An Unexpected Presentation of Serotonin Syndrome in a Patient Receiving ECT.

Serotonin syndrome is a toxidrome consisting of autonomic instability, altered mentation, hyperreflexia, clonus, and seizures. It is suspected to be due to either elevated serotonin concentrations or overstimulation of 5-hydroxytryptamine (5-HT) receptors. There are at least seven families of serotonin or 5-HT receptors along with multiple subtypes. The 5-HT1A and 5-HT2A serotonin receptor subtypes are heavily suspected to cause the broad spectrum of symptoms seen in serotonin syndrome. We present the case of a young woman treated with multiple psychotropic medications who developed serotonin syndrome (SS) after receiving electroconvulsive therapy (ECT). She had multiple psychiatric hospitalizations, and ECT was determined to be the appropriate course of treatment due to her treatment-resistant symptoms and catatonia. The case was unique as she tolerated multiple ECT treatments over a few weeks before the acute onset of serotonin syndrome following her eighth treatment, and she did not have any medication changes after the second ECT treatment. The patient's acute presentation of rigidity, elevated temperature, hyperreflexia, diaphoresis, confusion, and psychomotor agitation led to a diagnosis of serotonin syndrome. ECT is a neuromodulatory procedure approved for treatment-resistant depression and schizophrenia that involves electrically stimulating the brain with electrodes on the scalp to induce a seizure. The mechanism by which ECT confers therapeutic benefit for patients with neuropsychiatric conditions is not entirely understood. We discuss some of the literature on SS and ECT to better understand the potential for a causal relationship.

A Smooth Transition: Assessing Transition Readiness in Adolescents with Inflammatory Bowel Disease.

BACKGROUND: Inflammatory Bowel Disease (IBD) is an early onset condition that affects individuals of all ages. Approximately 15%-25% of patients present before the age of 20 years, with peak onset occurring during adolescence. AIMS: To evaluate transition readiness among adolescents diagnosed with IBD and identify barriers to transition. METHODS: We conducted a cross-sectional study of patients with IBD aged 12-21 years. Patients were stratified by age into three groups: A (12-14 years), B (14-17 years), and C (17 + years). Patients were asked to complete a questionnaire which assessed patient knowledge in three areas of transition: 'Taking Charge,' 'My Health,' and 'Using Health Care.' Fisher's Exact and Chi-Square tests were used to evaluate the associations between age and transition readiness. RESULTS: A total of 127 participants (68 males and 59 females) with a mean age of 16.14 years were included. Transition readiness increased with age from 60.7% in Group A to 63.2% and 77.9% in Groups B and C, respectively (p < 0.001). Patient confidence and the importance of transition increased with age, with means of 5.51, 6.17, and 6.94 in Groups A, B, and C (p = 0.02). Patient-reported knowledge of their health condition was > 70%, with no statistical differences between the groups (p = 0.65). Patient knowledge regarding 'Using Health Care' increased from 52% in Group A to 79% in Group C (p < 0.001). The greatest barriers to transitioning were carrying health information for Group A (100%) and obtaining provider referrals for Groups B (75%) and C (51%). CONCLUSION: This study demonstrated that transition readiness increases with age in adolescents with IBD.

Retroperitoneal liposarcoma: Case of a giant tumour inside the abdomen.

Retroperitoneal liposarcomas are rare malignant tumours that often grow rapidly in size and become symptomatic lat e in t he disease course, posing diagnostic a nd therapeutic challenges. Although abdominal imaging can rel iab ly diagnose the tumour, definitive diagnosis is only p ossib le th rough bio psy af ter surgical excision , w hich remains the primary treatment modality for these tumours. Long- term sur v ival is p rimarily determ ined throu gh histologic grade and post-resection tumour margins. We report t he case of a 43-year-o ld male patient, see n at Dr Ruth KM Pfau Hospital Karachi, who under went successful surgical excision for a well-differentiated retroperitoneal liposarcoma an d had no rad io gr aphic evidence o f local recurrence at both 3 and 12-month follow-ups.

