Publications by authors named "Angshuman Mukherjee"

14 Publications

  • Page 1 of 1

Response to comment on: Anatomical and functional outcomes one year after vitrectomy and retinal massage for large macular holes.

Indian J Ophthalmol 2021 10;69(10):2912

Department of Vitreoretina Services, Disha Eye Hospitals, Kolkata, West Bengal, India.

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http://dx.doi.org/10.4103/ijo.IJO_1558_21DOI Listing
October 2021

Response to comment on: Anatomical and functional outcomes one year after vitrectomy and retinal massage for large macular holes.

Indian J Ophthalmol 2021 10;69(10):2910-2911

Department of Vitreoretina Services, Disha Eye Hospitals, 88 Ghosh Para Road, Barrackpore, Kolkata, West Bengal, India.

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http://dx.doi.org/10.4103/ijo.IJO_1559_21DOI Listing
October 2021

Real-World Safety Outcomes of Intravitreal Ranibizumab Biosimilar (Razumab) Therapy for Chorioretinal Diseases.

Ophthalmol Ther 2021 Jun 17;10(2):337-348. Epub 2021 Apr 17.

Department of Vitreoretinal Services, Disha Eye Hospitals, Kolkata, 700120, India.

Introduction: To assess the safety profile of the intravitreal ranibizumab biosimilar molecule, Razumab (Intas Pharmaceuticals, Ahmedabad, India) in chorioretinal disorders under real-world conditions.

Methods: This was a multicenter, retrospective chart review which included patients from 15 centers receiving intravitreal Razumab (IVRz) injections from 2016 to 2020. Patient demographics, ocular examination data, and detailed safety information regarding serious adverse events (SAE) or serious adverse drug reactions (sADR), and non-serious AEs (nsAE) or non-serious ADRs (nsADR) occurring within 1 month of IVRz injections were compiled.

Results: A total of 6404 eyes of 6404 patients received 9406 IVRz injections [mean (± SD) = 1.49 (± 0.63)] during 4.25 years. Adverse events were reported after 1978 injections (21.03%): 64.16% nsAE, 32.96% nsADR, 2.37% sADR, and 0.51% SAE. The most frequent adverse events were subconjunctival hemorrhage (8.2% of total injections), transient blurring of vision (6.5% of total injections), and mild ocular pain (5.27% of total injections). Serious ocular (31 cases with retinal pigment epithelial tears [0.33%], two cases of non-infectious vitritis [0.02%], and one case of endophthalmitis [0.01%]) and systemic (seven patients with non-fatal myocardial infarction [0.12%] and six patients with non-fatal cerebrovascular accident [0.09%]) adverse events were infrequent.

Conclusion: The study reports the largest pooled safety data on IVRz use in a real-world scenario. The results did not raise any new ocular or systemic safety concerns for the biosimilar agent, with the incidence and spectrum of adverse reactions similar to those reported with other anti-vascular endothelial growth factor (anti-VEGF) drugs. The real-world evidence suggests that IVRz is a safe anti-VEGF agent in the management of chorioretinal disorders.
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http://dx.doi.org/10.1007/s40123-021-00345-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079600PMC
June 2021

Anatomical and functional outcomes one year after vitrectomy and retinal massage for large macular holes.

Indian J Ophthalmol 2021 04;69(4):895-899

Vitreoretina Services, Disha Eye Hospitals, Kolkata, West Bengal, India.

Purpose: The aim of this study was to report results of macular hole closure, visual benefit and longitudinal changes in foveal architecture over 1 year following macular hole surgery with retinal massage.

Methods: Records of patients with full thickness macular hole (FTMH) with minimum basal diameter of 550 μ who underwent vitrectomy, internal limiting membrane (ILM) peeling and retinal massage were drawn up. Retinal massage was performed after dye assisted ILM peeling, using a 27G flute needle with a long and soft silicone tip under air in a centripetal direction around the FTMH. At the end, 10% CF gas was used as tamponade. The foveal contour at 1 year follow up was recorded based on its cross sectional appearance on OCT and was classified into U, V and irregular types of closure as previously described.

