A 32-year-old female with a past medical history of constipation (predominant irritable bowel syndrome (IBS) and gastro-esophageal reflux disease (GERD)) presented with a complaint of pain in the lower abdomen. She lost 20 pounds in three months with a current body mass index (BMI) of 19.5 kg/m2 (ref: normal level 18.5-24.9). Computed tomography (CT) of the abdomen with contrast showed very little intra-abdominal fat, enlarged proximal duodenum, and decreased aorto-mesenteric angle of 15.4 0 suggestive of superior mesenteric artery (SMA) syndrome. Per general surgery, the patient was managed conservatively: initially Nil Per Os (NPO), slowly transitioned to a clear liquid diet, soft diet, and solid diet. She tolerated the diet, improved clinically, and was discharged home.
Objective This meta-analysis aimed to obtain the pooled estimate of fibrinogen levels in SSNHL cases and investigate its association with patient prognosis and recovery. Data sources We searched the databases PubMed, medRxiv, and Google Scholar for all relevant literature published until August 1, 2022. Review methods The primary objective of the meta-analysis was to assess the association of fibrinogen with the risk of SSNHL and recovery. The search results were screened and selected for review on the basis of eligibility criteria. SSNHL patients were defined as cases and healthy individuals as controls. Data on the level of fibrinogen in SSNHL and controls, as well as recovered and the non-recovered group were subjected to a meta-analysis on Review Manager Version 5.4.1 using a random and fixed-effects model. The pooled estimate was expressed as standardized mean difference (SMD) and forest plots were generated for interpretation Results Fourteen studies with a total of 2,077 participants fulfilled the eligibility. The overall risk of bias was moderate. The blood level of fibrinogen was significantly higher in SSNHL patients as compared to controls [SMD = 0.35; 95% CI = 0.04–0.67; p = 0.03]. Likewise, the recovered group had significantly lower fibrinogen prior to treatment as compared to the non-recovered group [SMD= -0.36; 95% CI= -0.58 to -0.14; p = 0.001]. Conclusion Higher fibrinogen levels were observed in SSNHL patients as compared to controls. Recovered patients had a lower fibrinogen level.
Background and aim Sensorineural hearing loss (SNHL) is the commonest hearing disorder prevalent. Borrelia burgdorferi is a spirochete whose infection has been shown to result in SNHL. This systematic review aims to investigate the prevalence and association of B. burgdorferi infection in SNHL. Methods A systematic literature search on the databases PubMed, Google Scholar, and UpToDate® was performed. Study selection process was done in accordance with the PRISMA guideline. In brief, studies were selected first by title and abstract screening followed by a full-text inspection. The quality assessment of the included studies was performed using the Joanna Briggs Institute Critical Appraisal tool. Data on study characteristics, patient demographics, audiological, microbiological, symptomatological, and therapeutical findings were extracted. Results The study search retrieved a total of 8,772 studies and 9 of them met out eligibility requirement. There were altogether 964 SNHL patients. 71 (7.3%) were tested positive for B. burgdorferi infection. The commonest symptoms in infected SNHL patients were tinnitus (53%) and vertigo (47%). Patients treated with steroids along with ceftriaxone showed a higher hearing recovery rate. Conclusion Borrelia burgdorferi infection is responsible for a substantial proportion of sensorineural hearing loss and should be investigated whenever no other reasons of hearing loss are established.
