Sevelamer, has been shown to have many pleiotropic actions on lipid panel, various inflammatory markers, and blood glucose levels in chronic kidney disease patients.We conducted a systematic review and meta-analysis to compare these pleiotropic effects of sevelamer to other phosphate binders used in chronic kidney disease patients. The relevant randomized controlled trials published from 1 January 2001 to 31 November 2019 on the following databases: Cochrane Central Register of Controlled Trials published in The Cochrane Library, PubMed, Scopus and Google Scholar were identified. All the included studies were independently assessed for eligibility and risk of bias. The modified data extraction form of Cochrane was used. This review included 44 studies for qualitative analysis and 28 reports for quantitative analysis. A meta-analysis of three studies (n = 180) showed that glycated haemoglobin had significantly decreased in sevelamer-treated patients (MD: 0.5%; p = <.001). Compared with calcium-based phosphate binders, sevelamer showed a significant reduction in low-density lipoprotein (MD: À19.43 mg/dL; p = <.001) and total cholesterol (MD: À19.98 mg/dL; p < .001). A significant increase in high-density lipoprotein (MD: 1.29 mg/dL; p = .05) was also prominent in sevelamer treated patients. However, we were not able to observe a significant change in other biochemical parameters such as TG, CRP, hs-CRP, FGF-23, IL-6 and albumin as, no statistically significant difference was observed.
Phenytoin is one of the most common and widely used anticonvulsant drug. The present case report explains the rare adverse effect of long term phenytoin treatment induced myelosuppression in a secondary care public hospital, Udhagamandalam, India. We report a case of 25 year old patient who was a known case of seizure for past 10 years. The patient was presented with complaints of two episodes of seizure, fever and abdominal pain to the intensive care unit. The patient was treated with intravenous fluids-dextrose normal saline and ringer lactate, intravenous routes of phenytoin, ciprofloxacin, metronidazole, ranitidine and tablet zinc. The patient's vital signs and blood parameters were monitored on a regular basis. The patient's blood pressure was fluctuating and blood parameters were found to be drastically reducing during the course of treatment with phenytoin. Blood transfusion was initiated in this patient for the treatment of myelosuppression due to which the blood parameters were seen normal during the discharge. In any patient presented with suspected drug induced myelosuppression, early diagnosis of cytopenia with a complete blood count is crucial. In such cases, appropriate symptomatic management along with timely withdrawal of drug remains the best option in current scenario. Being considered a classic antiepileptic, these kinds of serious haematological adverse effects of phenytoin on long term use is often overlooked. Reporting of these types of rare but potential adverse effects is necessary to create awareness among more clinicians.
Introduction: Majority of children and adolescents diagnosed with Type 1 Diabetes Mellitus (T1D) present with the classic symptoms of polyuria, polydipsia and polyphagia, associated with hyperglycemia. Concurrent conditions at the time of T1D diagnosis may alter its presentation and potentially lead to challenges in diagnosis and management. Clinical Case: We present a 17-year-old male with worsening fatigue and unintentional weight loss for two months, then one week of emesis and abdominal pain. Initial work-up by his primary care provider showed sodium 125 mmol/L (133–145), potassium 5.7 mmol/L (3.5–5.1), HCO3 20 mmol/L (21–31), anion gap 13 mmol/L (9–18), random glucose 141 mg/dL (70–199). Due to hyponatremia and dehydration, he was sent to a local emergency room where he was found to be mildly hypotensive at 87/57 mmHg. He received intravenous fluids for hydration and was sent home. On out-patient follow up, he appeared well despite being hypotensive. His additional labs revealed a random glucose of 330 mg/dl and elevated HbA1C of 8.3% (4.4–5.6). His urine was positive for glucose but negative for ketones. He was admitted for further management of new onset diabetes. On admission, he was well appearing and in no acute distress. Blood pressure was 86/57 mmHg, heart rate was 109 bpm, and other physical exam findings were unremarkable. Although his hyperglycemia improved after initiation of insulin therapy, his electrolyte abnormalities persisted, raising suspicion for adrenal insufficiency. An ACTH stimulation test was performed, with both baseline and 60-minute cortisol levels low at 1 ug/dl and 0.9 ug/dl, respectively, confirming adrenal insufficiency. He responded well to glucocorticoid and mineralocorticoid replacement. His electrolytes and blood pressure normalized. Further testing confirmed elevated levels of Glutamic Acid Decarboxylase antibodies 0.19 nmol/L (less than 0.02), Islet Antigen 2 Antibodies: 3.38 nmol/L (less than 0.02), and 21-Hydroxylase antibodies, consistent with T1D with concomitant Addison’s disease (AD). Conclusion: About 0.5% of patients with T1D have AD, but the diagnosis of T1D typically precedes AD for several years, thus the coexistence of both autoimmune conditions at diagnosis is rare.
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