Effects of colchicine in adults with metabolic syndrome: A pilot randomized controlled trial.

AIM: To evaluate the efficacy and safety of colchicine for improving metabolic and inflammatory outcomes in people with obesity and metabolic syndrome (MetS). MATERIALS AND METHODS: Adults with obesity and MetS, but who did not have diabetes, were randomized to colchicine 0.6 mg or placebo capsules twice daily for 3 months. The primary outcome was change in insulin sensitivity (SI ) as estimated by insulin-modified frequently sampled intravenous glucose tolerance tests. Secondary outcomes included changes in other metabolic variables and inflammatory markers. RESULTS: Of 40 participants randomized (21 colchicine, 19 placebo), 37 completed the trial. Compared with placebo, colchicine significantly reduced C-reactive protein (P <0.005), erythrocyte sedimentation rate (P <0.01), white blood cell count (P <0.005), and absolute neutrophil count (P <0.001). Change in SI was not significantly different between colchicine and placebo arms (difference: +0.21 × 10-5 ; CI -1.70 to +2.13 × 10-5 min-1 mU-1 mL; P = 0.82). However, changes in some secondary outcomes, including homeostatic model assessment of insulin resistance (P = 0.0499), fasting insulin (P = 0.07) and glucose effectiveness (P = 0.08), suggested metabolic improvements in the colchicine versus placebo group. Adverse events were generally mild and similar in both groups. CONCLUSIONS: This pilot study found colchicine significantly improved obesity-associated inflammatory variables and showed a good safety profile among adults with obesity and MetS who did not have diabetes. These results suggest a larger, adequately powered study should be conducted to determine whether colchicine improves insulin resistance and other measures of metabolic health in at-risk individuals.

Anti-Thyroid Peroxidase Reactivity Is Heightened in Pemphigus Vulgaris and Is Driven by Human Leukocyte Antigen Status and the Absence of Desmoglein Reactivity.

Pemphigus vulgaris (PV) belongs to an autoimmune disease cluster that includes autoimmune thyroid disease (AITD), suggesting common mechanisms driving autoimmune susceptibility. Our group has shown that PV patients exhibit significant reactivity to AITD-related anti-thyroid peroxidase (anti-TPO), and anti-TPO antibodies affect signaling pathways in keratinocytes similar to anti-desmoglein (Dsg) 3 antibodies. To further assess the relevance of anti-TPO reactivity in PV, we analyzed anti-TPO levels in 280 PV and 167 healthy control serum samples across a comprehensive set of variable and static parameters of disease activity and etiopathogenesis. PV patients have significantly higher activity rates (A.R.s) for anti-TPO than healthy controls, but levels do not differ between phases of clinical activity and remission. Patients that carry both the PV-associated human leukocyte antigen (HLA) alleles DRB1*0402 and DQB1*0503, or DQB1*0503 alone show a low prevalence of anti-TPO (A.R. 9.5 and 4.8%, respectively), while patients that lack expression of these alleles or carry DRB1*0402 alone have a much higher prevalence of anti-TPO (A.R. 23.1 and 15.8%, respectively), suggesting that the absence of DQB1*0503 may predispose patients to the development of anti-TPO antibodies. Similarly, anti-Dsg1-/3- patients have a higher anti-TPO A.R. (26.9%) than anti-Dsg1-/3+ (18.8%), anti-Dsg1+/3- (14.3%), and anti-Dsg1+/3+ (3.9%) patients. Our data suggest that anti-TPO reactivity in PV is driven by genetic markers that may be in linkage disequilibrium with the established PV-susceptibility alleles and that this association drives the selection of a combination of anti-Dsg and anti-TPO antibodies, with anti-TPO filling the gap in active patients that do not carry the established PV-associated autoantibodies and/or are lacking the established PV-HLA-susceptibility alleles.