Psychiatric medications are well established cause of diabetes. Our case had similar presentation. 67-year-old African-American male with history of hypertension and dementia was brought to the ER for auditory hallucination and bizarre behavior. His home medications were Hydrochlorothiazide, Nifedipine and Spironolactone. Psychiatry was consulted and he was admitted to psychiatric floor. He was diagnosed for first time with psychosis and depression. He was treated with citalopram 20 mg for depression; donepezil 10 mg for dementia and risperidone 0.5 mg twice a day for psychosis. 2 weeks later he developed difficulty swallowing and weakness, blood glucose level of 1263 mg/dl. All of his psychiatric medications were stopped except for citalopram 10 mg daily and patient was transferred to ICU. In the ICU, pH was 7.28 (normal 7.34-7.45), normal anion gap, bicarbonate 29mmol/L (normal 20-24), plasma osmolality 428 mOsm/kg (normal 280-320), HbA1c 10% (normal 4-5.6). He was intubated and managed as Hyperosmolar Hyperglycemic Non-Ketotic coma (HONK). He was started on insulin drip and later transitioned to Lantus and short-acting insulin. He improved and was then extubated. After 40 days, repeat A1C was 7.4%. The patient moved to another state and follow-up was lost. Discussion While the patient was on thiazide for a long time, he had a fairly good glucose control; his A1C ranged from normal to prediabetic (A1c 5.7%-6.4%). This makes thiazide unlikely cause of diabetes mellitus for him. The fact that right after 21 days of starting psych medications caused him to land in ICU for HONK, with A1c of 10% and glucose of 1273 mg/dl, strongly suggests that this is a case of psych medications induced T2DM. This is also supported by the fact that discontinuation of those medications lowered the A1c to 7.4% in 40 days. 3 weeks before the hospitalization his A1c was 5.1%. Metformin is demonstrated to be most promising long term medication in cases like this. Conclusion Psychiatric medications are important cause of drug induced diabetes and should always be thought as a cause of acute new onset diabetes. Stopping the offending drugs ensues good glycemic control.
41-year-old male with history of anxiety, bipolar disorder, depression, cognitive developmental delay, Idiopathic Thrombocytopenic Purpura (ITP), Vit D deficiency, tinnitus, suicidal attempt, auditory hallucination, borderline intellectual functioning comes to the PCP’s office for regular follow-up. The PCP has noted that the patient was hypocalcemic on multiple visits. On exam, vitals were in normal range, height 5 feet 2 inches, BMI 31 kg/m2.Despite the patient being on calcium and Vit D2 pills for a couple of months, his Calcium level were low ranging from 5.8–7.8mg/dl (normal 8.5-10.1) with normal albumin; ionized calcium was low 0.9-0.97mmol/l (normal 1.12-1.23); Magnesium was normal 2mEq/L (normal 1.5-2.5), phosphorus slightly high 5 mg/dL (normal 2.5-4.9), PTH (ParaThyroid Hormone level) was low-normal 18.8pg/ml (normal 11.1-79.5), vitamin D 25 OH low 16ng/ml (normal 30-100); 1,25 di OH vitamin D low 8ng/ml (normal25-40).Thyroid ultrasound showed 2 benign nodules, no further work-up done. TSH and free T4 were normal. FISH (Fluorescence In Situ Hybridization) came positive for DiGeorge syndrome (deletion at 22q11.2). He was treated with calcium 600 mg 4 pills daily, calcitriol 0.25 mcg two pills daily, Vit D2 50000 IU weekly and thiazide diuretic. His labs improved. DISCUSSIONHypocalcemia can be due to low magnesium level, drugs or associated with high or low PTH. The patient had normal magnesium and he was not on any medication that causes hypocalcemia. This rules out first two casues. Hypocalcemia with high PTH (pseudohypoparathyroidism or low vit D levels) doesn’t fall in our differential because our patient had low PTH. For hypocalcemia with low PTH, differentials include post-surgical condition (no surgical history), autoimmune (history and labs not suggestive of), infiltrative diseases (eg hemochromatosis- he had normal iron study, Wilson disease- normal copper level, granulomas- contrary he had low 1,25 Di OH vit D). Hypocalcemia secondary to genetic parthyroid gland anomaly was thought to be most likely in our patient. So FISH was pursued. Conclusion: For patients with cognitive issues, persistence of chronic hypocalcemia (with low PTH) despite treatment should prompt for genetic disorders like DiGeorge. DiGeorge is usually the diagnosis of children. Perhaps this is the first case of DiGeorge diagnosed so late at age of 41.
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