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PubMed2005

Hemosiderin pigmentation of tumour cells in cerebellar pilocytic astrocytoma associated with post-traumatic hemorrhage in adults.

The pilocytic astrocytoma is only rarely associated with gross intratumoral hemorrhage despite rich vasculature and blood vessel changes, accompanied often by perivascular depots of hemosiderin. We report an unusual case of pigmented cerebellar pilocytic astrocytoma presenting with posttraumatic hemorrhage in a 38-year-old man with no history related to the tumor. CT and MRI examination after head injury demonstrated unexpectedly the cystic lesion of 2 cm in diameter in the region of the right cerebellar hemisphere and vermis. The lesion was associated with hematoma and it was surgically removed 3 weeks after trauma. Histopathological examination revealed pilocytic astrocytoma tissue with broad hemorrhagic changes and with an unusual pattern of massive pigmentation of the cytoplasm of pilocytic astrocytes, consistent with hemosiderosis. Positive stains for iron and ferritin and ultrastructural study confirmed deposition of hemosiderin granules in the tumour cells. There was no evidence of melanin or melanosomes. This finding of hemosiderin accumulation in the cytoplasm of neoplastic astroglia seems to be analogous to post-hemorrhagic pigmentation of the normal Bergmann glia and subpial astrocytes. In the literature, the examples of neuroepithelial tumors with hemosiderin pigmentation of tumor cells have been rarely documented. To our knowledge, this is the first reported case of pigmented pilocytic astrocytoma exhibiting extensive intracellular hemosiderin deposition.

Adult↗
PubMed1997

[Hippocampal hemosiderin deposit due to large pituitary adenoma presenting temporal lobe epilepsy--a case report].

There have been reports of epilepsy associated with pituitary adenoma, but the epileptogenic zone and its histopathology have never been sufficiently described. We report a case of pituitary adenoma complicated by temporal lobe epilepsy, in which the epileptogenic focus was identified, resected, and examined histopathologically. The patient was a 38-year-old man on bromocriptine therapy for a huge pituitary adenoma (prolactin-producing) since 1985. He also had a history of temporal lobe epilepsy since 1989. CT images in 1985 revealed the tumor extending to the supra- and left para-sellar region. MR images in 1995 showed a significant decrease in the size of the tumor and a signal void area that was interpreted as a hemosiderin deposit in the left mesial temporal lobe. Ictal EEG demonstrated that seizure discharges were elicited at the left sphenoidal electrode and propagated to the both temporal lobes. Interictal SPECT revealed a local area of hypoperfusion in the left fronto-parietal lobe. An epileptogenic focus in the left mesial temporal lobe was diagnosed on the basis of the above examinations. The patient was treated by left anterior temporal lobectomy with partial hippocampectomy. Hemosiderin deposition in the hippocampus was suspected during surgery. Histopathological examination showed pyramidal cell loss and gliosis in the left hippocampus and confirmed the presence of hemosiderin in the CA1 region. The hemosiderin deposition in the hippocampus was inferred to have resulted from intratumoral hemorrhage due to bromocriptine therapy, and it may have caused the temporal lobe epilepsy in this patient. The outcome of surgery was freedom from seizures for eight months. Intra-tumoral hemorrhage in mesial temporal structures must be borne in mind as one of the epileptogenic mechanisms in pituitary adenoma, especially in cases in which hemosiderin is detected on MR images.

Adenoma↗
PubMed2005

[Study on hemosiderin deposition after intracerebral hemorrhage].

BACKGROUND AND PURPOSE: Hemosiderin degenerated from intracerebral hematoma (ICH) can be visualized as low intensity on gradient-echo T2*-weighted (T2*-w) MRI, which is sensitive for hemosiderin. We studied the factors associated with the hemosiderin deposition on T2*-w MRI after ICH. METHODS: We analyzed T2*-w MRIs in 72 outpatients with past ICH (46 males, 26 females, 28-89 (60.0 +/- 9.8) years old) consecutively came to our hospital. The odds ratio (OR) for the apparent thickness > or = 2.5 mm of low intensity surrounding ICH cavity was estimated, using the time after the onset of ICH (17 weeks - 26 years), and other factors. RESULTS: All of old ICHs were visible as low intensities on T2*-w MRI. Multivariate logistic regression analysis revealed that an elevated ratio of the apparent thickness > or = 2.5 mm of hemosiderin was found for the patients with time > or =5 years between T2*-w MRI and the onset (odds ratio (OR): 0.24, 95% confidence interval (CI): 0.06-0.99), intraventricular or subarachnoid hemorrhage related to ICH (OR: 0.16, 95% CI: 0.03-0.77), and the diameter of ICH > or =2 cm (OR: 33.7, 95% CI: 4.6-245). CONCLUSION: Though small sample size limited the power of analyses, our findings suggest that the amount of hemosiderin deposition after ICH may be associated with the time after the onset, intraventricular or subarachnoid hemorrhage related to ICH, and the diameter of ICH.

