Explore the vast range of titles available.

Abstract Context Subacute thyroiditis (SAT) is a thyroid disease of viral or postviral origin. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that began in Wuhan, China, has spread rapidly worldwide and Italy has been severely affected by this outbreak. Objectives The objective of this work is to report the first case of SAT related to SARS-CoV-2 infection. Methods We describe the clinical, laboratory, and imaging features of an 18-year-old woman who came to our attention for fever, neck pain radiated to the jaw, and palpitations occurring 15 days after a SARS-CoV-2–positive oropharyngeal swab. Coronavirus disease 2019 (COVID-19) had been mild and the patient had completely recovered in a few days. Results At physical examination the patient presented with a slightly increased heart rate and a painful and enlarged thyroid on palpation. At laboratory exams free thyroxine and free triiodothyronine were high, thyrotropin undetectable, and inflammatory markers and white blood cell count elevated. Bilateral and diffuse hypoechoic areas were detected at neck ultrasound. One month earlier, thyroid function and imaging both were normal. We diagnosed SAT and the patient started prednisone. Neck pain and fever recovered within 2 days and the remaining symptoms within 1 week. Thyroid function and inflammatory markers normalized in 40 days. Conclusions We report the first case of SAT after a SARS-CoV-2 infection. We alert clinicians to additional and unreported clinical manifestations associated with COVID-19.

Subacute thyroiditis (SAT) is a thyroid inflammatory disease, whose pathogenesis and determinants of the clinical course were unclear for many decades. The last few years have brought many clinically significant new data on the epidemiology, pathogenesis and management of SAT. Several human leukocyte antigen (HLA) alleles were demonstrated not only to increase the risk of SAT, but also to correlate with SAT clinical course and determine the risk of recurrence. The world-wide epidemic of the coronavirus disease 19 (COVID-19) has provided new observations that the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) can be a potent SAT-triggering factor, and that the clinical course of SAT in patients affected by COVID-19 is different from a typical one. Additionally, many new trends in the clinical course are emerging. In the last years, painless course of SAT is more and more often described, constituting a special challenge in patients hospitalized due to COVID-19. Despite an excellent availability of diagnostic methods, several difficulties in SAT differential diagnosis can be currently encountered and the proper diagnosis and treatment is frequently delayed. False positive diagnoses of SAT in patients with malignancies of poor prognosis constitute a life-threatening problem. Taking into account all the new aspects of SAT pathogenesis and of its clinical course, the new – modified – SAT diagnosis criteria have been proposed.

Background. Subacute sclerosing panencephalitis (SSPE) is a fatal complication of measles. We reviewed California cases from 1998–2015 to understand risk factors for SPPE and estimate incidence. Methods. SSPE cases had clinically compatible symptoms and measles antibody detection in cerebrospinal fluid (CSF) or medical record documentation of SSPE. Cases were identified though a state death certificate search, Centers for Disease Control and Prevention reports, or investigations for undiagnosed neurologic disease. Measles detection in CSF was performed by serology at the California Department of Public Health or at clinical laboratories. Results. Seventeen SSPE cases were identified. Males outnumbered females 2.4:1. Twelve (71%) cases had a history of measles-like illness; all 12 had illness prior to 15 months of age. Eight (67%) children were exposed to measles in California. SSPE was diagnosed at a median age of 12 years (3–35 years), with a latency period of 9.5 years (2.5–34 years). Among measles cases reported to CDPH during 1988–1991, the incidence of SSPE was 1:1367 for children <5 years, and 1:609 for children <12 months at time of measles disease. Conclusions. SSPE cases in California occurred at a high rate among unvaccinated children, particularly those infected during infancy. Protection of unvaccinated infants requires avoidance of travel to endemic areas, or early vaccination prior to travel at age 6–11 months. Clinicians should be aware of SSPE in patients with compatible symptoms, even in older patients with no specific history of measles infection. SSPE demonstrates the high human cost of \"natural\" measles immunity.

Subacute sclerosing panencephalitis (SSPE) is a chronic encephalitis occurring after infection with measles virus. The prevalence of the disease varies depending on uptake of measles vaccination, with the virus disproportionally affecting regions with low vaccination rates. The physiopathology of the disease is not fully understood; however, there is evidence that it involves factors that favour humoral over cellular immune response against the virus. As a result, the virus is able to infect the neurons and to survive in a latent form for years. The clinical manifestations occur, on average, 6 years after measles virus infection. The onset of SSPE is insidious, and psychiatric manifestations are prominent. Subsequently, myoclonic seizures usually lead to a final stage of akinetic mutism. The diagnosis is clinical, supported by periodic complexes on electroencephalography, brain imaging suggestive of demyelination, and immunological evidence of measles infection. Management of the disease includes seizure control and avoidance of secondary complications associated with the progressive disability. Trials of treatment with interferon, ribavirin, and isoprinosine using different methodologies have reported beneficial results. However, the disease shows relentless progression; only 5% of individuals with SSPE undergo spontaneous remission, with the remaining 95% dying within 5 years of diagnosis.

