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  1. Hi I’m a Cushings survivor..post Pitituary surgery 20 years since..Cushings came back in 2008 after 2004 three times surgery..Was put on medication until 2012 when I had gamma knife radiotherapy..Still have health issues which I know are related to my cushings disease..Arthritis and blood pressure and kidney cyst issues..Now suffering from gout since last year which I’m controlling with herbal remedies..Lost over 20kg since a few months doctors cannot find the solution and suffering from anxiety and depression..I think these problems are all because of my Cushings disease but doctors are not helping me or doing anything.. Need help desperately so posting here as I know Cushings survivors will understand and help..Regards Shagufta
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  2. I would have hoped that you could get better answers in the UK. I'm in the US - Virginia. Our doctors aren't very good, either
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  3. Hi I’m located in Bradford in the United Kingdom..where are you located?
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  4. Oh no, Shagufta! I cannot imagine what you're going through. Where are you located?
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  5. YOU’RE INVITED! Webinar on Dr. Theodore Friedman’s update on medical treatment for Cushing’s disease In this informative webinar, Dr. Friedman will discuss What medicines to use to treat Cushing’s disease Side effects and timing of the medicines The use of ketoconazole for a medication trial before surgery Longer-term treatment for Cushing’s How to determine when a patient should go to surgery Sunday • March 31 • 6 PM PDT here to join the meeting or https://us02web.zoom.us/j/4209687343?pwd=amw4UzJLRDhBRXk1cS9ITU02V1pEQT09&omn=88672684111 OR +16699006833,,4209687343#,,,,*111116# US (San Jose) OR Join on Facebook Live https://www.facebook.com/goodhormonehealth Slides will be available on the day of the talk here. There will be plenty of time for questions using the chat button. For more information, email us at mail@goodhormonehealth.com
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  6. Abstract Cushing’s syndrome is a constellation of features occurring due to high blood cortisol levels. We report a case of a 47-year-old male with a history of recurrent olfactory neuroblastoma (ONB). He presented with bilateral lower limb weakness and anosmia and was found to have Cushing’s syndrome due to high adrenocorticotropic hormone (ACTH) levels from an ectopic source, ONB in this case. Serum cortisol and ACTH levels declined after tumor removal. Introduction Olfactory neuroblastoma (ONB), or esthesioneuroblastoma, is a rare malignancy arising from neuroepithelium in the upper nasal cavity. It represents approximately 2% of all nasal passage tumors, with an incidence of approximately 0.4 per 2.5 million individuals [1]. ONB shares similar histological features with small round blue cell neoplasms of the nose. Ectopic hormone secretion is a very rare feature associated with these tumors. Five-year overall survival is reported to be between 60% and 80% [2,3]. The age distribution is either in the fifth to sixth decade of life [4,5], or in the second and sixth decades [6]. Features of Cushing’s syndrome (moon face, buffalo hump, central obesity hypertension, fragile skin, easy bruising, fatigue, muscle weakness) are due to high blood cortisol levels [7]. It can be either primary (cortisol-secreting adrenal tumor), secondary (adrenocorticotropic hormone (ACTH)-secreting pituitary tumor, also called Cushing disease), or ectopic ACTH secretion (from a non-pituitary source). All three types share similar features [8]. Ectopic ACTH syndrome (EAS) is due to an extra pituitary tumor, producing ACTH. It accounts for 12-17% of Cushing's syndrome cases [9]. Most cases of EAS-producing tumors are in the lungs, mediastinum, neuroendocrine tumors of the gastrointestinal tract, and pheochromocytomas [9]. Ectopic ACTH secretion from an ONB is very rare. As of 2015, only 18 cases were reported in the literature [10]. Here, we report such a case. Case Presentation Our patient is a 47-year-old Bangladeshi male, with a history of recurrent ONB that was resected twice in the past (transsphenoidal resection in 2016 and 2019) with adjuvant radiotherapy, no chemotherapy was given. He also had diabetes mellitus type 1 (poorly controlled) and hypertension. He presented with bilateral lower limb weakness, anosmia, decreased oral intake, loss of taste for one week, and bilateral submandibular swelling that increased in size gradually over the past two years. There was no history of fever, cough, abdominal pain, or exposure to sick contacts. The patient reported past episodes of similar symptoms, but details are unclear. The patient's family history is positive for diabetes mellitus type 1 in both parents. Lab tests in the emergency department showed hypokalemia and hyperglycemia as detailed in Table 1. He was admitted for further workup of the above complaints. Test Patient Results Reference Range Unit Status Hemoglobin 14.7 13-17 g/dL Normal White blood cell (WBC) 17.9 4-10 10*9/L High Neutrophils 15.89 2-7 10*9/L High Lymphocytes 1.07 1-3 10*9/L Normal Sodium 141 136-145 mmol/L Normal Potassium 2.49 3.5-5.1 mmol/L Low (Panic) Chloride 95 98-107 mmol/L Low Glucose 6.52 4.11-5.89 mmol/L Elevated C-reactive protein (CRP) 0.64 Less than 5 mg/L Normal Erythrocyte sedimentation rate (ESR) 2 0-30 mm/h Normal Creatinine 73 62-106 µmol/L Normal Uric acid 197 202.3-416.5 µmol/L Normal Alanine aminotransferase (ALT) 33.2 0-41 U/L Normal Aspartate aminotransferase (AST) 18.6 0-40 U/L Normal International Normalised Ratio (INR) 1.21 0.8-1.2 sec High Prothrombin time (PT) 15.7 12.3-14.7 sec High Lactate dehydrogenase (LDH) 491 135-225 U/L High Thyroid-stimulating hormone (TSH) 0.222 0.27-4.20 mIU/L Low Adrenocorticotropic hormone (ACTH) 106 ≤50 ng/L Elevated Cortisol (after dexamethasone suppression) 1750 Morning hours (6-10 am): 172-497 nmol, Afternoon hours (4-8 pm): 74.1-286 nmol nmol/L Elevated (failure of suppression) 24-hour urine cortisol (after dexamethasone suppression) 5959.1 <120 nmol/24 hrs nmol/24hr Elevated (failure of suppression) Table 1: Results of blood test at the time of hospitalization. Hypokalemia and high values of adrenocorticotropic hormone and cortisol were confirmed. On examination, the patient's vital signs were as follows: blood pressure was 154/77 mmHg, heart rate of 60 beats per minute, respiratory rate was 18 breaths per minute, oxygen saturation of 98% on room air, and a temperature of 36.7°C. The patient had a typical Cushingoid appearance with a moon face, buffalo hump, purple striae on the abdomen, central obesity, and hyperpigmentation of the skin. Submandibular lymph nodes were enlarged bilaterally. The examination of the submandibular lymph nodes showed a firm, fixed mass extending from the angle of the mandible to the submental space on the left