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Human immunodeficiency virus and other infectious diseases
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
Symptomatic disease includes persistent generalized lymphadenopathy, weight loss, fever, diarrhoea, neurological disease including encephalopathy and neuropathy, and a range of opportunistic infections and secondary cancers including: Pneumocystis pneumoniaCerebral toxoplasmosisCytomegalovirus (CMV) retinitisMycobacterium tuberculosis and Mycobacterium avium-intracellulareKaposi's sarcomaNon-Hodgkin's lymphomaCandidiasisCryptococcus
Infections
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The natural history of HIV/AIDS is summarized in Figure 20.3. About half of those individuals infected have a seroconversion illness that mimics acute infectious mononucleosis. During the latent phase, a proportion develop persistent generalized lymphadenopathy (PGL), which is a reactive hyperplasia affecting all lymph nodes. Histologically, there is follicular germinal cell hyperplasia of the B-cell follicles, reacting to virus in the follicle dendritic cells. The lymph nodes later atrophy.
Cervicofacial Infections
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Infection is associated with repeated opportunistic infections. Most cases of paediatric HIV infection are acquired from the mother by vertical transmission. Acute infection may mimic infectious mononucleosis. Persistent generalized lymphadenopathy including the cervical nodes becomes a feature as the disease progresses. Weight loss and recurrent fevers occur. Following HIV infection it may be years or decades before full acquired immune deficiency syndrome (AIDS) develops. There is significant evidence of increased life expectancy with early antiretroviral treatment.9
Protein Kinase C-Delta Defect in Autoimmune Lymphoproliferative Syndrome-Like Disease: First Case from the National Iranian Registry and Review of the Literature
Published in Immunological Investigations, 2022
Niusha Sharifinejad, Gholamreza Azizi, Nasrin Behniafard, Majid Zaki-Dizaji, Mahnaz Jamee, Reza Yazdani, Hassan Abolhassani, Asghar Aghamohammadi
Here, we described the first PRKCD-deficient case from the national Iranian registry (Abolhassani et al. 2018), with recurrent infections and periodic episodes of fever, lymphadenopathy, and urticarial rash. The laboratory data including low NK cell count, elevated double-negative T cell, and IgG level resembling ALPS clinical diagnosis. Another similar patient-reported by Kuehn et al. was a Hispanic male with recurrent infections starting in early childhood (Kuehn et al. 2013). He had persistent generalized lymphadenopathy and hepatosplenomegaly, accompanied by periodic fevers starting at three years of age. He had an intermittent facial rash in a butterfly distribution (erythematous macules) over the trunk and extremities. Flow cytometry revealed B cell lymphocytosis with a decrease in class-switched memory B cells. While the frequency of NK cells was normal, he was stably deficient in NK cell cytotoxic activity. The patient described by Salzer et al. was a 12-year-old boy of Turkish origin who had a clinical history of recurrent infections, generalized lymphadenopathy, and organomegaly (Salzer et al. 2013). He had multiple autoimmune disorders such as early onset membranous glomerulonephritis, relapsing polychondritis, hypothyroidism, and anti-phospholipid syndrome. According to laboratory data, IgG was slightly below the inferior normal range, with normal IgA and IgM. His total B-cell numbers were decreased and T cell immunophenotyping was normal.
Prevalence of succinate dehydrogenase deficiency in paragangliomas and phaeochromocytomas at a tertiary hospital in Cape Town: a retrospective review
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2021
Cassandra Bruce-Brand, Abraham C van Wyk
The SDH enzyme complex (mitochondrial complex II) catalyses the conversion of succinate to fumarate in the Krebs cycle.16 Loss of heterozygosity with inactivating germline mutations results in destabilisation of the SDH protein complex and abolishes its enzymatic activity leading to an accumulation of succinate.16,18–20 This results in reactive oxygen species causing free radical damage and activation of a pseudohypoxia pathway by increasing hypoxia-inducible factors.16,18–21 A third mechanism that has been proposed to explain how Krebs cycle dysfunction can lead to neoplasia is through a decrease in apoptosis.21 The SDH complex consists of four subunits, SDHA, SDHB, SDHC and SDHD. Hereditary PC/PGL syndrome can be caused by germline mutations in any of the SDH subunits as well as in SDHAF2, a mitochondrial protein that flavinates SDHA and promotes maturation of SDHB.16,21–24
Primary gastric lymphoma: A report of 16 pediatric cases treated at a single institute and review of the literature
Published in Pediatric Hematology and Oncology, 2020
Nilgün Kurucu, Canan Akyüz, Bilgehan Yalçın, İnci Y. Bajin, Ali Varan, Diclehan Orhan, İbrahim Karnak, Burça Aydın, Tezer Kutluk
Non-Hodgkin lymphomas (NHLs) account for 7–12% of all childhood malignancies. Almost all organs and tissues can be involved with lymphoma. Approximately one-third of NHL cases arise primarily from extranodal regions.2 Although the gastrointestinal tract is the most common extranodal site for childhood NHL, primary gastric lymphoma (PGL) is very rare. According to SEER (Surveillance, Epidemiology, and End Results) data, incidence of pediatric primary gastrointestinal lymphoma is 0.19/100.000.3 Most of those cases (47.6%) are located in the small intestine while only 10% arise in the stomach.3,4 The objective of this study was to report our institutional experience with primary pediatric gastric lymphomas over a 46-year period.