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Gamna-Gandy bodies
Micrograph of the spleen; Gamna-Gandy bodies and hemosiderin pigment.
Micrograph of the spleen showing Gamna-Gandy bodies (arrows) and hemosiderin pigment (arrowheads). H&E stain.
Classification and external resources

Gandy–Gamna nodules, Gandy–Gamna bodies or siderotic nodules are small yellow-brown, brown or rust-coloured foci found in the spleen in patients with splenomegaly due to portal hypertension and sickle cell disease. They consist of fibrous tissue with haemosiderin and calcium deposits, and probably form due to scarring at sites of small perivascular haemorrhages.[1] They are visible on MRI scanning due to the presence of haemosiderin.

Other names include hemosiderotic nodules[2], Gandy-Gamna-De Gaetani areas[3], sclerosiderotic areas of Gandy-Gamna[4], Gandy-Gamna lesions[5], sclerotic calciosiderosis[5], sclerosiderotic granulomatosis.[6] and because of their rusty colour on gross inspection, tobacco flecks.[7]

Etiology and structure[edit]

A multinucleated giant cell is seen in the left half of the picture, adjacent to a collection of pigment (circa 10 'o clock). H&E stain.

Gamna-Gandy bodies are thought to result from small local perivascular hemorrhages and necrosis in the splenic parenchyma, followed by fibrosis. Breakdown of hemoglobin produces hemosiderin deposits, that, together with calcium salt precipitates, impregnate degraded collagen and elastic fibres.[7][8] On section, many of the iron-containing filaments are continuous with normal elastic fibers.[9]

Tedeschi[10] indicated a number of components of the Gamna-Gandy bodies: various sizes of blood vessels with aberrations varying of a nonspecific type of vasculitis to sclerosis and hyalinisation with obliteration or narrowing of the lumina, calcium precipitates (demonstrated by the von Kossa stain) and hemosiderin deposits (demonstrated by the Gömöri iron stain), present in varying amounts in the walls of vessels and in stroma, and a prominent fibroblastic and macrophagic reaction with the production of multinucleated foreign body giant cells. These can have as many as 70 nuclei on one section, and can contain yellowish-green rods or crystalline material.[11] Spheroid, semilunar, or thread-like ("bamboo-shaped") fibers which resemble mycelial structures or parasitic eggs are the hallmark of the Gamna-Gandy bodies.[10]


On fresh sections, Gamna-Gandy bodies appear as circumscribed lesions measuring a couple of millimetres up to a centimetre or more, having a red rim, a pale inner zone and a brown center. These colours darken with exposure to oxygen.[7]

Image Dufour macroscopy GGB.

Mechanism of formation[edit]

To do: Piccin mechanism of distribution of GGB. (possibly image of spleen with red and white pulp)


MRI of the abdomen showing splenic Gamna-Gandy bodies in schistosomiasis.

Splenic Gamna-Gandy bodies have been found in the following disorders or pathological entities:

Gamna-Gandy bodies in a pedunculated adenomatous colorectal polyp, indicating hemorrhage, possibly by torsion. H&E stain, 200x magnification.

Although the spleen appears to be the organ in which Gamna-Gandy bodies are most often found, they have also been reported in other organs of the body:


Ultrasound, MRI/CT (picture Bhatt)

Clinical significance[edit]

Mimickers of GGB (Bhatt)


Kleinschmidt, argument that they are quite common if you look for them.[23]

In animals[edit]

Gamna-Gandy bodies have been incidental findings in the spleens of beagles used in toxicologic studies.[24] In another study of spontaneous findings in beagles used for toxicologic studies, an incidence of 43.1% of Gamna-Gandy-like bodies of the splenic capsule was reported.[25]


Gamna-Gandy bodies have been produced experimentally in the spleens of felines, canines and rabbits by intraparenchymatous injections of alcohol and calcium chloride, by caustics and by diathermy. Ligation of the splenic veins near the splenic hilum produced necrosis and variable amounts of Gamna-Gandy bodies in these animals; the best result was produced in canines.[26]


Gamna-Gandy bodies were first mentioned by Italian physician Marini in 1902 and by Stengel in 1904 in case reports of patients with splenomegaly and hepatic cirrhosis.[27][28] These bodies were given their eponymous name after they were reported by Charles Gandy (1872-1943) in 1905 and Carlo Gamna (1866-1950) in 1921, describing them in the spleen of a patient with biliary cirrhosis and in splenic blood vessels in hemolytic siderosis, respectively.[29][30] Gamna called them siderotic splenogranulomatosis, and explained their presence as resulting from small local hemorrhages, with degeneration and subsequent deposition of iron and calcium salts.[9][30]

Fungal origin[edit]

Hyphae of Penicillium sp. Early authors believed the thread-like iron incrustations sometimes seen in Gamna-Gandy bodies were fungal in origin.