side. Neurological examination showed weakness in both legs bilaterally (strength 3/5) and anosmia (checked by orthonasal smell test). The rest of the neurological exam was normal. Laboratory findings revealed (in Table 1) a marked hypokalemia of 2.49 mmol/L and hyperglycemia of 6.52 mmol/L. The serum cortisol level was elevated at 1587 nmol/L. Serum ACTH levels were raised at 106 ng/L (normal value ≤50 ng/L). Moreover, the high-dose dexamethasone suppression test failed to lower the serum ACTH levels and serum and urine cortisol. Serum cortisol level after the suppression test was 1750 nmol/L, while 24-hour urine cortisol after the test was 5959.1 nmol/24hr. Serum ACTH levels after the test also remained high at 100mg/L. This indicated failure of ACTH suppression by high-dose dexamethasone, which points towards ectopic ACTH production. Other blood tests (complete blood count, liver function tests) were insignificant. A computed tomography scan with contrast (CT scan) of the chest, abdomen, and pelvis, with a special focus on the adrenals, was negative for any malignancy or masses. CT scan of the neck showed bilaterally enlarged submandibular lymph nodes and an enlarged right lobe of the thyroid with nodules. Fine needle aspiration (FNA) of the thyroid nodules revealed a benign nature. Magnetic resonance imaging (MRI) of the brain showed a contrast-enhancing soft tissue lesion (18x18x10mm) in the midline olfactory groove area with extension into the frontal dura and superior sagittal sinus, suggesting recurrence of the previous ONB. There was evidence of previous surgery also. The pituitary gland was normal (Figures 1-2). Figure 1: A brain MRI (T1-weighted; without contrast; sagittal plane) shows a soft tissue lesion located in the midline olfactory groove area. Dural surface with extension into anterior frontal dura. MRI: Magnetic resonance imaging Figure 2: A brain MRI (T2-weighted; without contrast; axial plane) shows a soft tissue lesion located in the midline olfactory groove area. MRI: Magnetic resonance imaging Octreotide scintigraphy showed three focal abnormal uptakes in the submandibular cervical nodes. Additionally, there was a moderate abnormal uptake at the midline olfactory groove with bilateral extension (Figure 3). Figure 3: Whole-body octreotide scan (15 mCi 99mTc-Octreotide IV) demonstrates three focal abnormal uptakes: the largest (5.2 x 2.4 cm) in the left submandibular region, and two smaller ones on the right, suggestive of lymph node uptake. Additional abnormal uptake was seen along the midline of the olfactory groove region with bilateral extension. No other significant abnormal uptake was identified. On microscopic examination, an excisional biopsy after the transcranial resection surgery of the frontal skull base tumor showed nests and lobules of round to oval cells with clear cytoplasm, separated by vascular and hyalinized fibrous stroma (Figures 4A-4B). Tumor cells show mild to moderate nuclear pleomorphism, and fine chromatin (Figure 4C). A fibrillary neural matrix is also present. Some mitotic figures can be seen. Immunohistochemical stains revealed positive staining for synaptophysin (Figure 4D) and chromogranin (Figure 4E). Stains for CK (AE1/AE3), CD45, Desmin, and Myogenin are negative. Immunostaining for ACTH was focally positive (Figure 4F), while the specimen of the cervical lymph nodes showed the same staining, indicating metastases. The cytomorphologic and immunophenotypic features observed are consistent with a Hyams grade II ONB, with ectopic ACTH production. Figure 4: Histopathological and immunohistochemical findings of olfactory neuroblastoma. A (100x magnification) and B (200x magnification) - hematoxylin and eosin (H-E) staining shows cellular nests of round blue cells separated by hyalinized stroma. C (400x magnification) - nuclei show mild to moderate pleomorphism with fine chromatin. D (100x magnification) - an immunohistochemical stain for synaptophysin shows diffuse, strong cytoplasmic positivity within tumor cells. E (200x magnification) - tumor cells are positive for chromogranin. F (400x magnification) - ACTH cytoplasmic expression in tumor cells. ACTH: adrenocorticotropic hormone For his resistant hypokalemia, he had to be given intravenous (IV) and oral potassium chloride (KCL) repeatedly. The patient underwent transcranial resection of the frontal skull base tumor. The patient received cefazolin for seven days, and hydrocortisone for four days. After transcranial resection, his cortisol level decreased to 700 nmol/L. Furthermore, ACTH dropped, and serum potassium also normalized. Subsequently, the patient was transferred to the intensive care unit (ICU) for meticulous monitoring and continued care. In the ICU, the patient developed one episode of a generalized tonic-clonic seizure, which aborted spontaneously, and the patient received phenytoin and levetiracetam to prevent other episodes. A right-sided internal jugular vein and left transverse sinus thrombosis were also developed and treated with enoxaparin sodium. Following surgery, his low potassium levels improved, resulting in an improvement in his limb weakness. His other symptoms also gradually improved after surgery. Three weeks following the primary tumor resection, he underwent bilateral neck dissection with right hemithyroidectomy, for removal of the metastases. The patient opted out of chemotherapy and planned for an international transfer to his home country for further management. Other treatments that he received during hospitalization were ceftriaxone, azithromycin, and Augmentin®. Insulin was used to manage his diabetes, perindopril to regulate his blood pressure, and spironolactone to increase potassium retention. Omeprazole was administered to prevent GI bleeding and heartburn/gastroesophageal reflux disease relief after discharge. Discussion ONB was first described in 1924, and it is a rare neuroectodermal tumor that accounts for 2% of tumors affecting the nasal cavity [11]. Even though ONB has a good survival rate, long-term follow-up is necessary due to the disease's high recurrence rate [2]. ONB recurrence has been approximated to range between 30% and 60% after successful treatment of the primary tumor [12]. Recurrent disease is usually locoregional and tends to have a long interval to relapse with a mean of six years [12]. The first reported case of ectopic ACTH syndrome caused by ONB was in 1987 by M Reznik et al., who reported a 48-year-old woman with ONB who developed a Cushing-like syndrome 28 months before her death [13]. The occurrence of Cushing’s syndrome due to ectopic ACTH can occur either in the initial tumor or even years later during its course or after recurrence [3,6,9,14]. Similar to the case of Abe et al. [3], our patient also presented with muscle weakness due to hypokalemia, which is a feature of Cushing’s syndrome. Hypokalemia is present at diagnosis in 64% to 86% of cases of EAS and is resistant to treatment [9,14], as seen in our case. In our patient, the exact time of development