Results: Forty-one eyes of 41 patients with a mean age of 70.4 ± 6.9 years were included. The mean preoperative vision was 0.99 ± 0.07 logMAR and mean maximum basal diameter of the FTMH was 835 ± 208 μ. Macular hole closure was seen in all patients at 1-month follow up. The BCVA improved to 0.5 ± 0.1 log MAR at 6 months (P < 0.001) and then stabilized. The U shaped closure was the commonest pattern (n = 22, 54%), followed by V-shaped closure (n = 16, 39%) while irregular closure was seen in 3 eyes (7%).

Conclusion: Retinal massage after ILM peeling is a very simple, and as yet under-utilized manoeuvre that may improve hole closure rates and lead to potentially greater improvement in vision compared to existing techniques for large holes.
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http://dx.doi.org/10.4103/ijo.IJO_1680_20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8012922PMC
April 2021

Case Report of Henoch Schonlein Pupura in an Adult.

J Assoc Physicians India 2020 Jan;68(1):79

PT BDS PGIMS Rohtak.

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January 2020

Ultra-widefield image of a toxocara granuloma with an adjacent retinal break and retinal detachment.

Indian J Ophthalmol 2019 11;67(11):1884

Department of Vitreoretina Services, Disha Eye Hospitals, Kolkata, West Bengal, India.

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http://dx.doi.org/10.4103/ijo.IJO_1294_19DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836581PMC
November 2019

Ophthalmoplegic migraine: A critical analysis and a new proposal.

Ann Indian Acad Neurol 2012 Aug;15(Suppl 1):S2-6

Department of Neurology, Vivekananda Institute of Medical Science, Kolkatta, West Bengal, India.

The nosology, classification and pathophysiology of ophthalmoplegic migraine (OM) remains complex and debatable. A recently proposed classification of OM leaves several caveats. A critical analysis of all reported cases of OM (1993-2010) has been made incorporating the authors' own experience to arrive at a simple, unambiguous and easy to use diagnostic criteria and classification of OM. Between 2005 and 2010, 18 adult cases of OM had been seen whose clinical details are summarized. Most had sixth nerve palsies associated with migraine-like headaches lasting more than 4 days. Other possibilities were carefully excluded. All subjects responded to corticosteroids favorably. We prefer using the term ophthalmoplegia with migraine-like headache (OMLH) rather than OM. We classify OMLH as a migraine subtype (1.7) and into two groups-childhood-onset type (where third nerve palsies and nerve enhancement are common) and adult-onset type (where sixth nerve palsies are more common and nerve enhancement unusual). This clinico-radiological classification does not in any way hint at any difference in pathophysiology between the two groups.
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http://dx.doi.org/10.4103/0972-2327.99985DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444213PMC
August 2012

Spasticity mechanisms - for the clinician.

Front Neurol 2010 17;1:149. Epub 2010 Dec 17.

Department of Neurology, Vivekananda Institute of Medical Sciences Kolkata, India.

Spasticity, a classical clinical manifestation of an upper motor neuron lesion, has been traditionally and physiologically defined as a velocity dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex. Clinically spasticity manifests as an increased resistance offered by muscles to passive stretching (lengthening) and is often associated with other commonly observed phenomenon like clasp-knife phenomenon, increased tendon reflexes, clonus, and flexor and extensor spasms. The key to the increased excitability of the muscle stretch reflex (muscle tone) is the abnormal activity of muscle spindles which have an intricate relation with the innervations of the extrafusal muscle fibers at the spinal level (feed-back and feed-forward circuits) which are under influence of the supraspinal pathways (inhibitory and facilitatory). The reflex hyperexcitability develops over variable period of time following the primary lesion (brain or spinal cord) and involves adaptation in spinal neuronal circuitries caudal to the lesion. It is highly likely that in humans, reduction of spinal inhibitory mechanisms (in particular that of disynaptic reciprocal inhibition) is involved. While simply speaking the increased muscle stretch reflex may be assumed to be due to an altered balance between the innervations of intra and extrafusal fibers in a muscle caused by loss of inhibitory supraspinal control, the delayed onset after lesion and the frequent reduction in reflex excitability over time, suggest plastic changes in the central nervous system following brain or spinal lesion. It seems highly likely that multiple mechanisms are operative in causation of human spasticity, many of which still remain to be fully elucidated. This will be apparent from the variable mechanisms of actions of anti-spasticity agents used in clinical practice.
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http://dx.doi.org/10.3389/fneur.2010.00149DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478PMC
July 2011

Migraine pain location in adult patients from eastern India.

