Glucocorticoids are potent immunosuppressive and anti-inflammatory drugs used for various systemic and localized conditions. The use of glucocorticoids needs to be weighed against their adverse effect of aggravating hyperglycemia in persons with diabetes mellitus, unmask undiagnosed diabetes mellitus, or precipitate glucocorticoid-induced diabetes mellitus appearance. Hyperglycemia is associated with poor clinical outcomes, including infection, disability after hospital discharge, prolonged hospital stay, and death. Furthermore, clear guidelines for managing glucocorticoid-induced hyperglycemia are lacking. Therefore, this consensus document aims to develop guidance on the management of glucocorticoid-induced hyperglycemia. Twenty expert endocrinologists, in a virtual meeting, discussed the evidence and practical experience of real-life management of glucocorticoid-induced hyperglycemia. The expert group concluded that we should be proactive in terms of diagnosis, management, and post-steroid care. Since every patient has different severity of underlying disease, clinical stratification would help understand patient profiles and determine the treatment course. Patients at home with pre-existing diabetes who are already on oral or injectable therapy can continue the same as long as they are clinically stable and eating adequately. However, depending on the degree of hyperglycemia, modification of doses may be required. Initiating basal bolus with correction regimen is recommended for patients in non-intensive care unit settings. For patients in intensive care unit, variable rate intravenous insulin infusion could be temporarily used, but under supervision of diabetes inpatient team, and patients can be transitioned to subcutaneous insulin once stable baseline assessment and continual evaluation are crucial for day-to-day decisions concerning insulin doses. Glycemic variability should be carefully monitored, and interventions to treat patients should also aim at achieving and maintaining euglycemia. Rational use of glucose-lowering drugs is recommended and treatment regimen should ensure maximum safety for both patient and provider. Glucovigilance is required as the steroids taper during transition, and insulin dosage should be reduced subsequently. Increased clinical and economic burden resulting from corticosteroid-related adverse events highlights the need for effective management. Therefore, these recommendations would help successfully manage GC-induced hyperglycemia and judiciously allocate resources.

SummaryWe describe a case of lamellar ichthyosis with bilateral genu valgum. The association of genu valgum with congenital ichthyosis is rare. Our patient, a 22-year-old girl, had lamellar ichthyosis and was born with a collodion membrane. She developed progressive valgus deformity of the knees of 5 years duration associated with difficulty in walking. On evaluation, she had generalised scaly skin lesions along with bilateral genu valgum and biochemical evidence of vitamin D deficiency. Skin serves as an important site for vitamin D synthesis and thus skeletal deformities secondary to vitamin D deficiency may occur in cases of congenital ichthyosis, causing a diagnostic dilemma due to the unusual association. This case serves as a reminder that clinicians need to be aware of such an association in order to prevent, appropriately diagnose and adequately treat the rare case of congenital ichthyosis with rickets and osteomalacia. BACKGROUND

Background: To evaluate the clinical characteristics, treatment patterns, and clinical effectiveness and safety of high doses of metformin (1500-2500 mg/day) in Indian adults with type 2 diabetes mellitus (T2DM). Materials and methods: A retrospective, multicentric (n = 241), real-world study included patients with T2DM (aged >18 years) receiving high doses of metformin. Details were retrieved from patient’s medical records. Results: Out of 5695 patients, 62.7% were men with median age was 50.0 years. Hypertension (67.5%) and dyslipidemia (48.7%) were the prevalent comorbidities. Doses of 2000 mg (57.4%) and 1500 mg (29.1%) were the most commonly used doses of metformin and median duration of high-dose metformin therapy was 24.0 months. Metformin twice daily was the most frequently used dosage pattern (94.2%). Up-titration of doses was done in 96.8% of patients. The mean HbA1c levels were significantly decreased post-treatment (mean change: 1.08%; P < .001). The target glycemic control was achieved in 91.2% patients. A total of 83.0% had decreased weight. Adverse events were reported in 156 patients. Physician global evaluation of efficacy and tolerability showed majority of patients on a good to excellent scale (98.2% and 97.7%). Conclusion: Clinical effectiveness and safety of a high-dose metformin was demonstrated through significant improvement in HbA1c levels and weight reduction.

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Background: Thyroid function tests (TFTs) are one of the most frequently performed hormonal tests. Abnormal reports are commonly encountered even in the absence of thyroid dysfunction with medication use during testing being an important cause of this anomaly. Knowledge about the effects of different drugs on various components of TFTs will prevent unnecessary referrals, investigation and potentially dangerous therapeutic decisions. Objective: This narrative review aims to provide information to physicians regarding how various medicines can alter results of TFT even in the euthyroid state. Methods: Articles published up to April, 2020 in English language were identified through searches in PubMed and Google Scholar with a search strategy using keywords appropriate to analyze the effects of different medications on thyroid assays. Results: Medications ranging from over-the-counter vitamins to anti-cancer drugs are associated with anomalous TFTs in euthyroid individuals. This occurs through mechanisms of assay interference and alterations in levels or affinity of thyroid binding proteins (TBPs). High-dose biotin can mimic findings seen in thyrotoxicosis by interference with immunoassays utilizing streptavidin-biotin immobilizing systems. Heparin-induced increase in non-essential fatty acid causes displacement of thyroxine (T4) from TBP, effecting an artefactual increase in free hormone levels. Increases or decreases in thyroid-binding globulin (TBG), the key TBG, can cause a corresponding change in total T4 and tri-iodothyronine levels. Estrogen, selective estrogen receptor modulators, 5-fluorouracil, mitotane, clofibrate, heroin and methadone can increase while androgens, anabolic steroids, glucocorticoids, nicotinic acid and l-asparaginase can decrease TBG. Salicylates, frusemide, carbamazepine and phenytoin may displace T4 from TBP, producing a decline in the total hormone levels. Conclusions: Many categories of medications can interfere with analysis of TFTs through different mechanisms. Awareness about these drug-induced TFT fallacies is essential to avoid improper diagnosis and overtreatment of euthyroid patients.