of Cushing’s syndrome could not be ascertained due to the non-availability of previous records. However, according to the patient, he started developing abdominal obesity, pigmentation, and buffalo hump in 2021 about two years after his second surgery for ONB. The distinction between pituitary ACTH and ectopic ACTH involves utilizing CT/MRI of the pituitary, corticotropin-releasing hormone (CRH) stimulation test with petrosal sinus blood sampling, high dose dexamethasone suppression test, and checking serum K+ (more commonly low in ectopic ACTH) [2,15,16]. In our case, a CRH stimulation test was not available but CT/MRI brain, dexamethasone test, low serum potassium, plus the postoperative fall in cortisol levels, all pointed towards an ectopic ACTH source. Conclusions In conclusion, this case highlights the rare association between ONB and ectopic ACTH syndrome, which developed after tumor recurrence. The patient's unique presentation of bilateral lower limb weakness and hypokalemia can cause diagnostic challenges, emphasizing the need for comprehensive diagnostic measures. Surgical intervention proved crucial, with postoperative cortisol values becoming normal, highlighting the efficacy of this approach. The occurrence of ectopic ACTH production in ONB patients, although very rare, is emphasized, so that healthcare professionals who deal with these tumors are aware of this complication. This report contributes valuable insights shedding light on the unique ONB manifestation causing ectopic ACTH syndrome. The ongoing monitoring of the patient's clinical features will further enrich the understanding of the course of this uncommon phenomenon in the medical literature. References Thompson LD: Olfactory neuroblastoma. Head Neck Pathol. 2009, 3:252-9. 10.1007/s12105-009-0125-2 Abdelmeguid AS: Olfactory neuroblastoma. Curr Oncol Rep. 2018, 20:7. 10.1007/s11912-018-0661-6 Abe H, Suwanai H, Kambara N, et al.: A rare case of ectopic adrenocorticotropic hormone syndrome with recurrent olfactory neuroblastoma. Intern Med. 2021, 60:105-9. 10.2169/internalmedicine.2897-19 Yin Z, Wang Y, Wu Y, et al.: Age distribution and age-related outcomes of olfactory neuroblastoma: a population-based analysis. Cancer Manag Res. 2018, 10:1359-64. 10.2147/CMAR.S151945 Platek ME, Merzianu M, Mashtare TL, Popat SR, Rigual NR, Warren GW, Singh AK: Improved survival following surgery and radiation therapy for olfactory neuroblastoma: analysis of the SEER database. Radiat Oncol. 2011, 6:41. 10.1186/1748-717X-6-41 Elkon D, Hightower SI, Lim ML, Cantrell RW, Constable WC: Esthesioneuroblastoma. Cancer. 1979, 44:3-1087. 10.1002/1097-0142(197909)44:3<1087::aid-cncr2820440343>3.0.co;2-a Nieman LK, Biller BM, Findling JW, Newell-Price J, Savage MO, Stewart PM, Montori VM: The diagnosis of Cushing's syndrome: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2008, 93:1526-40. 10.1210/jc.2008-0125 Chabre O: Cushing syndrome: physiopathology, etiology and principles of therapy [Article in French]. Presse Med. 2014, 43:376-92. 10.1016/j.lpm.2014.02.001 Isidori AM, Lenzi A: Ectopic ACTH syndrome. Arq Bras Endocrinol Metabol. 2007, 51:1217-25. 10.1590/s0004-27302007000800007 Kunc M, Gabrych A, Czapiewski P, Sworczak K: Paraneoplastic syndromes in olfactory neuroblastoma. Contemp Oncol (Pozn). 2015, 19:6-16. 10.5114/wo.2015.46283 Finlay JB, Abi Hachem R, Jang DW, Osazuwa-Peters N, Goldstein BJ: Deconstructing olfactory epithelium developmental pathways in olfactory neuroblastoma. Cancer Res Commun. 2023, 3:980-90. 10.1158/2767-9764.CRC-23-0013 Ni G, Pinheiro-Neto CD, Iyoha E, et al.: Recurrent esthesioneuroblastoma: long-term outcomes of salvage therapy. Cancers (Basel). 2023, 15:1506. 10.3390/cancers15051506 Reznik M, Melon J, Lambricht M, Kaschten B, Beckers A: Neuroendocrine tumor of the nasal cavity (esthesioneuroblastoma). Apropos of a case with paraneoplastic Cushing's syndrome [Article in French]. Ann Pathol. 1987, 7:137-42. Kadoya M, Kurajoh M, Miyoshi A, et al.: Ectopic adrenocorticotropic hormone syndrome associated with olfactory neuroblastoma: acquirement of adrenocorticotropic hormone expression during disease course as shown by serial immunohistochemistry examinations. J Int Med Res. 2018, 46:4760-8. 10.1177/0300060517754026 Clotman K, Twickler MTB, Dirinck E, et al.: An endocrine picture in disguise: a progressive olfactory neuroblastoma complicated with ectopic Cushing syndrome. AACE Clin Case Rep. 2017, 3:278-83. 10.4158/EP161729.CR Chung YS, Na M, Ku CR, Kim SH, Kim EH: Adrenocorticotropic hormone-secreting esthesioneuroblastoma with ectopic Cushing’s syndrome. Yonsei Med J. 2020, 61:257-61. 10.3349/ymj.2020.61.3.257 From https://www.cureus.com/articles/226080-olfactory-neuroblastoma-causing-cushings-syndrome-due-to-the-ectopic-adrenocorticotropic-hormone-acth-secretion-a-case-report?score_article=true#!/
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  7. Abstract Background The aim of this study was to investigate the clinical features and treatment options for pediatric adrenal incidentalomas(AIs) to guide the diagnosis and treatment of these tumors. Methods The clinical data of AI patients admitted to our hospital between December 2016 and December 2022 were collected and retrospectively analyzed. All patients were divided into neonatal and nonneonatal groups according to their age at the time of the initial consultation. Results In the neonatal group, 13 patients were observed and followed up, and the masses completely disappeared in 8 patients and were significantly reduced in size in 5 patients compared with the previous findings. Four patients ultimately underwent surgery, and the postoperative pathological diagnosis was neuroblastoma in three patients and teratoma in one patient. In the nonneonatal group, there were 18 cases of benign tumors, including 9 cases of ganglioneuroma, 2 cases of adrenocortical adenoma, 2 cases of adrenal cyst, 2 cases of teratoma, 1 case of pheochromocytoma, 1 case of nerve sheath tumor, and 1 case of adrenal hemorrhage; and 20 cases of malignant tumors, including 10 cases of neuroblastoma, 9 cases of ganglioneuroblastoma, and 1 case of adrenocortical carcinoma. Conclusions Neuroblastoma is the most common type of nonneonatal AI, and detailed laboratory investigations and imaging studies are recommended for aggressive evaluation and treatment in this population. The rate of spontaneous regression of AI is high in neonates, and close observation is feasible if the tumor is small, confined to the adrenal gland and has no distant metastasis. Peer Review reports Background The incidence of adrenal incidentaloma (AI) is increasing due to the increased frequency of imaging and improved imaging sensitivity [1]. AI is relatively common in adults, and several organizations, such as the American Association of Clinical Endocrinologists/American Association of Endocrine Surgeons and the European Society Endocrinology, have proposed specific protocols to guide the evaluation, treatment, and follow-up management of AI in