Ann Indian Acad Neurol 2008 Apr;11(2):98-102

Department of Neurology, Vivekananda Institute of Medical Sciences, Kolkata, India.

Background: Sparse literature documenting the location of pain at the onset of migraine attacks and during established headaches is available.

Objectives: A prospective study (2003-05) on 800 adult migraine patients (International Classifications of Headache Disorders (ICHD), 2:1.1, 1.2.1 and 1.6.1) was conducted to document (a) sites of onset of pain and (b) location of pain during established attacks (in >50% occasions) through semistructured interviews.

Results: DEMOGRAPHY: N = 800; M:F = 144:656 (1:4.56); age, 16-42 years (mean, 26 years); duration of migraine, 1-18 years (mean, 6.8 years). 87% of the subjects were ethnic Bengalis from the eastern Indian state of West Bengal, Calcutta being the capital city. MIGRAINE TYPES: (on the basis of >50% headache spells): N = 800; 1.1:668 (83.5%); 1.2.1:18 (2.25%); 1.6.1:114 (14.25%). LOCATION OF PAIN AT ONSET: Unilateral onset was present in 41.38% of the patients; of these, 53.17% had eye pain; 8.16%, frontal pain and 38.67%, temporal pain. In 32.25% of the patients, bilateral/central location of pain, mostly bitemporal or at vertex was noted. Cervico-occipital pain onset was noted in 26.43% patients (predominantly occipital, 14.68%; predominantly cervical, 11.75%). LOCATION OF ESTABLISHED HEADACHES: In 47.4% of the patients, with unilateral ocular or temporal onset, pain remained at the same site. Pain became hemicranial in 32.9%. In most patients, unilateral frontal onset pain (55.5%) became bilateral or holocranial. Most bilateral ocular (69.4%) and temporal onset (69.7%) pains remained at the same location. However, most bifrontal (55.6%) and vertex onset (56.9%) pains subsequently became holocranial. Most occipital pains at onset became holocranial (45.3%), but cervical pains subsequently became either hemicranial (38.3%) or holocranial (36.2%).

Conclusions: This study documents location of pain at the onset and during established headaches in migraine patients largely from a specific ethnic group. Migraine with aura appears to be rare among ethnic Bengalis in eastern India. More than half had onset pain bilaterally/centrally and in the cervico-occipital regions. Only 40.5% experienced only unilateral pain. Cervico-occipital migraine pain appears to be common in ethnic Bengalis.
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http://dx.doi.org/10.4103/0972-2327.41876DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771967PMC
April 2008

Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations.

Carcinogenesis 2007 Mar 17;28(3):672-6. Epub 2006 Oct 17.

Molecular and Human Genetics Division, Indian Institute of Chemical Biology, Kolkata, India.

In West Bengal, India more than 6 million people are exposed to high levels of arsenic through drinking water. Since, only 15-20% of the exposed individuals show arsenic-induced skin lesions, it is assumed that genetic variation might play an important role in arsenic toxicity and carcinogenicity. Arsenic exposure often leads to the development of hyperkeratosis, the precursor of arsenic-induced skin cancer. ERCC2 (excision repair cross-complementing rodent repair deficiency, complementation group 2) is a nucleotide excision repair pathway gene, and its SNPs have been implicated in several types of epithelial cancers. We investigated the possible association of ERCC2 codon 751 A-->C polymorphism (lysine to glutamine) with arsenic-induced hyperkeratosis and correlated ERCC2 genotypes with increased frequencies of chromosomal aberration to ascertain whether any genotype leads to sub-optimal DNA repair. For this association study, 318 unrelated arsenic exposed subjects (165 with hyperkeratosis and 153 without any arsenic-induced skin lesions), drinking water contaminated with arsenic to a similar extent, were recruited. Genotyping was done through PCR-RFLP procedure. Lys/Lys genotype was significantly over-represented in the arsenic-induced hyperkeratosis-exhibiting group [odds ratio (OR) = 4.77, 95% confidence interval (CI) = 2.75-8.23]. A statistically significant increase in both CA/cell and percentage of aberrant cells was observed in the individuals with AA genotype compared to those with AC or CC genotype combined (P < 0.01) in each of the two study groups, as also, in the total study population. This study indicates that ERCC2 codon 751 Lys/Lys genotype is significantly associated with arsenic-induced premalignant hyperkeratosis and is possibly due to sub-optimal DNA repair capacity of the ERCC2 codon 751 Lys/Lys genotype.
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http://dx.doi.org/10.1093/carcin/bgl181DOI Listing
March 2007

Association of specific p53 polymorphisms with keratosis in individuals exposed to arsenic through drinking water in West Bengal, India.