Adult↗
PubMed1987

[Hemosiderin findings in the liver, spleen and lung in newborn infants and infants].

The content and distribution of hemosiderin in the liver, spleen and lungs of stillborn children, newborns and infants were determined histologically by Perl's method (Prussian blue reaction). We describe a study of 59 deaths up to the age of 2 years. The hemosiderin content depends on age and decreases with increasing age. No relevant differences were found in cases of sudden infant death syndrome (SIDS). In the liver hemosiderin is localized preponderantly in the periphery of the lobules. The spleen shows a diffuse siderosis of the red pulp. Minimal intrapleural, septal and perivasal depositions of hemosiderin can be found in the lung tissue. The significance of these findings is discussed.

Female↗
PubMed2000

Low-frequency low-field magnetic susceptibility of ferritin and hemosiderin.

Low-frequency low-field magnetic susceptibility measurements were made on four samples of mammalian tissue iron oxide deposits. The samples comprised: (1) horse spleen ferritin; (2) dugong liver hemosiderin; (3) thalassemic human spleen ferritin; and (4) crude thalassemic human spleen hemosiderin. These samples were chosen because Mössbauer spectroscopic measurements on the samples indicated that they exemplified the variation in magnetic and mineral structure found in mammalian tissue iron oxide deposits. The AC-magnetic susceptometry yielded information on the magnetization kinetics of the four samples indicating samples 1, 2, and 3 to be superparamagnetic with values of around 10(11) s(-1) for the pre-exponential frequency factor in the Néel-Arrhenius equation and values for characteristic magnetic anisotropy energy barriers in the range 250-400 K. Sample 4 was indicated to be paramagnetic at all temperatures above 1.3 K. The AC-magnetic susceptometry data also indicated a larger magnetic anisotropy energy distribution in the dugong liver sample compared with samples 1 and 3 in agreement with previous Mössbauer spectroscopic data on these samples. At temperatures below 200 K, samples 1-3 exhibited Curie-Weiss law behavior, indicating weak particle-particle interactions tending to favor antiparallel alignment of the particle magnetic moments. These interactions were strongest for the dugong liver hemosiderin, possibly reflecting the smaller separation between mineral particles in this sample. This is the first magnetic susceptometry study of hemosiderin iron deposits and demonstrates that the AC-magnetic susceptometry technique is a fast and informative method of studying such tissue iron oxide deposits.

Animals↗
PubMed1988

Brain hemosiderin and superficial siderosis of the central nervous system.

Brain tissue from five patients with superficial siderosis of the central nervous system was examined by immunocytochemistry for ferritin, glial fibrillary acidic protein (GFAP), alpha 1-antitrypsin, and alpha 1-antichymotrypsin, and by lectin affinity cytochemistry with biotinylated Ricinus communis agglutinin-1 (RCA-1). The sections were pretreated with 2,2'-dipyridyl and sodium hydrosulfite to remove iron and to reveal the antigenic sites. In siderotic cerebellar cortex, ferritin reaction product occurred in the hemosiderin matrix, the cell bodies and processes of Bergmann glia, and in microglia. Astrocytes other than Bergmann glia did not contain ferritin reaction product. RCA-1 stained microglia and hemosiderin whereas antisera to alpha 1-antitrypsin and alpha 1-antichymotrypsin only reacted with iron-depleted granules. The selective vulnerability of the eighth cranial nerve was explained by the presence of ferritin-reactive and lectin-positive microglia. Hemosiderin isolated from frozen cerebellum contained ferritin, GFAP, and vimentin. The presence of the intermediate filament proteins was likely due to co-localization with hemosiderin granules in Bergmann glia. The ability of the brain to biosynthesize ferritin in response to prolonged contact with hemoglobin iron is thought to be the most important factor in the pathogenesis of superficial siderosis. The great severity of the lesion in the exposed cerebellar cortex is readily explained by accelerated ferritin biosynthesis in Bergmann glia.

