Granuloma actinico de O'Brien / O'Brien actinic granuloma

Se comunica un caso de granuloma actínico en una paciente de sexo femenino, caucásica, la cual presentaba concomitantemente arteritis de la temporal y polimialgia reumática. Actualmente se considera que debido a la fisiopatogenia de las tres entidades mencionadas, podría tratarse la primera, de un marcador de las dos restantes.

We present a female, white, with an actinic granuloma, concomitantly with temporal arteritis and polymyalgia rheumatica. Today it is considered that, due to the phisiopathogenia of the three entities mentioned before, the first one could be used as a reference for the other two.

Comprehensive analysis of 112 melanocytic skin lesions demonstrates microsatellite instability in melanomas and dysplastic nevi, but not in benign nevi.

INTRODUCTION: the length of DNA repetitive sequences (microsatellite instability (MSI)) represent distinct tumorigenic pathways associated with several familial and sporadic tumors. MATERIAL AND METHODS: To investigate the prevalence and frequency of MSI in melanocytic lesions, the polymerase chain reaction (PCR)-based microsatellite assay was used to examine formalin-fixed, paraffin-embedded tissues of 30 benign melanocytic nevi, 60 melanocytic dysplastic nevi (MDN), and 22 primary vertical growth phase cutaneous malignant melanomas (CMM). Twenty-four microsatellite markers at the 1p, 2p, 3p, 4q and 9p chromosomal regions were used. RESULTS: MSI was found at 1p and 9p in MDN and CMM but not in benign melanocytic nevi. The overall prevalence of MSI was 17/60 (28%) in MDN and 7/22 (31%) in CMM. The frequency of MSI ranged from 2/24 (9%) to 4/24 (17%) and was most commonly found at D9S162. There was a statistically significant correlation between degree of atypia and frequency of MSI (p<0.001) in MDN. There were two MSI banding patterns: band shifts and additional bands. CONCLUSIONS: The data presented revealed the presence of low-frequency MSI (MSI-L) at the 1p and 9p regions in both MDN and CMM. Whether the MSI-L pattern reflects a defect in mismatch repair genes is still to be determined.

Insulin hyperresponsiveness in partially hepatectomized diabetic rats.

The present work analyzes the expression of insulin receptors and theirs related intracellular signaling molecules in partially hepatectomized-diabetic rats. Insulin binding through Scatchard analysis was studied using isolated hepatocytes of Control (Sham-operated), Hepatectomized, Diabetic and Diabetic-Hepatectomized male Wistar rats. In a set of in vivo experiments, the levels of alpha subunit of the insulin receptor, the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) were determined. [3H]-thymidine incorporation into DNA 24 or 48 h after surgery was assessed in all the experimental groups. Scatchard analysis showed that insulin receptor number was increased in diabetic and in hepatectomized rats in the same extent (64%, with respect to Controls). Diabetic-hepatectomized rats showed a dramatic increase of the receptor concentration (400%) and on the affinity constant (532%). Besides, the insulin receptor expression was increased in the treated groups, being the higher values those of the diabetic-hepatectomized rats. IRS-1 and PI3K showed similar increases. DNA synthesis was not impaired by the diabetes state. In conclusion, increased expression of IR and IRS-1 leads to increased association of PI3K in vivo in diabetic regenerating rats. The enhancement of this pathway may reveal an insulin hyperresponsiveness in these animals.

Inhibition by interferon alpha-2b of rat liver regeneration: effect on ornithine decarboxylase and total protein synthesis.

Polyamines are key factors in macromolecule synthesis during liver regeneration. It has been postulated that interferon-alpha (IFNalpha) decreases putrescine levels in regenerating liver by inhibiting ornithine decarboxylase (ODC) activity, the main enzyme in polyamine biosynthesis. In the present study, we analysed the effects of a pharmacological dose of IFNalpha on polyamine and ODC levels during the regenerative process following partial hepatectomy in rats. Synthesis of ODC by isolated hepatocytes from IFN-treated rats with regenerating livers was also assessed. Furthermore, we investigated the effect of IFNalpha-2b on DNA and total protein synthesis in 24-hr regenerating livers. No effect on DNA synthesis was observed at the dose of IFNalpha-2b used, but total protein synthesis decreased significantly in IFNalpha-2b-treated rats undergoing liver regeneration (7.0 +/- 2.0 and 12.1 +/- 1.7%. min(-1) in hepatectomized rats treated with IFNalpha-2b and saline, respectively). ODC levels were also reduced significantly (by 50%) in hepatectomized rats treated with IFNalpha-2b versus saline. In parallel with the ODC decrease, the concentrations of putrescine and spermidine (63 +/- 25 vs 101 +/- 15 nmol/g liver and 1.08 +/- 0.35 vs 2.14 +/- 0.22 micromol/g liver, respectively, in IFNalpha-2b- and saline-treated hepatectomized rats) showed similar, significant diminutions. Moreover, the incorporation of [35S]methionine into ODC was decreased dramatically in isolated hepatocytes from IFNalpha-2b-treated hepatectomized rats 12 hr after surgery. In conclusion, the protein synthesis rate in regenerating liver was impaired by therapeutic doses of IFNalpha-2b. In addition, the results presented in this study suggest that IFNalpha-2b negatively regulates ODC synthesis, causing a reduction in polyamine levels during liver regeneration.

