Telogen effluvium is characterized by excessive hair shedding usually following a stressful event. Ferritin has been used in clinical practice as a biomarker of nonanemic iron deficiency in cases of telogen effluvium. During the years of the COVID19 pandemic, telogen effluvium was reported as a part of post covid manifestations. As ferritin was also a biomarker for inflammation in cases with covid infection, this study was designed to evaluate the value of ferritin in cases with postcovid telogen effluvium one hundred patients recovering from covid 19 for 4-12 weeks were included in the study, detailed drug and laboratory history was obtained and serum ferritin level was measured. the mean serum level of ferritin among telogen effluvium patients was significantly lower than controls (68.52 ± 126 and 137 ± 137.597 ug/L respectively). Patients with telogen effluvium used significantly more azithromycin and ivermectin and significantly less vitamin C, D, lactoferrin and zinc than the controls Although serum ferritin is lower among telogen effluvium patients, it was still higher than the cutoff value for diagnosing nonanemic iron deficiency, we suggest that it will not be a good biomarkers in these cases. Our secondary outcomes showed that dietary supplements used during active infection such as vitamin C, D, lactoferrin and zinc might have a preventive value on postcovid hair loss, while azithromycin and ivermectin could have a negative long term effect on telogen effluvium.

Hemophagocytic lymphohistiocytosis (HLH) is a rare, and potentially fatal, syndrome, characterized by immune system dysregulation, with excessive activation of the macrophages and cytotoxic T cells. It can be classified into primary (genetic) and secondary (acquired) forms. HLH presents with fever, hepatosplenomegaly, cytopenia, and hyperferritinemia, with involvement of various organs. The initial symptoms of HLH are non-specific, but as, if untreated, it can progress rapidly to multiorgan failure, timely diagnosis is essential. We present here two cases of HLH in infants that illustrate the importance of early diagnosis and appropriate treatment, along with a short review of HLH.

BACKGROUND: Hemorrhagic fever with renal syndrome (HFRS) is a globally prevalent infectious disease caused by the hantavirus in rodents.
METHODS: This report describes a case of a 36-year-old male presenting with elevated ferritin, vitamin B12, and folic acid deficiency during the early onset phase of HFRS. Despite normal renal function at admission, the patient exhibited persistent fever and thrombocytopenia, leading to a potential misdiagnosis of an atypical HFRS presentation. Abnormal serum levels of ferritin, vitamin B12, and folic acid served as early indicators of renal dysfunction in patients with HRFS. The patient\'s condition improved rapidly with a combination of vitamin B6, methyl cobalamin, and folic acid, as evidenced by a subsequent decrease in the ferritin levels, from 3000 to 600 ng/mL, on days 4 and 24, respectively, and an increase in the vitamin B12 and folic acid levels to 200 pg/mL and 36.7 ng/mL, separately.
CONCLUSIONS: These findings suggest that ferritin, vitamin B12, and folic acid have the potential to serve as biomarkers for HFRS and play a predictive role in the diagnosis and treatment of the disease.

Adult-onset Still\'s disease (AOSD) causes fever, rash, pharyngalgia, and arthralgia through autoinflammation. Its complement titer has not previously received attention because this usually increases during the inflammatory process. Our female patient in her 60s was admitted to the hospital with fever, rash, arthralgia, and pharyngalgia. Her white blood cell count was 19,130/μL, hemoglobin was 11.0 g/dL, platelet count was 26.0 × 104/μL, and ferritin titer was 6,175 ng/mL. Anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies were negative. The presence of infectious diseases and malignancies was excluded. She was diagnosed with hypocomplementemia at the onset of AOSD because of her low complement component 4 (C4) titer (<5.0 mg/dL). Her complement component 3 (C3) titer was 104.5 mg/dL, which was within normal limits. There was no sign of thrombotic microangiopathy (TMA) or hemophagocytosis. She was treated with high-dose corticosteroids, including pulse methylprednisolone therapy, cyclosporine, methotrexate, and intravenous immunoglobulin, but was resistant to these, and her disease repeatedly flared up. Treatment with intravenous cyclophosphamide eventually led to remission. Post-treatment, her C4 titer increased to within the normal range. Although hypocomplementemia with TMA or hemophagocytosis has been reported in AOSD patients, our patient showed no sign of either at disease onset. Hypocomplementemia of AOSD may be a sign of high disease activity and could be a predictive marker for resistance to standard therapy.

