Drug-induced Causes Research Articles

Study the Effect of IL-1beta on Thyroid Hormones Levels in Women with Hypo- and Hyperthyroidism in the City of Ramadi

Thyroiditis is a medical condition of particular concern due to its diverse causes, including autoimmune factors, drug-induced inflammatory causes or fibrotic process, the most common of which is thyroiditis and includes hypothyroidism and hyperthyroidism. The study aimed to measure interleukin 1 beta (IL-1β) and compare it with the studied groups and the hormones TSH, T3, T4 and their relationship with IL-1β. The study included investigating the relationship between IL-1β and thyroid patients in females aged between (18-60) in the city of Ramadi as well as knowing the relationship between thyroid hormones (TSH, T4, T3) and IL-1β. 45 samples were collected from Ramadi Teaching Hospital. The current study showed that there was a significant increase in the level of IL-1β compared to the control group in hypothyroid patients at a significant level (P≤0.05), which was (2.3497ng/dl). There were no significant differences in the level of IL-1β in patients with hyperthyroidism at a significant level (P≤0.05), which was (ng/dl 2.0690) compared to the control group. The study showed that there is an inverse relationship between TSH and IL-1β (0.858) and a positive relationship between T4 and IL-1β (0.809) .We conclude from the study that interleukin 1 beta (IL-1β) has an effect on the thyroid gland, especially hypothyroidism, as it showed a highly significant increase in IL-1β in patients with hypothyroidism and no significant differences in IL-1β, as IL-1β affects thyroid hormones

Mortality in women with a history of incarceration in Norway: a 20-year national cohort study.

Women carry a substantial burden of psychiatric, somatic and lifestyle-related morbidity in the prison context. By describing causes of death and estimating the risk and burden of mortality compared with the general population, this study investigates how mortality operates in this highly marginalized and under-researched population. In this registry-based study of all women incarcerated in Norwegian prisons from 2000 to 2019 (N = 11 313), we calculated crude mortality rates, years of lost life and, by using mortality in age-matched women from the general population as a reference, age-standardized mortality ratios and years of lost life rates. Over a mean follow-up time of 10.7 years, at a median age of 50years, 9% of the population had died (n = 1005). Most deaths (80%) were premature deaths from an avoidable cause. Drug-induced causes and deaths from major non-communicable diseases (NCDs) were most frequent (both 32%). Compared with women in the general population, women with a history of incarceration were more likely to die from any cause. Trends in annual age-standardized years of lost life rates suggest that the mortality burden associated with major NCDs has gradually replaced drug-induced causes. Women with a history of incarceration die at a greater rate than their peers and largely from avoidable causes. The profile of causes contributing to the substantial burden of mortality placed on this population has changed over time and has important implications for future efforts to reduce morbidity and the risk of premature death following release from prison.

A stroke patient with persistently intermittent fever treated with gabapentin: A clinical case.

Fever is one of the most common complications in stroke patients and can generally be classified as either infectious or non-infectious. Infectious fevers are commonly caused by pulmonary infections, urinary tract infections, and secondary infections associated with medical interventions such as endotracheal intubation, urinary catheterization, and nasogastric tubes. Non-infectious fevers primarily manifest as central fevers, although in rare cases, they may also result from drug-induced causes. Existing research indicates that the most common cause of central fever is brainstem hemorrhage, followed by hemorrhage in the basal ganglia and thalamus, then cerebellar hemorrhage, large cortical infarction, and basilar artery occlusion, with intraventricular hemorrhage being relatively rare. Stroke patients' body temperatures can rise to 39°C within 12 hours after onset and peak within 24 hours. In this case, a stroke patient with acute cerebral infarction and secondary thalamic hemorrhage developed new sensory abnormalities in the left limbs and intermittent fever during hospitalization. Despite the use of antibiotics targeting a pulmonary infection, the patient's fever did not show significant improvement. Gabapentin was added to the treatment regimen to address the sensory abnormalities. Surprisingly, within four hours of gabapentin administration, the patient's body temperature normalized and remained stable during subsequent monitoring. This observation led us to hypothesize that gabapentin may have a potential role in alleviating central fever.