adults [2]. Although AI, a nonfunctioning adrenocortical adenoma, is most common in adults, neuroblastoma is the most common incidental tumor of the adrenal gland in children. In addition, in the neonatal period, which is a more complex stage of childhood, the biology of adrenal masses found in this age group is also more specific, and the nature of these masses can range from spontaneous regression to rapid progression to aggressive disease with metastatic dissemination and even death. Given that AI is the most common malignant tumor, the management of AI in children cannot be simply based on the measurements used in adult AI. In this study, we retrospectively analyzed the clinical data of pediatric AI patients in a single center to investigate the clinical characteristics and management of AI in children. Methods A total of 66 children with adrenal tumors were diagnosed and treated at the Department of Urology of the Children’s Hospital of Nanjing Medical University from December 2016 to December 2022. A total of 55 cases were detected during physical examination, or the patients were diagnosed and received treatment for diseases other than adrenal disease after excluding adrenal tumors detected due to typical clinical manifestations or signs such as centripetal obesity and precocious puberty. Research protocols involving human materials were approved by the Medical Ethics Committee of the Children’s Hospital of Nanjing Medical University. All clinical information, radiological diagnosis, laboratory test results, intervention results, and follow-up data were collected from the department’s database. All the children underwent ultrasonography and CT scanning, and 11 children underwent MRI. In addition to routine tests such as blood routine and biochemical indexes, the examination and evaluation of adrenal endocrine hormones and tumor markers included (1) plasma cortisol and ACTH levels, (2) plasma catecholamine and metabolite determination, (3) plasma renin and plasma aldosterone, (4) urinary vanillylmandelic acid/homovanillic acid(VMA/HVA), and (5) AFP, CEA, NSE, and CA19-9. Five patients underwent a low-dose dexamethasone suppression test. Seventeen of the 55 patients were treated with watch-waiting therapy, 4 of the 17 ultimately underwent surgery, 4 of the 38 patients underwent tumor biopsy, and 34 underwent adrenalectomy. The data were analyzed using Graph Pad Prism 8. The measurement data are expressed as ‾x ± sd. The maximum diameter of the tumors, age of the patients with benign and malignant tumors, and maximum diameter of the tumors between the laparoscopic surgery group and the open surgery group were compared using paired t tests, and the percentages of the count data were compared using Fisher’s exact test. Results In this study, all patients were divided into two groups according to their age at the time of consultation: the neonate group and the nonneonate group. Neonate group: There were 7 male and 10 female patients, 7 of whom were diagnosed via prenatal examination and 10 of whom were diagnosed after birth. Five patients were diagnosed with lesions on the left side, 12 patients were diagnosed with lesions on the right side, and the maximal diameters of the masses ranged from 16 to 48 mm. The characteristics of the AIs in the neonate group are presented in Table 1. Table 1 Characteristics of AI in the neonates group Full size table Among the 17 patients, 8 had cystic masses with a maximum diameter of 16∼48 mm, 5 had cystic-solid masses with a maximum diameter of 33∼39 mm, and 4 had solid masses with a maximum diameter of 18∼45 mm. Two patients with solid adrenal gland masses suggested by CT scan had obvious elevations in serum NSE and maximum diameters of 44 and 45 mm, respectively. These patients underwent adrenal tumor resection, and the pathology diagnosed that they had neuroblastomas(NB). In one patient, the right adrenal gland was 26 × 24 × 27 mm in size with slightly elevated echogenicity at 38 weeks after delivery, and the mass increased to a size of 40 × 39 × 29 mm according to the 1-month postnatal review. MRI suggested that the adrenal gland tumor was associated with liver metastasis, and the pathology of the tumor suggested that it was NB associated with liver metastasis after surgical resection (stage 4 S, FH). One child was found to have 25 × 24 × 14 mm cystic echoes in the left adrenal region during an obstetric examination, and ultrasound revealed 18 × 11 mm cystic solid echoes 5 days after birth. Ultrasound revealed 24 × 15 mm cystic solid echoes at 2 months. Serum NSE and urinary VMA were normal, and the tumor was excised due to the request of the parents. Pathology suggested a teratoma in the postoperative period. A total of 13 children did not receive surgical treatment or regular review via ultrasound, serum NSE or urine VMA. The follow-up time ranged from 1 to 31 months, with a mean of 9.04 ± 7.61 months. Eight patients had complete swelling, and 5 patients were significantly younger than the previous patients. Nonneonate group: There were 24 male and 14 female patients in the nonneonate group; 24 patients had lesions on the left side, 14 patients had lesions on the right side, and the maximal diameters of the masses ranged from 17 to 131 mm. Most of these tumors were found during routine physical examinations or incidentally during examinations performed for various complaints, such as gastrointestinal symptoms, respiratory symptoms, or other related conditions. As shown in Table 2, abdominal pain was the most common risk factor (44.7%) for clinical onset, followed by routine physical examination and examination for respiratory symptoms. Table 2 Clinical presentations leading to discovery of AI in non-neonate group Full size table Among the 38 patients, 10 had NBs with maximum diameters ranging from 20 to 131 mm, 9 had ganglion cell neuroblastomas with maximum diameters ranging from 33.6 to 92 mm, 9 had ganglion cell neuromas with maximum diameters ranging from 33 to 62 mm, 2 had adrenal adenomas with maximum diameters ranging from 17 to 70 mm, 1 had a cortical carcinoma with a maximum diameter of 72 mm, 2 had adrenal cysts with maximum diameters ranging from 26 to 29 mm, 2 had mature teratomas with maximum diameters of 34 and 40 mm, 1 had a pheochromocytoma with a diameter of 29 mm, 1 had a nerve sheath tumor with a diameter of 29 mm, and 1 patient with postoperative pathological confirmation of partial hemorrhagic necrosis of the adrenal gland had focal calcification with a maximum diameter of 25 mm (Table 3). Table 3 Distribution of different pathologies among AI with various sizes in non-neonate group Full size table The mean age of children with malignant tumors was significantly lower than that of children with benign tumors (57.95 ± 37.20 months vs. 105.0 ± 23.85 months; t = 4.582, P < 0.0001). The maximum diameter of malignant tumors ranged from 20 to 131 mm, while that of benign tumors ranged from 17 to 72 mm, and the maximum diameter of malignant tumors was significantly greater than