Mutat Res 2006 Oct 22;601(1-2):102-12. Epub 2006 Aug 22.

Molecular and Human Genetics Division, Indian Institute of Chemical Biology, 4, Kolkata, India.

Although, more than six million people are endemically exposed to inorganic arsenic in West Bengal, India by drinking heavily contaminated groundwater, only about 300,000 people show arsenic induced skin lesions. This suggests that genetic variability plays an important role in arsenic induced skin lesions and skin cancers. Arsenic induced keratosis is considered as a possible precancerous state of in situ carcinoma. Several reports have suggested the role of p53 polymorphisms as potential marker for risk assessment of different types of cancers. This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water. A total of 366 unrelated individuals (177 individuals with arsenic induced keratosis and 189 individuals with no arsenic induced skin lesions) were recruited from North 24 Parganas, Nadia and Murshidabad districts between January 2003 and February 2005 for the study of the genotypic distribution of three p53 polymorphisms (16bp duplication at intron 3, codon 72 Arg/Pro and G>A at intron 6 [nt 13,494]) by PCR-RFLP. The arginine homozygous genotype at codon 72, and homozygous genotype of no duplication polymorphism at intron 3 were over represented in the individuals with keratosis compared with individuals with no skin lesions (OR=2.086; 95% CI=1.318-3.299 and OR=2.086; 95% CI=1.257-3.457, respectively). This study indicates that individuals carrying the arginine homozygous genotype at codon 72, and/or no duplication homozygous genotype at intron 3 are at risk for the development of arsenic induced keratosis.
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http://dx.doi.org/10.1016/j.mrfmmm.2006.06.014DOI Listing
October 2006

Comparison of health effects between individuals with and without skin lesions in the population exposed to arsenic through drinking water in West Bengal, India.

J Expo Sci Environ Epidemiol 2007 May 12;17(3):215-23. Epub 2006 Jul 12.

Division of Molecular and Human Genetics, Indian Institute of Chemical Biology, Kolkata, India.

A study was conducted to explore the effect of arsenic causing conjunctivitis, neuropathy and respiratory illness in individuals, with or without skin lesions, as a result of exposure through drinking water, contaminated with arsenic to similar extent. Exposed study population belongs to the districts of North 24 Parganas and Nadia, West Bengal, India. A total of 725 exposed (373 with skin lesions and 352 without skin lesions) and 389 unexposed individuals were recruited as study participants. Participants were clinically examined and interviewed. Arsenic content in drinking water, urine, nail and hair was estimated. Individuals with skin lesion showed significant retention of arsenic in nail and hair and lower amount of urinary arsenic compared to the group without any skin lesion. Individuals with skin lesion also showed higher risk for conjunctivitis ((odd's ratio) OR: 7.33, 95% CI: 5.05-10.59), peripheral neuropathy (OR: 3.95, 95% CI: 2.61-5.93) and respiratory illness (OR: 4.86, 95% CI: 3.16-7.48) compared to the group without any skin lesion. The trend test for OR of the three diseases in three groups was found to be statistically significant. Again, individuals without skin lesion in the exposed group showed higher risk for conjunctivitis (OR: 4.66, 95% CI: 2.45-8.85), neuropathy (OR: 3.99, 95% CI: 1.95-8.09), and respiratory illness (OR: 3.21, 95% CI: 1.65-6.26) when compared to arsenic unexposed individuals. Although individuals with skin lesions were more susceptible to arsenic-induced toxicity, individuals without skin lesions were also subclinically affected and are also susceptible to arsenic-induced toxicity and carcinogenicity when compared to individuals not exposed to arsenic.
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http://dx.doi.org/10.1038/sj.jes.7500510DOI Listing
May 2007

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic-induced cancer through drinking water.