Adult↗
PubMed1997

Hemosiderin deposition in portal endothelial cells is a histologic marker predicting poor response to interferon-alpha therapy in chronic hepatitis C.

Interferon (IFN)-alpha is regarded as an efficient therapy for chronic hepatitis C, despite the fact that less than 50% of patients receiving IFN-alpha are known to show an initial biochemical response, and several adverse reactions related to this therapy are becoming a serious clinical problem. For a more efficient and safer treatment of IFN-alpha, several pretreatment factors to predict a favorable or unfavorable response to IFN-alpha therapy are now being evaluated, such as hepatitis C virus (HCV)-RNA levels in serum and the genotypes of HCV. Recently, the hepatic iron concentration has been reported to influence the outcome of IFN-alpha therapy for chronic viral hepatitis. In the present study, whether hemosiderin deposition in liver is a histologic predictor of response to IFN-alpha therapy was evaluated, as well as which anatomical location showing the hemosiderin deposition was more closely related to the response to this therapy. Two factors, high titer of HCV-RNA in serum and hemosiderin deposition in portal endothelial cells, were found to be predictable factors of poor response to IFN-alpha therapy, and these two factors were found to be related to each other. Results showed that the hemosiderin deposition in portal endothelial vessels is an easily evaluable histologic finding, and clinicians and histopathologists are encouraged to use this finding when selecting patients with chronic hepatitis C suitable for IFN-alpha therapy.

Adult↗
PubMed1985

Distribution of ferritin and hemosiderin in the liver, spleen and bone marrow of normal, phlebotomized and iron overloaded rats.

The distribution of ferritin has been studied in many tissues, but has not yet been established on the cellular level. We investigated the cellular distribution of ferritin in the liver, spleen and bone marrow using the immunoperoxidase method, and compared it with that of hemosiderin. We also examined changes in the distribution of these proteins after phlebotomy and iron overload. In normal rats, ferritin was seen in centrilobular hepatocytes, Kupffer cells, macrophages in the red and white pulp of the spleen and central macrophages in bone marrow. Hemosiderin was observed almost exclusively in the red pulp and partly in tangible body macrophages of the white pulp. After phlebotomy, neither ferritin nor hemosiderin were detectable in these cells except for ferritin-positive cells in the white pulp, which showed little change after either phlebotomy or iron overload. In iron overloaded rats, both ferritin and hemosiderin increased in hepatocytes and reticulo-endothelial (RE) cells. Ferritin-positive cells in the liver were mainly located in the periportal area. These results indicated that hepatocytes and RE cells except for those in the white pulp may play an important role in iron storage, and that ferritin-positive cells in the white pulp may have a function other than iron reserve. They also suggested that the zonal distribution of ferritin-positive hepatocytes may be due to microcirculation in the hepatic lobules.

Anemia↗
PubMed1993

Demonstration of the deposition of hemosiderin in the kidneys of patients with paroxysmal nocturnal hemoglobinuria by magnetic resonance imaging.

Hemosiderinuria caused by intravascular hemolysis is a characteristic clinical feature of an acquired hemolytic disorder, paroxysmal nocturnal hemoglobinuria (PNH). We examined the deposition of hemosiderin (iron) in the kidneys of 6 patients with PNH using magnetic resonance imaging (MRI). Three patients with autoimmune hemolytic anemia (AIHA), a hemolytic disorder showing extravascular hemolysis, served as controls. In five of the six patients with PNH, a characteristic T2-weighted MRI of the kidneys, suggesting the deposition of iron (hemosiderin) predominantly in the renal cortex, was obtained. Hemosiderin-deposition was not revealed in the kidneys of any of the patients with AIHA. We conclude that MRI is a sensitive means of detecting hemosiderin deposited in the renal cortex of patients with PNH and that this feature is considerably specific for diseases showing intravascular hemolysis, as represented by PNH.