that of benign tumors (65.15 ± 27.61 mm v 37.59 ± 12.98 mm; t = 3.863, P = 0.0004). Four biopsies, 5 laparoscopic adrenal tumor resections and 11 open adrenal tumor resections were performed for malignant tumors, and 16 laparoscopic adrenal tumor resections and 2 open procedures were performed for benign tumors. The maximum diameter of the tumors ranged from 17 to 62 mm in 21 children who underwent laparoscopic surgery and from 34 to 99 mm in 13 children who underwent open resection; there was a statistically significant difference in the maximum diameter of the tumors between the laparoscopic surgery group and the open surgery group (35.63 ± 10.36 mm v 66.42 ± 20.60 mm; t = 5.798, P < 0.0001). Of the 42 children with definitive pathologic diagnoses at surgery, 23 had malignant tumors, and 19 had benign tumors. There were 15 malignant tumors with calcification on imaging and 5 benign tumors. The percentage of malignant tumors with calcifications in was significantly greater than that of benign tumors (65.22% v 26.32%; P = 0.0157). In the present study, all the children underwent CT, and 31 patients had postoperative pathological confirmation of NB. A total of 26 patients were considered to have neurogenic tumors according to preoperative CT, for a diagnostic compliance rate of 83.97%. Three children were considered to have cortical adenomas by preoperative CT, and 1 was ultimately diagnosed by postoperative pathology, for a diagnostic compliance rate of 33.33%. For 4 patients with teratomas and adrenal cysts, the CT findings were consistent with the postoperative pathology. According to our research, NB 9-110HU, GNB 15-39HU, GB 19-38HU, ACA 8HU, adrenal cyst 8HU, and cellular achwannoma 17HU. Discussion According to the clinical practice guidelines developed by the European Society of Endocrinology and European Network for the Study of Adrenal Tumors, AI is an adrenal mass incidentally detected on imaging not performed for a suspected adrenal disease [3]. The prevalence of AI is approximately 4%, and the incidence increases with age [4]. Most adult AIs are nonfunctioning benign adrenal adenomas (up to 75%), while others include functioning adrenal adenomas, pheochromocytomas, and adrenocortical carcinomas [5]. In contrast to the disease spectrum of adult AI cases, NB is the most common tumor type among children with AI, and benign cortical adenomas, which account for the vast majority of adult AI, accounting for less than 0.5% of cases in children [6]. According to several guidelines, urgent assessment of an AI is recommended in children because of a greater likelihood of malignancy [3, 7]. When an adult patient is initially diagnosed with AI, it should be clear whether the lesion is malignant and functional. In several studies, the use of noncontrast CT has been recommended as the initial imaging method for adrenal incidentaloma; a CT attenuation value ≤ 10 HU is used as the diagnostic criterion for benign adenomas; and these methods have a specificity of 71-79% and a sensitivity of 96-98% [8, 9]. A CT scan of tumors with diameters greater than 4 to 6 cm, irregular margins or heterogeneity, a CT attenuation value greater than 10 HU, or a relative contrast enhancement washout of less than 40% 10 or 15 min after administration of contrast media on enhanced CT is considered to indicate potential malignancy [7]. As the most common AI in children, NB often appears as a soft tissue mass with uneven density on CT, often accompanied by high-density calcified shadows, low-density cystic lesions or necrotic areas. CT scans can easily identify more typical NBs, and for those AIs that do not show typical calcified shadows on CT, it is sometimes difficult to differentiate neurogenic tumors from adenomas. In these patients, except for the 1 patient with adrenal cysts who had a CT value of 8 HU, very few of the remaining AI patients had a CT value less than 10 HU. Therefore, the CT value cannot be used simply as a criterion for determining the benign or malignant nature of AI, and additional imaging examinations, such as CT enhancement, MRI, and FDG-PET if necessary, should be performed immediately for AI in children. Initial hormonal testing is also needed for functional assessment, and aldosterone secretion should also be assessed when the patient is hypertensive or hypokalemic [7]. Patients with AI who are not suitable for surgery should be observed during the follow-up period, and if abnormal adrenal secretion is detected or suggestive of malignancy during this period, prompt adrenal tumor resection is needed. For adult patients with AI, laparoscopic adrenal tumor resection is one of the most effective treatments that has comparative advantages in terms of hospitalization time and postoperative recovery speed; however, there is still some controversy over whether to perform laparoscopic surgery for some malignant tumors with large diameters, especially adrenocortical carcinomas, and some studies have shown that patients who undergo laparoscopic surgery are more prone to peritoneal seeding of tumors [10]. The maximum diameter of an adult AI is a predictor of malignancy, and a study by the National Italian Study Group on Adrenal Tumors, which included 887 AIs, showed that adrenocortical carcinoma was significantly correlated with the size of the mass, and the sensitivity of detecting adrenocortical carcinoma with a threshold of 4 cm was 93% [11]. According to the National Institutes of Health, patients with tumors larger than 6 cm should undergo surgical treatment, while patients with tumors smaller than 4 cm should closely monitored; for patients with tumors between 4 and 6 cm, the choice of whether to be monitored or surgically treated can be based on other indicators, such as imaging [12]. A diameter of 4 cm is not the initial threshold for determining the benign or malignant nature of a mass in children. In a study of 26 children with AI, Masiakos et al. reported that 9 of 18 benign lesions had a maximal diameter less than 5 cm, 4 of 8 malignant lesions had a maximal diameters less than 5 cm, and 2 had a diameter less than 3 cm. The mean maximal diameter of benign lesions was 4.2 ± 1.7 cm, whereas the mean maximum diameter of malignant lesions was 5.1 ± 2.3 cm. There was no statistically significant difference between the two comparisons; therefore, this study concluded that children with AI diameters less than 5 cm cannot be treated expectantly [6]. Additionally, this study revealed that malignant lesions occurred significantly more frequently than benign lesions in younger children (mean age 1.7 ± 1.8 years v 7.8 ± 5.9 years; P = 0.02). In the nonneonatal group of this study, 20 patients with malignant tumors had maximum diameters ranging from 20 to 131 mm, 10 had malignant tumors larger than 60 mm, and 3 had tumors smaller than 40 cm; 18 patients with benign tumors had maximum diameters ranging from 17 to 70 mm, 5 had diameters ranging from 40 to 60 mm, and 5 had diameters larger than 60 mm. Therefore, it is not recommended to use the