Involvement of mu class glutathione S-transferase subunit M2 (rGST M2) levels in the initiation and promotion of hepatocellular carcinogenesis in old rats.

Age-associated differences in the response of the initiation and promotion of hepatocellular carcinogenesis in the rat were analyzed. Male Wistar rats 5 and 18 months-old were used throughout. They underwent an experimental design of multistage model of hepatocarcinogenesis: hepatic cells were initiated with the complete carcinogen Aflatoxin B1 (0.5mg/Kg b.w.) and the promotion was performed through a combined treatment of proliferation (partial hepatectomy, 65%) and administration of the tumorigenic promoter phenobarbital (0.1% in drinking water for 21 days). After the treatment, rats were sacrificed and the following parameters were determined: activity and subunit composition of the glutathione S-transferase enzyme system, the number of liver preneoplastic foci and the proliferation cell index. The combined treatment (initiation + promotion) lowered the expression of the mu class GST (rGST M1, rGST M2). The inhibition in rGST M2 in old animals (which in basal conditions had already been lower) was significant. On the other hand, the treatment increased the alpha class GST (rGST A, rGST A3). The number of preneoplastic foci was higher in old rats (number of foci/cm(2): 6.9+/-0.3 vs 3.9+/-0.3 in young rats, p< 0.05). The proliferation cell index did not show age-related differences. Because rGST M2 deficiency coexisted with induced expression of alpha class, the livers would be resistant to some toxic insults, being selectively sensitive to potentially genotoxic substances for which M2 is an essential detoxification pathway. The transition to a rGST M2-deficient phenotype during aging could induce higher responsiveness to genotoxic effects, and might favor the likelihood of further progression, indicating a higher susceptibility of aged animals to the development of carcinogenesis.

[In vivo apoptotic effect of alpha-2b interferon (IFN) on rat preneoplastic liver ]. / Efecto apoptotico in vivo del interferon alfa-2b (IFN) sobre higados preneoplasicos de rata.

In order to know whether IFN alpha prevents in vivo oncogenesis in the very-early-stage cancer cells, we evaluated the action of IFN alpha-2b on preneoplastic foci in rats. Animals were divided into six groups: subjected to an initiation-promotion model of cancer development (G1), treated with IFN alpha-2b during: a) initiation-promotion (G2), b) initiation (G3), promotion (G4); subjected only to an initiation stage (G5) and treated with IFN alpha-2b during this period (G6). The number and area of rGST P-positive foci were reduced and the Apoptotic index was increased in G2, 3 and 6. Bcl-2 and Bcl-XL protein levels were decreased in IFN alpha-2b-treated rats. Increased levels of mitochondrial Bax protein were observed in G2, 3 and 6. In conclusion, preneoplastic hepatocytes in the IFN alpha-2b-treated rats undergo programmed cell death as a result of a significant increase of Bax and its translocation to the mitochondria.

Efecto apoptotico in vivo del interferon alfa-2b (IFN) sobre higados preneoplasicos de rata. / [In vivo apoptotic effect of alpha-2b interferon (IFN) on rat preneoplastic liver ]

In order to know whether IFN alpha prevents in vivo oncogenesis in the very-early-stage cancer cells, we evaluated the action of IFN alpha-2b on preneoplastic foci in rats. Animals were divided into six groups: subjected to an initiation-promotion model of cancer development (G1), treated with IFN alpha-2b during: a) initiation-promotion (G2), b) initiation (G3), promotion (G4); subjected only to an initiation stage (G5) and treated with IFN alpha-2b during this period (G6). The number and area of rGST P-positive foci were reduced and the Apoptotic index was increased in G2, 3 and 6. Bcl-2 and Bcl-XL protein levels were decreased in IFN alpha-2b-treated rats. Increased levels of mitochondrial Bax protein were observed in G2, 3 and 6. In conclusion, preneoplastic hepatocytes in the IFN alpha-2b-treated rats undergo programmed cell death as a result of a significant increase of Bax and its translocation to the mitochondria.

