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   2019| December  | Volume 14 | Issue 5  
    Online since December 2, 2019

 
 
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REVIEW ARTICLES
Drug-induced vasculitis
Durga Prasanna Misra, Pallavi Patro, Aman Sharma
December 2019, 14(5):3-9
DOI:10.4103/0973-3698.272156  
Vascular injury due to drugs is recognized as a distinct entity under the Chapel Hill Consensus Conference 2012 definitions for vasculitis. Drug-induced vasculitis (DIV) may affect various types of vessels. Isolated cutaneous leukocytoclastic vasculitis is most commonly seen in association with antibiotics and nonsteroidal anti-inflammatory drugs. Drug-induced antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis has been classically associated with cocaine (alone or contaminated with levamisole), antithyroid drugs (propylthiouracil, methimazole, carbimazole) and hydralazine; minocycline often mimics medium-vessel vasculitis, with ANCA positivity. Drug-induced large-vessel vasculitis remains rare; however, it has been reported with anticancer agents targeting immune pathways, including immune checkpoint inhibitors. Cerebral vasculitis has been associated with oral or topical sympathomimetic drug use. Operational pathogenetic mechanisms in DIV include immune complex deposition, abnormal generation of neutrophil extracellular traps, and bypassing of normal immune checkpoints like that between programmed cell death ligand 1 on dendritic cells and programmed cell death 1 on T-lymphocytes. DIV can have an unpredictable course, and a significant proportion of patients require immunosuppressive therapy in addition to drug withdrawal.
  2,157 321 -
Drug-induced myopathy
Manesh Manoj, Rasmi Ranjan Sahoo, Kasturi Hazarika, Prashant Bafna, Anupam Wakhlu
December 2019, 14(5):27-36
DOI:10.4103/0973-3698.272157  
A number of medications, including very commonly used ones, have been described as causing myopathy. Drug-induced myopathy is defined as an acute or subacute adverse effect of a drug on the muscular system, which may range from asymptomatic increase in serum creatine kinase and simple myalgias to life-threatening rhabdomyolysis. It is necessary for the treating physician to recognize these manifestations early and manage promptly; in order to prevent treatment-related morbidity and mortality. A PubMed search was conducted using the MeSH terms “drug AND myopathy” and “drug AND rhabdomyolysis.” The consensus of the authors was sought to finalize a group of 60 articles for further review. With the large number of drugs available to the treating physician today, and the significant drug interactions that can occur, knowledge about the various drugs causing myopathy, their characteristic features if any, and the optimal management of these adverse effects is imperative.
  1,951 224 -
Drug-induced psoriasis
Sunil Dogra, Divya Kamat
December 2019, 14(5):37-43
DOI:10.4103/0973-3698.272159  
Psoriasis is known to be triggered by a number of factors including drugs. Some therapeutic agents for the treatment of psoriasis are also known to have a paradoxical effect and alter the course of the disease. The drugs may either cause de novo psoriasis or are responsible for aggravating preexisting psoriasis. The distinction is not always clear-cut and is clinically often indistinguishable from psoriasis vulgaris. The morphological types can vary from plaque psoriasis to pustular psoriasis and even erythroderma. There are certain established agents which are known to trigger psoriasis. Many of the biological agents and targeted therapies available today can trigger psoriasis by activating signaling pathways. The lag time between the intake of drug and onset of psoriasis is highly variable and thus requires a high index of suspicion. Due to the various systemic comorbidities, patients with psoriasis often receive polypharmacy and hence it is important for dermatologists, rheumatologists, and physicians to be aware of the possible triggers.
  1,850 231 -
Drug-Induced Interstitial Lung Disease
Wei-I Lee, Pravin Hissaria
December 2019, 14(5):19-26
DOI:10.4103/0973-3698.272161  
Drug-induced interstitial lung disease (DIILD) represents a rare but potentially fatal adverse drug reaction. A large number of drugs have been implicated to have this potential risk, including chemotherapeutics and disease-modifying antirheumatic drugs. The clinical presentations, laboratory investigations, pulmonary function test result, and imaging and histopathological findings associated with drug-induced pulmonary fibrosis are nonspecific. The diagnosis is achieved after the exclusion of alternative diagnosis, such as infection, pulmonary edema, and connective tissue diseases. However, sometimes, the underlying diseases (e.g., rheumatoid arthritis) and the drugs used to treat the disease (e.g., methotrexate) can both cause ILD; it is often difficult to tease out causality especially if baseline pulmonary assessment (respiratory function test and imaging) is incomplete prior to the commencement of the drug therapy. Many efforts have been put into investigating the pathogenesis of the DIILD, particularly as animal model of bleomycin-induced pulmonary fibrosis has been used as a surrogate for idiopathic pulmonary fibrosis. However, more research is required to improve our understanding of pathogenesis in order to develop more sensitive and specific diagnostic tests as well as to establish evidence-based treatment approach.