Acute bilateral toxic endothelitis in binge alcohol consumption – A case series

Endothelitis has a vast range of etiologies, including infective, chemical-induced, drug-induced, systemic, and toxic causes. Toxic endothelitis secondary to alcohol binge consumption is rare and is reported less frequently in the literature. We report a series of three cases with bilateral defective vision due to corneal edema and endothelitis following binge alcohol consumption. All cases showed dramatic improvement with frequent topical steroid application alone. We hypothesize the cause for corneal edema as transient suppression of corneal endothelial cell metabolism rather than apoptosis, with later regain of functions following alcohol cessation and control of further inflammatory insults with intensive steroids.

Clinical management of nonobstructive azoospermia: An update.

Approximately 1% of the general male population has azoospermia, and nonobstructive azoospermia accounts for the majority of cases. The causes vary widely, including chromosomal and genetic abnormalities, varicocele, drug-induced causes, and gonadotropin deficiency; however, the cause is often unknown. In azoospermia caused by hypogonadotropic hypogonadism, gonadotropin replacement therapy can be expected to produce sperm in the ejaculate. In some cases, upfront varicocelectomy for nonobstructive azoospermia with varicocele may result in the appearance of ejaculated spermatozoa; however, the appropriate indication should be selected. Each guideline recommends microdissection testicular sperm extraction for nonobstructive azoospermia in terms of successful sperm retrieval and avoidance of complications. Sperm retrieval rates generally ranged from 20% to 70% but vary depending on the causative disease. Various attempts have been made to predict sperm retrieval and improve sperm retrieval rates; however, the evidence is insufficient. Further evidence accumulation is needed for salvage treatment in cases of failed sperm retrieval. In Japan, there is inadequate provision on the right to know the origin of children born from artificial insemination of donated sperm and the rights of sperm donors, as well as information on unrelated family members, and the development of these systems is challenging. In the future, it is hoped that the pathogenesis of nonobstructive azoospermia with an unknown cause will be elucidated and that technology for omics technologies, human spermatogenesis using pluripotent cells, and organ culture methods will be developed.

Abstract #1406613: Recurrent Thyroiditis in a Patient with Multiple sclerosis on Natalizumab

Thyroiditis, or self-limiting inflammation of the thyroid gland consists of 3 phases: hyperthyroidism, from release of hormone from damaged cells; hypothyroidism, when thyroid stores are depleted and euthyroidism with restoration of thyroid function. Etiology can include infectious, drug-induced or autoimmune causes such as multiple sclerosis (MS). In fact, 20-25% of untreated MS patients have autoimmune thyroiditis [1]. Moreover, drugs used to treat MS such as alemtuzumab and interferon have been reported to cause thyroid disease [2]. A 42-year-old female with MS on natalizumab for 10 years presented with right sided neck pain radiating to her jaw for 3 months and difficulty swallowing. Family history was pertinent for hypothyroidism in her father, and MS in her brother. She was exposed to nuclear radiation at age 3 from the Chernobyl disaster. On presentation, vital signs and physical exam were unremarkable. Thyroid ultrasound noted an ill-defined 4.2X1.3X1.9 cm hypoechoic nodule in the right mid-pole. Fine needle aspiration of the nodule showed subacute granulomatous thyroiditis (SAH). Labs showed TSH 0.02mIU/L [0.4-4.5], FT4 1.5ng/dL [0.8-1.8] and elevated total T3 204ng/dL [76-181]. TSI< 89 [140%]. Naproxen was given for pain control. Repeat labs 1 month later showed TSH 0.83mIU/L, FT4 1.1 ng/dL and total T3 196ng/dL, consistent with resolution of thyroiditis and clinically correlated with resolution of her pain. However, a month later she presented with worsening left sided neck pain and left thyromegaly associated with speech difficulty, diaphoresis, and constipation. Repeat thyroid ultrasound showed decreased size of right thyroid nodule 1.1X1.1X0.9cm and findings consistent with thyroiditis. She was treated with prednisone with complete resolution of symptoms. Labs post treatment showed elevated TSH 6.01mIU/L, total T3 106ng/dL, and FT4 0.8ng/dL consistent with the recovery phase of thyroiditis. Anti-TPO antibody level was < 1 [< 9 IU/mL]. Labs 1 month later showed normal TSH and FT4 levels. Natalizumab, a humanized monoclonal antibody commonly used to treat MS, has rarely been associated with thyroid disease. Alterations in thyroid function are thought to be due to direct toxicity on the thyroid, its blood supply or indirectly mediated by the immune system [2]. Although MS can be associated with thyroiditis, our patient did not present with the typical pattern of thyroiditis. Instead, she reported symptoms consistent with inflammation of one lobe of thyroid followed by resolution, and thereafter developed inflammation and pain of the other lobe, raising suspicion of potential involvement of natalizumab due to her atypical presentation.