size of the largest diameter of the tumor to decide whether to wait and observe or intervene surgically for children with AI. Instead, it is necessary to consider the age of the child; laboratory test results, such as whether the tumor indices are elevated or not; whether the tumor has an endocrine function; etc.; and imaging test results to make comprehensive judgments and decisions. Preoperative aggressive evaluation and prompt surgical treatment are recommended for nonneonatal pediatric AI patients. Adrenal hematoma and NBs are the most common types of adrenal area masses in children, while pheochromocytoma, adrenal cyst, and teratoma are rarer masses [13]. In clinical practice, adrenal hematoma and NB are sometimes difficult to differentiate, especially when adrenal masses are found during the prenatal examination and neonatal period, and such children need to be managed with caution. The Children’s Oncology Group (COG ANBL00B1) implemented the watchful waiting treatment for children under 6 months of age with a solid adrenal mass < 3.1 cm in diameter (or a cystic mass < 5 cm) without evidence of distant metastasis, and if there is a > 50% increase in the adrenal mass volume, there is no return to the baseline VMA or HVA levels, or if there is a > 50% increase in the urinary VMA/HVA ratio or an inversion, surgical resection should be performed [14]. Eighty-three children in this study underwent expectant observation, 16 of whom ultimately underwent surgical resection (8 with INSS stage 1 NB, 1 with INSS stage 2B, 1 with INSS stage 4 S, 2 with low-grade adrenocortical neoplasm, 2 with adrenal hemorrhage, and 2 with extralobar pulmonary sequestration). Most of the children who were observed had a reduced adrenal mass volume. Of the 56 patients who completed the final 90 weeks of expectant observation, 27 (48%) had no residual mass, 13 (23%) had a residual mass volume of 0–1 ml, 8 (14%) had a mass volume of 1–2 ml, and 8 (14%) had a volume of > 2 ml; ultimately, 71% of the residual masses had a volume ≤ 1 ml and 86% had a residual volume ≤ 2 ml. In this study, a total of 16 patients were included in the watchful waiting treatment group; 3 patients underwent surgical treatment during the follow-up period, and 13 patients ultimately completed watchful waiting treatment. After 1–31 months of follow-up, 8 patients’ swelling completely disappeared, and 5 patients’ swelling significantly decreased. After strict screening for indications and thorough follow-up review, AIs in the neonatal period can be subjected to watchful waiting treatment, and satisfactory results can be achieved. For benign adrenal tumors, laparoscopic surgery is superior to open surgery in terms of successful resection, whereas the feasibility of minimally invasive surgery for AI with preoperative suspicion of malignancy is controversial. The European Cooperative Study Group for Pediatric Rare Tumors recommends that minimally invasive surgery be considered only for early childhood tumors and should be limited to small, localized tumors; additionally, imaging should suggest no invasion of surrounding tissue structures or lymph nodes; and this strategy requires surgeons with extensive experience in oncologic and adrenal surgery [15]. NB is the most common pediatric AI, and open tumor resection remains the mainstay of treatment. For small, early tumors without evidence of invasion on preoperative examination, laparoscopic resection may be considered if the principles of oncologic surgery can be adhered to. If the patient responds to chemotherapy, the decision to perform laparoscopic tumor resection can also be re-evaluated after chemotherapy. According to the current study, the recurrence and mortality rates of laparoscopic surgery are comparable to those of open surgery [16, 17]. The relative contraindications for laparoscopic NB resection include a tumor diameter greater than 6 cm, venous dilatation, and the involvement of adjacent organs or blood vessels [18]. Patients who undergo open adrenalectomy have higher overall survival and recurrence-free survival rates than patients who undergo laparoscopic adrenalectomy [19]. Open adrenalectomy remains the gold standard for surgical resection of adrenocortical carcinoma, whereas laparoscopic adrenalectomy should be reserved for highly selected patients and performed by surgeons with appropriate expertise [20]. Cortical tumors are particularly rare among children with AIs and are sometimes not clearly distinguishable from neurogenic tumors on preoperative imaging; in such patients, the presence of subclinical Cushing’s syndrome needs to be carefully evaluated preoperatively; otherwise, a perioperative adrenal crisis may occur [21]. In patients in whom the possibility of an adrenocortical tumor was considered preoperatively, the assessment for subclinical Cushing’s syndrome mainly involved assessing the serum dehydroepiandrosterone sulfate level and performing an overnight dexamethasone suppression test. A procedure for evaluating pediatric AI is shown in Fig. 1. Imaging is the first step in the evaluation of AI in children. CT can be used to clarify the nature of most tumors. MRI can be used to evaluate imaging risk factors (IDRFs) for NB. Bone marrow cytomorphology is recommended for all children with AI, along with microscopic residual neuroblastoma testing and further bone scanning if the bone marrow examination is positive. In addition, serum tumor marker levels and other relevant tests should be performed, and hormone levels should be evaluated. If adrenal adenomas cannot be completely excluded during the preoperative examination, a 1 mg overnight dexamethasone suppression test should be performed to exclude subclinical Cushing’s syndrome. In patients with hypertensive hypokalemia, the presence of aldosteronism should be evaluated by testing plasma aldosterone concentrations and plasma renin activity. Adrenal masses found in the neonatal period can be observed if the tumor is small, confined to the adrenal gland and shows no evidence of distant metastasis, while tumors that increase significantly in size during the follow-up period or that are associated with persistently elevated tumor markers require aggressive surgical treatment. Fig. 1 Algorithm for the evaluation and management of a pediatric adrenal incidentaloma. *DST overnight :20µg/kg dexamethasoneweight ˂40 kg,1 mg dexamethasone if ≥ 40 kg. CT = computed tomographic;MRI = magnetic resonance imaging;NSE = neuron-specific enolase;AFP = alpha-fetoprotein;CEA = carcinoembryonic antigen;CA19-9 = cancerantigen19-9;ACTH = adrenocorticotropic hormone;PAC = plasma aldosterone concentration; PRA = plasma renin activity;DST = dexamethasone suppression test Full size image Data availability The datasets analyzed during the current study are not public, but are available from the corresponding author on reasonable request. Abbreviations CT: computed tomographic MRI: magnetic resonance imaging ACTH: adrenocorticotropic hormone VMA: vanillylmandelic acid HVA: homovanillic Acid AFP: alpha-fetoprotein CEA: carcinoembryonic antigen NSE: neuron-specific enolase CA19-9: cancerantigen19-9 FH: favorable histology HU: Hounsfiled Unit COG: Children’s Oncology Group INSS: International Neuroblastoma Staging System References Barzon L, Sonino N, Fallo F, Palu G, Boscaro M. Prevalence and natural history of adrenal incidentalomas. Eur J Endocrinol. 