Abstract Context Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected more than 18 million people worldwide and the pandemic is still spreading. After the first case we reported, we observed 4 additional cases of subacute thyroiditis (SAT) related to SARS-CoV-2 infection. Objectives The objective of this work is to describe additional cases of SAT associated with SARS-CoV-2 infection to alert physicians that SAT may be a manifestation of SARS-CoV-2 infection. Methods We describe clinical, biochemical, and imaging features of 4 patients with SAT related to SARS-CoV-2 infection. Results All patients were female (age, 29-46 years). SAT developed 16 to 36 days after the resolution of coronavirus disease 2019 (COVID-19). Neck pain radiated to the jaw and palpitations were the main presenting symptoms and were associated with fever and asthenia. One patient was hospitalized because of atrial fibrillation. Thyroid function tests (available for 3 individuals) were suggestive of destructive thyroiditis, and inflammatory markers were high. At neck ultrasound the thyroid was enlarged, with diffuse and bilateral hypoechoic areas and (in 3 patients) absent vascularization at color Doppler. Symptoms disappeared a few days after commencement of treatment (prednisone in 3 patients and ibuprofen in 1). Six weeks after the onset of SAT, all patients were asymptomatic and inflammatory markers had returned to normal range. Two patients were euthyroid, whereas 2 were diagnosed with subclinical hypothyroidism. Conclusions SAT may be an underestimated manifestation of COVID-19. Clinicians should keep in mind the possible occurrence of SAT during and after SARS-CoV-2 infection.

Introduction The emergence of Subacute Thyroiditis (SAT) in the wake of COVID-19 has presented a unique set of challenges for clinicians and researchers. This study delves into the intricate interplay between COVID-19 and SAT, examining a wealth of cases from observational studies. Methods We conducted a comprehensive literature review utilizing PubMed/MEDLINE, EMBASE, and Scopus databases, encompassing studies available up to January 2, 2025. The search strategy incorporated a combination of keywords such as “Subacute Thyroiditis” and “COVID-19,” complemented by synonyms and Mesh terms. Relevant studies, investigating COVID-19-associated SAT were included. Results After a meticulous review of 964 papers, 46 records were included in the final analysis, consisting of 37 case reports and 9 case series. Our study, covered 75 individuals aged 18 to 85. Investigated patients presenting diverse symptoms, including anterior cervical pain and palpitations, displaying varying timelines from COVID-19 onset to SAT symptoms. Treatment approaches, involving prednisone and non-steroidal anti-inflammatory drugs (NSAIDs), led to recovery in many cases, but some individuals experienced a transition to hypothyroidism. The diagnostic and laboratory investigations across revealed diverse profiles, thyroid imaging findings, inflammatory markers, thyroid function tests, and the presence of anti-thyroid antibodies. Conclusion The complexity of SAT is emphasized, particularly in the context of COVID-19. The consistent trend toward recovery of thyroid function not only suggests potential treatment efficacy but also emphasizes the necessity for vigilant symptom monitoring, especially in individuals with a history of COVID-19. Future studies should further investigate the details of SAT post-COVID-19, improving approaches to diagnosis, treatment, and patient care.

Microglia have been implicated in various neurological and psychiatric disorders in rodent and human postmortem studies. However, the dynamic actions of microglia in the living human brain have not been clarified due to a lack of studies dealing with in situ microglia. Herein, we present a novel technique for developing induced microglia-like (iMG) cells from human peripheral blood cells. An optimized cocktail of cytokines, GM-CSF and IL-34, converted human monocytes into iMG cells within 14 days. The iMG cells have microglial characterizations; expressing markers, forming a ramified morphology and phagocytic activity with various cytokine releases. To confirm clinical utilities, we developed iMG cells from a patient of Nasu-Hakola disease (NHD), which is suggested to be directly caused by microglial dysfunction and observed that these cells from NHD express delayed but stronger inflammatory responses compared with those from the healthy control. Altogether, the iMG-technique promises to elucidate unresolved aspects of human microglia in various brain disorders.