A review on drug-induced dry eye disease.

Dry eye disease encompasses a broad range of etiologies and disease subtypes which have similar clinical manifestations. Medications can cause dry eye disease or symptoms of dryness as a side effect by either interfering with the lacrimal gland or meibomian gland function, or both, and by other mechanisms that affect the ocular surface homeostasis. This is important to know and recognize as eliminating the offending medication can reverse the symptoms and, in many cases, prevent further deterioration of the ocular surface inflammation. This review focuses on drugs like systemic isotretinoin and taxanes, which cause meibomian gland dysfunction; immune checkpoint inhibitors that cause lacrimal gland dysfunction; gliptins and topical antiglaucoma medications that cause cicatrizing conjunctivitis; and epidermal growth factor receptor inhibitors, fibroblast growth factor receptor inhibitors, and belantamab mafodotin, which cause mucosal epitheliopathy. Many of these medications, particularly the newer anticancer agents, have only recently been introduced for clinical use, and knowledge and awareness of their ocular side effects are still evolving. This review aims to update ophthalmologists on the drug-induced causes of dry eye disease or symptoms of dryness, which is avoidable by discontinuation of the incriminating agent or can be mitigated by reducing the dose or frequency of usage.

Medical Therapy and Scleral Windows for Uveal Effusion Syndrome: A Case Series and Literature Review.

Uveal effusion syndrome (UES) is arare ocular disease causing idiopathic uveal effusion, often with associated ciliochoroidal and retinal detachment. UES diagnosis is challenging because of overlapping features with other ocular inflammatory, neoplastic, iatrogenic, and drug-induced causes of uveal effusion. While several successful surgical treatments have been described, such as full-thickness or partial-thickness sclerectomy, medical therapies may also have a therapeutic role. To provide an updated review of the published literature on the course of the disease, medical and surgical management strategies, as well as newer treatment modalities.

S2167 Chronic, Massive Pneumoperitoneum in a Patient Without Signs of Peritonitis: A Case Report

Introduction: Pneumoperitoneum is the presence of free air in the abdominal cavity. This alarming symptom can be due to a wide variety of etiologies, including infection, trauma, perforation, and others. However, pneumatosis intestinalis, which is the presence of free air in the extraluminal space, can be due to other pathology unrelated to the GI tract. It can be seen in pulmonary disease, such as COPD and asthma, autoimmune conditions, and drug-induced causes as well. It can present with more benign symptoms. We present a case of chronic pneumatosis intestinalis that was present in the patient for over 2 years and presented with relatively minor, nonspecific symptoms. Case Description/Methods: This patient was a 62-year-old male who presented with concerns of bloating and cramping, ongoing for 2 years. Previous work-ups had not revealed a clear cause for his ongoing symptoms. He had undergone CT of the abdomen, which was significant for massive pneumoperitoneum, as well as fluid-filled prominent loops of small bowel concerning for ileus or obstruction. There was no site of bowel perforation that could be visualized. Upper endoscopy and colonoscopy had been performed, which showed normal mucosa and colonic diverticulosis. After further workup at an additional institution, diagnostic laparotomy was recommended to further evaluate his small bowel. At the lower anterior diaphragm, the peritoneal surface had subperitoneal emphysema, suggesting a potential thoracic source for the pneumoperitoneum. Thoracic surgery were consulted for exploratory right-sided thoracoscopy since he was noted to have peritoneal blebs along the diaphragm most notably, with one also being identified on the liver. It was concluded that the etiology was most likely due to an alveolar-peritoneal fistula through the right hemidiaphragm (Figure). Discussion: Pneumatosis Intestinalis can be a benign presenting symptom. Pneumoperitoneum can be due to primary (idiopathic) or secondary causes. Secondary causes are numerous, and these can be seen in the setting of COPD, immunodeficiency, or acute GI pathology. Increased pressure in the abdomen or the mediastinum can result in gas diffusing across tissues and into the bowel wall. Treatment and management varies depending on the patient's presentation. More serious abdominal pathology requires surgical management, while benign causes in the setting of chronic lung pathology can be asymptomatic, or present with mild symptoms that require only conservative medical management.Figure 1.: Pneumatosis Intestinalis on CT Scan.

