Sitagliptin induced splenic infarcts

  Sitagliptin belongs to the class of dipeptidyl pepti­dase-4 (DPP-4) inhibitors. DPP-4 inhibitors are remark­ably well tolerated oral antihyperglycemic drugs with an adverse effect profile similar to that of placebo. No adverse effects have been reported even with overdose of sitagliptin in suicide attempts. We present here case summary of a 35-year-old female with type 2 diabetes mellitus and major depressive disorder who presented with multiple splenic infarcts after ingestion of sitag­liptin 700 mg and metformin 14 g with suicidal intent. To the best of our knowledge, there are no published reports of splenic infarcts as an adverse event of sit­agliptin. (Clin Diabetol 2017; 6, 6: 215–217

Zawały śledziony spowodowane stosowaniem sitagliptyny

  Sitagliptyna należy do klasy inhibitorów dipeptydy­lopeptydazy-4 (DPP-4). Inhibitory DPP-4 są bardzo dobrze tolerowanymi doustnymi lekami przeciwhi­perglikemicznymi, a ich profil działań niepożądanych jest podobny jak przy stosowaniu placebo. Działań niepożądanych nie obserwowano nawet w przypad­kach przedawkowania sitagliptyny w celu popełnienia samobójstwa. W niniejszej pracy przedstawiono przy­padek 35-letniej kobiety z cukrzycą typu 2 i ciężkim zaburzeniem depresyjnym, u której stwierdzono liczne zawały śledziony po zażyciu — w celu popełnienia samobójstwa — 700 mg sitagliptyny i 14 mg metfor­miny. Według najlepszej wiedzy autorów dotychczas nie publikowano żadnych doniesień na temat zawałów śledziony jako działania niepożądanego sitagliptyny

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

BACKGROUND: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. METHODS: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). FINDINGS: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29-146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0- 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25-1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39-1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65-1·60]; p=0·92). INTERPRETATION: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention. FUNDING: British Heart Foundation

Role of cervical ultrasonography in primary hyperparathyroidism

Aim: To evaluate the role of USG in the preoperative localization of parathyroid adenomas in patients with symptomatic hyperparathyroidism and to compare its usefulness with that of scintigraphy scan and postoperative findings. Material and methods : Twenty-five patients with symptomatic primary hyperparathyroidism were subjected to USG of the neck and nuclear scintigraphy, followed by surgery. The results were independently analyzed and compared with per-operative findings. Results : The 25 patients had a total of 28 abnormal glands: 22 solitary adenomas, and 6 multiple adenomas (two each in three patients). USG detected 20 out of 22 solitary adenomas and three out of six multiple adenomas. USG missed five abnormal glands, two of which were in the neck and three in the mediastinum. Scintigraphy was positive in 26 abnormal glands, out of which 22 were single and four were multiple. Two abnormal glands were missed: one in the neck and one in the mediastinum. Conclusion: As limited neck dissection for primary hyperparathyroidism becomes increasingly popular, USG has been found to be a sensitive, specific, and easily available noninvasive investigation for parathyroid localization. It can be easily offered to patients as a method for preoperative localization prior to limited parathyroid surgery outside tertiary care settings

Sella turcica size in women with sheehan syndrome—A case–control study

Introduction: Sheehan syndrome is a common cause of hypopituitarism in developing countries. Among risk factors, in addition to post-partum haemorrhage, a smaller sellar volume is also believed to predispose to pituitary necrosis. Some earlier studies have reported smaller sellar volume in these patients but involved a small number of patients and lacked matched controls. The main of the present study was to study the sellar volume in a large cohort of patients with Sheehan syndrome and compare it with age- and parity-matched controls. Methods: Fifty women with Sheehan syndrome and an equal number of age- and parity-matched controls were studied. Baseline investigations, relevant hormonal assay, and MRI of pituitary were studied in all. Results: Sellar volume was significantly lower in patients with Sheehan syndrome (334.50 ± 129.08 mm3 in patients as against 456.64 ± 169.25 mm3 in controls, P = 0.000). Far more women with Sheehan syndrome than controls had decreased sellar volume (40% vs. 12%). Conclusions: Patients with Sheehan syndrome have a smaller sellar volume that may be a non-modifiable risk factor for the development of post-partum pituitary necrosis

Lithium toxicity and myxedema crisis in an elderly patient

While thyroid dysfunction is a frequent complication of lithium treatment, myxedema crisis is a rare occurrence with a handful of cases described. Here, we describe a patient receiving lithium for about a decade for bipolar disorder, who presented with myxedema crisis and lithium toxicity. In this patient, myxedema crisis was likely precipitated by lithium toxicity and community acquired pneumonia. The effects of lithium on thyroid are briefly reviewed. Objective: To describe an elderly male who was diagnosed with myxedema crisis and lithium toxicity. Case Report: A 70-year-old male was admitted in our hospital with history of gradual onset progressive decrease in level of consciousness and altered behavior for last 1 month. Patient also had history of respiratory tract symptoms for 1 week. Patient was a known case of diabetes and bipolar affective disorder for which he had been receiving insulin and lithium for 10 years. One year earlier, patient was admitted in our ward for glycemic control and evaluation of complications and was found to be clinically and biochemically euthyroid; he never returned for follow up until the present admission. On examination patient had incoherent speech, hypothermia, and bradycardia. Thyroid function showed thyroid-stimulating hormone >150 IU/ml, Tetraiodothyronine (T4) <1 ΅g/dl, anti-thyroid peroxidase titer of 60 IU/ml. The serum lithium level was 2.9 nmol/L (therapeutic level 0.2-1.2 nmol/L). He was managed with levothyroxine, starting with a loading oral dose of 500 ΅g through ryles tube followed by 100 ΅g daily, IV antibiotics and fluids; lithium was stopped after consultation with a psychiatrist. From day 5, patient started showing progressive improvement and by day 10, he had a Glasgow Coma Scale of 15/15, normal electrolyte, serum creatinine of 1.8 mg/dl and serum lithium level of 0.5 nmol/L. Conclusion: Lithium-induced hypothyroidism may be life-threatening, thyroid function should be monitored before and during lithium therapy and drug should be discontinued and appropriate therapy instituted if hypothyroidism develops