We describe the case of an infant who presented with simple rhinovirus/enterovirus bronchiolitis whose condition worsened with rapid progression to multiple organ dysfunction syndrome (MODS). The patient was presumed to have either primary or secondary hemophagocytic lymphohistiocytosis (HLH), and treatment was initiated using dexamethasone, anakinra, and intravenous immunoglobulin to modulate the immune system. Due to the organ dysfunction, the use of etoposide was avoided and instead, emapalumab, an interferon gamma antagonist, was administered at a dose of 6 mg/kg. The patient\'s organ failure improved, and the levels of inflammatory markers decreased. The flow cytometry analysis revealed that cytotoxic cells lacked perforin expression, and subsequent genetic analysis confirmed homozygous pathogenic mutations in the perforin gene. This case highlights the potential avoidance of etoposide in cases of primary HLH, the possible benefit of an elevated initial dose of emapalumab, and the contribution offered by a multi-specialty team approach to complex diagnosis.

BACKGROUND: Oral potentially malignant disorders (OPMD) are lesions associated with an increased risk of transformation (MT) into cancer.
OBJECTIVE: A study was made of the salivary levels of adenosine deaminase (ADA), ferritin (FRR) and total proteins (TP) in healthy individuals and in patients with oral potentially malignant disorders (OPMD), assessing the potential role of saliva as a diagnostic tool.
METHODS: A total of 91 subjects participated in the study, divided into two groups-59 patients with OPMD (oral leukoplakia or oral lichen planus) and 32 healthy controls-with measurements being made of salivary ADA, ferritin (FRR) and total proteins (TP).
RESULTS: There were no significant differences in salivary mean ADA between the OPMD group 0.85 ± 2.18 UI/I and the controls 0.71 ± 1.72 UI/I (p = 0.934), though the levels of both FRR mean OPMD, 12.66 ± 10.50 (µg/L), versus control, 7.19 ± 4.44 (p = 0.001), and TP, 23.41 ± 17, versus control, 14.15 ± 15.19, were significantly higher in the OPMD group (p = 0.001). Patients with oral lichen planus showed significant differences in terms of FRR (p = 0.009) and TP (p = 0.003). The ferritin in LPO with a cut-off point of 8.5C showed a sensitivity and specificity of 54.3% and 82.3, respectively. The area under the curve (AUC) was 0.69 (95% confidence interval (95% CI): 0.58-0.82; p = 0.003).
CONCLUSIONS: Ferritin and total proteins may constitute potential salivary biomarkers for oral lichen planus, though further studies are still needed in this field. In addition, saliva testing is a reliable and noninvasive diagnostic tool and appears to be a reliable strategy offering an interesting alternative for the screening of large populations.

Iron overload disorders can present as non-specific symptoms and develop gradually but, if untreated, can be very fatal. The common causes include multiple blood transfusions for chronic anemia and increased iron absorption, including hereditary hemochromatosis (HH). HH is one of the common causes of iron overload disorders and usually presents with liver cirrhosis in a setting of significantly elevated ferritin and elevated transferrin saturation. Alcoholic hepatitis is a clinical syndrome of progressive inflammatory liver injury associated with long-term heavy intake of ethanol. However, in patients with alcohol abuse, excessive alcohol consumption can disrupt iron metabolism releasing large amounts of iron into circulation. This can cause severely elevated ferritin due to disruption of iron metabolism, simulating iron overload disorders such as HH, especially if the patient also has liver cirrhosis. Even though a high transferrin saturation of greater than 45% is recommended as a cutoff transferrin value as high sensitivity for detecting iron overload disorders, it has a low specificity and positive predictive value and often identifies people with other causes of acutely elevated ferritin levels such as alcohol liver disease and hepatitis. Recognizing this feature and timely management can spare the patient from unnecessary phlebotomies and prompt treatment for alcoholic hepatitis. We present an interesting case of severe alcoholic hepatitis mimicking HH with severely elevated ferritin levels and transferrin saturation with underlying liver cirrhosis.