Mortality, Causes of Death, and Predictors of Death among Patients On and Off Opioid Agonist Treatment: Results from a 19-Year Cohort Study

Background: Mortality is increased among people with opioid use disorder but reduced while on opioid agonist treatment (OAT). However, the impact of patient and treatment characteristics on mortality and causes of death is insufficiently studied. Objectives: The objective of this study was to explore mortality and causes of death and examine the impact of patient and treatment characteristics on mortality in an OAT cohort with high retention in treatment. Methods: Design: longitudinal cohort study. Setting: Norway. Observation period: time from OAT start as of 1998 until death or end of 2016, 2,508 person-years (PY) in total. Sample: 200 persons starting OAT 1998–2007. Data sources: hospital records, interviews, the Norwegian Cause of Death Registry, Statistics Norway. Results: Retention: 86.4% of the observation period was on OAT, 9.0% off, 4.6% unknown OAT status. All-cause crude mortality rate per 100 PY during the whole observation period was 1.64 (95% CI: 1.19–2.20), for deaths of somatic cause 0.88 (0.56–1.31), for drug-induced deaths 0.44 (0.23–0.76), and traumatic deaths 0.24 (0.10–0.50). Off-versus-on-OAT all-cause mortality ratio was 2.31 (1.00–4.85). On OAT, 58% of the deaths were of somatic cause and 21% drug-induced; off OAT, 38% of somatic cause and 50% drug-induced. Increasing baseline age and rate of somatic hospital treatment episodes were independently associated with increased all-cause mortality risk, while increasing rate of in-patient psychiatric treatment episodes was associated with reduced risk. Increasing duration of nicotine and cannabis use and alcohol dependence as well as increasing severity of polydrug use were associated with increased all-cause and somatic mortality adjusted for age and sex. Conclusion: The long observation period made it possible to demonstrate the importance of long-term retention in OAT to reduce mortality. Further, the preponderance of somatic and reduction of drug-induced causes of death during OAT underlines the need for follow-up of chronic diseases and health-promoting lifestyle changes. These findings add to the knowledge about long-term OAT effects, not least in ageing OAT populations.

IOIBD Recommendations for Clinical Trials in Ulcerative Proctitis: The PROCTRIAL Consensus

Clinical trials evaluating biologics and small molecules in patients with ulcerative colitis are predominantly excluding ulcerative proctitis. The objective of the Definition and endpoints for ulcerative PROCtitis in clinical TRIALs initiative was to develop consensus statements for definitions, inclusion criteria, and endpoints for the evaluation of ulcerative proctitis in adults. Thirty-five international experts held a consensus meeting to define ulcerative proctitis, and the endpoints to use in clinical trials. Based on a systematic review of the literature, statements were generated, discussed, and approved by the working group participants using a modified Delphi method. Consensus was defined as at least 75% agreement among voters. The group agreed that the diagnosis of ulcerative proctitis should be made by ileocolonoscopy and confirmed by histopathology, with the exclusion of infections, drug-induced causes, radiation, trauma, and Crohn's disease. Ulcerative proctitis was defined as macroscopic extent of lesions limited to 15 cm distance from the anal verge in adults. Primary and secondary endpoints were identified to capture response of ulcerative proctitis to therapy. A combined clinical and endoscopic primary endpoint for the evaluation of ulcerative proctitis disease activity was proposed. Secondary endpoints that should be evaluated include endoscopic remission, histologic remission, mucosal healing, histologic endoscopic mucosal improvement, disability, fecal incontinence, urgency, constipation, and health-related quality of life. In response to the need for guidance on the design of clinical trials in patients with ulcerative proctitis, the Definition and end points for ulcerative PROCtitis in clinical TRIALs consensus provides recommendations on the definition and endpoints for ulcerative proctitis clinical trials.