2003;149(4):273–85. Article CAS PubMed Google Scholar Maas M, Nassiri N, Bhanvadia S, Carmichael JD, Duddalwar V, Daneshmand S. Discrepancies in the recommendedmanagement of adrenalincidentalomas by variousguidelines. J Urol. 2021;205(1):52–9. Article PubMed Google Scholar Fassnacht M, Tsagarakis S, Terzolo M, et al. European Society of Endocrinology clinical practice guidelines on the management of adrenal incidentalomas, in collaboration with the European network for the study of adrenal tumors. Eur J Endocrinol. 2023;189(1):G1–42. Article PubMed Google Scholar Young WFJr. Clinical practice. The incidentally discovered adrenal mass. N Engl J Med. 2007;356(6):601–10. Article Google Scholar Rowe NE, Kumar R, Schieda N, et al. Diagnosis, management, and follow-up of the incidentallydiscoveredadrenalmass: CUAguidelineendorsed by the AUA. J Urol. 2023;210(4):590–9. Article PubMed Google Scholar Masiakos PT, Gerstle JT, Cheang T, Viero S, Kim PC, Wales P. Is surgery necessary for incidentally discovered adrenal masses in children?J. Pediatr Surg. 2004;39(5):754–8. Article Google Scholar Lee JM, Kim MK, Ko SH et al. Clinical guidelines for the management of adrenal incidentaloma. Endocrinol Metab. 2017;32(2). Terzolo M, Stigliano A, Chiodini I, et al. AME position statement on adrenal incidentaloma. Eur J Endocrinol. 2011;164(6):851–70. Article CAS PubMed Google Scholar Boland GW, Blake MA, Hahn PF, Mayo-Smith WW. Incidental adrenal lesions: principles, techniques, and algorithms for imaging characterization. Radiology. 2008;249(3):756–75. Article PubMed Google Scholar Payabyab EC, Balasubramaniam S, Edgerly M, et al. Adrenocortical cancer: a molecularlycomplexdiseasewheresurgerymatters. Clin Cancer Res. 2016;22(20):4989–5000. Article CAS PubMed Google Scholar Angeli A, Osella G, Alì A, Terzolo M. Adrenal incidentaloma: an overview of clinical and epidemiological data from the National Italian Study Group. Horm Res. 1997;47(4–6):279–83. Article CAS PubMed Google Scholar Grumbach MM, Biller BM, Braunstein GD, et al. Management of the clinically inapparent adrenal mass (incidentaloma). Ann Intern Med. 2003;138(5):424–9. Article PubMed Google Scholar Zhang K, Zhang Y, Zhang Y, Chao M. A retrospective analysis of the clinical characteristics of 207 hospitalized children with adrenal masses. Front Pediatr. 2023;11:1215095. Article PubMed PubMed Central Google Scholar Nuchtern JG, London WB, Barnewolt CE, et al. A prospective study of expectant observation as primary therapy for neuroblastoma in young infants: a Children‘s oncology group study. Ann Surg. 2012;256(4):573–80. Article PubMed Google Scholar Virgone C, Roganovic J, Vorwerk P, et al. Adrenocortical tumours in children and adolescents: the EXPeRT/PARTNER diagnostic and therapeutic recommendations. Pediatr Blood Cancer. 2021;68(suppl 4):e29025. Article PubMed Google Scholar Chang S, Lin Y, Yang S, et al. Safety and feasibility of laparoscopic resection of abdominal neuroblastoma without image-defined risk factors: a single-center experience. World J Surg Oncol. 2023;21(1):113. Article PubMed PubMed Central Google Scholar Zenitani M, Yoshida M, Matsumoto S, et al. Feasibility and safety of laparoscopic tumor resection in children with abdominal neuroblastomas. Pediatr Surg Int. 2023;39(1):91. Article PubMed Google Scholar International Pediatric Endosurgery Group. IPEG guidelines for the surgical treatment of adrenal masses in children. J Laparoendosc Adv Surg Tech A. 2010;20(2):vii–ix. Google Scholar Nakanishi H, Miangul S, Wang R, et al. Open versuslaparoscopicsurgery in the management of adrenocorticalcarcinoma: a systematicreview and meta-analysis. Ann Surg Oncol. 2023;30(2):994–1005. Article PubMed Google Scholar Gaillard M, Razafinimanana M, Challine A, et al. Laparoscopic or openadrenalectomy for stage I-IIadrenocorticalcarcinoma: a retrospectivestudy. J Clin Med. 2023;12(11):3698. Article PubMed PubMed Central Google Scholar Utsumi T, Iijima S, Sugizaki Y, et al. Laparoscopic adrenalectomy for adrenal tumors with endocrine activity: perioperative management pathways for reduced complications and improved outcomes. Int J Urol. 2023;30(10):818–26. Article CAS PubMed Google Scholar Download references Acknowledgements We would like to express our deepest gratitude to all the patients and their parents who participated in this study. Their patience and cooperation were instrumental to the success of this research. We thank our colleagues in the Department of Radiology for their invaluable contributions in diagnosing and monitoring the progression of adrenal incidentalomas. We sincerely appreciate the hard work of the pathologists in diagnosing and classifying tumors, which laid the foundation for our study. Finally, we would like to thank our institution for providing the necessary resources and an enabling environment to conduct this research. Funding Not applicable. Author information Authors and Affiliations Department of Urology, Children’s Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, Jiangsu, China Xiaojiang Zhu, Saisai Liu, Yimin Yuan, Nannan Gu, Jintong Sha, Yunfei Guo & Yongji Deng Contributions X.J.Z. and Y.J.D designed the study; S.S.L., Y.M.Y., N.N.G., and J.T.S. carried out the study and collected important data; X.J.Z. analysed data and wrote the manuscript; Y.F.G. and Y.J.D.gave us a lot of very good advices and technical support; All authors read and approved the final manuscript. Corresponding author Correspondence to Yongji Deng. Ethics declarations Competing interests The authors declare no competing interests. Ethics approval and consent to participate Ethics approval for this study was granted by the Ethics Committee of Children’s Hospital of Nanjing Medical University. Informed written consent was obtained from all the guardians of the children and we co-signed the informed consent form with their parents before the study. We confirmed that all methods were performed in accordance with relevant guidelines and regulations. Conflict of interest There are no conflicts of interest. Additional information Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Reprints and permissions From https://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-024-04673-7
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  8. This article costs $70 to buy https://doi.org/10.1136/bcr-2024-259687 Doctors should suspect Cushing’s syndrome when they see patients with purple stretch marks and metabolic conditions such as diabetes, even if those symptoms aren’t the reasons for a medical visit, physicians in Japan wrote in a case study describing how they reached that diagnosis for a woman in her early 30s.