Aluminum effects upon calbindin D9k-linked duodenal calcium transport in diabetic male rats.

In order to elucidate if the inhibition mechanisms of Aluminum (Al) on intestinal calcium flux involve some possible action on calbindin-D9k, a series of in vivo and in vitro experiments were carried out in normal and in streptozotocin-induced diabetic male rats. The dose-response curves obtained from the in vitro studies indicate that, in the diabetic group (which has a lower content of calbindin-D9k), the effect of Al on JCa(ms) has a small dependence on rising Al concentration (0-10 microM). The parameters obtained from those curves: Emax (maximum reduction percentage of JCa(ms)) and ED50 (Al concentration that produces half of the highest inhibition) were significantly diminished in this group compared to control. Both s.c. injections of calcitriol (D3) at doses of 0.08 and 0.40 microg/kg body wt. per day and insulin (10 IU/kg body wt. per day), increase the inhibitory effect of Al to levels that did not differ from controls. In vivo gavage of 60 mg/kg body wt. per day of aluminum chloride for 1 week reveals that the degree of reduction of intestinal CaBP9k by Al is directly correlated to duodenal content of this protein (r2 = 0.683, P = 0.022).

Putrescine decreases cytochrome P450 3A4 levels during liver regeneration in the rat.

BACKGROUND/AIMS: The mechanism by which many cytochrome P450 (CYP) isozymes decrease during liver regeneration is unclear. Peptides and growth factors are thought to be involved. Putrescine, the first polyamine synthesised by ornithine decarboxylase, peaks early following partial hepatectomy and is known to play an essential role in hepatic regeneration. Gamma amino butyric acid was reported as a physiologic inhibitor of ornithine decarboxylase. In this work we studied the possible involvement of putrescine in the CYP reduction during liver regeneration. METHODS: Hepatectomised, putrescine-treated sham, and GABA-treated hepatectomised rats were used throughout. Total hepatic cytochrome P450, o-dealkylase activities (CYP1A1 and CYP2B1/2), nifedipine oxidase activity (CYP3A4), and Western blot assays of their respective apoproteins were analysed in liver microsomes. Putrescine levels in hepatic tissue were also measured. RESULTS: Partial hepatectomy and putrescine treatment induced a significant diminution in total CYP (50% and 30% of sham-operated rats, respectively). Gamma amino butyric acid treatment prevented this decrease in partially hepatectomised rats. Nifedipine oxidase activity of partially hepatectomised and putrescine-treated rats significantly decreased to 43% and 60% of that in sham-operated rats, respectively. Again, gamma amino butyric acid prevented the diminution in partially hepatectomised rats. No significant changes were observed in o-dealkylase activities. CONCLUSIONS: These results show that inducible CYP1A1 and CYP2B1/2, which are important in carcinogen metabolisation, are preserved after partial hepatectomy. However, constitutive CYP3A4, which represents 50% of total CYP and metabolises drugs like nifedipine, warfarin, acetaminophen, cyclosporin and FK-506, is reduced during liver regeneration. Our experiments suggest that endogenous putrescine is, at least, partly responsible for this decrease.

Hepatic protein synthesis and serum aminoacid levels during liver regeneration in young and old malnourished rats.

The aim of the present study was to measure protein synthesis in regenerating liver and to evaluate the impact of malnutrition in young and old rats. Two groups of male Wistar rats were used: young rats (4 months old) and old rats (18 months old). The rats were allocated to malnutrition or ordinary food intake for 1 week. Half of each group was sham-operated and the other was partially hepatectomized 2 days before the end of diet manipulation. Hepatic protein synthesis was significantly increased in all hepatectomized groups compared with their respective sham group: young well-nourished hepatectomized rats, 44%; young malnourished hepatectomized rats, 55%; old well-nourished hepatectomized rats, 47%; and old malnourished hepatectomized rats only 21%. Hepatic DNA content was unchanged in all groups and liver RNA content was higher in young malnourished hepatectomized rats (21%, P < 0.05). Serum total amino acid concentration did not change in young well-nourished hepatectomized and young malnourished hepatectomized rats. This value did not show significant changes between old well-nourished hepatectomized and old well-nourished sham, but it increased 14% (P < 0.05) in old malnourished hepatectomized. It was concluded that (a) regeneration is not impaired by malnutrition in young rats and may even be better than in rats eating a normal diet, and (b) the deleterious effect of aging is revealed once old animals are exposed to malnutrition. It is manifested in the decreased rate in hepatic protein synthesis observed in old malnourished hepatectomized rats and in the augmentation of total serum amino acid concentration, where the hypercatabolism induced by hepatectomy is significantly greater.