  1,672 240 -
Autoimmune/autoinflammatory syndrome induced by adjuvants: what is it and why the controversy?
Sajal Ajmani
December 2019, 14(5):76-81
DOI:10.4103/0973-3698.272150  
Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA) is a group of autoimmune diseases with possible adjuvant-associated causes, such as siliconosis, macrophagic myofasciitis syndrome, Gulf War syndrome, sick building syndrome, and postvaccination autoimmune phenomena. Over time, an international registry with over 500 patients has been established for this conglomeration of rare syndromes. In spite of this, the very existence of ASIA has been debated at times and the diagnostic criteria have come under criticism. The cause-effect relationship between adjuvants and autoimmune phenomenon is difficult to prove due to lack of precisely defined time range between exposure and disease and also due to numerous exposures to adjuvants a person may have in his or her lifetime. The current article attempts at reviewing the clinical features, diagnostic criteria, and evidence for/against the existence of the disease.
  1,692 141 -
Drug-induced bone disorders: A systematic review
Anshita Aggarwal, Meha Sharma, Indira Maisnam, Soumitra Ghosh, Sameer Aggarwal, Saptarshi Bhattacharya, Deep Dutta
December 2019, 14(5):44-51
DOI:10.4103/0973-3698.272152  
Drug-induced bone disorders are a group of disorders characterized by osteomalacia or osteoporosis, with the common denominator being the iatrogenic nature of the disease. Drug-induced bone disorders are either due to the drug directly effecting the bone microarchitecture (osteoblastic or osteoclastic activity) or indirectly by interfering with Vitamin D metabolism, Vitamin D/calcium absorption, and excess calcium loss or due to altered hormone states which promote bone loss (hypogonadism, hyperthyroidism, somatostatin excess states, insulin deficiency, increased systemic inflammation, and oxidative stress). References for this review were identified through searches of PubMed, Medline, and Embase for articles published until July 2019 using the terms “drug induced bone disorders” (MeSH Terms) AND “osteoporosis” (All Fields) OR “osteomalacia” (All Fields). Anti-epileptics, proton pump inhibitors, glucocorticoids, immunosuppressants (calcineurin inhibitors), anticoagulants, glitazones, SGLT2 inhibitors, somatostatin analogs, anticancer medications, and protein kinase inhibitors are some of the commonly used medications associated with bone mineral loss. An increased awareness, minimizing the use of these medications in patients at increased risk of fractures, keeping dosage and duration of therapy to the lowest, ensuring Vitamin D and calcium adequacy either through diet or supplements, and prophylactic use of bisphosphonates (where indicated) can play a major role in preventing morbidity associated with drug-induced bone disorders.
  1,544 151 -
Drug-Induced Musculoskeletal Syndromes and Soft-Tissue Rheumatism
Rudra Prosad Goswami, Parasar Ghosh
December 2019, 14(5):82-89
DOI:10.4103/0973-3698.272160  
Drug-induced musculoskeletal syndromes represent a broad clinical spectrum, ranging from asymptomatic biological abnormalities to severe organ-threatening manifestations. Many drugs have been implicated in inducing rheumatological adverse events. For some compounds, there is pathological or epidemiological evidence for a causal link, and for others, the association is based on anecdotal reports. Several different types of musculoskeletal symptoms occur ranging from chondropathy to arthritis to periarticular symptoms. The most common afflictions are hyperuricemia and gout arising from a variety of commonly used medications such as antitubercular drugs, diuretics, and low-dose aspirin. Although virtually all drug classes may induce some form of musculoskeletal disorders, a significant chunk is corticosteroids, especially injectable, antibiotics, lipid-lowering agents, and newer generation antidiabetics. Knowledge of drug-induced musculoskeletal disorders avoids burdening the patient with an array of unnecessary investigations and allows optimal management of the patients, which includes early discontinuation of the offending agent.
  1,281 166 -
Drug-induced lupus
Kavadichanda Chengappa G
December 2019, 14(5):10-18
DOI:10.4103/0973-3698.272154  
Drug-induced lupus erythematosus (DILE) is an important differential to consider in a clinical setting of mild lupus. Numerous drugs ranging from the classically described procainamide and hydralazine to novel biological agents such as anti-tumor necrosis factors and immune checkpoint inhibitors are implicated in causing DILE. Various pathophysiologic mechanisms such as decreased central tolerance, molecular cross-reactivity, and epigenetic modifications of immune cells are known to play a role in the precipitation of drug-induced autoimmunity. Early recognition and prompt withdrawal of the offending agent is often sufficient to treat these autoimmune manifestations. A thorough knowledge of DILE is essential to ensure better patient care and better understand the role of xenobiotics in precipitating autoimmunity.
