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Query: UMLS:C0038002 (splenomegaly)
9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gamna-Gandy (G-G) bodies are classically defined as spheroidal yellow-brown foci consisting of dense fibrous tissue and collagenous fibers encrusted with iron pigments and calcium salts. These siderotic nodules were first described in the spleen early in the twentieth century and for a short time were considered to be caused by fungal infection due to the presence of unusual "bamboo-like and articulated" fibers in the lesions that vaguely mimicked mycelia forms. This notion was proven to be incorrect in the 1930s and G-G bodies are now considered to result from organization of small hemorrhages. Although originally reported in splenomegaly, G-G bodies are well-recognized findings in atrial myxomas where they form linear arrays of mineral-encrusted fibers, often at the edge of resolving hemorrhages. They rarely have been reported in lymph nodes, thymoma, thyroid adenoma, and renal cell carcinoma. Curiously, published examples of G-G bodies in central nervous system (CNS) neoplasms or vascular malformations have not appeared, despite the known tendency for bleeding, even recurrent episodes of bleeding, in several types of these lesions. Since 1999 I have accrued all the examples of G-G bodies that I have observed in my practice of surgical neuropathology. These cases are presented here and the historical aspects of the entity are reviewed.
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PMID:Gamna-Gandy bodies in surgical neuropathology specimens: observations and a historical note. 1498 96

Gamna-Gandy bodies (GGBs), also known as hemosiderotic nodules, were first described in 1921 in association with sickle cell disease. Since then, they have been documented to occur in association with other pathological processes such as hemolytic anemia, congestive splenomegaly, hereditary hemochromatosis; and acquired hemosiderosis. Despite a uniquely characteristic microscopic appearance that is easily recognized by routine histopathologic examination, the precise significance of GGBs remains unknown. As such, documentation of GGBs in patients either by pathology or radiology should herald the presence of a systemic disorder such as sickle cell anemia or hemochromatosis wherein portal hypertension and/or congestive splenomegaly are present. In this article, we briefly present two autopsy cases from two patients with distinctly different clinical presentations wherein classic Gamna-Gandy bodies are illustrated on routine histopathologic examination.
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PMID:Splenic nodules at autopsy. 2401 27

Hereditary spherocytosis (HS) and sickle cell disease (SCD) are associated with splenomegaly and spleen dysfunction in pediatric patients. Scant data exist on possible correlations between spleen morphology and function in HS and SCD. This study aimed to assess the histologic and morphometric features of HS and SCD spleens, to get possible correlations with disease pathophysiology. In a large series of spleens from SCD, HS, and control patients, the following parameters were considered: (i) macroscopic features, (ii) lymphoid follicle (LF) density, (iii) presence of perifollicular marginal zones, (iv) presence of Gamna-Gandy bodies, (v) density of CD8-positive sinusoids, (vi) density of CD34-positive microvessels, (vii) presence/distribution of fibrosis and smooth muscle actin (SMA)-positive myoid cells, and (viii) density of CD68-positive macrophages. SCD and HS spleens had similar macroscopic features. SCD spleens had lower LF density and fewer marginal zones than did HS spleens and controls. SCD also showed lower CD8-positive sinusoid density, increased CD34-positive microvessel density and SMA-positive myoid cells, and higher prevalence of fibrosis and Gamna-Gandy bodies. HS had lower LF and CD8-positive sinusoid density than did controls. No significant differences were noted in red pulp macrophages. By multivariate analysis, most HS spleens clustered with controls, whereas SCD grouped separately. A multiparametric score could predict the degree of spleen changes irrespective of the underlying disease. In conclusion, SCD spleens display greater histologic effacement than HS, and SCD-related changes suggest impaired function due to vascular damage. These observations may contribute to guide the clinical management of patients.
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PMID:Spleen histology in children with sickle cell disease and hereditary spherocytosis: hints on the disease pathophysiology. 2777 75