Anti-sulfatide antibodies are autoantibodies that are associated with various neurological disorders. They have been identified in several conditions including Guillain-Barré syndrome, multiple sclerosis, and chronic inflammatory demyelinating polyneuropathy. Subacute combined degeneration of the spinal cord is mainly caused by vitamin B12 deficiency. Chronic atrophic gastritis is a complex condition characterized by atrophy and inflammation of the gastric mucosa. To date, there have been no reported cases of patients with subacute combined degeneration of the spinal cord co-occurring with chronic atrophic gastritis and positive anti-sulfatide antibodies. A 58-year-old male patient presented with symmetrical progressive numbness of his limbs. Although he did not experience gait instability, he had difficulty performing fine motor tasks in his upper limbs. We reviewed the patient's medical history and analyzed the results of his blood tests, imaging studies, and gastroscopic. The patient met the criteria for subacute combined degeneration of the spinal cord, chronic atrophic gastritis, macrocytic anemia, and anti-sulfatide antibody positivity. His symptoms improved after treatment. This is the first report on the coexistence of positive anti-sulfatide antibodies and subacute combined degeneration of the spinal cord, including chronic atrophic gastritis and macrocytic anemia, which will enhance our understanding of the relationships between these conditions.

The aim of this study was to compare the clinical presentations, nerve conduction studies, neuroimaging findings of subacute combined degeneration (SCD) caused by N O abuse and primary vitamin B12 deficiency. The goal is to improve diagnostic accuracy, tailored therapeutic interventions, and ultimately enhancing patient outcomes in cases of SCD caused by N O abuse. This study was a retrospective case-control study which enrolled 23 patients diagnosed with N O-induced subacute combined degeneration (N O-SCD) and 20 patients with vitamin B12 deficiency-induced subacute combined degeneration (Vit B12-SCD) between 2015 and 2023. Clinical manifestations, physical examinations, laboratory tests, nerve conduction studies, and spinal cord MRI imaging results were collected. Additionally, age-matched healthy control groups were also included for comparative electrophysiological analysis, consisting of 23 young individuals and 21 elderly individuals corresponding to the N O-SCD and Vit B12-SCD groups, respectively. The study found that compared to Vit B12-SCD, N O-SCD patients exhibited more severe and extensive neurological damage. Both N O-SCD and Vit B12- SCD patients may present with numbness or abnormal sensations, limb weakness, difficulty walking and inability to walk, but these are more severe and widespread in N O-SCD patients. N O-SCD patients showed significant decreases in limb strength, with common walking difficulties and paralysis. Additionally, N O abuse patients more frequently exhibited psychiatric symptoms, especially memory loss, hallucinations and confusion. Both Vit B12-SCD and N O-SCD can cause peripheral nerve demyelination and axonal damage, but it is more severe in the N O-SCD group, with more damage in the lower limbs than in the upper limbs. The extensive nature of axonal damage also indicated a poor prognosis. The degree of spinal cord damage in the N O-SCD group was more severe and affected longer segments. These results suggest that in addition to affecting vitamin B12, N O also causes neurological damage through other mechanisms. In summary, N O-SCD leads to more severe clinical symptoms, peripheral nerve damage, and spinal cord injury than Vit B12-SCD. These differences guide the clinical treatment of N O-SCD, requiring not only vitamin B12 supplementation but also an addition in neuroprotective treatments.

Subacute thyroiditis (SAT) is an inflammatory thyroid disease. The main purpose of the treatment is to relieve pain and control the inflammatory process. The aim of the present study was to evaluate the therapeutic effects of steroid and non-steroidal anti-inflammatory drugs (NSAIDs) in SAT. Initial laboratory data, treatment response, and long-term results of 295 SAT patients treated with ibuprofen or methylprednisolone were evaluated. After the exclusion of 78 patients, evaluation was made of 126 patients treated with 1800 mg ibuprofen and 91 patients treated with 48 mg methylprednisolone. In 59.5% of 126 patients treated with ibuprofen, there was no adequate clinical response at the first control visit. In 54% of patients, the treatment was changed to steroids in mean 9.5 days. Symptomatic remission was achieved within two weeks in all patients treated with methylprednisolone. The total recurrence rate was 19.8%, and recurrences were observed more frequently in patients receiving only steroid therapy than in patients treated with NSAID only (23% vs. 10.5% p:0.04). Persistent hypothyroidism developed in 22.8% of patients treated only with ibuprofen and in 6.6% of patients treated with methylprednisolone only. Treatment with only ibuprofen (p:0.039) and positive thyroid peroxidase antibody (anti-TPO) (p:0.029) were determined as the main risk factors for permanent hypothyroidism. NSAID treatment is not as effective as steroid treatment in early clinical remission. Steroid treatment was detected as a protective factor against permanent hypothyroidism. Therefore, steroid therapy may be considered especially in anti-TPO positive SAT patients and patients with high-level acute phase reactants.