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Biopsy etc. Procedures and Bronchography.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Although most hamartomas are 'like rubber in texture' and difficult to puncture with a needle, a few are vascular and are likely to bleed, down the needle or around the lesion (sometimes causing a sudden apparent increase in size on a post-biopsy CT section or chest radiograph).
Developmental Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James H. Tonsgard, Nikolas Mata-Machado
Cataracts usually do not require removal. Poor eyelid closure due to VIIth nerve injury can be surgically facilitated. Frequent eyedrops help with dryness. No treatment is currently available for retinal hamartomas.
Paper 1
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
The presence of fat and description of ‘punctate calcification’ is typical for a hamartoma, which is a benign entity. Hamartomas are usually asymptomatic and most are detected incidentally. Typically they are peripheral; a minority (10%) are endobronchial. Malignant transformation is very rare. According to the most recent 2015 British Thoracic Society guidelines, nodules with clear benign features can be discharged without further imaging. Hamartomas can demonstrate avidity on FDG PET in 20% of cases but this investigation is not warranted and likely to cause confusion rather than aid diagnosis.
Recurrent respiratory epithelial adenomatoid hamartoma of the nasal cavity
Published in Baylor University Medical Center Proceedings, 2022
Dhananjay Kumar, K. K. Handa, Aru Handa, Poonam Gautam
A hamartoma is a benign malformation or congenital error of tissue development and is indigenous to a specific part of the body. The term was first used by Albrecht in 1904. It is common in the lung, kidney, liver, spleen, and intestine but rare in the head and neck region, particularly the nasal cavity and paranasal sinuses. Respiratory epithelial adenomatoid hamartoma (REAH) is the most common hamartoma of the sinonasal tract, first recognized by Wenig and Heffner in 1995. It is defined as a tumor originating from the surface epithelium with excessive proliferation of glandular elements but not originating from the seromucinous gland. The usual age of occurrence is the third to ninth decade, and the male-to-female ratio is 3:2. Most REAHs are unilateral and occur in the posterior nasal septum; less commonly they arise in the middle meatus, lateral nasal wall, ethmoid sinus, maxillary sinus, inferior turbinate, and nasopharynx.1 The clinical presentation includes nasal obstruction, congestion, epistaxis, rhinorrhea, chronic sinusitis, facial pain, headache, and olfactory dysfunction. REAH can be misdiagnosed as inverted papilloma or well-differentiated adenocarcinoma clinically as well as histopathologically. Thus, it is important to make the correct diagnosis, as complete excision through a conservative approach is the treatment of choice for REAH.2
Long-term follow-up of adult patient with neurofibromatosis type 1 with retinal astrocytic hamartoma using spectral-domain optical coherence tomography: a review of the literature and a report of a case
Published in Ophthalmic Genetics, 2021
Solmaz Abdolrahimzadeh, Martina Formisano, Luca Scuderi, Siavash Rahimi
The exact nosographic definition of neural proliferation of the retina associated or unrelated to TSC and NF1 is difficult, if not impossible. Classically, clinically benign lesions are called hamartoma and locally aggressive lesions are called astrocytoma. However, due to the limited number of reported cases and the scarcity of histopathological analysis, the boundary between these entities is not straightforward and clinically aggressive lesions have been also called hamartoma. The classification of these lesions, by nature, is based on histopathological grounds; however, there are only few descriptions in the literature that are rather dated and describe very basic morphological features, some with electron microscopy findings, but no immunohistochemical analysis (6,34,35). The authors do not mention if there was nuclear atypia, necrosis, and mitoses. The neoplasms reported in these articles were composed of spindle-shaped cells immersed in a fibrillar network formed by the cellular processes, consistent with astrocytic proliferation. The authors called these lesions hamartoma. Martin et al. used the term “hamartoma” without histopathological analysis of the neoplasms (36).
Juvenile cataract in association with tuberous sclerosis complex
Published in Ophthalmic Genetics, 2020
A. L. Geffrey, K. R. Geenen, E. Abati, S. H. Greenstein, D. K. VanderVeen, R. L. Levy, S. L. Davidson, M. P. McGarrey, E. A. Thiele, M. E. Aronow
A 7-week-old female presented to the emergency room with infantile spasms (IS). Magnetic resonance imaging (MRI) of the brain revealed cortical tubers in the right frontal lobe and a subependymal nodule (SEN), leading to the clinical diagnosis of TSC. Genetic testing confirmed a disease-causing mutation in TSC2 (c.4919 A > G substitution in exon 37; histidine replaced by arginine). At 12 weeks of age, due to refractory seizure activity, she underwent a right frontal craniotomy with resection of a cortical tuber. Following admission for surgery, she had a baseline in-office ocular examination in anticipation of initiating vigabatrin. Examination revealed a 1 mm central opacity most consistent with an anterior subcapsular cataract in the right eye. The remainder of the ocular examination, including dilated fundus examination, was normal in both eyes. Specifically, no astrocytic hamartomas or achromic patches were observed. At 6 months follow-up, the cataract was stable. She continues to have complete ophthalmic examinations at regular intervals due to vigabatrin use and to monitor the cataract and any signs of amblyopia.