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Objective: To compare the efficacy of agomelatine with escitalopram in the treatment of major depressive disorder (MDD), improve sleep in MDD patients and study the adverse effects of agomelatine. Materials and Methods: Randomized, parallel-group, open-label study. The primary efficacy outcome was change from baseline to last post-baseline value in Hamilton depression rating scale and Leeds sleep evaluation questionnaire scale. Both parametric and nonparametric tests were applied for analysis. Results: Within-group and between-groups comparison of the mean HAMD17 scores showed statistically significant changes (P < 0.0001). Escitalopram showed early onset of response and remission compared to agomelatine at 10^th week (P < 0.0001) and 14^th week (P < 0.0001), respectively. In agomelatine, within-group and between-groups change of the mean LSEQ score was statistically significant at subsequent follow-up visits (P < 0.0001). Conclusion: Escitalopram is superior to agomelatine in efficacy, considering the early response, early remission, and better relief from symptoms of MDD in adults. Agomelatine may be preferred in MDD patients having insomnia as a predominant symptom. Liver function monitoring should be done in patients on long-term agomelatine therapy.

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This case report outlines a very rare case of losartan-induced severe hyponatremia in a 73-year-old type 2 diabetic patient. The patient was initiated with 50 mg daily oral losartan monotherapy for newly diagnosed moderate hypertension. After 3.5 months of taking the drug, he presented to the emergency department in a drowsy state with severe generalized weakness and occasional palpitations. He was a known diabetic for the last 3 years and well controlled by oral metformin alone. On examination, his serum sodium level was found to be 123 meq/L. There were no evidences of any other possible metabolic, infective, organic or other pathologic causes giving rise to that condition, except losartan itself. De-challenge was done and he was treated vigorously resulting in reversal of the diseased state. Naranjo adverse drug reaction probability scale suggested that it was “probable” that oral losartan was responsible for the development of severe hyponatremia in this patient.

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Fungal infection of the nail as well as nail bed is termed as 'onychomycosis'. It is caused by dermatophytes, non-dermatophytic fungal species and yeasts like Candida albicans. It is traditionally treated by topical antifungals, systemic agents like ketoconazole, griseofulvin, itraconazole, fluconazole, etc. Chemical avulsion or surgical removal of nail can also be tried to treat this disease. In spite of all these treatment options available, podiatrists were always in search of an ideal drug molecule with lesser side effects and which may improve the patient compliance. This exhaustive search led to the discovery of a better antifungal agent, known as “Tavaborole.” A systematic literature search was carried out using databases such as PubMed, Cochrane Reviews, Google Scholar, etc. Detailed information about onychomycosis and tavaborole was gathered. Tavaborole is the first oxaborole antifungal agent approved by FDA in July 2014. It is marketed under the trade name “Kerydin.” It acts by inhibiting protein synthesis in the fungus. It inhibits an enzyme known as cytosolic leucyl-transfer RNA synthetase, or LeuRS, which plays a key role in fungal essential protein synthesis. Dermatitis at the site of topical application, erythema, exfoliation and ingrowing toe nail has been reported in 1% of subjects. Tavaborole may offer a promising role in the treatment of onychomycosis and may compell podiatrists to offer its use in onychomycosis. The present study describes about chemical nature, mechanism of action and two completed phase 3 clinical trial findings of Tavaborole.

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Antidepressant withdrawal mania is not a commonly reported occurrence. To date, there is only one published report of hypomanic episode on withdrawal of mirtazapine. A case is presented herein of a patient who experienced manic episode on withdrawal of mirtazapine.

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A 47 year old lady with hyperthyroidism for past 1½ years was initially on Carbimazole 20 mg orally then changed to 30 mg (during Hysterectomy) but was taking 10 mg for last 1 year. She had intermittent fever with severe B/L bifrontal headache since 3 weeks. Routine investigations showed anaemia, neutropenia, leucopenia and CRP elevation. Peripheral smear showed normocytic normochromic anaemia with Rouleaux formation, leucopenia with 2% atypical cells and mild thrombocytosis. Widal test, RA factor (Rheumatoid factor) test, Ig M (Immunoglobulin M) dengue, Ig M Lepto, TORCH infections (Toxoplasmosis, Other (Syphilis, varicella-zoster, parvovirus B19), Cytomegalovirus and Herpes infections), ANA (Antinuclear antibody) screen cANCA (Cytoplasmic antineutrophil cytoplasmic antibodies) and pANCA (Perinuclear Anti-Neutrophil Cytoplasmic Antibodies) tests were negative. Bone marrow aspiration showed normo to hypercellular marrow with 15% atypical cells and plasma cells. Multiple myeloma workup was done. Carbimazole was withheld. Conclusion: Drug induced agranulocytosis occurs with in 1-2 months of taking the antithyroid medication but onset delayed by 1½ year. De-challenge resulted normalization of blood parameters.