Thread-like structures are sometimes found in Gamna-Gandy bodies, prompting belief by some that these were mycelial hyphae, and that the causative agent of splenomegaly was fungal in origin (giving rise to terms such as splenomycosis and mycotic splenomegaly). Others regarded these filaments as mycelial but believed the fungus to be a secondary invader and not of etiologic significance. The fungal belief was strengthened by findings of fungi of the Aspergillus and Helminthosporium genera in some enlarged spleens. Abrikossoff reviewed these findings and could not find compelling evidence for either presence of Aspergillus nor an etiological link with splenomegaly, concluding that the threads were incrustations of iron in tissue fibers.[31]

Reimann and Kurotchkin examined these findings in 1931 and found that the Helminthosporium was without virulence for laboratory animals, and could not culture any fungi in primary chronic splenomegaly without liver cirrhosis, nor in selected other splenic diseases. The appearance of the filaments in the Gamna-Gandy bodies did not conform with that of hyphae cultured from the same spleen. Introducing Helminthosporium in laboratory monkeys in various ways did not produce any Gamna-Gandy bodies in the spleen. Reimann and Kurotchkin thus concluded that Gamna-Gandy bodies are not caused by the growth or presence of fungi.[9]

Additional images[edit]

External links[edit]


  1. ^ "Gandy-Gamna bodies". Mondofacto online medical dictionary. Retrieved March 30, 2009. 
  2. ^ Dennis KA, Cheek B, Leroy M, McGoey RR (2013). "Splenic nodules at autopsy". J La State Med Soc. 165 (3): 142–4. PMID 24015427. 
  3. ^ Bottacin C (1958). "Report on the Gandy-Gamna-De Gaetani areas in the spleen in splenomegaly caused by hemolytic jaundice; fibrosclerosiderotic areas containing bile pigments [Article in Italian]". Endocrinol Sci Cost. 24 (5): 334–44. PMID 13597844. 
  4. ^ Cavallini A (February 1958). "Unusual case of accessory spleen in the liver with sclerosiderotic area of Gandy-Gamna [Article in Italian]". Minerva Med. 49 (16): 687–90. PMID 13541053. 
  5. ^ a b Herrera JM (December 1963). "Observations on sclerotic calciosiderosis of the spleen, the "Gandy-Gamna lesion" in sickle-cell disease [Article in Spanish]". Arch Med Panamenos. 11 (12): 262–90. PMID 14161959. 
  6. ^ a b c Tedeschi LG, Sherman JD, Tedeschi CG (March 1965). "Sclerosiderotic granulomatosis in thymoma". Arch Pathol. 80: 235–40. PMID 14322944. 
  7. ^ a b c Dufour JF, Dinkel HP, Zimmermann A (October 2003). "Image of the month. Gamma-Gandy bodies". Gastroenterology. 125 (4): 1010, 1294. PMID 14517782. 
  8. ^ Bhatt S, Simon R, Dogra VS (December 2005). "Gamna-Gandy bodies: sonographic features with histopathologic correlation". J Ultrasound Med. 25 (12): 1625–9. PMID 17121963. 
  9. ^ a b c d Reimann HA, Kurotchkin TJ (October 1931). "The relationship of fungi to chronic splenomegaly of unknown origin". Am J Med Sci. 131: 107–114.  line feed character in |title= at position 29 (help)
  10. ^ a b c Tedeschi LG (March 1971). "The Gamna nodule". Hum Pathol. 2 (1): 182–3. PMID 5095245. 
  11. ^ a b Morgan DR, Lieber MM, Stewart HL (May 1935). "Siderotic nodules (Gandy-Gamna bodies) in primary renal carcinoma". Am J Pathol. 11 (3): 583–94. PMC 1910961Freely accessible. PMID 19970219. 