Sex-related differences in the effect of aluminum on calcium transport in the small intestine of the rat.

Everted sacs of distinct segments of small intestine from male and female rats were incubated with 2 microM of aluminum (Al). In duodenum, Al significantly diminished calcium flux (JCams) in cycling females (31%, P < 0.01) and in males (17%, P < 0.05). Incubation under anaerobic conditions nullified the inhibition of Al on JCams both in male and in female duodenal sacs. Jejunal and ileal JCams measured under aerobic conditions were not modified by the presence of Al in mucosal fluid compared to Al-free controls, neither in males nor in cycling females. In ovariectomized female rats treated with estrogen the studies of dose-response curves showed that the sensitivity to the effect of Al on JCams was raised (the dose that produced half maximum response diminished) with increasing 17 beta-estradiol serum levels, without changes in the maximum response. In castrated male rats injected with testosterone, the effect of Al on duodenal JCams was found to be independent of testosterone levels. In summary, our results demonstrated that the Al inhibition on duodenal JCams was influenced by sexual hormone levels in females but was independent of them in males.

Role of calcium fluxes in the action of glucagon on cytosolic glutathione S-transferase activity in rat liver slices.

In a previous study we demonstrated that the administration of 20 micrograms/kg b.wt. of glucagon to rats caused a significant diminution of hepatic cytosolic glutathione S-transferase (GST) activity. This inhibition was non-competitive and reversible. We suggested that the effect would be mediated by cytosolic effectors. The present work was performed to characterize the mechanism involved in this inhibition. Liver tissue slices (170 to 200 mg) were incubated during different periods of time (0, 5, 10, 15, 20 and 30 min.) with several concentrations of glucagon (10(-5) M, 10(-8) M and 10(-10) M), dibutiryl cyclic AMP (10(-4) M, 10(-6) M and 10(-9) M), divalent cation ionophore A23187 (10(-4) M, 10(-6) M and 10(-9) M) or vasopressin (10(-7) M, 5 x 10(-7) M and 10(-8) M). The incubation was done with or without calcium in the medium. In all cases the cytosolic GST activity were determined in liver slices. The percentage of inhibition of GST activity was directly related to the increase of concentration of the test substances. An inhibition between 40% to 45% after 10 min. of incubation with the highest concentrations was observed (except vasopressin which caused 10% of inhibition). 10(-10) M glucagon did not produce a decrease of GST activity. The inhibition disappeared in calcium-free incubated slices, but direct relationship between plasma-membrane calcium influx and inhibition of GST activity (r = 0.950, P < 0.001, n = 24) could be obtained. By using calmodulin antagonists, we conclude that the inhibition process of the enzyme was mediated by calmodulin. In summary, we propose that plasma-membrane calcium influx induced by high concentrations of glucagon activates calmodulin, which promotes a modification (actually a methylation, according to other authors) on GST, thereby causing a decrease in its activity.

Acute regulation of hepatic glutathione S-transferase by insulin and glucagon.

The intravenous administration of insulin plus glucose in anesthetized rats caused, within 30 min, an increase of about 56% in hepatic cytosolic glutathione S-transferase (GST) activity, but it did not affect the microsomal enzyme. The injection of glucagon resulted, at the same time, in a 43% drop in the hepatic cytosolic GST, without affecting the microsomal GST. The insulin-dependent increase in cytosolic GST activity was abolished by the pretreatment of the animals with an inhibitor of protein synthesis (cycloheximide). A kinetic analysis revealed a non-competitive inhibition caused by glucagon upon the cytosolic enzyme. In addition, the presence of insulin did not interfere with the effectiveness of glucagon, and vice versa. We propose that: (1) the effect of insulin on hepatic cytosolic GST activity requires protein synthesis; (2) glucagon produces an inhibition of hepatic cytosolic GST, which could be mediated by cytosolic effectors such as adenosine 3'-5'-cyclic monophosphate (cAMP); (3) the effects of glucagon and insulin were not mutually exclusive; (4) hepatic microsomal GST is regulated by different mechanism(s).

