Intersecting Pathways: Nonalcoholic Fatty Liver Disease and Psoriasis Duet-A Comprehensive Review.

Psoriasis is a chronic, immune-mediated, inflammatory disease that has a major impact on patients' quality of life. Common psoriasis-associated comorbidities include cardiovascular diseases, psoriatic arthritis, inflammatory bowel syndromes, type-2 diabetes, and metabolic syndrome. Nonalcoholic fatty liver disease (NAFLD) is affecting a substantial portion of the population and is closely linked with psoriasis. The interplay involves low-grade chronic inflammation, insulin resistance, and genetic factors. The review presents the pathophysiological connections between psoriasis and nonalcoholic fatty liver disease, emphasizing the role of cytokines, adipokines, and inflammatory cascades. The "hepato-dermal axis" is introduced, highlighting how psoriatic inflammation potentiates hepatic inflammation and vice versa. According to the new guidelines, the preliminary examination for individuals with psoriasis should encompass evaluations of transaminase levels and ultrasound scans as part of the initial assessment for this cohort. Considering the interplay, recent guidelines recommend screening for NAFLD in moderate-to-severe psoriasis cases. Treatment implications arise, particularly with medications impacting liver function. Understanding the intricate relationship between psoriasis and NAFLD provides valuable insights into shared pathogenetic mechanisms. This knowledge has significant clinical implications, guiding screening practices, treatment decisions, and the development of future therapeutic approaches for these chronic conditions.

COVID-19 infection: from stress-related cortisol levels to adrenal glands infarction.

Cortisol is a key element in acute stress including a severe infection. However, in coronavirus-associated disease, 20% of subjects experience hypocortisolemia due to direct or immune damage of pituitary and adrenal glands. One extreme form of adrenal insufficiency is found in 2∕3 of cases with viral and post-viral adrenal infarction (AI) (with∕without adrenal hemorrhage) that is mostly associated with a severe coronavirus disease 2019 (COVID-19) infection; it requires prompt glucocorticoid intervention. Some reports are incidental findings at computed tomography (CT)∕magnetic resonance imaging (MRI) scans for non-adrenal complications like pulmonary spreading and others are seen on post-mortem analysis. This is a review of PubMed-accessible, English papers focusing on AI in addition to the infection, between March 1, 2020 and November 1, 2021. Exclusion criteria were acute adrenal insufficiency without the histopathological (HP) and∕or imaging report of adrenal enlargement, necrosis, etc., respective adrenal failure due to pituitary causes, or non-COVID-19-related adrenal events. We identified a total of 84 patients (different levels of statistical evidence), as follows: a retrospective study on 51 individuals, two post-mortem studies comprising nine, respectively 12 patients, a case series of five subjects, seven single-case reports. HP aspects include necrosis associated with ischemia, cortical lipid degeneration (+/- focal adrenalitis), and infarcts at the level of adrenal cortex, blood clot into vessels, acute fibrinoid necrosis in arterioles and capsules, as well as subendothelial vacuolization. Collateral potential contributors to adrenal damage are thrombotic events, coagulation anomalies, antiphospholipid syndrome, endothelial dysfunction, severe COVID-19 infection with multiorgan failure, etc. Clinical picture is variable from acute primary adrenal insufficiency to asymptomatic or mild evolution, even a retrospective diagnostic; it may be a part of long COVID-19 syndrome; glucocorticoid therapy for non-adrenal considerations might mask cortisol deficient status due to AI∕hemorrhage. Despite its rarity, the COVID-19-associated AI/hemorrhage represents a challenging new chapter, a condition that is essential to be recognized due to its gravity since prompt intervention with glucocorticoid replacement is lifesaving.

The New Entity of Subacute Thyroiditis amid the COVID-19 Pandemic: From Infection to Vaccine.