Aged↗
PubMed1980

Experimental hemosiderosis: relationship between skin pigmentation and hemosiderin.

Iron (totalling 7.5 mg per mouse in three doses) was injected into hairless mice to determine the relationship between skin pigmentation and hemosiderin deposition. The skin color reached its maximum 24 to 48 hours after the last injection and then gradually faded over the subsequent 8 months. In the skin, hemosiderin granules were present extracellularly between collagen bundles as well as within dermal macrophages, Langerhans cells and indeterminate dendritic cells of the epidermis. A larger amount of iron was deposited in the facial than in the dorsal skin, resulting in darker pigmentation of the former. This study suggests that brownish discoloration of skin in hemochromatosis might be attributable in some degree to accumulation of hemosiderin and that pronounced hyperpigmentation of the face in hemochromatosis might be due to increased activation of melanocytes by a high content of hemosiderin.

Animals↗
PubMed2000

Differentiation between hemosiderin- and ferritin-bound brain iron using nuclear magnetic resonance and magnetic resonance imaging.

MRI is an optimal clinical (research) tool to provide information on brain morphology and pathology and to detect metal ions that possess intrinsic magnetic properties. Non-heme iron is abundantly present in the brain in three different forms: "low molecular weight" complexes, iron bound to "medium molecular weight complexes" metalloproteins such as transferrin, and "high molecular weight" complexes as ferritin and hemosiderin. The total amount and form of iron may differ in health and disease, and MRI can possibly quantify and monitor such changes. Ferritin-bound iron is the main storage form of iron and is present predominantly in the extrapyramidal nuclei where its amounts normally increase as a function of age. Ferritin is water soluble and shortens both, T1 and T2 relaxation, with as result a signal change on the MR images. Hemosiderin, a degradation product of ferritin, is water-insoluble with a stronger T2 shortening effect than ferritin. The larger cluster size of hemosiderin and its water-insolubility also explain a lack of significant T1-shortening effect on T1-weighted images. Using both in vitro specimens and intact brain tissue in vivo we demonstrate here that MRI may be able to distinguish between ferritin- and hemosiderin-bound iron.

Aged↗
PubMed2001

Abundant intracytoplasmic hemosiderin in both histiocytes and neoplastic cells: A diagnostic pitfall in fine-needle aspiration of cystic papillary renal-cell carcinoma.

Benign renal tubular cells and renal-cell carcinomas (RCC) may have intracytoplasmic hemosiderin (ICH). The RCC subtype most commonly reported to contain ICH is papillary carcinoma (PRCC). PRCC, usually a low-grade neoplasm, may be associated with cystic degeneration, hemorrhage, and presence of abundant hemosiderin-laden macrophages (HLM). We report a case of PRCC with massive ICH and HLM that created a diagnostic challenge to differentiate from a hemorrhagic cyst. Review of 14 additional nephrectomy specimens with PRCC disclosed ICH in 3 cases. All had coexisting cystic change and hemorrhage. Preoperative FNA had been performed in one of these cases, and both ICH and HLM were found. Papillary epithelial cell features, however, were well-defined in this case. PRCC should be considered in the differential diagnosis of cystic renal lesions with hemosiderin-laden cells. Differentiation of HLM from neoplastic cells with massive ICH may be difficult, especially when epithelial fragments are scanty.

Biopsy, Needle↗
PubMed1995

Hemosiderin deposition in portal endothelial cells: a novel hepatic hemosiderosis frequent in chronic viral hepatitis B and C.

We have recently noted a hitherto undescribed hepatic hemosiderosis confined to endothelial cells of the portal tract in chronic viral hepatitis. In this study, this lesion was surveyed in 156 liver biopsy specimens from patients with chronic hepatitis C and in 21 liver biopsy specimens from patients with chronic hepatitis B. As controls, we examined 110 liver biopsy specimens from patients with primary biliary cirrhosis (PBC), 36 from patients with alcoholic liver injury, nine from patients with autoimmune hepatitis (AIH), and five from patients with primary hemochromatosis. Hemosiderin deposition was found in the endothelial cells of venous vessels in portal tracts regardless of the presence or degree of hemosiderin deposition in hepatic parenchyma. This phenomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C and in eight of 21 (38%) cases of chronic hepatitis B. In controls, this lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and alcoholic liver injury (11%). The incidence of this lesion showed significant differences between chronic hepatitis C, B, and AIH, and between PBC and alcoholic liver injury. There was a positive correlation between the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder chronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectively, in more severe cases. However, this correlation was not evident in either PBC or alcoholic liver injury. This hemosiderin deposition was positively correlated with the degree of piecemeal necrosis in chronic hepatitis C, and to a lesser degree, the positive correlation was shown in chronic hepatitis B. These findings suggest that the progression of chronic hepatitis and the piecemeal necrosis in chronic hepatitis C and B, followed by the release of hepatocellular iron to portal and periportal areas, are directly or indirectly responsible for endothelial hemosiderosis. Further studies focusing on this peculiar phenomenon in relation to choice of therapy and evaluation of chronicity of viral hepatitis are encouraged.