Is intestinal cytosolic glutathione S-transferase an alternative detoxification pathway in two-thirds hepatectomized rats?

The present study was designed to investigate the effect of partial (two-thirds) hepatectomy (PH) on hepatic and intestinal glutathione S-transferases (GSTs) activities. A significant decrease of cytosolic hepatic GSTs activity was observed after the PH. The lowest value of hepatic GSTs was obtained 48 h after the surgery. On the other hand, intestinal GSTs activities increased after PH, reaching the highest values 48 h after the hepatic lobes resection. The hepatic GSTs activities diminution was attributed, in part, to the high accumulation of bile acids in the liver tissue of hepatectomized rats, also demonstrated by a higher retention of [14C] taurocholate. The kinetic analysis performed with 1-chloro-2,4-dinitrobenzene (CDNB) as substrate showed two sets of parameters, indicating the presence of isozymes of high and low affinities. Vmax1 and Vmax2 were lower in PH rats suggesting a non competitive inhibition mechanism. The inhibitory effect of bile acids decreased during liver regeneration process of hepatectomized rats disappearing at 7 days after PH. Conversely, in non regenerating rats (GABA treated) the inhibitory mechanism was still observed at 7 days after the surgery. The increase of intestinal GSTs activities (isozymes of high and low affinities) was attributed to the presence of polyamines, mainly putrescine, produced during the hepatic regeneration process. In this regard, it was showed that GABA treatment, which inhibits polyamine synthesis, completely abolished the increase on intestinal GSTs activities. Finally, the treatment with exogenous putrescine showed that in hepatectomized and sham-operated rats, the polyamine induced GSTs activities in both tissues. In PH rats, the putrescine dependent increase of hepatic GSTs was masked by the inhibitory effect of bile acids. In addition, a summation effect of endogenous and exogenous putrescine was probably the reason of the induction of intestinal GSTs after PH. The GSH/GSSG ratio did not change during the treatments, as well as the microsomal GST activity of both tissues. The work points out the hypothetical detoxification power of the intestine during the hepatocellular insufficiency which follows a two-thirds hepatectomy.

Differential effects of blood insulin levels on microsomal enzyme activities from hepatic and extrahepatic tissues of male rats.

Microsomal glutathione S-transferase, UDP-glucuronyl transferase, and aniline hydroxylase activities were determined in liver, renal cortex, and small intestine of control, streptozotocin-diabetic, alloxan-diabetic, and untreated insulin-injected male Wistar rats. Renal microsomal glutathione S-transferase activity showed a direct linear relationship with insulin blood levels, in agreement with our previous report on cytosolic glutathione S-transferase. This result suggests a possible regulatory mechanism of insulin that needs to be further examined. The hepatic microsomal UDP-glucuronyl transferase was only decreased in streptozotocin-diabetic rats and was not restored by insulin treatment. Intestinal UDP-glucuronyl transferase exhibited an opposite response in streptozotocin-treated animals that was not normalized by the administration of insulin. Hepatic aniline hydroxylase showed the same behaviour as intestinal UDP-glucuronyl transferase. These results suggest that streptozotocin and (or) its metabolites have a direct effect on hepatic and intestinal UDP-glucuronyl transferase activity and on hepatic aniline hydroxylase activity. On the other hand, insulin regulation of enzyme activity varies from one organ to another.

Studies on the mechanism of bile salt-independent bile flow impairment in streptozotocin-induced hepatotoxicity.

The main factors involved in the impairment of formation of the bile salt-independent bile flow (BSIF) in streptozotocin (SZ)-treated rats were examined. Twenty-four hours after SZ injection (50 mg/kg body wt, i.v.) bile flow, bile salt output and biliary excretion of the major inorganic electrolytes (sodium, chloride and bicarbonate) were significantly diminished. The relationship between bile flow and bile salt output obtained during the administration of sodium taurocholate at stepwise-increasing rates indicated that bile salt-independent bile flow (y-intercept) was diminished by 37% in SZ-treated rats. The relationship between electrolyte output and bile salt output showed that the fractions of sodium, chloride and bicarbonate excreted independently of bile salt (y-intercept) decreased to 59%, 47% and 67% of the control values respectively, while the amount of electrolyte secreted per unit of bile salt secreted was unaffected in SZ-treated rats. The hepatic activity of Na+,K(+)-adenosine triphosphatase (Na+,K(+)-ATPase) was decreased by 59% (P less than 0.05) in SZ-treated rats. Nicotinamide administered prior to SZ prevented the hyperglycemia indicative of SZ-induced diabetes, but had no effect on the decrease in Na+,K(+)-ATPase activity caused by the drug. These results suggest that SZ itself, and not its diabetogenic effect, decreases the BSIF by a mechanism that involves impairment of the biliary electrolyte excretion, which could be the result of the inhibition of the hepatic Na+,K(+)-ATPase activity.