  12. ^ a b Laurent O, Lubrano J, de Beauregard M, Aubry S, Kastler B, Delabrousse É (October 2011). "Gamna-Gandy bodies in cirrhosis: a meaningless finding? [Article in French]". J Radiol. 92 (10): 909–14. PMID 22000612. doi:10.1016/j.jradio.2011.05.010. 
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  15. ^ Lambertucci JR, Voieta I, Andrade LM (May–June 2008). "Gamna-Gandy bodies in hepatosplenic schistosomiasis mansoni [Article in Spanish]". Rev Soc Bras Med Trop. 41 (3): 320–1. PMID 18719819. doi:10.1590/S0037-86822008000300021. 
  16. ^ Gonzalez TD, Mourão Santos JE, Sales DM, Takemoto K, Capobianco J, Brant PE, Colleoni R, Ahmed M, D'Ippolito G (March–April 2008). "Ultrasonographic assessment of splenic siderotic nodules in schistosomal patients with portal hypertension". Radiologia Brasileira. 41 (2): 69–73. 
  17. ^ Varma D, Khurana N, Singh T (January 2004). "Gamna Gandy bodies of spleen seen in CML: a causal association--a case report". Indian J Pathol Microbiol. 47 (1): 51–2. PMID 15471130. 
  18. ^ Roubidoux MA (MArch-April 1994). "MR of the kidneys, liver, and spleen in paroxysmal nocturnal hemoglobinuria". Abdom Imaging. 19 (2): 168–73. PMID 8199554.  Check date values in: |date= (help)
  19. ^ Anvari MS, Boroumand MA, Karimi A, Abbasi K, Ahmadi H, Marzban M, Movahedi M, Moshtaghi N, Salehiomran A, Davoodi S, Shirzad M, Abbasi SH (October 2009). "Histopathologic and Clinical Characterization of Atrial Myxoma: A Review of 19 Cases". LabMedicine. 40 (10): 596–9. doi:10.1309/LM02GA6LCOEHGWPR. 
  20. ^ Jiménez Heffernan JA, Salas C, Tejerina E, Viguer JM (June 2010). "Gamna-Gandy bodies from cardiac myxoma on intraoperative cytology". Cytopathology. 21 (3): 203–5. doi:10.1111/j.1365-2303.2009.00674.x. 
  21. ^ a b Jiménez-Heffernan JA, Tejerina E, de la Morena E, Sanz Ortega E (October–December 2010). "Gamna-Gandy bodies in an adenomatous colorectal polyp". Indian J Pathol Microbiol. 53 (4): 876–7. PMID 21045462. doi:10.4103/0377-4929.72028. 
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  23. ^ a b c Kleinschmidt-DeMasters BK (February 2004). "Gamna-Gandy bodies in surgical neuropathology specimens: observations and a historical note". J Neuropathol Exp Neurol. 63 (3): 106–12. PMID 14989596. doi:10.4103/0377-4929.72028. 
  24. ^ a b Sato J, Doi T, Wako Y, Hamamura M, Kanno T, Tsuchitani M, Narama I (March 2012). "Histopathology of incidental findings in beagles used in toxicity studies". J Toxicol Pathol. 25 (1): 103–34. PMID 22481862. doi:10.1293/tox.25.103. 
  25. ^ Maita K, Masuda H, Suzuki Y (April 1977). "Spontaneous lesions detected in the beagles used in toxicity studies". Jikken Dobutsu. 26 (2): 161–7. PMID 560313. 
  26. ^ Fasiani GM, Oselladore G (May 1932). "Uber die experimentelle Erzeugung siderofibroser Milzveranderungen.". Virchows Arch. f. path. Anat. 284 (2): 474–490. 
  27. ^ Marini G (1902). "Sopra un caso di splenomegalia con cirrosi epatica". Arch Sci Med (Torino). 26: 105–116. 
  28. ^ Stengel A (October 1904). "Varieties of splenic anaemia". Am J Med Sci. 128 (3): 497–533. 
  29. ^ Gandy C (1905). "Lesions particulieres de la rate dans un cas de cirrhose biliare". Bull Soc Anat Paris. 80: 872–9. 
  30. ^ a b Gamna C (1921). "Sopra alcune lesioni dei vasi nella siderosi emolitica delle milza". Minerva Med. 84: 291. 
  31. ^ Abrikossoff AI (1928). "Uber "Splenomykosen" und "Mykotische Splenomegalien"". Virchows Arch. f. path. Anat. 272: 593–612.