Vibrio vulnificus is a Gram-negative bacterium, a member of the Vibrionaceae family. V. vulnificus is the main cause of seafood-related deaths in the United States because it can cause severe wound infections or sepsis. This microorganism is highly dependent on iron availability. Therefore, patients with high body iron levels are more susceptible to the infection. Prompt treatment with cephalosporins as well as doxycycline is usually administered. We present a case of V. vulnificus bacteremia in a patient heterozygous for HFE p.C282Y mutation and underlying alcoholic liver cirrhosis.

Progressive multifocal leukoencephalopathy (PML) is a severe demyelinating disease caused by JC virus infection of oligodendrocytes. Little has been reported on iron deposits in patients with PML. Herein, we report a case of PML with massive iron deposition in the juxtacortical regions attaching white matter lesions in a 71-year-old woman who developed bilateral visual disturbance and progressive aphasia after 16 months of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone treatment for follicular lymphoma. Magnetic resonance imaging revealed white matter lesions in the left parietal and other lobes with massive iron deposition in the juxtacortical lesions. A PCR test for JC virus was positive, confirming the diagnosis of PML. Despite treatment with mefloquine and mirtazapine, the patient died six months later. At autopsy, demyelination was found dominantly in the left parietal lobe. Moreover, hemosiderin-laden macrophages and reactive astrocytes containing ferritin were abundant in the juxtacortical regions adjacent to the white matter lesions. This is a previously unreported case of PML after lymphoma, in which iron deposition was confirmed both radiologically and pathologically.

BACKGROUND: Severe influenza, especially influenza pneumonia, causes large numbers of deaths each year. Some patients who develop severe influenza have no known risk factors. In this study we investigated risk factors for mortality of patients with influenza A-related pneumonia who have different basic conditions. We also evaluated the power of pneumonia severity assessment tools in Chinese patients hospitalized with influenza A-related pneumonia. Together, these results could provide a basis for a screening method that has improved ability for the early identification of critical patients who will have poor prognoses in clinical practice.
METHODS: This single-center, retrospective case-control study included 152 adult patients with severe influenza over six influenza seasons. Data for diagnoses and demographics, as well clinical data, laboratory findings, treatment methods, 30-day and 60-day outcomes of the patients were collected. Patients who had any of the risk factors for severe influenza were included in the high-risk group, and those that had no known risk factors were included in the low-risk group.
RESULTS: The PSI, CURB-65 and PIRO-CAP tools all underestimated the mortality rate of patients hospitalized with influenza A-related pneumonia, and this underestimate was more pronounced for low-risk patients. D-dimer (Odds ratio [OR] = 1.052, 95% confidence interval [CI] 1.001-1.106, p = 0.045) and direct bilirubin (OR = 1.143, 95%CI 1.049-1.246, p = 0.002) were independent risk factors for mortality of patients with influenza A-related pneumonia. When used in combination with ferritin and D-dimer, the area under receiver operator characteristic curve (AUCROC) was 0.851 (95%CI 0.780-0.922, p < 0.001), 0.840 (95%CI 0.763-0.916, p < 0.001) and 0.829 (95%CI 0.748-0.911, p < 0.001) for PSI, CURB-65 and PIRO-CAP, respectively, which was higher than that obtained using PSI, CURB-65 and PIRO-CAP alone.
CONCLUSIONS: The findings demonstrate that currently used community-acquired pneumonia (CAP) scoring systems could underestimate the risk of influenza A-related pneumonia mortality. D-dimer was shown to be an independent risk factor of mortality for influenza A-related pneumonia in hospitalized patients, and a combination of D-dimer with ferritin could improve the predictive value of PSI, CURB-65 and PIRO-CAP for adverse prognoses of patients with influenza A-related pneumonia.