Int J Cancer 2006 May;118(10):2470-8

Indian Institute of Chemical Biology, Kolkata, and West Bank Hospital, Howrah, India.

In West Bengal, India, more than 300,000 arsenic-exposed people are showing symptoms of arsenic toxicity, which include cancers of skin and different internal organs. Since only 15-20% of the exposed population manifest arsenic-induced skin lesions, it is thought that genetic variation might play an important role in arsenic toxicity and carcinogenicity. A total of 422 unrelated arsenic-exposed subjects (244 skin-symptomatic and 178 asymptomatic) were recruited for this study. Cytogenetic damage, as measured by chromosomal aberrations in lymphocytes and micronuclei formation in oral mucosa cells, urothelial cells and binucleated lymphocytes, was studied in unexposed, skin-symptomatic and asymptomatic individuals with similar socioeconomic status. Identification of null mutations in GSTT1 and GSTM1 genes were carried out by PCR amplification. GSTP1 SNPs, implicated in susceptibility to various cancers, were assessed by PCR-RFLP method. Symptomatic individuals had higher level of cytogenetic damage compared to asymptomatic individuals and asymptomatic individuals had significantly higher genotoxicity than unexposed individuals. No difference in allelic variants in GSTT1 and GSTP1 was observed between these 2 groups. Incidence of GSTM1 null gene frequencies was significantly higher in the asymptomatic group. Individuals with GSTM1-positive (at least one allele) had significantly higher risk of arsenic-induced skin lesions (odds ratio, 1.73; 95% confidence interval, 1.24-2.22). These results show a protective role of GSTM1 null in arsenic toxicity. This study also indicates that asymptomatic individuals are sub clinically affected and are also significantly susceptible to arsenic-induced genotoxicity.
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http://dx.doi.org/10.1002/ijc.21640DOI Listing
May 2006

Familial pediatric rapidly progressive extrapyramidal syndrome: is it Hallervorden-Spatz disease?

Pediatr Neurol 2003 Aug;29(2):170-2

Department of Neurology, Vivekananda Institute of Medical Sciences, Calcutta, India.

The clinical features of two children of a family with rapidly progressive extrapyramidal-pyramidal-dementia complex have been described. Inheritance seems most likely to be autosomal recessive. Magnetic resonance imaging results of brain were negative. Even so, the authors argued in favor of a diagnosis of Hallervorden-Spatz disease because the cases fulfilled the clinical criteria for diagnosis of this disease. Apart from the negative magnetic resonance findings, the other unusual feature was the early development of levodopa-induced dyskinesia. Few conditions need to be considered in the differential diagnosis of a childhood-onset rapidly progressive extrapyramidal syndrome. Such conditions include Wilson's disease, Hallervorden-Spatz disease (HSD), juvenile form of Huntington's disease, juvenile neuronal ceroid lipofuscinosis, early-onset Machado-Joseph disease neuroacanthocytosis, storage disorders, and variant form of dopa-response dystonias (DRD). Rarer conditions are Leigh's disease, Lafora body disease, and dentato-rubro-pallido-luysian atrophy. HSD is a rare disorder characterized by progressive extrapyramidal dysfunction and dementia. Onset is most commonly in late childhood or early adolescence. The disease can be familial or sporadic. When familial, it is inherited recessively and has been linked to chromosome 20. Recently, a mutation in the pantothenate kinase (PANK2) gene on band 20pl3 has been described in patients with typical HSD. HSD produces typical magnetic resonance imaging (MRI) changes in brain, aiding in antemortem diagnosis. The typical finding is of bilaterally symmetrical hyperintense signal changes in the external segment of globus pallidus, with surrounding hypointensity on T(2)-weighted image. These imaging features are fairly diagnostic and have been termed the "eye-of-the tiger sign". The hyperintensity represents pathologic changes, including gliosis, demyelination, neuronal loss, and axonal swelling, and the surrounding hypointensity is caused by loss of signal secondary to iron deposition. Described herein are the clinical aspects of a family with autosomal recessive inheritance with rapidly progressive extrapyramidal-pyramidal-dementia complex but with negative brain MRI results. The diagnosis should be considered a variant form of HSD.
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http://dx.doi.org/10.1016/s0887-8994(03)00231-5DOI Listing
August 2003
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