Adult↗
PubMed1959

The cellular transformation of injected colloidal iron complexes into ferritin and hemosiderin in experimental animals; a study with the aid of electron microscopy.

As revealed by electron microscopy and electron diffraction, the physical state of ferric hydroxide micelles contained in iron-dextran, saccharated iron oxide, and hydrous ferric oxide ("ferric hydroxide") differs notably from the state of the ferric hydroxide in ferritin or hemosiderin. By virtue of this difference one can trace the intracellular transformation of colloidal iron, administered parenterally, into ferritin and hemosiderin. One hour after intraperitoneal injection of iron-dextran or saccharated iron oxide into mice, characteristic deposits were present in splenic macrophages, in sinusoidal endothelial cells of spleen and liver, and in vascular endothelial cells of various renal capillaries. Four hours after injection, small numbers of ferritin molecules were identifiable about intracellular aggregates of injected iron compounds; and by the 6th day, ferritin was abundant in close proximity to deposits of injected iron compounds. The latter were frequently situated in cytoplasmic vesicles delimited by single membranes. These vesicles were most frequently found in tissue obtained during the first 6 days after injection; and in certain of the vesicles ferritin molecules surrounded closely packed aggregates of injected material. Much unchanged ferric hydroxide was still present in macrophages and vascular endothelial cells 3 to 4 weeks after injection. While electron microscopy left no doubt about the identity of injected ferric hydroxide on the one hand, and of ferritin or hemosiderin on the other, histochemical tests for iron failed in this respect. Precipitation of ferric hydroxide (hydrous ferric oxide) from stabilized colloidal dispersions of iron-dextran was brought about in vitro by incubation with minced mouse tissue (e.g. liver), but not by incubation with mouse serum or blood. Subcutaneous injections of hydrous gel of ferric oxide into mice initially produced localized extracellular precipitates. Most of the material was still extracellular 16 days after injection, though part of it was phagocytized by macrophages near the site of injection; but apparently none reached the spleen in unaltered form. Five days after injection and thereafter, much ferritin was present in macrophages about the site of injection and in the spleen. The findings show that iron preparations widely used in therapy can be identified within cells, and that their intracellular disposition and fate can be followed at the molecular level. Considered in the light of previous work, they indicate that the characteristic structure of the ferric hydroxide micelles in molecules of ferritin is specific, and develops during the union of apoferritin with ferric hydroxide. Apparently this union does not depend upon specific cell components.

Animals↗
PubMed2000

Pulmonary hemosiderin in deceased infants: baseline data for further study of infant mortality.

Infant lung samples were obtained prospectively at autopsy by medical examiner pathologists in five areas of the United States. Tissues were submitted regardless of the cause of death. Lung sections were stained with Prussian blue to detect deposits of hemosiderin. Fifty-nine cases were evaluated for the study. The four sections examined for each case were taken from the anterior and posterior aspects of the right and left upper lung. Three pathologists independently scanned the lung sections microscopically using a 10x objective lens (with 10x ocular lens) and indicated an "iron score" by indicating for each section if it showed no staining for iron-hemosiderin (Score 0), occasional staining with most fields negative (Score 1), focally abundant staining with most fields having no staining (Score 2), focally abundant staining with most fields showing positive staining (Score 3), or prominent staining throughout the section (Score 4). There was good agreement between pathologists on the iron score for each case. A total iron score was calculated by adding the scores based on each pathologist's observations. The mean total iron score was 6 (range, 1-44), with the range of possible total iron scores being 0 to 48. There was no significant difference between the four lung sections in a given case. Six cases had total iron scores that were at least twice the mean (i.e., total iron score > 12); in five of these cases death was caused by conditions other than sudden infant death syndrome, including one case in which asphyxia was the cause of death. These data are consistent with other reports that pulmonary hemosiderin in deceased infants is suggestive of a cause of death other than sudden infant death syndrome. The data may be useful as baseline data for further studies of infant mortality involving possible pathologic changes in the lungs.