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Objective: To examine the role of Na⁺-K⁺-ATPase and K⁺ channels in mediating vasorelaxation in the superior mesenteric artery of Capra hircus. Materials and Methods: Goat superior mesenteric artery (GSMA) was cut into 1.5–2 mm circular rings and mounted in a thermostatically controlled (37°C ± 0.5°C) organ bath containing 20 ml of modified Krebs-Henseleit saline (MKHS) (pH 7.4), with continuous aeration under 1.5 g tension for 90 min. Endothelium-intact (ED+) or endothelium-denuded (ED−) GSMA ring was contracted with phenylephrine (PE) or 5-hydroxytryptamine (5-HT) (1µM–0.1 mM) in the absence or presence of ouabain (0.1 µM). KCl (1µM–10 mM) was added cumulatively to K⁺-free MKHS-pre-contracted (ED+/−) rings in the absence or presence of ouabain (0.1µM) or barium (1µM) or 4-aminopyridine (1µM). Results: Ouabain did not alter the basal tone of the arterial ring. The contractile response induced by PE (E_max: 50.46 ± 2.68, pD2: 5.53 ± 0.04) and 5-HT (E_max: 30.86 ± 1.33, pD2: 6.17 ± 0.03) in ED+ ring was significantly (P < 0.001) augmented in ED− rings (PE: E_max: 93.30 ± 2.11, pD2: 6.41 ± 0.04; 5-HT: E_max: 95.07 ± 0.99, pD2: 6.27 ± 0.03). The contractile response induced by PE and 5-HT in ED+ or ED− rings in the presence of ouabain was almost identical with that of ED− rings. Vasorelaxation of KCl (E_max: 2.90 ± 1.14, pD2: 3.9 ± 0.03) was significantly attenuated in the presence of ouabain (E_max: 73.8 ± 5.16, pD2: 4.3 ± 0.04), Ba²⁺ (E_max: 16.34 ± 4.7, pD2: 3.22 ± 0.02), 4-AP (E_max: 18.16 ± 2.4, pD2: 3.68 ± 0.03), ouabain and Ba²⁺ (E_max: 70.09 ± 3.66, pD2: 4.41 ± 0.04), and ouabain and 4-AP (E_max: 66.98 ± 4.61, pD2: 4.13 ± 0.06). Conclusion: The vasorelaxation in GSMA is mediated by the endothelium-derived hyperpolarizing factor (EDHFs) such as ouabain-sensitive Na⁺-K⁺-ATPase, K_IRand K_vchannels.

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Calciphylaxis or uremic arteriolopathy is a complex process typically seen in patients with end-stage renal disease, but has also been reported in patients with normal renal function. However, therapies for calciphylaxis are based on reports of traditional patients (i.e., end-stage renal disease). A mainstay of therapy, sodium thiosulfate (STS), has been shown to be effective for the treatment of calciphylaxis. Without a standardized therapy reported for nondialysis patients there is a need for evidence-based therapy. Here, we report a case of a 63-year-old woman with an acute injury on chronic kidney disease (CrCl_Baseline = 48 mL/min, CrCl_AKI = 36 mL/min), not requiring dialysis, with warfarin-induced calciphylaxis. After 4 weeks of therapy with STS, sevelamer, alendronate, and enzymatic debridement the patient subjectively reported slight improvement of the necrotic ulcers but developed cellulitis on her nonaffected limb. Additionally, after 12 weeks of therapy she was readmitted for renal failure and subsequently required dialysis.

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Malignant hyperpyrexia syndrome (MHS) is a rare entity and may not be encountered by the anaesthesiologists throughout their professional career. Whenever it manifests can be a challenging task to manage and prove to be fatal when a timely diagnosis and required therapeutic measures are not taken. Althoughthe dantrolene should be available wherever anaesthesia is practiced, considering the rarity of the syndrome this may not be the scenario always. We are reporting a case of MHS in a pediatric patient to highlight the facts that prompt clinical diagnosis, ongoing supportive treatment, discontinuation of all the anaesthetic agents and and stringent perioperative monitoring along with postoperative oral dantrolene may provide an answer to the MHS crisis in the face of an unavailability of the IV dantrolene; as may be the case in many rural and developing set-ups.

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A 74-year-old female with trigeminal neuralgia developed hypertension after the initiation of carbamazepine therapy. The time sequence of start of the suspected drug and onset of hypertension are consistent with the diagnosis. The hypertension did not resolve with antihypertensive therapy or dose reduction of carbamazepine. Patient recovered after the carbamazepine therapy was discontinued. The positive rechallenge and positive dechallenge showed association of carbamazepine therapy with hypertension as its adverse effect. This is a rare case that we report of carbamazepine-induced hypertension and this report may act as alerting mechanism to the health care professionals especially neurologists.

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Kounis syndrome is a clinical condition due to hypersensitivity that culminates into acute coronary syndrome (ACS) which can be fatal. A 36-year-old male with no conventional coronary risk factors presented elsewhere with a history of fever for 4 days, cough with expectoration, diarrhea and was treated with cephalosporin (Inj. Cefotaxime as an infusion) along with analgesics. He experienced generalized itching 5 minutes after cefotaxime infusion followed by sweating, headache, chest pain with facial and periorbital swelling for which he was rushed to our hospital. On examination he was afebrile with a low blood pressure. Electrocardiogram taken at an outside hospital revealed incomplete right bundle branch block and ST depression V3–V5. Investigations showed increase in troponin T. He was managed with anti-histamines and standard protocol for treatment of ACS. Coronary angiogram revealed normal coronaries. The patient improved symptomatically with treatment and was discharged on an anti-platelet, nitrate and a statin.

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Pleural effusion caused by drug is an uncommon event in clinical practice. Etoricoxib induced pleural effusion is an extremely rare. We describe a patient with pleural effusion as an adverse drug reaction of etoricoxib.

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