021 edition) [.
Chinese Journal of Neuroimmunology and Neurology, 2021, 28(06): 423-43 Link: https://pubm.
ncb.
n.
n.
gov/26092914/https://k.
cn.
net/kcms/detail/deta.
aspx?dbcode=CJFQ&dbname=CJFDLAST2022&filename=ZSMB202106002&v=Mjc3NzlQUHo3R2JMRzRITkRNcVk5RlpvUjhlWDFMdXhZUzdEaDFUM3FUcldNMUZyQ1VSN2lmWXVkdkZpamhVcjc=