The Young were not Spared: What Death Certificates Reveal about Non-Covid Excess Deaths.

From April 2020 through at least the end of 2021, Americans died from non-Covid causes at an average annual rate of 97 000 in excess of previous trends. Hypertension and heart disease deaths combined were elevated 32 000. Diabetes or obesity, drug-induced causes, and alcohol-induced causes were each elevated 12 000 to 15 000 above previous (upward) trends. Drug deaths especially followed an alarming trend, only to significantly exceed it during the pandemic to reach 108 000 for calendar year 2021. Homicide and motor-vehicle fatalities combined were elevated almost 10 000. Various other causes combined to add 18 000. While Covid deaths overwhelmingly afflict senior citizens, absolute numbers of non-Covid excess deaths are similar for each of the 18 to 44, 45 to 64, and over-65 age groups, with essentially no aggregate excess deaths of children. Mortality from all causes during the pandemic was elevated 26% for working-age adults (18-64), as compared to 18% for the elderly. Other data on drug addictions, non-fatal shootings, weight gain, and cancer screenings point to a historic, yet largely unacknowledged, health emergency.

C95. The electrocardiographic changes in a hypertensive COVID-19 patient who received beta-blocker and favipiravir: a case report

BackgroundVarious electrocardiographic manifestations have been reported in COVID-19 which either result from myocarditis or insult-induced re-emerging of pre-existing condition. Some antiviruses used off-labelly for COVID-19, including favipiravir, are considered to be proarrhythmic. Meanwhile, anti-hypertensive drugs such as beta-blocker may induce bradyarrhythmia.Case SummaryA 69-year-old male with confirmed COVID-19 and a history of uncontrolled hypertension presented with blood pressure of 216/111mmHg at admission. No sign and symptom of acute target organ damage had been reported. His electrocardiography showed normal sinus rhythm (heart rate [HR] 60bpm). The echocardiographic finding revealed normal heart function. He received favipiravir for 5 days, intravenous nicardipine (0.5mcg/kgBW/hour), and peroral amlodipine (1x10mg), candesartan (1x16mg), and bisoprolol (1x2.5mg). During hospitalization, the HR fluctuated between 52-109. On the sixth day, a total atrioventricular (AV) block with junctional escape rhythm (HR 66bpm) was present. Both favipiravir and bisoprolol were ceased simultaneously. The AV block persisted for 4 days then transformed into a junctional rhythm for the next 3 days and sinus bradycardia (HR 48bpm) thereafter. No pacing was performed.DiscussionThe possible differential diagnoses in this case include sick sinus syndrome (SSS), COVID-19-induced myocarditis, and drug-induced. The SSS might explain the wide variability of the HR. There were some reports presenting the sinus node dysfunction as a manifestation of SARS-CoV-2 infection. Further evaluation using Holter and/or electrophysiological study is warranted. Drug-induced cause may be excluded because the bradyarrhythmia remained after the cessation of both beta-blocker and favipiravir.

