Uday Khopkar's research while affiliated with King Edward Memorial Hospital and other places

... Its causative organism is Mycobacterium leprae. [1][2][3][4][5][6][7][8][9][10][11] There is skin involvement in the form of hypopigmented patches and loss of sensation over the affected areas, which commonly include the skin, peripheral nerves, mucosa of the upper respiratory tract, and eyes. 2,[4][5][6][7][8][9][11][12][13] It also involves the peripheral nervous system, mostly in the form of nerve thickening. ...

... 6 The prevailing belief is that Prototheca species infect humans either through direct contact with exposed areas or via traumatic inoculation of materials contaminated with the algae. 1,[7][8][9][10] This infection typically manifests in three primary forms: intra-cutaneous to subcutaneous nodules and plaques, olecranon bursitis, and systemic (disseminated) disease. 11 Notably, the skin emerges as the organ most frequently affected. ...

... Nearly 35 years later, the first evidence to support his hypothesis was confirmed with the identification of AR CARD9 deficiency in four patients with pheohyphomycosis due to P. verrucosa [447]. This inborn error of immunity has since been identified in pheohyphomycosis due to Exophiala [448][449][450][451], other Phialophora species [452], Aureobasidium [453], Alternaria [454,455], and Exserohilum [456], as well as more esoteric dematiaceous fungi, including Pallidocercospora crystallina, Ochroconis musae, and Corynespora cassiicola [449,[457][458][459]. Intriguingly, disseminated infection with C. cassiicola (with extension into the CNS) has also been reported in a patient with compound heterozygous mutations in CLEC7A (encoding Dectin-1, which is a fungal pattern recognition receptor that signals through CARD9) [460]. Other pheohyphomyces have also been reported with single heterozygous variants in CLEC7A or CARD9, although with distinct fungal etiologies than those for AR CARD9 deficiency [460]. ...

... Bullous pemphigoid (BP) is a common autoimmune subepidermal bullous disease characterized by immunoglobulin G (IgG) autoantibodies mainly against the NC16A domain of BP180 (type XVII collagen, 180 kDa), causing tense bullae [1,2]. IgG anti-BP180 NC16A antibodies are related to the disease severity of BP [3][4][5][6][7][8][9][10][11][12][13][14][15][16]. ...

... Although dracunculiasis has been considered to have been an eradicated disease in Rajasthan state, India, since 1997, 8 and in India since 1999, 12,13 with the WHO declaration that India had eradicated dracunculiasis being made in 2000, 14 some sporadic cases have continued to be reported. Following the declaration that Rajasthan was dracunculiasis free in 1997, three cases were detected in the Dungarpur district, Rajasthan, in July 1997, 8,15 in 1999, 15 and in 2006. ...

... Dermoscopic findings outlined by the authors included multiple pink to whitish areas surrounded by a finely pigmented network. Similar structures were also encountered in other anatomical locations [44]. ...

... The histology shows a well-defined area of vascular proliferation with large epithelioid endothelial cells with abundant eosinophilic cytoplasm, accompanied by an inflammatory infiltrate of lymphocytes and eosinophils [1,3,5,7]. Surgery had been considered to be the best treatment modality for ALHE, but the recurrence is frequent also, there are other modalities such as intralesional bleomycin, corticosteroids, propranolol, imiquimod and pulsed dye laser [10][11][12][13][14][15][16][17][18]. The objective of this paper is to report 4 new cases with focus on the clinical and histological characteristics of AHLE. ...

... Since the 1990s, some of these formulations went into clinical use: AmB lipid complex with the commercial name Abelcet ® [183,184], which is formed in a ribbon-like shape [185]; there is also a colloidal dispersion of AmB and cholesteryl sulfate that forms disk complexes and is sold under the commercial name of Amphotec ® or Amphocil ® [186][187][188][189][190]; a liposomal formulation of AmB in cholesterol-containing lipid vesicles sold under the name of Ambisome ® [191][192][193][194]; and a multilamellar vesicle formulation, with a different lipid mixture and sold under the name Fungisome TM [195][196][197][198][199][200]. In the case of Nys, a liposomal formulation called Nyotran ® [201][202][203][204][205] is currently undergoing phase III clinical trials [178], and the available results are promising. ...

... Frequency of outcomes[75][76][77][78][79][80][81] . ...

... 6 Furthermore, there was no information on the gene mutations in two individual cases (Cases 19, Table 2 and Table S1). 15,16 In all, we analysed the FAM111B gene mutations in thirty-four cases. Even though, 55% of these mutations resulted from a paternal and maternal inheritance, compared with the 42% of spurious (i.e. de novo) mutations, suggesting this syndrome may also result from a non-mendelian pattern of inheritance ( Table 2). ...