Possible role of blood insulin levels on glutathione S-transferase activities from different tissues of male rats.

The activity of in vitro glutathione S-transferase towards 1-chloro-2,4-dinitrobenzene was examined in liver, renal cortex, and small intestine (duodenum, jejunum, ileum) after the in vivo treatment of male Wistar rats with streptozotocin or alloxan. The studies were performed at 2, 10, 24, and 48 h and 7 and 15 days after streptozotocin treatment or 24 and 48 h after alloxan treatment. The results indicated that while the blood levels of insulin-glucose did not show variations, there were no alterations of the glutathione S-transferase activity in the tissues tested. On the other hand, when the treatments caused modifications on blood insulin-glucose levels, there were changes of glutathione S-transferase activity in all tissues (except in the ileum) in such a way that a direct relationship between plasma insulin levels and glutathione S-transferase activity could be demonstrated. These results were also confirmed through insulin administration to control and diabetic rats. The data demonstrate a possible regulation of glutathione S-transferase activity by blood insulin and (or) glucose levels in the tissues tested.

Effect of aflatoxin B1 treatment in vivo on the in vitro activity of hepatic and extrahepatic glutathione S-transferase.

The effect of aflatoxin B1 (AFB1) on the glutathione S-transferase activity (GST) and on non-protein thiol levels of different tissues was studied in adult male Wistar rats. Animals received a single dose of the toxin (100 or 500 micrograms/kg body wt., p.o.), and were studied 6 or 24 h after administration. GST was determined in liver, renal cortex, duodenum, jejunum-ileum and distal ileum, using 3 substrates: 1-chloro-2,4-dinitrobenzene (CDNB), trans-4-phenyl-3-buten-2-one (PBO) and 1,2-epoxyethylbenzene (STOX). The non-protein thiol content of all tissues tested increased with the lowest dose at 6 h, returning to normal values at 24 h, while the higher dose produced a significant decrease in reduced thiol levels at 6 h, returning to normal values at 24 h. AFB1 administration induced, independently of dose and tissue, total GST (CDNB) and epoxide-transferase activity (STOX) while A--C-type transferases (PBO) were inhibited. Almost all activities returned to normal values at 24 h. In cases of enzyme induction there was in general an increase in Vmax and a decrease in apparent Km. The opposite was seen in cases of inhibition. In conclusion, the results provide evidence that extrahepatic GST could be important in the overall process of detoxification of AFB1. The behavior seen in hepatic and extrahepatic tissues revealed the functions of catalysis (B-type transferases) and covalent bond formation, as well as inactivation by probable AFB1 metabolites (A--C-type transferases).

Poroma ecrino originado en un nevus sebaceo de Jadassohn / Eccrine poroma originated in a nevus sebaceus of Jadassohn

Se presenta el caso de un Nevus sebáceo de Jadassohn, en el tercer estadío, con desarrollo a su nivel de una neoplasia anexial sudorípara, con caracteres de poroma ecrino. Se observa asociada, imágenes de desarrollo clonal intraepidérmico del mismo tumor (Fenómeno de Jadassohn). La aparición de neoplasias anexiales de distintas líneas histogenéticas en el Nevus sebáceo de Jadassohn, es un argumento más en favor del origen del mismo en el germen epitelial primario

Poroma ecrino originado en un nevus sebaceo de Jadassohn / Eccrine poroma originated in a nevus sebaceus of Jadassohn

Se presenta el caso de un Nevus sebáceo de Jadassohn, en el tercer estadío, con desarrollo a su nivel de una neoplasia anexial sudorípara, con caracteres de poroma ecrino. Se observa asociada, imágenes de desarrollo clonal intraepidérmico del mismo tumor (Fenómeno de Jadassohn). La aparición de neoplasias anexiales de distintas líneas histogenéticas en el Nevus sebáceo de Jadassohn, es un argumento más en favor del origen del mismo en el germen epitelial primario (AU)