C95. The electrocardiographic changes in a hypertensive COVID-19 patient who received beta-blocker and favipiravir: a case report

BackgroundVarious electrocardiographic manifestations have been reported in COVID-19 which either result from myocarditis or insult-induced re-emerging of pre-existing condition. Some antiviruses used off-labelly for COVID-19, including favipiravir, are considered to be proarrhythmic. Meanwhile, anti-hypertensive drugs such as beta-blocker may induce bradyarrhythmia.Case SummaryA 69-year-old male with confirmed COVID-19 and a history of uncontrolled hypertension presented with blood pressure of 216/111mmHg at admission. No sign and symptom of acute target organ damage had been reported. His electrocardiography showed normal sinus rhythm (heart rate [HR] 60bpm). The echocardiographic finding revealed normal heart function. He received favipiravir for 5 days, intravenous nicardipine (0.5mcg/kgBW/hour), and peroral amlodipine (1x10mg), candesartan (1x16mg), and bisoprolol (1x2.5mg). During hospitalization, the HR fluctuated between 52-109. On the sixth day, a total atrioventricular (AV) block with junctional escape rhythm (HR 66bpm) was present. Both favipiravir and bisoprolol were ceased simultaneously. The AV block persisted for 4 days then transformed into a junctional rhythm for the next 3 days and sinus bradycardia (HR 48bpm) thereafter. No pacing was performed.DiscussionThe possible differential diagnoses in this case include sick sinus syndrome (SSS), COVID-19-induced myocarditis, and drug-induced. The SSS might explain the wide variability of the HR. There were some reports presenting the sinus node dysfunction as a manifestation of SARS-CoV-2 infection. Further evaluation using Holter and/or electrophysiological study is warranted. Drug-induced cause may be excluded because the bradyarrhythmia remained after the cessation of both beta-blocker and favipiravir.

Acute onset hemiballismus/hemichorea due to various etiologies: A case series

Chorea is irregular, non-rhythmic, involuntary movements that can spread from one part of the body to another for a short time. Ballismus, on the other hand, is characterized with high amplitude choreic movements in the proximal extremities. The mechanism of acute hemichorea/hemiballismus has not been clearly explained. It is generally caused by lesions in the contralateral subthalamic nucleus (STN) and its afferent and efferent connections. Although vascular causes are the most common etiology, toxic-metabolic, inflammatory, infectious, demyelinating, and drug-induced causes have also been reported.

COVID-19-Induced Cardiovascular Damage Differs from other Prevalent Viruses

Viral infections persist globally, among all ages, gender, and ethnicity. Of particular importance is COVID-19, associated with asymptomatic to severe symptoms, including complications/mortality. Cardiovascular disease (CVD) involves heart and blood vessel disorders including coronary heart disease, cerebrovascular disease, peripheral artery disease, thrombosis, and more. CVD associated with severe COVID-19 includes heart failure, coronary artery disease, cardiomyopathy, hypertension, and cerebrovascular disease/stroke. Data were acquired from PubMed, Google Scholar, Centers for Disease Prevention and Control, and Lexi-Comp using the search terms “COVID-19 and cardiovascular pathology;” “COVID-19 induced CVD;” “Viral infection induced CVD;” and “Viral infection induced heart damage.” COVID-19-induced CVD mechanisms include direct viral entry, inflammation, cytokine storm, hypoxia, interferon-mediated immune response, plaque destabilization, stress, and drug-induced causes. Other viral pathologies causing CVD include atherosclerosis, inflammation, cytokine storm, and plaque destabilization. Individual parameters, such as old age, males, and higher body mass index (BMI), are more likely to experience viral-associated complications, possibly explained by patient risk factors or comorbidities. Populations at higher risk include older males with an elevated BMI. Viral mechanisms associated with CVD are similar but differ in disease severity, potentially explained by diverse cytokine profiles where COVID-19 activates different types at higher quantities.

Pseudomyopia and Its Association With Anxiety.