This is a review of full-length articles strictly concerning subacute thyroiditis (SAT) in relation to the SARS-CoV-2 virus infection (SVI) and COVID-19 vaccine (COV) that were published between the 1st of March 2020 and the 21st of March 2022 in PubMed-indexed journals. A total of 161 cases were reported as follows: 81 cases of SAT-SVI (2 retrospective studies, 5 case series, and 29 case reports), 80 respective cases of SAT-COV (1 longitudinal study, 14 case series, 17 case reports; also, 1 prospective study included 12 patients, with 6 patients in each category). To our knowledge, this represents the largest cohort of reported cases until the present time. SAT-SVI was detected in adults aged between 18 and 85 years, mostly in middle-aged females. SAT-COVID-19 timing classifies SAT as viral (synchronous with infection, which is an original feature of SATs that usually follow a viral infection) and post-viral (during the recovery period or after infection, usually within 6 to 8 weeks, up to a maximum 24 weeks). The clinical spectrum has two patterns: either that accompanying a severe COVID-19 infection with multi-organ spreading (most frequent with lung involvement) or as an asymptomatic infection, with SAT being the single manifestation or the first presentation. Either way, SAT may remain unrecognized. Some data suggest that more intense neck pain, more frequent fever, and more frequent hypothyroidism at 3 months are identified when compared with non-SAT-SVI, but other authors have identified similar presentations and outcomes. Post-COVID-19 fatigue may be due to residual post-SAT hypothyroidism. The practical importance of SAT-SVI derives from the fact that thyroid hormone anomalies aggravate the general status of severe infections (particular concerns being tachycardia/arrhythmias, cardiac insufficiency, and ischemic events). If misdiagnosed, SAT results in unnecessary treatment with anti-thyroid drugs or even antibiotics for fever of unknown cause. Once recognized, SAT does not seem to require a particular approach when compared with non-COVID-19 cases, including the need for glucocorticoid therapy and the rate of permanent hypothyroidism. A complete resolution of thyroid hormone anomalies and inflammation is expected, except for cases with persistent hypothyroidism. SAT-COV follows within a few hours to a few weeks, with an average of 2 weeks (no particular pattern is related to the first or second vaccine dose). Pathogenesis includes molecular mimicry and immunoinflammatory anomalies, and some have suggested that this is part of ASIA syndrome (autoimmune/inflammatory syndrome induced by adjuvants). An alternative hypothesis to vaccine-related increased autoimmunity is vaccine-induced hyperviscosity; however, this is supported by incomplete evidence. From what we know so far concerning the risk factors, a prior episode of non-SVI-SAT is not associated with a higher risk of SAT-COV, nor is a previous history of coronavirus infection by itself. Post-vaccine SAT usually has a less severe presentation and a good outcome. Generally, the female sex is prone to developing any type of SAT. HLA susceptibility is probably related to both new types of SATs. The current low level of statistical evidence is expected to change in the future. Practitioners should be aware of SAT-COV, which does not restrict immunization protocols in any case.

Association between genetic variants and depression in a Romanian cohort.

Major depressive disorder (MDD) is beyond doubt a common, disabling, and costly condition. MDD associates hypothalamic-pituitary-adrenal (HPA) axis alterations. We sought to investigate two candidate variants which could have a role in the genetic susceptibility for stress or corticoid-induced MDD: glucocorticoid receptor (GR) - nuclear receptor subfamily 3 group C member 1 (NR3C1) rs41423247 and brain-derived neurotrophic factor rs6265 BDNF:c.442G>A Val66Met. We enrolled 82 Romanian subjects, 1:2 male to female ratio, 53.54±8.98 years old, diagnosed with an episode of major depression at the Clinical Neuropsychiatry Hospital in Craiova, Romania, and 286 healthy controls, 34.28±16.34 years old. All subjects were genotyped using specific ThermoFisher Scientific assays on a ViiA™ 7 real-time polymerase chain reaction (PCR) system. The impact of certain genetic variants may be ethnic-specific. In our Romanian cohort, rs41423247 NR3C1:c.1184+646C>G has a minor allele frequency of 29.2%, and rs6265 BDNF:c.442G>A of 22.2%. Neither reached significance in our study, under any of the association models - dominant, recessive, or allelic. Interpretation of our negative findings requires caution: literature provides arguably more evidence for the association between the analyzed polymorphisms; our study has sample size challenges, from which refined phenotyping limitations derive.

TSH and T4 Levels in a Cohort of Depressive Patients.

Depression is a significant contributor to the overall burden of disease on a global scale. Thyroid hormones thyroxine (T4) and triiodothyronine (T3) have been shown to play a critical role in the development and normal function of the brain. It has been suggested that dysregulation of thyroid function could be associated with depression, especially hypothyroidism, but not all studies support this hypothesis. We enrolled a cohort of 96 subjects with major depressive disorder and tested TSH and FT4 levels for 80 of them in order to assess the status of the hypothalamic-pituitary-thyroid axis (HPT). We found 7 cases (8.75% of the tested) of subclinical hyperthyroidism and 1 case (1.25%) of overt hyperthyroidism. While we did not find supporting evidence for association between TSH and FT4 levels and depression, our findings question whether screening depressive patients for HPT axis anomalies could be clinically relevant, if anything, in a regional context.

Circulating Cortisol in a Cohort of Depressive Patients.

It has long been suspected that the hypothalamic pituitary adrenal (HPA) axis plays a role in the pathophysiology of depression. Whether this association exists or not, and if it does, the degree of its significance, remain highly disputed. The issue is further complicated as no consensus currently exists on cortisol sampling timepoints or methods. Our study aimed to evaluate HPA functionality by evaluating plasma cortisol levels in a cohort of patients diagnosed with Major Depressive Disorder (MDD). We enrolled 96 subjects admitted for a major depressive episode and tested serum cortisol levels for 80 of them. We found that only 15 (12%) had values that were outside the normal reference range, with 14 of these being below the normal threshold. We also interviewed the patients and obtained self-reported information regarding previous depressive episodes, treatment administration, anxiety, suicidal ideas and suicidal gestures. Our study did not find a significant association between cortisol levels and the number of previous depressive episodes, the presence of feelings of anxiety, suicidal ideas or suicidal gestures. While our cohort did not find an association between cortisol levels and depression other authors have reported significantly different results and as such, more research is needed in order to establish or infirm this hypothesis.