  1,209 173 -
Drug-induced fibrosing syndromes: A scoping review
Sakir Ahmed, Prasanta Padhan, Partisha Gupta
December 2019, 14(5):52-58
DOI:10.4103/0973-3698.272153  
There are numerous case reports implicating drugs in the pathogenesis of scleroderma-like fibrotic syndromes. A MEDLINE and SCOPUS search was made in an attempt to review these drugs. The entire spectrum of sclerodermatous disorders ranging from localized morphea, fasciitis, and linear scleroderma to the classical diffuse systemic sclerosis with typical autoantibody formation have been reported in association with drugs. Some drugs such as bleomycin and pentazocine have been established to cause fibrosis and are used to create animal models of systemic sclerosis. There are controversies regarding the role of others such as beta-blockers. Certain chemotherapeutic agents and ergot derivatives can also lead to fibrosing disorders. The new checkpoint inhibitors have been shown to develop systemic sclerosis like disease among other “immune related adverse effects.” The mechanisms leading to fibrosis are poorly understood in case of most drugs due to paucity of data. This limits therapeutic strategies. However, many of these syndromes regress if the causative drug is withdrawn early. Thus, it is imperative for clinicians to have knowledge about these syndromes and identify them early.
  1,208 129 -
Glucocorticoids: A review of its adverse effects including bone loss
Amit Dua, Parthajit Das, Vinod Ravindran
December 2019, 14(5):90-98
DOI:10.4103/0973-3698.272158  
Glucocorticoids (GCs) play a crucial role in the management of many inflammatory, immunological, and autoimmune diseases. Apart from symptomatic relief, they also act as disease-modifying agents as in arthritis and potent immunosuppressive agents as in vasculitides and systemic lupus erythematosus. However, they have been overused, misused, and abused because of their easy availability, low cost, and rapid action. On the other hand, they are also associated with a variety of adverse effects such as osteoporosis, increase risk of infections, cataract, glaucoma, myopathy, glucose intolerance, dyslipidemia, cardiovascular diseases, psychiatric disturbances, and adrenal suppression. GC-induced osteoporosis (GIOP) with increased fracture risk needs special mention, as it causes significant morbidity. In this review, we bring the readers up-to-date information with regard to the major adverse effects of systemic GCs with a special reference to prevention and management of GIOP.
  1,086 153 -
Drug reaction with eosinophilia and systemic symptoms syndrome
KC Shanoj, Sneha Joseph, Padmanabha Shenoy
December 2019, 14(5):59-66
DOI:10.4103/0973-3698.272151  
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a delayed form of severe cutaneous adverse reaction (SCAR) seen in association with certain drugs, especially anticonvulsants and allopurinol. Unlike other SCARs, DRESS is associated with significant systemic involvement such as fever, lymphadenopathy, eosinophilia, renal failure, transaminitis, and myocarditis. Because of delayed onset of symptoms and a persistent course even after discontinuation of culprit drug, DRESS can mimic a variety of rheumatological disorders. Even though glucocorticoids are the mainstay of treatment, unlike other SCARs, DRESS is associated with a high incidence of viral reactivation, especially with members of the human Herpesviridae family. Early identification of the viral activation and prompt therapy is critical in the management of DRESS.
  1,072 135 -
Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum for the rheumatologist
Jyoti Ranjan Parida, Saumya Ranjan Tripathy
December 2019, 14(5):67-75
DOI:10.4103/0973-3698.272155  
Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) represent a spectrum of mucocutaneous manifestations characterized by widespread epidermal and/or mucosal detachment from dermis. It occurs due to Type IV hypersensitivity leading to keratinocyte apoptosis. Many extrinsic and intrinsic defects in the apoptotic pathway have been postulated to result in its dysregulation. The characteristic skin lesions of SJS/TEN include ill-defined, coalescing, red macules with necrotic centers followed by extensive epidermal detachment. Mucosa is involved in up to 90% of cases causing erosions and crusts that may precede or follow skin lesions. Supportive care is the mainstay of treatment and if not started promptly may result in high mortality and morbidity. Although many immunosuppressive drugs have been tried in treatment, no treatment has proven beneficial except cyclosporine which has been shown to retard the progression of SJS/TEN. A patient with SJS/TEN as a presenting feature poses two-fold challenge to a rheumatologist as it could be a manifestation of lupus or side effects of a myriad of drugs used by the rheumatologist.
  1,039 98 -
PREFACE
Drug-induced rheumatic syndromes
Anupam Wakhlu, Rasmi Ranjan Sahoo, Durga Prasanna Misra
December 2019, 14(5):1-2
DOI:10.4103/0973-3698.238193  
  591 265 -