Pseudomyopia is an inappropriately excessive accommodation of the eye due to overstimulation or ciliary spasm, which leads to a marked approximation of the far point. Common symptoms of pseudomyopia include eye strain or fatigue, and it is classified as organic or functional. The latter is due to eye strain and functional increase in the ciliary tonus. Pseudomyopia can vary from being a transient condition or continue to progress to myopia. Head trauma is the most common cause followed by psychiatric illnesses, neurologic diseases, and drug-induced causes. There is an association between psychological stress-inducing events and pseudomyopia as it affects the autonomic nervous system. The human body counteracts anxiety by activating the parasympathetic nervous system, causing ciliary muscle contraction. Underlying psychiatric diseases in pseudomyopia patients have been reported in the past in multiple studies. Generalized anxiety disorder is the most common psychiatric illness associated with pseudomyopia with a positive correlation between anxiety-somatization scores and accommodation amount of the eye. It is strongly advised that a psychiatric consultation should be included in the multidisciplinary evaluation of every case. If patients have coexisting anxiety disorders, a multidisciplinary approach using psychiatric consultations, work environment changes, ocular exercises, and cycloplegic drugs can be used. This review aims to shed light on the association of psychiatric disorders such as anxiety with pseudomyopia.

Genetic and drug-induced hypomagnesemia: different cause, same mechanism.

Magnesium (Mg2+) plays an essential role in many biological processes. Mg2+ deficiency is therefore associated with a wide range of clinical effects including muscle cramps, fatigue, seizures and arrhythmias. To maintain sufficient Mg2+ levels, (re)absorption of Mg2+ in the intestine and kidney is tightly regulated. Genetic defects that disturb Mg2+ uptake pathways, as well as drugs interfering with Mg2+ (re)absorption cause hypomagnesemia. The aim of this review is to provide an overview of the molecular mechanisms underlying genetic and drug-induced Mg2+ deficiencies. This leads to the identification of four main mechanisms that are affected by hypomagnesemia-causing mutations or drugs: luminal transient receptor potential melastatin type 6/7-mediated Mg2+ uptake, paracellular Mg2+ reabsorption in the thick ascending limb of Henle's loop, structural integrity of the distal convoluted tubule and Na+-dependent Mg2+ extrusion driven by the Na+/K+-ATPase. Our analysis demonstrates that genetic and drug-induced causes of hypomagnesemia share common molecular mechanisms. Targeting these shared pathways can lead to novel treatment options for patients with hypomagnesemia.

Post-mortem toxicological analyses of blood samples from 107 patients receiving opioid agonist treatment: substances detected and pooled opioid and benzodiazepine concentrations.

To present the substances and their concentrations detected post-mortem in patients receiving opioid agonist treatment (OAT) stratified by cause of death, estimate the pooled opioid and benzodiazepine concentrations using established conversion factors for blood concentrations from the Norwegian Road Traffic Act, and explore the association between drug-induced cause of death and the pooled opioid and benzodiazepine concentrations. Cross-sectional nationwide study. Norway. One hundred and seven patients who died during OAT (i.e. within 5 days after the last intake of OAT medication) between 1 January 2014 and 31 December 2015, with post-mortem femoral blood available for toxicology. Data were collected from hospital records, the Norwegian Cause of Death Registry and autopsy reports. Presence of alcohol and non-alcohol substances in the bloodstream at time of death, determined through records of toxicology of post-mortem femoral blood. A median of four substances was detected across the causes of death. At least one benzodiazepine was detected in 81 (76%) patients. The median pooled opioid concentration was significantly higher in drug-induced deaths compared with other causes of death (362 ng/mL versus 182 ng/mL, P < 0.001), in contrast to the pooled benzodiazepine concentration (5466 versus 5701 ng/mL, P = 0.353). The multivariate regression analysis showed that only increasing pooled opioid concentration (ng/ML) was associated with increased odds of a drug-induced cause of death (odds ratio, 1.003; 95% confidence interval: 1.001-1.006). In Norway, overall opioid concentration seems to play an important role in drug-induced deaths during opioid agonist treatment in patients prescribed methadone or buprenorphine. Patients prescribed buprenorphine tend to replace their agonist with full agonists, while patients prescribed methadone tend to have high opioid concentrations from methadone as the only opioid.

Haemophilus influenzae Conjunctivitis Secondary to Pneumonia in the Setting of Lymphoplasmacytic Lymphoma

Haemophilus influenzae Conjunctivitis Secondary to Pneumonia in the Setting of Lymphoplasmacytic Lymphoma