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  9. Medically reviewed by Daniel More, MD You may notice that your face appears puffy or more round on certain days. This can happen as your weight and hormones fluctuate or when you experience allergies or a temporary illness. However, if the puffiness persists or if your facial swelling is severe, this may be a sign of moon face—a condition that causes your face to become rounder due to fluid buildup. Symptoms Moon face causes swelling in your face as a result of excess fluid buildup. You may notice extra puffiness in your cheeks, forehead, and chin. When your facial features enlarge, it creates a round shape that mimics the look of the moon—hence the name, "moon face." It’s important to pay attention to the way your face feels. Sometimes, moon face is mild and not easily noticeable. But other times, moon face can be painful or affect your breathing. Keep track of any pain and swelling you're experiencing. Before seeing a healthcare provider, it can also help to document the following: What pain you're feeling Where the pain is located When your swelling began What improves and worsens your pain and swelling Any other symptoms that accompany puffiness These notes can help your healthcare provider understand the severity of your symptoms and recommend appropriate treatment options. Causes A variety of factors can cause moon face—ranging from mild everyday reactions to more serious conditions. Infections Underlying infections and medical conditions can cause facial swelling and increase your risk of moon face. These include: Conjunctivitis, or “pink eye” Infection in your salivary glands (the glands that produce saliva) Sinusitis, or swelling of your sinuses Styes that cause swelling around your eye Tooth abscesses, or infections in your teeth that cause a pocket of pus Cellulitis, a type of bacterial skin infection Cushing's Syndrome Among the most common causes of moon face is Cushing's syndrome—a condition that occurs when your body makes too much cortisol, which is commonly referred to as the "stress hormone." One of the most common symptoms of Cushing's syndrome is moon face, but you might also experience darkening of the skin, weight gain, and muscle weakness. Corticosteroids If your body doesn’t produce enough cortisol, your healthcare provider may prescribe corticosteroids. These anti-inflammatory drugs can also help treat several conditions such as arthritis, severe allergies, multiple sclerosis, lupus, certain kinds of cancer, and other conditions related to your lungs, skin, eyes, blood, kidneys, thyroid, stomach, or intestines. One of the most common corticosteroids is Deltasone (prednisone). Excess amounts or long-term use of corticosteroids can cause moon face to occur. Medical Side Effects Besides corticosteroids, other types of medication and medical treatment can also cause moon face. Specifically, you may develop moon face as a reaction to a blood transfusion or a range of medications, such as Bayer (aspirin) and certain types of antibiotics. You can also experience moon face after head, nose, or jaw surgery. Weight Changes Both severe malnutrition (not eating enough to get the nutrients you need) and obesity may lead to moon face. Some people with malnutrition develop kwashiorkor—a condition that can lead to swelling of your arms, legs, and face. This can happen because not eating enough food or drinking enough water can cause low levels of fluid and force your body to retain excess salt, which can cause swelling. People with obesity may also be more likely to develop moon face. It's estimated that approximately three out of every four people with Cushing's syndrome experience obesity. When Cushing's syndrome causes excess weight on your body, you may also be at an increased risk of developing fat deposits in your face. Other Causes Other common causes of moon face include: Allergic reactions Burns or injuries to the face Angioedema—a condition that causes swelling under the skin due to an issue with your immune system functioning Myxedema, which is a severe form of hypothyroidism—a condition that occurs when your thyroid gland doesn't make enough thyroid hormone and causes symptoms like skin changes and weight gain Superior vena cava (SVC) syndrome—a condition that causes facial and neck swelling because your SVC (a type of vein in your body) becomes compressed and isn't able to drain or pump blood back to the heart How to Get Rid of Moon Face Because moon face is a symptom of other underlying health conditions, it’s best to consult a healthcare provider to understand what's causing your facial swelling and learn about treatment options. For example, if your moon face is the result of an injury, you might try using ice to reduce the swelling. In addition, propping your head up with extra pillows while you sleep may help improve fluid drainage and reduce swelling. But, if a condition like Cushing's syndrome is causing moon face, medication or surgery may help improve facial swelling. How to Prevent Moon Face There isn't one surefire way to prevent moon face—mostly because a variety of factors can cause symptoms to develop. If you are at risk or concerned about a particular cause of facial swelling, speak with your healthcare provider about your options. If you’re prescribed a corticosteroid, there are particular steps you can take to reduce your chances of developing moon face. When taking a prescribed corticosteroid like prednisone, pay close attention to your symptoms and let your healthcare provider know early if you are developing any symptoms of Cushing's syndrome, including moon face. The earlier they are able to recommend alternative treatment, the better your chances of preventing long-term swelling. When to Contact a Healthcare Provider It’s important to seek care from your provider if you have specific symptoms associated with moon face, including: Swelling that comes on suddenly, causes pain, or is severe Long-lasting swelling Signs of infection, including fever, redness, or tenderness What To Expect at Your Appointment If you seek medical care for moon face, your healthcare provider will likely begin your appointment by taking your medical history and performing a physical exam. They may also ask about: How long your face has been swollen and when it began Things that improve or worsen your symptoms What allergies you have Which medications you take Any recent facial injury, medical test, or surgery Additional symptoms you're experiencing Once they gather this information, your provider can order the necessary testing, understand the underlying cause of your symptoms, and offer treatment options for moon face. A Quick Review Moon face is a condition that occurs when fluid builds up under your skin and causes facial swelling. Several factors can cause moon face, like reactions to medication or surgery, allergies, infections, weight changes, and underlying health conditions. If you have symptoms of moon face or notice your face getting puffy without a clear reason, talk to your provider. They can help you pinpoint the underlying cause and recommend treatment. Adapted from https://www.yahoo.com/lifestyle/moon-face-180000163.html
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