Autopsy↗
PubMedDate not supplied

Giant cell tumors of bone containing large amounts of hemosiderin: MR-pathologic correlation.

We present three giant cell tumors of bone that contained large amounts of hemosiderin and compare their MR appearance with intraoperative findings and histological characterization. Histologically, hemosiderin was found in multinucleated giant cells, mononuclear stromal cells, and xanthoma cells. All cases showed markedly decreased signal areas on both T1- and T2-weighted MR imaging due to hemosiderin deposition; this made evaluation of the integrity of the adjacent cortices difficult. In one case, extraosseous tumor extension appeared as a signal void area on MR imaging. Findings on immunohistochemical studies suggested the giant cells may have a histiocytic nature. Because the tumor cells themselves have a phagocytic nature, the decreased signal areas in and around giant cell tumors should be regarded as active tumor tissues in delineating the tumor on MR imaging.

Adult↗
PubMed2005

Hemosiderin deposits in chronic graft-vs.-host disease related myopathy.

Chronic graft-vs.-host disease (cGVHD) occurs in 20-50% of patients who survive for at least 100 d after allogeneic stem cell transplantation (SCT). cGVHD includes scleroderma-like skin changes, chronic cholangitis, obstructive lung disease and general wasting syndrome. Polymyositis or myopathy are rare manifestations of cGVHD with approximately 40 reported cases. Polymyositis accompanied by hemosiderin deposits in cGVHD has been reported only once, and there are no reports on lipofuscin deposits in skeletal muscle cells in cGVHD. We report here on a 56-yr-old male who underwent allogeneic SCT in 1999 for osteomyelofibrosis and progressive hematopoietic insufficiency. In February 2004, the patient was hospitalized for progressive muscular weakness with loss of the ability to walk. Laboratory tests demonstrated normal values for serum creatine kinase, aldolase and lactic dehydrogenase; the ferritin level was highly elevated. The femoral muscle biopsy showed mostly perifascicular atrophy as well as numerous subsarcolemmal hemosiderin and lipofuscin deposits. Intravenous administration of the chelating agent deferoxamine was ineffective. Three weeks later the patient died of aspiration pneumonia. Interestingly, autopsy disclosed moderate hemosiderin deposits in the liver, the organ usually involved in hemosiderosis.

Biopsy↗
PubMed2003

[Analysis of dot-like hemosiderin spots using brain dock system].

BACKGROUND AND PURPOSE: Dot-like low intensity spots (a dot-like hemosiderin spot: dotHS) on T2*-weighted MR images (T2*WI), which is regarded as a sensitive method for hemosiderin detection, have been histologically diagnosed as old microbleeds associated with microangiopathies. The clinical significance of the dotHS, however, is still under debate. Therefore, we investigated the factors associated with dotHS. METHODS: We investigated 209 healthy volunteers in our hospital (sex: 106 males, 103 females; age: 38 to 78 years old, mean age: 56.4 +/- 8.3 years old) using "Brain Dock", a formalized screening system for asymptomatic brain diseases. The Odds ratio (OR) was estimated from multiple logistic regression analyses using the dotHS and variables. RESULTS: T2*WI demonstrated dotHS in 7.7% of volunteers, and the mean number of dotHS was 0.16 +/- 0.78. The hemosiderin was preferentially deposited in the basal ganglia and thalamus. Age > or = 65 years old (OR: 5.9; 95% confidence interval [CI]: 1.4-25.9; p = 0.02), hypertension (OR: 7.0; 95% CI: 1.4-34.7; p = 0.02), and headache (OR: 5.8; 95% CI: 1.4-24.6; p = 0.02) were all found to be independently associated with dotHS. CONCLUSIONS: The dotHS was significantly associated with several factors, including age, hypertension and headache.

Adult↗